Acute Kidney Injury
1. Definition and Staging
2. Prevention and Treatment
3. Dialysis Intervention
4. Specific Clinical Settings
  - 4.1 Contrast-induced AKI
  - 4.2 Hepatorenal syndrome
Chronic Kidney Disease
1. Definition and Classification
2. Risk Factors
3. Clinical Assessment and GFR Estimation
4. Screening for Early CKD
5. When to Refer for Specialist Care
6. General Management Strategies
  - 6.1 Blood pressure control
  - 6.2 Anti-proteinuric measures
  - 6.3 Lipid lowering
  - 6.4 Correction of anaemia
  - 6.5 Bone metabolism
  - 6.6 Hyperuricaemia management
  - 6.7 Nutritional considerations
7. Diabetic Kidney Disease
  - 7.1 Primary prevention
  - 7.2 Retardation of progression
  - 7.3 Glycaemic control in DKD with CKD stage 3B or higher (eGFR <45 mL/min)
8. Precautions for Special Investigations
  - 8.1 Use of intravenous gadolinium-containing contrast
  - 8.2 Bowel preparation for colonoscopy
Glomerulonephritides
1. General Considerations
  - 1.1 Kidney biopsy
  - 1.2 Proteinuria assessment
  - 1.3 Potential complications
  - 1.4 Special precaution
2. Specific Primary/Systemic Glomerulonephritides
  - 2.1 Minimal change disease
  - 2.2 Focal segmental glomerulosclerosis
  - 2.3 Membranous nephropathy
  - 2.4 Membranoproliferative glomerulonephritis
  - 2.5 Immunoglobulin A nephropathy
  - 2.6 ANCA-associated vasculitis
  - 2.7 Anti-glomerular basement membrane disease
  - 2.8 Lupus nephritis
Audit Items
1. Renal Biopsy
2. Chronic Kidney Disease
3. Acute Kidney Injury

A. ACUTE KIDNEY INJURY

About one-third of the acute kidney injury (AKI) burden occurs in the perioperative context, and the incidence of AKI continues to rise. While mortality rates in AKI have improved, the figures remain significant. Crucial factors that determine the prognosis include timing of onset, severity and duration of injury, recovery status and recurrence. AKI is associated with an increased hospital mortality, risk of hospital readmissions and risk of chronic kidney disease (CKD).

1. Definition and Staging

AKI is defined as any of (Not Graded):
- Increase in serum creatinine (SCr) by ≥26.5 μmol/L within 48 h; or
- Increase in SCr to ≥1.5 times baseline within the prior 7 days; or
- Urine volume < 0.5 mL/kg/h for 6 h.
- AKI is staged for severity according to (Not Graded):

Stage

SCr

Urine output

1.5–1.9 times baseline

≥26.5 μmol/L increase

<0.5 mL/kg/h for 6–12 h

2.0–2.9 times baseline

<0.5 mL/kg/h for ≥12 h

3.0 times baseline

Increase to ≥354 μmol/L

Initiation of dialysis

In patients <18 years, decrease in estimated glomerular filtration rate (eGFR) to <35 mL/min per 1.73 m² (Schwartz formula)

<0.3 mL/kg/h for ≥24 h

Anuria for ≥12 h

This definition of both AKI and its staging originals from a proposal to simplify and unify both the RIFLE1 and AKIN2 systems, when literature has demonstrated similar stepwise increments in mortality and need for renal replacement therapy (RRT) associated with staging used in either criteria.3-5 Indeed, the two criteria identified somewhat different patients, and data suggest that the use of both help identify more AKI patients than using either alone.6 Although the urine output criteria remain less well validated than the creatinine-based criteria,7 studies using both SCr and urine output show an increased AKI incidence, suggesting that the use of SCr alone may miss a number of patients.

SCr level can vary rapidly as a result of diet, activity and interferences in assay from chromogens. Changes in muscle mass and fluid balance can all affect the serum levels, while urine output in the very obese subjects also needs to be cautioned. Clinical judgment is thus crucial in the interpretation.
It is recommended that the first documented SCr value of the episode would be treated as the ‘baseline’.8
There is evidence demonstrating that the evaluation of urine output in 6-h blocks is as accurate as hourly observation, and this is particularly relevant in the non-intensive care unit (ICU) setting, and would obviate the need for bladder catheterization.9
Patients should be staged according to the criteria that would give them the highest stage.
The cause of AKI should try to be determined. (Not Graded)

Generally, discontinuation of nephrotoxic agents whenever possible, maintenance of volume status and perfusion pressure, functional haemodynamic monitoring and that of SCr and urine output, avoiding hyperglycaemia and resort to alternatives avoiding radio-contrast procedures should all be considered for patients at high risk of or have developed AKI. Patients with AKI require diagnostic workup, and stage 2/3 patients require change in drug dosing as renal impairment advances and consideration for RRT.
It is recommended that patients be stratified for risk of AKI according to their susceptibilities and exposures (R), and managed accordingly in order to reduce such risk. (Not Graded)

Exposures that may cause AKI include sepsis, critical illness, circulatory shock, burns, trauma, cardiac surgery (especially with cardiopulmonary bypass), major non-cardiac surgery, nephrotoxic drugs, radio-contrast media, poisonous plants and animals. Even with these exposures, the risk of AKI would vary between different patient groups and in different clinical context.
For patients at increased risk for AKI, monitor their SCr and urine output to detect (and stage severity) AKI, at individualized frequency and duration based on patient risk and clinical course. (Not Graded)

The use of SCr and urine output would be meaningful when these are monitored regularly at a defined fashion, but clinical practice would usually be dictated by clinical judgment based on the clinical setting and indication, with a tendency for high-risk and critically ill patients being monitored more frequently. The availability of time-dependent biomarkers would be helpful.
Manage patients with AKI according to the stage and cause. (Not Graded)

High risk	Avoid nephrotoxic agents Optimize volume status and monitor haemodynamic status Monitor SCr and urine output Control stress hyperglycaemia Avoid iodinated contrast media and consider alternative imaging
Stage 1	Diagnostic workup
Stage 2/3	Adjust drug dosing for renal impairment Consider timing for RRT Consider ICU admission

The proposed stepwise approach to management based on the degree of severity of AKI requires validation.7

Evaluate patients 2 months after AKI to look for return to baseline, or development of new CKD or worsening of pre-existing CKD. (R)

There is strong association of AKI with subsequent development of CKD and end-stage renal disease (ESRD).10, 11 Prediction tools have been tested to help identify patients with AKI who are at high risks of CKD.10, 12-14

2. Prevention and Treatment

For initial fluid replacement in hypovolemic (not haemorrhagic) patients at risk for, or with, AKI, isotonic crystalloids rather than albumin or starches are recommended. (R)

Recent data from multi-centre, open-label trial continues to support this recommendation.15-17 The Acute Dialysis Quality Initiative group recently concluded on the evidence for harm with hetastarch (hydoxyethyl starch) or albumin administration in traumatic brain injury cases.18 While 0.9% saline may result in a chloride-induced tubule-glomerular feedback–mediated vasoconstriction and metabolic acidosis compared with more physiologically balanced and buffered crystalloids, supporting evidence is mainly derived from post hoc analyses of large patient data sets, rather than prospective, controlled trials.19
Vasopressors are recommended in volume-resuscitated patients with vasomotor shock at risk for, or with, AKI. (R)

Current clinical data are insufficient to conclude on the best vasoactive agent in preventing AKI.20-23
Protocoled therapies with specific physiological goals (haemodynamic and tissue oxygenation targets) are suggested to reduce perioperative AKI in high-risk patients. (D)

The results from few multi-centre trials that looked at protocoled resuscitation with or without an oximetric central venous oxygen saturation monitoring (early goal-directed therapy) failed to suggest survival benefit in patients with septic shock who have received timely antibiotics and usual fluid resuscitation.24-26 In high-risk patients in the perioperative setting, while studies using different protocoled therapies with specific physiological goals (haemodynamic and tissue oxygenation targets)27 have been shown to significantly reduce post-operative AKI, there is no evidence to support the identification of the best regime.
In patients with stress hyperglycaemia, the target plasma glucose for insulin therapy is suggested to be 6.1–8.3 mmol/L, and to avoid hypoglycaemia. (D)

It is important to avoid the danger of potentially serious hypoglycaemia. While the target blood glucose between 6.1 and 8.3 mmol/L have not been directly studied in randomized controlled trial (RCT), they are interpolated from the comparisons tested in the trials.28, 29
An energy intake of 20–30 kcal/kg per day is suggested, and enteral feeding is preferred. (D)

Though the optimal energy intake has not been well determined, data from both retrospective and randomized trials in AKI patients support a total energy intake of at least 20, but not to exceed 25–30 kcal/kg per day.30, 31 Studies have suggested that enteral feeding is associated with improved outcome and survival in ICU patients.32-34
Protein intake is suggested to be 0.8–1.0 g/kg per day in non-catabolic patients not on dialysis, 1.0–1.5 g/kg per day in dialysis patients and up to 1.7 g/kg per day in hypercatabolic patients or patients on continuous renal replacement therapy (CRRT). (D)

Since malnutrition is associated with increased mortality in critically ill patients, nutritional protein administration is not recommended to be restricted as a means to attenuate the rise in serum urea level when renal function declines. On the other hand, there is little evidence that hypercatabolism can be overcome by increasing protein intake to higher than physiological levels.35, 36 During RRT, nutritional support should include replacement for the losses during the procedures, especially with modalities associated with high filtration rates, including CRRT, sustained low efficiency dialysis (SLED) or peritoneal dialysis (PD).37
The use of diuretics to prevent (R) or treat (D) AKI is not recommended, except in the presence of volume overload or acute decompensated heart failure (ADHF).

Though diuretics theoretically may reduce renal tubular oxygen consumption and attenuate intra-tubular obstruction, the benefits of its use has remained contentious in AKI prevention. In the setting of cardiac surgery, a double-blind RCT has demonstrated a higher rate of AKI being associated with the use of furosemide.38, 39 Studies have suggested that diuretics given to treat post-operative AKI is best avoided.40, 41 This also applies to patients on CRRT.42, 43 In patients with ADHF, there were no significant differences in symptom relief or renal safety when diuretic therapy was administered by bolus compared with continuous infusion.44 Although high-dose therapy (2.5 times the usual oral dose given intravenously) improved diuresis, with a trend towards improved symptom relief, there was associated increase in renal adverse events compared with low-dose therapy (usual oral dose given intravenously).45 Individual careful clinical judgment is needed.
The use of low-dose dopamine to prevent or treat AKI is not recommended. (R)

The early positive results in the use of dopamine for renal protection in the critically ill have been opposed by quality RCT trial and meta-analysis.45-47 The use of either dopamine or synthetic natriuretic peptide on top of standard therapy in ADHF is also not associated with enhanced pulmonary decongestion or improved renal function.48 This is also true in the setting of AKI after cardiac surgery.49, 50
The use of fenoldopam to prevent or treat AKI is not suggested. (D)

Fenoldopam mesylate is a dopamine type-1 receptor agonist with similar haemodynamic renal effects as low-dose dopamine, without systemic α- or β-adrenergic stimulation. While early data suggests a lower incidence of AKI was associated with the use of fenoldopam, data from adequately powered multi-centre trials with clinically significant endpoints do not support recommending fenoldopam to either prevent or treat AKI,51, 52 noting in particular the concern of the associated hypotension.
The use of atrial natriuretic peptide to prevent or treat AKI is not suggested. (D)

Studies demonstrating benefits of recombinant human atrial natriuretic peptide in reduced need for dialysis and improved dialysis-free survival after cardiac surgery53 or solid organ transplantation tend to be underpowered, its routine use for the prevention or treatment of AKI cannot be recommended, the concern of hypotension aside.53-56
The use of off-pump coronary artery bypass graft in order to prevent post-operative AKI is not suggested. (D)

While the conclusion from systematic review and meta-analysis of studies looking at off-pump surgery compared with on-pump surgery in cardiopulmonary bypass suggest a 43% reduction in the risk of post-operative AKI, it has been cautioned that the definitions of AKI were variable and that the RCT included were associated with lower than normal event rates.57-60 More data is thus awaited to reach a recommendation.

3. Dialysis Intervention

Use traditional indications for RRT that include fluid status, electrolyte and acid–base balance, clinical context. (Not Graded)

The optimal timing of initiation of RRT has yet to be determined, and is largely a clinical decision. In recent prospective studies, conflicting results have been obtained, with different definitions of early versus conventional initiation of dialysis being used.61-64 Thus, while traditional indications for RRT used for patients with CKD may not necessarily be valid for AKI, the best timing for RRT may only be confirmed through prospective RCT when there are candidate biomarkers, enabling the selection of the right target patients and the offer of therapy at the right time. There is a general trend to commence RRT earlier in the more critically ill.65, 66
The use of diuretics to enhance kidney function recovery is not suggested. (D)

One RCT has evaluated the role of furosemide by continuous infusion at a rate of 0.5 mg/kg/h on top of continuous veno-venous hemofiltration (CVVH). While treated patients had a significantly increased urinary volume and greater sodium excretion compared to the controls, there were no differences in the need for repeated CVVH, or renal recovery during ICU or hospital stay.42
The use of anti-coagulation during RRT, except those with bleeding risk, is recommended: (R)
1. For intermittent RRT, either unfractionated or low-molecular-weight heparin, is recommended. (R)
2. For CRRT, regional citrate anti-coagulation is suggested. (D)
3. For CRRT in patients who have contraindications for citrate, either unfractionated or low-molecular-weight heparin, is suggested. (D)
Studies have shown that frequent clotting affected RRT treatment efficacy, increased circuit ‘down time’, and increased transfusion requirements and cost.67

The advantages of unfractionated heparin include low cost, wide availability, easy administration and monitoring and availability of antidote. Its disadvantages include unpredictable and complex pharmacokinetics, risk of heparin-induced thrombocytopenia, heparin resistance from low circulating anti-thrombin III levels and increased risk of haemorrhage. Data from studies in chronic haemodialysis (HD) comparing unfractionated with low-molecular-weight heparin concluded that both are equally safe in terms of bleeding complications and effectiveness in maintaining circuit patency.68

Recent meta-analyses concluded that regional citrate anticoagulation (RCA) decreased the risk of bleeding compared with heparin anti-coagulation, improved circuit patency, especially in patients with increased bleeding risk, provided that appropriate protocols for monitoring are in place to eliminate the risk of citrate toxicity.69 Unexpectedly, there are studies showing improved renal recovery and hospital survival associated with the use of RCA, awaiting further confirmation.70

Patients with severe liver failure may have difficulty metabolizing the calcium–citrate complex, resulting in citrate accumulation, characterized by low ionized calcium levels, and high anion gap metabolic acidosis.
For patients with increased bleeding risk, regional citrate anti-coagulation during CRRT, unless with contraindications, is suggested. (D)
Both continuous and intermittent RRT are complementary therapies in AKI patients. (Not Graded)

Both intermittent HD and CRRT should be regarded as complementary modalities of RRT, as supported by the absence of definitive data favouring either one, in terms of hospital or ICU mortality, length of hospitalization and renal recovery in survivors.71, 72 Also, availability, expertise, resources, cost and physician preference would influence the clinical choice. Transitions between both modalities would be based on the changing clinical status of the patient, technical considerations such as circuit ‘down time’, and clinical needs of the patients such as rescheduling of diagnostic or therapeutic procedures.
CRRT instead of intermittent HD, is the suggested modality for both haemodynamically unstable patients and patients with raised intracranial pressure. (D)

CRRT, rather than intermittent HD, resulted in a significantly higher mean arterial pressure and a lower requirement of vasopressor therapy.71 SLED is generally well tolerated in the settings where CRRT is commonly used and may have a role when other forms of CRRT are not available, but data from comparative studies are limited. Intermittent HD in patients with raised intracranial pressure (acute brain injury or brain oedema) may compromise cerebral perfusion pressure as a result of HD-associated hypotension or by aggravating cerebral oedema and intracranial pressure through rapid intracellular volume and solute shifts.73-76
A Kt/V of 3.9 per week for intermittent HD is recommended (R), and the actual delivery should be closely monitored (R).

Two well-conducted RCT looking at the dialytic dose of intermittent HD in AKI failed to demonstrate improvement in mortality or renal recovery when the dialysis dose was increased, either by a higher Kt/V above 3.9 weekly or by maintaining a serum urea level <15 mmol/L.77, 78 It is thus recommended to offer thrice-weekly Kt/V of 1.3 for intermittent HD in AKI. More frequent dialysis treatments may, however, be required in order to optimize fluid control, in hypercatabolic individuals or in the presence of severe hyperkalaemia or acidaemia. Positive fluid balance has been shown to be an independent risk factor for mortality in AKI patients.79
An effluent volume of 20–25 mL/kg/h for CRRT is recommended. (R)

The two large, multi-centre RCT, the Veterans Affairs/National Institutes of Health Acute Renal Failure Trial Network Study77 and the Randomized Evaluation of Normal versus Augmented Level Renal Replacement Therapy (RENAL) trial80 did not confirm that a more intensive therapy (CVVHDF with effluent flow exceeding 20–25 mL/kg/h) was associated with improved patient survival or recovery of renal function. However, studies in CRRT have shown that delivery usually falls substantially short of the prescribed dose81 as a result of technical problems such as poor blood flows, reduced haemofilter efficiency with time or filter clotting. It is thus generally recommended to prescribe a higher dose at 25–30 mL/kg/h, in order to achieve the recommended target.

4. Specific Clinical Settings

4.1 Contrast-induced AKI

In patients suspected to have contrast-induced (CI)-AKI, look out for other possible causes of AKI too. (Not Graded)

The incidence may be as high as 25% in patients with pre-existing renal impairment or together with other risk factors such as diabetes, congestive heart failure, advanced age and concurrent administration of nephrotoxic drugs.82-84 Patients who develop CI-AKI have a greater risk for death or prolonged hospitalization.85, 86 Monitoring of SCr following contrast exposure is essential, looking for new-onset CKD.87
Assess the risk for CI-AKI and always screen for renal impairment in patients planned for a procedure that involves intravascular (i.v. or i.a.) administration of iodinated contrast medium, and consider alternative examinations in patients at increased risk. (Not Graded)

While the CI-AKI Consensus Working Panel suggested that the risk of CI-AKI becomes clinically important when the baseline SCr concentration is ≥115 mmol/L in men and ≥ 88.4 mmol/L in women, equivalent to an eGFR <60 mL/min per 1.73 m², there are recent data suggesting that patients with SCr concentration >159 mmol/L are the group at risk.88 When a recent SCr is not available, a simple questionnaire or a dipstick testing for urine protein may be useful for identifying pre-existing kidney disease.89, 90 The risk of CI-AKI appears to be greater after arterial compared to venous administration of contrast media, with an overall CI-AKI incidence of about 5% after procedures that involve intravenous low-osmolar contrast media.91 Controversial risk factors include diabetes, hypertension, congestive heart failure, advanced age, volume depletion (including the use of loop diuretics), haemodynamic instability, concurrent use of nephrotoxic drugs, metabolic syndrome, multiple myeloma, female gender, cirrhosis and large volume or high osmolality of the contrast media.
The use of either iso-osmolar or low-osmolar iodinated contrast media, but not high-osmolar iodinated contrast media (R), at the lowest possible dose (Not Graded) in patients at increased risk is recommended.

Repeated exposure should preferably be delayed for 48 h in patients without risk factors for CI-AKI, and for 72 h in those with risk factors. If AKI develops after contrast-media administration, repeat exposure should be postponed until the SCr level has returned to baseline.92

A meta-analysis looking at 24 randomized studies suggests that low-osmolar contrast media are less nephrotoxic than high-osmolar agents in patients with pre-existing renal impairment.93 Clinical heterogeneity in terms of baseline risk profile, definitions of CI-CKI and timing of SCr measurement, among the studies comparing the iso-osmolar contrast media with low-osmolar agents in high-risk patients make it difficult to reach a conclusive recommendation.94-97

We suggest that in high-risk patients, a repeat SCr is performed 12 and 72 h after administration of contrast media. (D)98, 99
Intravenous fluid (unless clinically contraindicated), either isotonic sodium chloride or sodium bicarbonate, is recommended for patients at increased risk. (R)

Despite the absence of RCT that directly evaluate the role of intravenous fluids versus placebo in the prevention of AKI, comparisons observed in trials looking at different fluids, when matched with historical untreated control subjects suggest a large benefit from fluids.100 The possible exception would be patients with fluid overload. Even though there is no clear evidence from the literature to guide the choice of the optimal rate and duration of fluid administration in CI-AKI prevention, a ‘good’ urine output (>150 mL/h) in the 6 h after the radiological procedure has been associated with reduced rates of AKI.101 As crystalloids given intravenously would not be retained in the vascular space for long, this target urine flow rate requires an infusion rate of around 1.0–1.5 mL/kg/h for 3–12 h before and 6–12 h after the contrast exposure.

Isotonic 0.9% saline solution has been proven to be superior to 0.45% saline solution102, 103 in CI-AKI prevention. For the comparison between sodium bicarbonate and saline, meta-regression suggests that small studies tend to demonstrate the superiority of bicarbonate, even though there were no consistent effects in terms of the risk for dialysis, heart failure and total mortality.104 The additional burden and potential harm from errors in preparing the bicarbonate solutions at the bedside or by local pharmacy, may further argue against the use of this fluid at present. The on-going, large, multi-centre, randomized, double-blind controlled trial comparing isotonic sodium bicarbonate with isotonic saline, along with N-acetylcysteine (NAC) versus placebo, for CI-AKI prevention, the PRESERVE study, has scheduled to enrol 8000 participants. The fluid prescription personalized to the volume status of individual patients represents a promising approach when compared with the usual weight-based fluid prescriptions of specified duration pre-contrast and post-contrast exposure. One such trial utilized the invasively measured left ventricular end diastolic pressure in high-risk patients undergoing cardiac catheterization.105 The other approaches tested include device-assisted fluid administration matched with urine output106 or inferior vena cava volume measurement.
We suggest using oral NAC, together with intravenous fluid, in patients at increased risk. (D)

The effect of NAC on the incidence of CI-AKI is quite variable, with most of the published studies being relatively small in size. With marked heterogeneity in the studies recruited, it is not surprising that many but not all meta-analyses revealed a net benefit.107 There is at present no evidence that either oral or intravenous NAC can alter hard outcomes including mortality and need for RRT after contrast-media administration to patients at risk for CI-AKI. The overall benefit of NAC is not consistent or overwhelming.108 However, oral NAC has a good safety profile and is inexpensive. Also, studies of NAC combined with bicarbonate administration have shown substantially reduced overall incidence of CI-AKI, but not that of dialysis-dependent renal failure, when compared to the combination of NAC with saline.109, 110
The use of statins as an alternative to volume expansion is not suggested. (Not Graded)

Although recent RCT are associated with significant study limitations including the focus on relatively low-risk populations, they consistently demonstrate the efficacy of rosuvastatin for prevention of CI-AKI, including among the subgroups of CKD patients, echoing the results from previous meta-analyses. Studies devoted to patients with stage 3–4 CKD, however, would be crucial to support a definitive conclusion.111, 112
The use of prophylactic HD or haemofiltration for contrast-media removal in patients at increased risk is not suggested. (D)

While there are conflicting data on the use of prophylactic intermittent HD in the incidence of CI-AKI, leading to either increased harm113 or tendency towards being useful,114, 115 a recent meta-analysis of studies using peri-procedural extracorporeal blood purification techniques concluded that such treatments did not decrease the incidence of CI-AKI.116

4.2 Hepatorenal syndrome

Use of vasoconstrictors such as terlipressin, norepinephrine or midodrine plus octreotide combined with volume resuscitation by infusion of 20–25% albumin is recommended for type 1 hepatorenal syndrome (HRS) in the setting of liver cirrhosis. (R)

HRS type 1 represents a severe form of AKI in chronic liver disease characterized by systemic and splanchnic haemodynamic abnormalities without concomitant structural kidney injury. The diagnosis requires demonstration of a recent rise in SCr and exclusion of other causes of AKI such as hypovolaemia, drugs and parenchymal renal disease. There are data showing that early initiation of treatment with vasoconstrictor therapy coupled with albumin infusion might improve patient survival and renal outcomes.117, 118

B. CHRONIC KIDNEY DISEASE

1. Definition and Classification

The National Kidney Foundation defined CKD as either kidney damage or GFR <60 mL/min per 1.73 m² for ≥3 months.119 Kidney damage is defined as pathological abnormalities or the presence of markers of damage, including abnormalities in blood or urine tests or imaging studies. Damage to the kidney can be within the parenchyma, large blood vessels or collecting systems. The markers of kidney damage often provide a clue to the probable site of damage within the kidney and in association with other clinical findings, the aetiology of kidney disease.

In 2012, Kidney Disease: Improving Global Outcomes (KDIGO) re-defined CKD as abnormalities of kidney structure or function, present for more than 3 months, with implications for health. CKD is classified based on Cause, GFR category and Albuminuria category (CGA).120

The markers for kidney injury were specified as follows:

Albuminuria (albumin excretion rate (AER) ≥30 mg/24 h; albumin-creatinine ratio (ACR) ≥30 mg/g (≥3 mg/mmol))
Urine sediment abnormalities, especially renal tubular cells, red blood cells (RBC)/white blood cell casts, dysmorphic RBC
Electrolyte and other abnormalities due to tubular disorders
Abnormalities detected by histology
Structural abnormalities detected by imaging
History of kidney transplantation

The stages of CKD were arbitrarily classified as follows:

GFR category	GFR (mL/min per 1.73 m²)	Description
G1†	≥90	Normal or ↑ GFR
G2†	60–89	Mild ↓ GFR
G3a G3b	45–59 30–44	Mild-to-moderate ↓ GFR Moderate-to-severe ↓ GFR
G4	15–29	Severe ↓ GFR
G5	<15 or dialysis	Kidney failure

† In the absence of evidence of kidney damage, neither GFR category G1 nor G2 fulfil the criteria for CKD.

The albuminuria categories in CKD were classified as follows:

Albuminuria category†	AER (mg/24 h)	ACR (approximately) in mg/mmol	ACR (approximately) in mg/g	Description
A1	<30	<3	<30	Normal or mild ↑
A2	30–300	3–30	30–300	Moderate ↑
A3	>300	>30	>300	Severe ↑

† Correlates with renal prognosis.

The classification was also expanded by KDOQI (2012) to reveal treatment status, as follows:

CKD categories	Definition
CKD	CKD of any stage,119-123 with or without a kidney transplant, including both non–dialysis dependent CKD (CKD 1–5ND) and dialysis-dependent CKD (CKD 5D)
CKD ND	Non–dialysis-dependent CKD of any stage,119-123 with or without a kidney transplant (i.e. CKD excluding CKD 5D)
CKD T	Non–dialysis-dependent CKD of any stage119-123 with a kidney transplant

Specific examples and meanings:

CKD 1, 2, 3, 4	Specific stages of CKD, CKD ND or CKD T
CKD 3–4 and so on	Range of CKD stages
CKD 5D	Dialysis-dependent CKD 5
CKD 5HD	HD-dependent CKD 5
CKD 5PD	Peritoneal dialysis–dependent CKD 5

2. Risk Factors

Studies reveal that a substantial proportion of people without known history of CKD may actually harbour subclinical CKD. Individuals at increased risk of developing CKD should undergo testing for markers of kidney damage, and to estimate the level of GFR. The risk factors include but are not limited to the following conditions:

Advanced age
Diabetes
Hypertension
Heart failure
Smoking
Obesity
Autoimmune disease, for example systemic lupus erythematosus, vasculitis
Neoplasia
Systemic or recurrent urinary tract infections
Hereditary kidney disease
Recovery from AKI
Reduced kidney mass
Ongoing exposure to nephrotoxic agents, for example analgesics
Dyslipidaemia
Low birth weight
Race, for example African Americans, Aboriginals, etc.
Severe socioeconomic disadvantage
Family history of CKD/ESRD

All of the above are known risk factors with the exception that recent observations showed that are Associations with and prognostic impact of CKD in heart failure, with CKD being more common in preserved than in mid-range and reduced ejection fraction.121

3. Clinical Assessment and GFR Estimation

Reporting of eGFRcreat in addition to SCr in adults is preferred and the equation used should be specified. (R)

The original Modification of Diet in Renal Disease (MDRD) study equation122 required more variables (including blood urea nitrogen and serum albumin) than was thought to be practicable for routine clinical practice, and an abbreviated four-variable version was eventually adopted and widely used in clinical practice.123 The MDRD study equation was limited to only estimating GFR in CKD patients, as GFR is underestimated when applied to patients with kidney function better than 60 mL/min per 1.73 m². Subsequently, KDIGO recommended the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation124 designed to overcome the shortcomings of the MDRD study equation. CKD-EPI was derived from an ethnically broader population and included both healthy participants and subjects with CKD. Even then, it must be borne in mind that the validity of the CKD-EPI equation in non-European and non-African ethnicities remains uncertain. Other methods of improving the accuracy of the estimating equations include the use of an alternative or additional serum biomarker, and also muscle mass quantification to adjust for variations in SCr. Thus, the CKD-EPI collaboration group further developed an equation that used both SCr and cystatin C.125 Several investigators in Asia (including China, Japan, Korea, Taiwan and Thailand) assessed the performance of the various GFR estimating equations, in particular, the MDRD study equation, the CKD-EPI equation (creatinine only), and the CKD-EPI equations (creatinine and cystatin C). Since cystatin C measurement is not widely available in Hong Kong, we will adopt the most current KDIGO guideline that recommended using the CKD-EPI SCr-based GFR estimating equation.
Measuring SCr using a specific assay with calibration traceable to international standards and minimal bias compared to isotope-dilution mass spectrometry reference methodology is suggested. (D)
In most patients, well-defined clinical scenarios together with non-invasive tests, for example serological and imaging studies, provide a sufficient basis to formulate a working diagnosis of CKD. (R)
Kidney biopsy may be indicated when a definitive diagnosis would either change the treatment or provide useful information on prognosis. (R)
In general, evaluation of patients with CKD requires understanding of the aetiology that triggers CKD, stage of the disease, comorbid conditions, complications of disease including cardiovascular morbidity, and risks for progression. Periodic assessment of GFR is also important as it allows estimation of the rate of change of renal function. (R)
Review of medications should be performed regularly with regard to dosage adjustment based on the stage of CKD, and detection of potentially adverse effects on kidney function or complications of CKD. (R)

4. Screening for Early CKD

Screening for CKD be targeted and performed in individuals at increased risk of developing CKD, including those with diabetes mellitus, hypertension and established cardiovascular disease (see item 2 above). (D)

The screening tools should include history taking, blood pressure (BP) recording, urine dipstick testing for protein and red cells, and measurement of SCr. Other screening tests should be included for specific at-risk groups, for example urine microalbumin in diabetic subjects, or urinary albumin:creatinine ratio in dipstick-positive individuals.126, 127

5. When to Refer for Specialist Care

Patients with CKD should be referred to a specialist for consultation and co-management if the clinical action plan cannot be prepared, the prescribed evaluation of the patient cannot be carried out, or the recommended treatment cannot be instituted. (R)

The criteria for specialist referral vary with individual practice and available resources.

In general, the following scenarios deserve consideration of referral:
CKD 4 or higher
Anticipation of the need of initiation of renal replacement therapy within 1 year
AKI or abrupt sustained fall in GFR
Significant proteinuria, for example >1 g/24 h
Urinary red cell casts, for example RBC >20 per high power field sustained and not readily explained
CKD and hypertension refractory to treatment with four or more anti-hypertensive agents
Persistent abnormalities of serum potassium not otherwise explained
Recurrent urinary tract infections
Hereditary kidney disease, for example autosomal dominant polycystic kidney disease (ADPKD)

6. General Management Strategies

The management of progression of CKD is aimed at tackling a myriad of factors known to be associated with progression. These measures have been shown to modify cardiovascular health and CKD concomitantly or separately. Addressing CV risk factors may indirectly and directly impact CKD progression, and vice-versa. Strategies include general lifestyle measures, salt restriction, BP control and blockade of the renin-angiotensin-aldosterone system. In addition, control of other metabolic parameters such as blood sugar, lipid, anaemia, bone metabolism, uric acid and acidosis are also important.120

6.1 Blood pressure control

BP targets should be tailored according to age, tolerability and the level of proteinuria. (D)
An angiotensin receptor blocker (ARB) or angiotensin-converting enzyme (ACE)-I is suggested for both diabetic and non-diabetic patients with CKD and urine albumin excretion >300 mg/24 h (or equivalent), unless the use of renin–angiotensin system (RAS) blockers is limited by intractable hyperkalaemia. (R)
For diabetic and non-diabetic patients with AER less than 30 mg/24 h (or equivalent), the suggested BP target is ≤140/90 mmHg. For diabetic and non-diabetic patients with UAE ≥30 mg/24 h (or equivalent), the suggested BP target is ≤130/80 mmHg. (D)

Available evidence is inconclusive but does not prove that a blood pressure target of less than 130/80 mmHg improves clinical outcomes more than a target of less than 140/90 mmHg in adults with CKD.128

6.2 Anti-proteinuric measures

The level of proteinuria has been shown to correlate with renal prognosis in both diabetic and non-diabetic CKD.129

Every attempt should be made to lower proteinuria. (R)
Treatment with a RAS blocker (ACEi or ARB) appears to be the only proven therapeutic option. (D)
Combination of ACEi/ARB, ARB/mineralocorticoid receptor blocker or ARB/direct renin inhibitor is in general not recommended due to potential adverse events, mainly AKI, hyperkalaemia or hypotension. (D)

6.3 Lipid lowering

Adults over 50 years old with CKD G3a–G5 ND could be treated with a statin or statin/ezetimibe combination. (D)

Recent studies have shed light on lipid management in patients with CKD. Although definitive evidence is still lacking, these studies suggest that lipid lowering could only confer tangible cardiovascular protection during early rather than late CKD.130
For those in GFR categories G1–G2, treatment with a statin is desirable. (D)
In younger subjects below 50 years of age with CKD ND, statin treatment is recommended if there is an additional cardiovascular risk factor, namely known coronary heart disease, diabetes, prior ischemic stroke or an estimated 10-years incidence of coronary death or non-fatal myocardial infarction (MI) >10%. (D)
For dialysis-dependent patients and kidney transplant recipients, follow-up measurement of lipid levels is not required for most patients, and treatment with a statin should be individualized. For those to be treated, dosage adjustment for reduced GFR is generally required. (D)
The dose of statin should be titrated to achieve the target level of Low-density lipoprotein (LDL) cholesterol, which in turn is determined by each patient's presumed coronary risk. (D)
For renoprotection, lowering LDL cholesterol by 1 mmol/L did not slow kidney disease progression within 5 years in a wide range of patients with CKD in a large randomized study using simvastatin/ezetimibe combination. (ungraded)

Exploratory analyses of the SHARP study, however, showed no significant effect of lipid lowering on the rate of change in eGFR.131 A more recent study (PLANET I)* found atorvastatin to have more renoprotective effects than high-dose rosuvastatin in patients with diabetes who have progressive renal disease.132

6.4 Correction of anaemia

The first principle is to address all correctable causes of anaemia (such as iron deficiency and occult inflammatory states) prior to initiation of an erythropoiesis-stimulating agent (ESA). It is also important to balance the potential benefits of reducing blood transfusions and anaemia-related symptoms against the risk of side effects such as hypertension, stroke and vascular access loss. Landmark clinical trials of the last decade have shed light on the optimal target haemoglobin levels in the CKD population.133-135

For CKD ND patients, initiation of ESA should be individualized based mainly on symptoms, but also on prior response to iron therapy and the risk of blood transfusion. (D)
For CKD 5D patients, ESA can be commenced as haemoglobin falls below 9 g/dL. The target haemoglobin level should be around 11.5 g/dL. The route of administration should be intravenous or subcutaneous for CKD 5HD, and subcutaneous for CKD ND and CKD 5PD patients. (D)

6.5 Bone metabolism

Dietary phosphate reduction should be implemented during CKD 3–4 when plasma intact parathyroid hormone (iPTH) levels exceed 70 pg/mL (7.7 pmol/L) (stage 3) or >110 pg/mL (12.1 pmol/L) (stage 4). (D)

The major disorders can be classified into those associated with high bone turnover and high PTH levels (including osteitis fibrosa, the hallmark lesion of secondary hyperparathyroidism and mixed lesion) and low bone turnover and low or normal PTH levels (osteomalacia and adynamic bone disease). The abnormalities that lead to bone disease begin to occur at earlier stages of CKD. Elevated levels of PTH and phosphorus, reduced levels of calcium and reduced urinary phosphate excretion have been described among patients with GFR <70 mL/min or lower.119
Vitamin D or analogues are useful in treating secondary hyperparathyroidism (SHPT) (D)

Treatment of SHPT with oral or intravenous calcitriol or paricalcitol can reduce the elevated levels of iPTH, and may be useful to treat various clinical features of symptomatic secondary hyperparathyroidism, such as improved features of hyperparathyroid bone disease as reflected by reductions of serum alkaline phosphatase (and/or bone-specific alkaline phosphatase).
The desirable iPTH threshold for commencing treatment in CKD 5HD and CKD 5PD patients is 300 pg/mL (33.0 pmol/L), and the target iPTH is 150–300 pg/mL (16.5–33.0 pmol/L). (D)
For patients with the corrected CaxPO4 product above the target range, a trial of alternative vitamin D analogs, such as paricalcitol, is recommended. (R)
Calcimimetic agents can be considered when vitamin D or its analogue is ineffective or contraindicated. (Not Graded)

There is less data on the use of calcimimetic agents. Treatment with cinacalcet reduces levels of PTH, CaxPO4 product and may reduce rates of parathyroidectomy and fracture. The use of cinacalcet may be associated with development of adynamic bone disease when iPTH values are <10.6 pmol/L (<100 pg/mL).

6.6 Hyperuricaemia management

There is insufficient evidence to support the routine use of uric acid lowering agents in retarding the progression of CKD in either symptomatic or asymptomatic hyperuricaemia. (Not Graded)

There is also insufficient evidence to suggest that HLA-B*5801 genotyping is less costly and more effective than treatment without genotyping in terms of reducing the occurrence of allopurinol-induced severe cutaneous adverse reactions and related complications.

6.7 Nutritional considerations

Dietary intervention should be considered in CKD patients in the context of maintaining a satisfactory nutritional status.

For patients with early CKD, a normal protein diet, consisting of 0.75–1.0 g/kg per day, with adequate caloric intake is desirable. Dietary sodium intake should be limited to 100 mmol/day (or 2.3 g sodium or 6 g salt per day), as it reduces blood pressure and albuminuria, and enhances the anti-proteinuric efficacy of RAS blockers. (D)
The recommended daily allowance of dietary protein intake at 0.75 g/kg per day appears reasonable in patients with GFR >30 mL/min per 1.73 m² (CKD 1–3). (D)

There is insufficient evidence to recommend for or against routine prescription of dietary protein restriction to slow the progression CKD.
A lower protein intake of 0.6 g/kg per day can be considered for patients with lower GFR (CKD 4 and 5) to slow progression and minimize accumulation of uremic toxins. (D)

Individual decision-making is required after balancing the potential risks and benefits. There is recent anecdotal experience that ketoanalogue-supplemented vegetarian very low-protein diet (0.3 g/kg) could retard the progression of CKD compared with conventional low-protein diet.136
Patients with CKD should receive expert dietetic advice and information tailored to the stage of CKD and the need to intervene on sodium, phosphate, potassium and fluid intake. (R)

7. Diabetic Kidney Disease

7.1 Primary prevention

Optimal glycaemic control is recommended, though this has to be balanced against the risk of hypoglycaemia particularly in susceptible individuals such as elderly subjects. (R)

Hyperglycaemia, the defining metabolic feature of diabetes, is a fundamental cause of vascular target organ complications, including diabetic kidney disease (DKD). Previous and recent studies have confirmed the efficacy of intensive glycaemic control in preventing or retarding the onset of DKD.137, 138 Intensive treatment of hyperglycaemia carries with it an inherently increased risk of hypoglycaemia.139
RAS blockers may be considered as a preventive measure against DKD. (D)

The use of RAS blocker even before the onset of microalbuminuria has also been shown to delay the onset of DKD. It must be borne in mind, however, that unmodifiable factors, such as genetic predisposition, operate in the context of DKD.139

7.2 Retardation of progression

RAS blockade is desirable in reducing albuminuria and the risk of renal end points in established DKD. (R)
Treatments that produce a lasting decrease in albuminuria excretion may slow the progression of DKD even in the absence of hypertension, although most people with diabetes and albuminuria have hypertension. (D)
Combination of ACEi/ARB, ARB/mineralocorticoid receptor antagonist (MRA) or ARB/direct renin inhibitor is in general not recommended due to potential adverse events. (D)

Although the level of residual proteinuria is a significant prognostic indicator, these anti-proteinuric measures have been reported to carry significant untoward effects such as hyperkalaemia, hypotension or even AKI.140
The non-steroidal MRA could have a lower incidence of hyperkalaemia. (Not Graded)

The only RAS blocker that may be potentially combined with an ACEi or ARB is the novel non-steroidal MRA finerenone141 that has greater receptor selectivity than spironolactone and better receptor affinity than eplerenone in vitro with a lower incidence of hyperkalaemia than spironolactone.
An HbA1c target of ≤7.0% is desirable to prevent or delay the onset or progression of microvascular complications including DKD. (R)
In patients at risk of hypoglycaemia, for example the elderly, and in individuals with comorbidities or limited life expectancy, the HbA1c target should be relaxed to ≥7.0%. (D)

7.3 Glycaemic control in DKD with CKD stage 3B or higher (eGFR <45 mL/min)

Metformin in a dose adapted to renal function as a first line agent should be mandated. (R)

Meticulous management of glycaemic control is required for this category of patients.
When improvement of glycaemic control is deemed appropriate, a drug with a low risk for hypoglycaemia should be chosen as an additional agent. (D)
Temporary withdrawal of metformin should be exercised in conditions that foster any form of AKI, for example systemic infection, impending dehydration, exposure to contrast media. (R)
The sodium-glucose co-transporter 2 (SGLT2) inhibitor is generally not recommended for this range of renal function. (Not Graded)

8. Precautions for Special Investigations

8.1 Use of intravenous gadolinium-containing contrast

Intravenous gadolinium contrast should not be used in patients with eGFR <15 mL/min per 1.73 m², and is not recommended for high risk patients with eGFR <30 mL/min per 1.73 m², hepatorenal syndrome, and AKI. It should be used with caution at the minimum dose in lower risk patients with eGFR 30–45 mL/min per 1.73 m². Patients with eGFR >45 mL/min have negligible risk. (D)

Use of intravenous gadolinium contrast is associated with increased risk of NSF in patients with significant renal function impairment. The condition is characterized by diffuse fibrosis of the skin and other tissues and the exact aetiology is unknown.142

8.2 Bowel preparation for colonoscopy

Oral phosphate-containing bowel preparations should not be used in people with a GFR <60 mL/min per 1.73 m². (R)

Advanced CKD is a risk factor for acute phosphate nephropathy from consumption of oral phosphate-containing bowel preparations, which should not be used in people with low GFR.

C. GLOMERULONEPHRITIDES

1. General Considerations

1.1 Kidney biopsy

Kidney biopsy is mandatory for making a definitive histopathological diagnosis. Exceptions include steroid-sensitive nephrotic syndrome in children unless the clinical response is atypical, and where biopsy is contraindicated in adults. Adequacy of the biopsy relates to the size of the tissue necessary to diagnose a specific histopathological pattern with a reasonable level of confidence, and to allow assessment of the degree of acute or chronic damage. The Oxford Classification for IgA nephropathy for example mandates obtaining at least eight glomeruli on the biopsy.143 Repeat kidney biopsy during therapy or following a relapse should only be considered if it may guide a change in therapy. There is no systematic evidence to support recommendations for when or how often it is necessary.

1.2 Proteinuria assessment

There is a lack of consensus whether urine albumin or protein excretion is the preferred measurement to assess glomerular injury. 24-h protein excretion remains the gold standard as it averages the variation of proteinuria due to the circadian rhythm, physical activity, and posture. Although this method is subject to error due to over- or under-collection, the simultaneous measurement of urine creatinine may improve its reliability. Protein-creatinine ratio (PCR) or ACR on a spot urine sample, or a first void morning urine sample, is a practical alternative to 24-h urine collection. It is increasingly used in clinical practice and in clinical trials because the sample is easy to obtain and is not affected by urine concentration influenced by variations in water intake.144 Over the sub-nephrotic range, there is a correlation between PCR and 24-h protein excretion,145 but is unreliable in patients with high protein excretion and should not be used in the clinical setting unless 24 h urine collection is unavailable. Nephrotic-range proteinuria is nearly always arbitrarily defined as proteinuria >3.5 g per 24 h.

1.3 Potential complications

1.3.1 Hypertension

Lifestyle modification (salt restriction, weight normalization, regular exercise and smoking cessation) should be an integral part of the therapy for blood pressure control. The ideal goal for blood pressure is not firmly established but current recommendations suggest that 130/80 mmHg should be the treatment goal. There are limited data to support a lower target of 125/75 mmHg if there is proteinuria >1 g/day.128

1.3.2 Symptomatic nephrotic oedema

The mainstay of treatment is diuretics and moderate dietary sodium restriction (1.5–2 g (60–80 mmol) sodium per 24 h). Oral loop diuretics with once- or twice-daily administration are usually preferred. However, in severe nephrotic syndrome, gastrointestinal absorption of the diuretic may be uncertain because of intestinal-wall oedema, and i.v. diuretic, by bolus injection or infusion, may be necessary to induce an effective diuresis. Alternatively, combining a loop diuretic with a thiazide diuretic or with metolazone is often an effective oral regimen.144 Albumin infusions may be combined with diuretics to treat diuretic resistance, but are of unproven benefit.

1.3.3 Acute kidney injury

Severely nephrotic patients may develop AKI as a result intravascular contraction despite a grossly oedematous state. Albumin infusion with intravenous diuretic such as furosemide may provide transient symptomatic relief. Renal vein thrombosis is another potential cause of AKI due to a hypercoagulable state. The risk of thrombotic events increases significantly as serum albumin falls below 25 g/L.144 Immobility as a consequence of oedema or hospitalization can further aggravate the risk. Prophylactic low-dose anti-coagulation is common practice.

1.4 Special precaution

Hepatitis serologies must be routinely obtained at diagnosis. (R)

Hepatitis B virus (HBV) reactivations have been reported widely, even including liver failure and death, in patients who received immunosuppressive and biological agents.146 In particular, HBsAg+ or anti-HBc+ patients are at high risk of HBV reactivation if they are to receive rituximab, or moderate (10–20 mg prednisone daily or equivalent) or high dose (>20 mg daily prednisone daily or equivalent) corticosteroids for ≥4 weeks. Some literature even suggests a threshold of 2 weeks.147, 148
HBV carriers who do not meet the criteria for antiviral treatment must receive prophylaxis before receiving such therapy. (R)
Entecavir is preferred to lamivudine because of their better resistance profile during long-term immunosuppressant treatments. (D)
For patients to be treated with high-dose corticosteroid or immunosuppression, pneumocystis pneumonia (PCP) prophylaxis should be instituted after ascertaining the G6PD status. (Not Graded)

2. Specific Primary/Systemic Glomerulonephritides

2.1 Minimal change disease

Corticosteroid is the desirable first-line treatment. (R)

The suggested dosage for the initial episode of minimal change disease (MCD) is prednisolone at a single daily dose of 1 mg/kg (maximum 80 mg daily). This initial high dose should be maintained for a minimum period of 4 weeks if complete remission (CR) is achieved, or for a maximum of 16 weeks of CR is not achieved. In patients who remit, corticosteroids should be tapered over a period of up to 6 months following remission.
For frequently relapsing or steroid-dependent, addition of calcineurin inhibitor (CNI, cyclosporin or tacrolimus) for 1–2 years is recommended. (R)

Mycophenolate (MMF) or cyclophosphamide (CTX) for the same duration are alternatives, particularly for patients who cannot tolerate high dose corticosteroids. Levamisole may also be considered.149
For steroid-resistant MCD, addition of calcineurin inhibitor can be considered. (D)

Before adding CNI, one must also re-evaluate for other causes of the nephrotic syndrome and consider repeating kidney biopsy for the possibility of focal segmental glomerulosclerosis (FSGS) or other pathologies.
For the initial episode of nephrotic syndrome from MCD, statins are not recommended for nephrotic dyslipidaemia. In addition, RAS blockers are not recommended as an adjunct to lower proteinuria in normotensive patients. (D)

2.2 Focal segmental glomerulosclerosis (idiopathic)

Every effort should be made to exclude secondary causes. (R)
The recommended treatment is corticosteroid given at a single daily dose of 1 mg/kg (maximum 80 mg). (D)

The initial high dose of corticosteroids should be maintained for a minimum of 4 weeks, and continued for up to 16 weeks, as tolerated, or until CR has been achieved. In patients who remit, corticosteroids should be tapered over a period of up to 6 months following remission.
For steroid-resistant FSGS, addition of calcineurin inhibitor (cyclosporin or tacrolimus) can be attempted for 4–6 months. (D)

If there is response to treatment, CNI should be maintained for at least 1 year. Mycophenolate may be an alternative, particularly in patients who are intolerant to CNI. For steroid and CNI/MMF resistant and heavily nephrotic patients, treatment with abatacept (a CTLA-4-Ig fusion protein, a co-stimulatory inhibitor that target B7-1, CD80) may be considered, bearing in mind that mixed results have been reported.150

2.3 Membranous nephropathy (idiopathic)

Every effort should be made to exclude secondary causes. (R)
Immunosuppressive treatment can be started right away for patients with clinical features of frank nephrotic syndrome. (D)

Initial therapy should consist of a 6-month course of corticosteroid and cyclophosphamide. Calcineurin inhibitor (cyclosporin or tacrolimus) can be an alternative to cyclophosphamide. Patients who do not respond well to either of these regimens can be crossed over to the other one, that is steroid/CTX to steroid/CNI and vice-versa.151
We suggest not using alternating monthly cycles of intravenous followed by oral corticosteroid and chlorambucil due to the high incidence of side effects. (R)
For treatment resistant cases, rituximab,152 a monoclonal antibody against the cell surface antigen CD20 of B cells, or adrenocorticotropic hormone may be considered. (Not Graded)

2.4 Membranoproliferative glomerulonephritis

Every effort should be made to exclude secondary causes. (R)
In nephrotic patients, treatment with corticosteroids and oral CTX or MMF should be considered. (D)

2.5 Immunoglobulin A nephropathy

Patients with isolated microscopic haematuria and normal blood pressure and renal function do not require specific treatment. (R)
For patients with significant proteinuria, optimization of supportive care, namely RAS blockade, low salt diet and stringent blood pressure control (<130/80 mmHg for proteinuria <1 g/day and 125/75 mmHg for proteinuria >1 g/day), is recommended (R).

Intensive supportive care has been reported to induce at least partial remission in up to one third of patients in STOP-IgAN.153
Patients with persistent proteinuria ≥1 g/day despite 6 months of optimized supportive care and eGFR >30 mL/min per 1.73 m² can be treated with a 6-month course of corticosteroid (D).

There are mixed results with steroid usage in IgAN. While the recent European STOP-IgAN153 study showed no effect, the Chinese TESTING study154, 155 demonstrated some anti-proteinuric effects although an untoward side effect profile was observed in the latter study that involved pulse steroid therapy. A retrospective analysis of the European VALIGA cohort suggested that corticosteroid may also be efficacious in IgAN patients with lower GFR.156 Another European study using an enteric formulation of budesonide also demonstrated significant renoprotective effects after 9 months of therapy.157
For steroid-resistant patients, MMF may be individually considered in Chinese subjects without advanced tubulointerstitial changes,158-160 but it is not recommended for Caucasians.161 (Not Graded)
For IgAN/MCD overlap syndrome, treatment should be analogous to that of MCD (see item 1). (R)
For crescentic IgAN with clinical features of rapidly progressive glomerulonephritis (RPGN), corticosteroids (intravenous followed by oral) and cyclophosphamide is recommended, analogous to the treatment of ANCA-associated vasculitis (AAV). (D)

There is insufficient evidence to support the use of the following approaches: anti-platelet therapy, fish oil, azathioprine and tonsillectomy.

2.6 ANCA-associated vasculitis

Initial treatment should consist of pulse corticosteroid and CTX. (R)

Corticosteroid and rituximab is an alternative for patients in whom CTX is undesirable or ineffective. This stems from initial proof of efficacy of rituximab from small, prospective trials and retrospective surveys conducted in AAV patients with relapsing and refractory disease in which high remission rates allowed reduction of steroid dosages and withdrawal of immunosuppressants. Subsequent randomized trials comparing rituximab versus CTX for inducing remission of new or relapsing AAV led to the licensing of rituximab for this indication.162
Plasmapheresis is desirable for patients with rapidly deteriorating renal function, evidence of pulmonary haemorrhage or overlap syndrome with anti-glomerular basement membrane (GBM) nephritis. (R)

In a large trial of 137 patients with a new diagnosis of ANCA-associated systemic vasculitis confirmed by renal biopsy and SCr >500 μmol/L, plasma exchange was associated with a reduction in risk for progression to ESRD of 24% (95% confidence interval 6.1–41), from 43% to 19%, at 12 months when compared with intravenous methylprednisolone, though patient survival and severe adverse event rates were similar in both groups.163
Maintenance treatment should consist of corticosteroid and azathioprine. MMF is an alternative. (R)
Decision on changing immunosuppressive dosage should take into account the clinical picture in addition to the ANCA titre, but not the titre alone. (R)
Kidney transplantation should be deferred until CR has been achieved for 1 year irrespective of the ANCA titre. (D)

2.7 Anti-glomerular basement membrane disease

Initial treatment should consist of pulse corticosteroid and CTX plus plasmaphersis. (R)

Treatment should be commenced as early as possible to reduce the chance of irreversible renal failure. Patients who are already dialysis-dependent on presentation have a poorer renal prognosis and immunosuppressive therapy has to be individualized.
Kidney transplantation should be deferred until anti-GBM antibodies are undetectable for 1 year. (Not Graded)

2.8 Lupus nephritis

Immunosuppressive treatment for lupus nephritis (LN) includes corticosteroids alone or combined with cyclophosphamide or mycophenolate mofetil. Emerging therapy may even include calcineurin inhibitors and biological agents that target key pathogenetic mechanisms of the disease with the objectives of inducing remission, preserving kidney function and preventing relapses and other complications.164, 165 These latter approaches are not yet fully incorporated into the current guideline due to the paucity of long-term data.

Treatment decisions for LN are largely dictated by the histological grade of the renal lesion. (R)
For class I and class II LN with proteinuria below 3 g/day, treatment will be determined in accordance with the extrarenal manifestation of the disease. If proteinuira is >3 g/day, corticosteroids or CNIs may be applied as for MCD (see item 1). (R)
For class III and class IV LN, initial treatment with corticosteroids combined with either MMF or CTX is recommended. (R)
Maintenance therapy should include low-dose corticosteroid (e.g. ≤10 mg/day prednisolone) and MMF or azathioprine continued for at least 12 months. (D)
If there is disease relapse while on maintenance therapy, the dose of immunosuppression can be increased (R).
If CR is not achieved within 12 months or if there is disease relapse after long periods of quiescence, a repeat renal biopsy is worthwhile to look for a change of histological class of LN. (Not Graded)
For class V LN, treatment may consist of corticosteroids and any of the following immunosuppressants: CTX, CNI, MMF or azathioprine. (D)
For class V + IV LN, multi-target therapy consisting of MMF, tacrolimus and corticosteroids may be considered. (Not Graded)
For treatment of resistant LN not responding to any of the desired protocol, rituximab, IVIg or CNI may be considered. (D)
In pregnant women, MMF, CTX and RAS blockers should not be used. (R)
Corticosteroids and hydroxychloroquine can be maintained throughout pregnancy. (D)
Patients who get pregnant while already on MMF or CTX should be switched to azathioprine. (R)
Disease flare during pregnancy should be treated with an increased dose of corticosteroids. (D)
Anti-platelet therapy can be considered for all pregnant patients. (D)

D. Audit Items

1. Renal Biopsy

Number of renal biopsy performed and by whom in the renal unit
Appropriateness and techniques of biopsy
Complications-type, rate and need for intervention
Adequacy of specimen obtained

2. Chronic Kidney Disease

Blood pressure control
Glycaemic control in diabetic nephropathy patients
Appropriate use of ACEI/AII
Biochemical control-calcium, phosphate, PTH and bicarbonate
Correction of anaemia and iron status

3. Acute Kidney Injury

Appropriateness of prophylaxis used for CI nephropathy
Proportion of patients who receive nephrotoxic drugs
Types and complications of the dialytic access
Type and efficacy of anti-coagulation used in the extracorporeal circulation
Outcome
- Percentage with residual CKD
- Percentage requiring RRT within 3–6 months.

ACKNOWLEDGEMENTS

Dr SK Mak would like to acknowledge Dr Ping-nam Wong for his support for preparing the final draft.

* Correction added June 2019, after original publication: spelling of ‘PLANET I’ corrected.

REFERENCES

1Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P, Acute Dialysis Quality Initiative Workgroup. Acute renal failure – Definition, outcome measures, animal models, fluid therapy and information technology needs: The second international consensus conference of the acute dialysis quality initiative (ADQI) group. Crit. Care 2004; 8: R204–12.
10.1186/cc2872
PubMed Web of Science® Google Scholar
2Mehta RL, Kellum JA, Shah SV et al. Acute kidney injury network: Report of an initiative to improve outcomes in acute kidney injury. Crit. Care 2007; 11: R31.
10.1111/j.1600-6143.2004.00433.x
PubMed Web of Science® Google Scholar
3 Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int. Suppl. 2012; 2: 1–138.
Google Scholar
4 The Ad-Hoc Working Group of ERBP, Fliser D, Laville M, Covic A et al. A European Renal Best Practice (ERBP) position statement on the Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guidelines on acute kidney injury: Part 1: Definitions, conservative management and contrast-induced nephropathy. Nephrol. Dial. Transplant. 2012; 27: 4263–72.
10.1093/ndt/gfs375
PubMed Web of Science® Google Scholar
5National Institute for Health and Care Excellence. NICE guideline: Acute kidney injury: prevention, detection and management. [Cited 22 March 2016.] Available from URL: nice.org.uk/guidance/cg169
Google Scholar
6Joannidis M, Metnitz B, Bauer P et al. Acute kidney injury in critically ill patients classified by AKIN versus RIFLE using the SAPS 3 database. Intensive Care Med. 2009; 35: 1692–702.
10.1007/s00134-009-1530-4
PubMed Web of Science® Google Scholar
7Palevsky PM, Liu KD, Brophy PD et al. KDOQI US commentary on the 2012 KDIGO clinical practice guideline for acute kidney injury. Am. J. Kidney Dis. 2013; 61: 649–72.
10.1053/j.ajkd.2013.02.349
PubMed Web of Science® Google Scholar
8Siew ED, Matheny ME, Ikizler TA et al. Commonly used surrogates for baseline renal function affect the classification and prognosis of acute kidney injury. Kidney Int. 2010; 77: 536–42.
10.1038/ki.2009.479
PubMed Web of Science® Google Scholar
9Macedo E, Malhotra R, Claure-Del Granado R et al. Defining urine output criterion for acute kidney injury in critically ill patients. Nephrol. Dial. Transplant. 2011; 26: 509–15.
10.1093/ndt/gfq332
PubMed Web of Science® Google Scholar
10Coca SG, Yusuf B, Shlipak MG, Garg AX, Parikh CR. Long-term risk of mortality and other adverse outcomes after acute kidney injury: A systematic review and meta-analysis. Am. J. Kidney Dis. 2009; 53: 961–73.
10.1053/j.ajkd.2008.11.034
PubMed Web of Science® Google Scholar
11Ishani A, Xue JL, Himmelfarb J et al. Acute kidney injury increases risk of ESRD among elderly. J. Am. Soc. Nephrol. 2009; 20: 223–8.
10.1681/ASN.2007080837
PubMed Web of Science® Google Scholar
12Amdur RL, Chawla LS, Amodeo S, Kimmel PL, Palant CE. Outcomes following diagnosis of acute renal failure in U.S. veterans: Focus on acute tubular necrosis. Kidney Int. 2009; 76: 1089–97.
10.1038/ki.2009.332
PubMed Web of Science® Google Scholar
13Wald R, Quinn RR, Luo J et al. Chronic dialysis and death among survivors of acute kidney injury requiring dialysis. JAMA 2009; 302: 1179–85.
10.1001/jama.2009.1322
CAS PubMed Web of Science® Google Scholar
14Chawla LS, Amdur RL, Amodeo S, Kimmel PL, Palant CE. The severity of acute kidney injury predicts progression to chronic kidney disease. Kidney Int. 2011; 79: 1361–9.
10.1038/ki.2011.42
PubMed Web of Science® Google Scholar
15Finfer S, Bellomo R, Boyce N et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N. Engl. J. Med. 2004; 350: 2247–56.
10.1056/NEJMoa040232
CAS PubMed Web of Science® Google Scholar
16Annane D, Siami S, Jaber S et al. Effects of fluid resuscitation with colloids vs crystalloids on mortality in critically ill patients presenting with hypovolemic shock: The CRISTAL randomized trial. JAMA 2013; 310: 1809–17.
10.1001/jama.2013.280502
CAS PubMed Web of Science® Google Scholar
17Caironi P, Tognoni G, Masson S et al. Albumin replacement in patients with severe sepsis or septic shock. N. Engl. J. Med. 2014; 370: 1412–21.
10.1056/NEJMoa1305727
CAS PubMed Web of Science® Google Scholar
18Raghunathan K, Murray PT, Beattie WS et al. Choice of fluid in acute illness: What should be given? An international consensus. Br. J. Anaesth. 2014; 113: 772–83.
10.1093/bja/aeu301
CAS PubMed Web of Science® Google Scholar
19Myburgh JA, Mythen MG. Resuscitation fluids. N. Engl. J. Med. 2013; 369: 1243–51.
10.1056/NEJMra1208627
CAS PubMed Web of Science® Google Scholar
20Redl-Wenzl EM, Armbruster C, Edelmann G et al. The effects of norepinephrine on hemodynamics and renal function in severe septic shock states. Intensive Care Med. 1993; 19: 151–4.
10.1007/BF01720530
CAS PubMed Web of Science® Google Scholar
21Albanese J, Leone M, Delmas A et al. Terlipressin or norepinephrine in hyperdynamic septic shock: A prospective, randomized study. Crit. Care Med. 2005; 33: 1897–902.
10.1097/01.CCM.0000178182.37639.D6
CAS PubMed Web of Science® Google Scholar
22Lauzier F, Levy B, Lamarre P et al. Vasopressin or norepinephrine in early hyperdynamic septic shock: A randomized clinical trial. Intensive Care Med. 2006; 32: 1782–9.
10.1007/s00134-006-0378-0
CAS PubMed Web of Science® Google Scholar
23De Backer D, Biston P, Devriendt J et al. Comparison of dopamine and norepinephrine in the treatment of shock. N. Engl. J. Med. 2010; 362: 779–89.
10.1056/NEJMoa0907118
CAS PubMed Web of Science® Google Scholar
24Yealy DM, Kellum JA, Huang DT et al. A randomized trial of protocol-based care for early septic shock. N. Engl. J. Med. 2014; 370: 1683–93.
10.1056/NEJMoa1401602
CAS PubMed Web of Science® Google Scholar
25Peake SL, Delaney A, Bailey M et al. Goal-directed resuscitation for patients with early septic shock. N. Engl. J. Med. 2014; 371: 1496–506.
10.1056/NEJMoa1404380
CAS PubMed Web of Science® Google Scholar
26Mouncey PR, Osborn TM, Power GS et al. Trial of early, goal-directed resuscitation for septic shock. N. Engl. J. Med. 2015; 372: 1301–11.
10.1056/NEJMoa1500896
CAS PubMed Web of Science® Google Scholar
27Brienza N, Giglio MT, Marucci M, Fiore T. Does perioperative hemodynamic optimization protect renal function in surgical patients? A meta-analytic study. Crit. Care Med. 2009; 37: 2079–90.
10.1097/CCM.0b013e3181a00a43
PubMed Web of Science® Google Scholar
28Schetz M, Vanhorebeek I, Wouters PJ, Wilmer A, van den Berghe G. Tight blood glucose control is renoprotective in critically ill patients. J. Am. Soc. Nephrol. 2008; 19: 571–8.
10.1681/ASN.2006101091
CAS PubMed Web of Science® Google Scholar
29Van den Berghe G, Schetz M, Vlasselaers D et al. Clinical review: Intensive insulin therapy in critically ill patients: NICE-SUGAR or Leuven blood glucose target? J. Clin. Endocrinol. Metab. 2009; 94: 3163–70.
10.1210/jc.2009-0663
CAS PubMed Web of Science® Google Scholar
30Macias WL, Alaka KJ, Murphy MH, Miller ME, Clark WR, Mueller BA. Impact of the nutritional regimen on protein catabolism and nitrogen balance in patients with acute renal failure. J. Parenter. Enteral Nutr. 1996; 20: 56–62.
10.1177/014860719602000156
CAS PubMed Google Scholar
31Fiaccadori E, Maggiore U, Rotelli C et al. Effects of different energy intakes on nitrogen balance in patients with acute renal failure: A pilot study. Nephrol. Dial. Transplant. 2005; 20: 1976–80.
10.1093/ndt/gfh956
PubMed Web of Science® Google Scholar
32Metnitz PG, Krenn CG, Steltzer H et al. Effect of acute renal failure requiring renal replacement therapy on outcome in critically ill patients. Crit. Care Med. 2002; 30: 2051–8.
10.1097/00003246-200209000-00016
PubMed Web of Science® Google Scholar
33Scheinkestel CD, Kar L, Marshall K et al. Prospective randomized trial to assess caloric and protein needs of critically ill, anuric, ventilated patients requiring continuous renal replacement therapy. Nutrition 2003; 19: 909–16.
10.1016/S0899-9007(03)00175-8
CAS PubMed Web of Science® Google Scholar
34Fiaccadori E, Maggiore U, Giacosa R et al. Enteral nutrition in patients with acute renal failure. Kidney Int. 2004; 65: 999–1008.
10.1111/j.1523-1755.2004.00459.x
PubMed Web of Science® Google Scholar
35Scheinkestel CD, Adams F, Mahony L et al. Impact of increasing parenteral protein loads on amino acid levels and balance in critically ill anuric patients on continuous renal replacement therapy. Nutrition 2003; 19: 733–40.
10.1016/S0899-9007(03)00107-2
CAS PubMed Web of Science® Google Scholar
36Bellomo R, Tan HK, Bhonagiri S et al. High protein intake during continuous hemodiafiltration: Impact on amino acids and nitrogen balance. Int. J. Artif. Organs 2002; 25: 261–8.
10.1177/039139880202500403
CAS PubMed Web of Science® Google Scholar
37Salahudeen AK, Kumar V, Madan N et al. Sustained low efficiency dialysis in the continuous mode (C-SLED): Dialysis efficacy, clinical outcomes, and survival predictors in critically ill cancer patients. Clin. J. Am. Soc. Nephrol. 2009; 4: 1338–46.
10.2215/CJN.02130309
PubMed Web of Science® Google Scholar
38Lassnigg A, Donner E, Grubhofer G, Prester IE, Drum IW, Hiesmayr M. Lack of renoprotective effects of dopamine and furosemide during cardiac surgery. J. Am. Soc. Nephrol. 2000; 11: 97–104.
10.1681/ASN.V11197
CAS PubMed Web of Science® Google Scholar
39Ho KM, Sheridan DJ. Meta-analysis of frusemide to prevent or treat acute renal failure. BMJ 2006; 333: 420.
10.1136/bmj.38902.605347.7C
CAS PubMed Web of Science® Google Scholar
40Lombardi R, Ferreiro A, Servetto C. Renal function after cardiac surgery: Adverse effect of furosemide. Ren. Fail. 2003; 25: 775–86.
10.1081/JDI-120024293
CAS PubMed Web of Science® Google Scholar
41Ho KM, Power BM. Benefits and risks of furosemide in acute kidney injury. Anaesthesia 2010; 65: 283–93.
10.1111/j.1365-2044.2009.06228.x
CAS PubMed Web of Science® Google Scholar
42van der Voort PH, Boerma EC, Koopmans M et al. Furosemide does not improve renal recovery after hemofiltration for acute renal failure in critically ill patients: A double blind randomized controlled trial. Crit. Care Med. 2009; 37: 533–8.
10.1097/CCM.0b013e318195424d
CAS PubMed Web of Science® Google Scholar
43Uchino S, Bellomo R, Morimatsu H et al. Discontinuation of continuous renal replacement therapy: A post hoc analysis of a prospective multicenter observational study. Crit. Care Med. 2009; 37: 2576–82.
10.1097/CCM.0b013e3181a38241
PubMed Web of Science® Google Scholar
44Felker GM, Lee KL, Bull DA et al. Diuretic strategies in patients with acute decompensated heart failure. N. Engl. J. Med. 2011; 364: 797–805.
10.1056/NEJMoa1005419
CAS PubMed Web of Science® Google Scholar
45Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh J. Low-dose dopamine in patients with early renal dysfunction: A placebo-controlled randomised trial. Australian and New Zealand Intensive Care Society (ANZICS) clinical trials group. Lancet 2000; 356: 2139–43.
10.1016/S0140-6736(00)03495-4
CAS PubMed Web of Science® Google Scholar
46Kellum JA, M Decker J. Use of dopamine in acute renal failure: A meta- analysis. Crit. Care Med. 2001; 29: 1526–31.
10.1097/00003246-200108000-00005
CAS PubMed Web of Science® Google Scholar
47Marik PE. Low-dose dopamine: A systematic review. Intensive Care Med. 2002; 28: 877–83.
10.1007/s00134-002-1346-y
CAS PubMed Web of Science® Google Scholar
48Chen HH, Anstrom KJ, Givertz MM et al. Low-dose dopamine or low-dose nesiritide in acute heart failure with renal dysfunction: The ROSE acute heart failure randomized trial. JAMA 2013; 310: 2533–43.
10.1001/jama.2013.282190
CAS PubMed Web of Science® Google Scholar
49Tang AT, El-Gamel A, Keevil B, Yonan N, Deiraniya AK. The effect of ‘renal-dose’ dopamine on renal tubular function following cardiac surgery: Assessed by measuring retinol binding protein (RBP). Eur. J. Cardiothorac. Surg. 1999; 15: 717–22.
10.1016/S1010-7940(99)00081-0
CAS PubMed Web of Science® Google Scholar
50Woo EB, Tang AT, el-Gamel A et al. Dopamine therapy for patients at risk of renal dysfunction following cardiac surgery: Science or fiction? Eur. J. Cardiothorac. Surg. 2002; 22: 106–11.
10.1016/S1010-7940(02)00246-4
PubMed Web of Science® Google Scholar
51Tumlin JA, Finkel KW, Murray PT, Samuels J, Cotsonis G, Shaw AD. Fenoldopam mesylate in early acute tubular necrosis: A randomized, double-blind, placebo-controlled clinical trial. Am. J. Kidney Dis. 2005; 46: 26–34.
10.1053/j.ajkd.2005.04.002
CAS PubMed Web of Science® Google Scholar
52Bove T, Zangrillo A, Guarracino F et al. Effect of fenoldopam on use of renal replacement therapy among patients with acute kidney injury after cardiac surgery: A randomized clinical trial. JAMA 2014; 312: 2244–53.
10.1001/jama.2014.13573
PubMed Web of Science® Google Scholar
53Sward K, Valsson F, Odencrants P et al. Recombinant human atrial natriuretic peptide in ischemic acute renal failure: A randomized placebo-controlled trial. Crit. Care Med. 2004; 32: 1310–5.
10.1097/01.CCM.0000128560.57111.CD
CAS PubMed Web of Science® Google Scholar
54Allgren RL, Marbury TC, Rahman SN et al. Anaritide in acute tubular necrosis. Auriculin anaritide acute renal failure study group. N. Engl. J. Med. 1997; 336: 828–34.
10.1056/NEJM199703203361203
CAS PubMed Web of Science® Google Scholar
55Lewis J, Salem MM, Chertow GM et al. Atrial natriuretic factor in oliguric acute renal failure. Anaritide acute renal failure study group. Am. J. Kidney Dis. 2000; 36: 767–74.
10.1053/ajkd.2000.17659
CAS PubMed Web of Science® Google Scholar
56Nigwekar SU, Kulkarni H, Thakar CV. Natriuretic peptides in the management of solid organ transplantation associated acute kidney injury: A systematic review and meta-analysis. Int. J. Nephrol. 2013; 2013: 949357.
10.1155/2013/949357
PubMed Google Scholar
57Shroyer AL, Grover FL, Hattler B et al. On-pump versus off-pump coronary-artery bypass surgery. N. Engl. J. Med. 2009; 361: 1827–37.
10.1056/NEJMoa0902905
CAS PubMed Web of Science® Google Scholar
58Nigwekar SU, Kandula P, Hix JK, Thakar CV. Off-pump coronary artery bypass surgery and acute kidney injury: A meta-analysis of randomized and observational studies. Am. J. Kidney Dis. 2009; 54: 413–23.
10.1053/j.ajkd.2009.01.267
PubMed Web of Science® Google Scholar
59Seabra VF, Alobaidi S, Balk EM, Poon AH, Jaber BL. Off-pump coronary artery bypass surgery and acute kidney injury: A meta-analysis of randomized controlled trials. Clin. J. Am. Soc. Nephrol. 2010; 5: 1734–44.
10.2215/CJN.02800310
PubMed Web of Science® Google Scholar
60Chawla LS, Zhao Y, Lough FC, Schroeder E, Seneff MG, Brennan JM. Off-pump versus on-pump coronary artery bypass grafting outcomes stratified by preoperative renal function. J. Am. Soc. Nephrol. 2012; 23: 1389–97.
10.1681/ASN.2012020122
PubMed Web of Science® Google Scholar
61Bouman CS, Oudemans-Van Straaten HM, Tijssen JG et al. Effects of early high-volume continuous venovenous hemofiltration on survival and recovery of renal function in intensive care patients with acute renal failure: A prospective, randomized trial. Crit. Care Med. 2002; 30: 2205–11.
10.1097/00003246-200210000-00005
PubMed Web of Science® Google Scholar
62Bagshaw SM, Uchino S, Bellomo R et al. Timing of renal replacement therapy and clinical outcomes in critically ill patients with severe acute kidney injury. J. Crit. Care 2009; 24: 129–40.
10.1016/j.jcrc.2007.12.017
PubMed Web of Science® Google Scholar
63Jamale TE, Hase NK, Kulkarni M et al. Earlier-start versus usual-start dialysis in patients with community-acquired acute kidney injury: A randomized controlled trial. Am. J. Kidney Dis. 2013; 62: 1116–21.
10.1053/j.ajkd.2013.06.012
PubMed Web of Science® Google Scholar
64Vaara ST, Reinikainen M, Wald R, Bagshaw SM, Pettilä V, FINNAKI Study Group. Timing of RRT based on the presence of conventional indications. Clin. J. Am. Soc. Nephrol. 2014; 9: 1577–85.
10.2215/CJN.12691213
PubMed Web of Science® Google Scholar
65Thakar CV, Rousseau J, Leonard AC. Timing of dialysis initiation in AKI in ICU: International survey. Crit. Care 2012; 16: R237.
10.1186/cc11906
PubMed Web of Science® Google Scholar
66Legrand M, Darmon M, Joannidis M, Payen D. Management of renal replacement therapy in ICU patients: An international survey. Intensive Care Med. 2013; 39: 101–8.
10.1007/s00134-012-2706-x
PubMed Web of Science® Google Scholar
67Oudemans-van Straaten HM, Ostermann M. Bench-to-bedside review: Citrate for continuous renal replacement therapy, from science to practice. Crit. Care 2012; 16: 249–57.
10.1186/cc11645
PubMed Web of Science® Google Scholar
68Lim W, Cook DJ, Crowther MA. Safety and efficacy of low molecular weight heparins for hemodialysis in patients with end-stage renal failure: A meta-analysis of randomized trials. J. Am. Soc. Nephrol. 2004; 15: 3192–206.
10.1097/01.ASN.0000145014.80714.35
PubMed Web of Science® Google Scholar
69Wu MY, Hsu YH, Bai CH, Lin YF, Wu CH, Tam KW. Regional citrate versus heparin anticoagulation for continuous renal replacement therapy: A meta-analysis of randomized controlled trials. Am. J. Kidney Dis. 2012; 59: 810–8.
10.1053/j.ajkd.2011.11.030
CAS PubMed Web of Science® Google Scholar
70Oudemans-van Straaten HM, Bosman RJ, Koopmans M et al. Citrate anticoagulation for continuous venovenous hemofiltration. Crit. Care Med. 2009; 37: 545–52.
10.1097/CCM.0b013e3181953c5e
CAS PubMed Web of Science® Google Scholar
71Rabindranath K, Adams J, Macleod AM et al. Intermittent versus continuous renal replacement therapy for acute renal failure in adults. Cochrane Database Syst. Rev. 2007: CD003773.
CAS PubMed Web of Science® Google Scholar
72Lins RL, Elseviers MM, Van der Niepen P et al. Intermittent versus continuous renal replacement therapy for acute kidney injury patients admitted to the intensive care unit: Results of a randomized clinical trial. Nephrol. Dial. Transplant. 2009; 24: 512–8.
10.1093/ndt/gfn560
CAS PubMed Web of Science® Google Scholar
73Ronco C, Bellomo R, Brendolan A, Pinna V, la Greca G. Brain density changes during renal replacement in critically ill patients with acute renal failure. Continuous hemofiltration versus intermittent hemodialysis. J. Nephrol. 1999; 12: 173–8.
CAS PubMed Web of Science® Google Scholar
74Bagshaw SM, Peets AD, Hameed M, Boiteau PJE, Laupland KB, Doig CJ. Dialysis disequilibrium syndrome: Brain death following hemodialysis for metabolic acidosis and acute renal failure: A case report. BMC Nephrol. 2004; 5: 9.
10.1186/1471-2369-5-9
PubMed Google Scholar
75Lin CM, Lin JW, Tsai JT et al. Intracranial pressure fluctuation during hemodialysis in renal failure patients with intracranial hemorrhage. Acta Neurochir. Suppl. 2008; 101: 141–4.
10.1007/978-3-211-78205-7_24
CAS PubMed Web of Science® Google Scholar
76Davenport A. Continuous renal replacement therapies in patients with acute neurological injury. Semin. Dial. 2009; 22: 165–8.
10.1111/j.1525-139X.2008.00548.x
CAS PubMed Web of Science® Google Scholar
77Palevsky PM, Zhang JH, O'Connor TZ et al. Intensity of renal support in critically ill patients with acute kidney injury. N. Engl. J. Med. 2008; 359: 7–20.
10.1056/NEJMoa0802639
CAS PubMed Web of Science® Google Scholar
78Faulhaber-Walter R, Hafer C, Jahr N et al. The Hannover dialysis outcome study: Comparison of standard versus intensified extended dialysis for treatment of patients with acute kidney injury in the intensive care unit. Nephrol. Dial. Transplant. 2009; 24: 2179–86.
10.1093/ndt/gfp035
PubMed Web of Science® Google Scholar
79Bouchard J, Soroko SB, Chertow GM et al. Fluid accumulation, survival and recovery of kidney function in critically ill patients with acute kidney injury. Kidney Int. 2009; 76: 422–7.
10.1038/ki.2009.159
PubMed Web of Science® Google Scholar
80Bellomo R, Cass A, Cole L et al. Intensity of continuous renal-replacement therapy in critically ill patients. N. Engl. J. Med. 2009; 361: 1627–38.
10.1056/NEJMoa0902413
PubMed Web of Science® Google Scholar
81Venkataraman R, Kellum JA, Palevsky P. Dosing patterns for continuous renal replacement therapy at a large academic medical center in the United States. J. Crit. Care 2002; 17: 246–50.
10.1053/jcrc.2002.36757
PubMed Web of Science® Google Scholar
82Mehran R, Nikolsky E. Contrast-induced nephropathy: Definition, epidemiology, and patients at risk. Kidney Int. Suppl. 2006; 100: S11–5.
10.1038/sj.ki.5000368
CAS PubMed Web of Science® Google Scholar
83McCullough PA, Adam A, Becker CR et al. Risk prediction of contrast-induced nephropathy. Am. J. Cardiol. 2006; 98: 27K–36K.
10.1016/j.amjcard.2006.01.022
PubMed Web of Science® Google Scholar
84Rudnick MR, Goldfarb S, Tumlin J. Contrast-induced nephropathy: Is the picture any clearer? Clin. J. Am. Soc. Nephrol. 2008; 3: 261–2.
10.2215/CJN.04951107
PubMed Web of Science® Google Scholar
85Weisbord SD, Chen H, Stone RA et al. Associations of increases in serum creatinine with mortality and length of hospital stay after coronary angiography. J. Am. Soc. Nephrol. 2006; 17: 2871–7.
10.1681/ASN.2006030301
CAS PubMed Web of Science® Google Scholar
86McCullough PA. Radiocontrast-induced acute kidney injury. Nephron Physiol. 2008; 109: 61–72.
10.1159/000142938
CAS PubMed Web of Science® Google Scholar
87Drey N, Roderick P, Mullee M, Rogerson M. A population-based study of the incidence and outcomes of diagnosed chronic kidney disease. Am. J. Kidney Dis. 2003; 42: 677–84.
10.1016/S0272-6386(03)00916-8
PubMed Web of Science® Google Scholar
88Bruce RJ, Djamali A, Shinki K, Michel SJ, Fine JP, Pozniak MA. Background fluctuation of kidney function versus contrast-induced nephrotoxicity. AJR Am. J. Roentgenol. 2009; 192: 711–8.
10.2214/AJR.08.1413
PubMed Web of Science® Google Scholar
89Choyke PL, Cady J, DePollar SL, Austin H. Determination of serum creatinine prior to iodinated contrast media: Is it necessary in all patients? Tech. Urol. 1998; 4: 65–9.
CAS PubMed Google Scholar
90Lameire N, Adam A, Becker CR et al. Baseline renal function screening. Am. J. Cardiol. 2006; 98: 21K–6K.
10.1016/j.amjcard.2006.01.021
PubMed Web of Science® Google Scholar
91Katzberg RW, Lamba R. Contrast-induced nephropathy after intravenous administration: Fact or fiction? Radiol. Clin. North Am. 2009; 47: 789–800.
10.1016/j.rcl.2009.06.002
PubMed Web of Science® Google Scholar
92Goldenberg I, Matetzky S. Nephropathy induced by contrast media: Pathogenesis, risk factors and preventive strategies. Can. Med. Assoc. J. 2005; 172: 1461–71.
10.1503/cmaj.1040847
PubMed Web of Science® Google Scholar
93Barrett BJ, Carlisle EJ. Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media. Radiology 1993; 188: 171–8.
10.1148/radiology.188.1.8511292
CAS PubMed Web of Science® Google Scholar
94Jo SH, Youn TJ, Koo BK et al. Renal toxicity evaluation and comparison between visipaque (iodixanol) and hexabrix (ioxaglate) in patients with renal insufficiency undergoing coronary angiography: The RECOVER study: A randomized controlled trial. J. Am. Coll. Cardiol. 2006; 48: 924–30.
10.1016/j.jacc.2006.06.047
CAS PubMed Web of Science® Google Scholar
95Heinrich MC, Haberle L, Muller V et al. Nephrotoxicity of iso-osmolar iodixanol compared with nonionic low-osmolar contrast media: Meta- analysis of randomized controlled trials. Radiology 2009; 250: 68–86.
10.1148/radiol.2501080833
PubMed Web of Science® Google Scholar
96Reddan D, Laville M, Garovic VD. Contrast-induced nephropathy and its prevention: What do we really know from evidence-based findings? J. Nephrol. 2009; 22: 333–51.
CAS PubMed Web of Science® Google Scholar
97Mehran R, Nikolsky E, Kirtane AJ et al. Ionic low-osmolar versus nonionic iso-osmolar contrast media to obviate worsening nephropathy after angioplasty in chronic renal failure patients: The ICON (ionic versus non-ionic contrast to obviate worsening nephropathy after angioplasty in chronic renal failure patients) study. JACC Cardiovasc. Interv. 2009; 2: 415–21.
10.1016/j.jcin.2009.03.007
PubMed Web of Science® Google Scholar
98Ribichini F, Graziani M, Gambaro G et al. Early creatinine shifts predict contrast-induced nephropathy and persistent renal damage after angiography. Am. J. Med. 2010; 123: 755–63.
10.1016/j.amjmed.2010.02.026
CAS PubMed Web of Science® Google Scholar
99Stacul F, van der Molen AJ, Reimer P et al. Contrast induced nephropathy: Updated ESUR contrast media safety committee guidelines. Eur. Radiol. 2011; 21: 2527–41.
10.1007/s00330-011-2225-0
PubMed Web of Science® Google Scholar
100Better OS, Rubinstein I. Management of shock and acute renal failure in casualties suffering from the crush syndrome. Ren. Fail. 1997; 19: 647–53.
10.3109/08860229709109030
CAS PubMed Web of Science® Google Scholar
101Stevens MA, McCullough PA, Tobin KJ et al. A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy: Results of the P.R.I.N.C.E. study. Prevention of radiocontrast induced nephropathy clinical evaluation. J. Am. Coll. Cardiol. 1999; 33: 403–11.
10.1016/S0735-1097(98)00574-9
CAS PubMed Web of Science® Google Scholar
102Mueller C, Buerkle G, Buettner HJ et al. Prevention of contrast media-associated nephropathy: Randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch. Intern. Med. 2002; 162: 329–36.
10.1001/archinte.162.3.329
CAS PubMed Web of Science® Google Scholar
103Weisbord SD, Palevsky PM. Prevention of contrast-induced nephropathy with volume expansion. Clin. J. Am. Soc. Nephrol. 2008; 3: 273–80.
10.2215/CJN.02580607
CAS PubMed Web of Science® Google Scholar
104Zoungas S, Ninomiya T, Huxley R et al. Systematic review: Sodium bicarbonate treatment regimens for the prevention of contrast-induced nephropathy. Ann. Intern. Med. 2009; 151: 631–8.
10.7326/0003-4819-151-9-200911030-00008
PubMed Web of Science® Google Scholar
105Brar S, Aharonian V, Mansukhani P et al. Haemodynamic-guided fluid administration for the prevention of contrast-induced acute kidney injury: The POSEIDON randomized controlled trial. Lancet 2014; 383: 1814–23.
10.1016/S0140-6736(14)60689-9
PubMed Web of Science® Google Scholar
106Murray PT, Thakar CV. Acute kidney injury and critical care nephrology. NephSAP 2015; 14: 97–160.
Google Scholar
107Fishbane S. N-acetylcysteine in the prevention of contrast-induced nephropathy. Clin. J. Am. Soc. Nephrol. 2008; 3: 281–7.
10.2215/CJN.02590607
CAS PubMed Web of Science® Google Scholar
108Thiele H, Hildebrand L, Schirdewahn C et al. Impact of high-dose N-acetylcysteine versus placebo on contrast-induced nephropathy and myocardial reperfusion injury in unselected patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. The LIPSIA-N-ACC (prospective, single-blind, placebo-controlled, randomized Leipzig immediate percutaneous coronary intervention acute myocardial infarction N-ACC) trial. J. Am. Coll. Cardiol. 2010; 55: 2201–9.
10.1016/j.jacc.2009.08.091
CAS PubMed Web of Science® Google Scholar
109Briguori C, Airoldi F, D'Andrea D et al. Renal insufficiency following contrast media administration trial (REMEDIAL): A randomized comparison of 3 preventive strategies. Circulation 2007; 115: 1211–7.
10.1161/CIRCULATIONAHA.106.687152
CAS PubMed Web of Science® Google Scholar
110Brown JR, Block CA, Malenka DJ, O'Connor GT, Schoolwerth AC, Thompson CA. Sodium bicarbonate plus N-acetylcysteine prophylaxis: a meta-analysis. JACC Cardiovasc. Interv. 2009; 2: 1116–24.
10.1016/j.jcin.2009.07.015
PubMed Web of Science® Google Scholar
111Leoncini M, Toso A, Maioli M, Tropeano F, Villani S, Bellandi F. Early high-dose rosuvastatin for contrast-induced nephropathy prevention in acute coronary syndrome: Results from the PRATO-ACS study (protective effect of rosuvastatin and antiplatelet therapy on contrast-induced acute kidney injury and myocardial damage in patients with acute coronary syndrome). J. Am. Coll. Cardiol. 2014; 63: 71–9.
10.1016/j.jacc.2013.04.105
CAS PubMed Web of Science® Google Scholar
112Han Y, Zhu G, Han L et al. Short-term rosuvastatin therapy for prevention of contrast-induced acute kidney injury in patients with diabetes and chronic kidney disease. J. Am. Coll. Cardiol. 2014; 63: 62–70.
10.1016/j.jacc.2013.09.017
CAS PubMed Web of Science® Google Scholar
113Reinecke H, Fobker M, Wellmann J et al. A randomized controlled trial comparing hydration therapy to additional hemodialysis or N-acetyl- cysteine for the prevention of contrast medium-induced nephropathy: The dialysis-versus-diuresis (DVD) trial. Clin. Res. Cardiol. 2007; 96: 130–9.
10.1007/s00392-007-0473-4
CAS PubMed Web of Science® Google Scholar
114Kawashima S, Takano H, Iino Y, Takayama M, Takano T. Prophylactic hemodialysis does not prevent contrast-induced nephropathy after cardiac catheterization in patients with chronic renal insufficiency. Circ. J. 2006; 70: 553–8.
10.1253/circj.70.553
PubMed Web of Science® Google Scholar
115Lee PT, Chou KJ, Liu CP et al. Renal protection for coronary angiography in advanced renal failure patients by prophylactic hemodialysis. A randomized controlled trial. J. Am. Coll. Cardiol. 2007; 50: 1015–20.
10.1016/j.jacc.2007.05.033
PubMed Web of Science® Google Scholar
116Cruz DN, Perazella MA, Ronco C. The role of extracorporeal blood purification therapies in the prevention of radiocontrast-induced nephropathy. Int. J. Artif. Organs 2008; 31: 515–24.
10.1177/039139880803100607
CAS PubMed Web of Science® Google Scholar
117Nadim MK, Durand F, Kellum JA et al. Management of the critically ill patient with cirrhosis: A multidisciplinary perspective. J. Hepatol. 2016; 64: 717–35.
10.1016/j.jhep.2015.10.019
PubMed Web of Science® Google Scholar
118Sanyal AJ, Boyer TD, Frederick RT et al. Reversal of hepatorenal syndrome type 1 with terlipressin plus albumin vs. placebo plus albumin in a pooled analysis of the OT-0401 and REVERSE randomised clinical studies. Aliment. Pharmacol. Ther. 2017; 45: 1390–402.
10.1111/apt.14052
CAS PubMed Web of Science® Google Scholar
119 National Kidney Foundation. National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI) guidelines. Available from URL: https://www.kidney.org/professionals/guidelines
Google Scholar
120 Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. Suppl. 2013; 3: 1–150.
10.1038/kisup.2012.73
Google Scholar
121Löfman I, Szummer K, Dahlström U, Jernberg T, Lund LH. Associations with and prognostic impact of chronic kidney disease in heart failure with preserved, mid-range, and reduced ejection fraction. Eur J Heart Fail. 2017; 19: 1606–14.
10.1002/ejhf.821
PubMed Web of Science® Google Scholar
122Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: A new prediction equation. Modification of diet in renal disease study group. Ann. Intern. Med. 1999; 130: 461–70.
10.7326/0003-4819-130-6-199903160-00002
CAS PubMed Web of Science® Google Scholar
123Levey AS, Greene T, Kusek JW, Beck GJ. A simplified equation to predict glomerular filtration rate from serum creatinine. J. Am. Soc. Nephrol. 2000; 11:155A.
PubMed Google Scholar
124Levey AS, Stevens LA, Schmid CH et al. A new equation to estimate glomerular filtration rate. Ann. Intern. Med. 2009; 150: 604–12.
10.7326/0003-4819-150-9-200905050-00006
PubMed Web of Science® Google Scholar
125Inker LA, Schmid CH, Tighiouart H et al. Estimating glomerular filtration rate from serum creatinine and cystatin C. N. Engl. J. Med. 2012; 367: 20–9.
10.1056/NEJMoa1114248
CAS PubMed Web of Science® Google Scholar
126 The Kidney Health Australia. Caring for Australasians with renal impairment (KHA-CARI) guidelines. Available from URL: http://www.cari.org.au/
Google Scholar
127Li PK, Kwan BC, Leung CB et al. Prevalence of silent kidney disease in Hong Kong: The screening for Hong Kong asymptomatic renal population and evaluation (SHARE) program. Kidney Int. Suppl. 2005; 94: S36–40.
10.1111/j.1523-1755.2005.09410.x
PubMed Google Scholar
128Upadhyay A, Earley A, Haynes SM, Uhlig K. Systematic review: Blood pressure target in chronic kidney disease and proteinuria as an effect modifier. Ann. Intern. Med. 2011; 154: 541–8.
10.7326/0003-4819-154-8-201104190-00335
PubMed Web of Science® Google Scholar
129Astor BC, Matsushita K, Gansevoort RT et al. Lower estimated glomerular filtration rate and higher albuminuria are associated with mortality and end-stage renal disease. A collaborative meta-analysis of kidney disease population cohorts. Kidney Int. 2011; 79: 1331–40.
10.1038/ki.2010.550
CAS PubMed Web of Science® Google Scholar
130Baigent C, Landray MJ, Reith C et al. The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease (Study of Heart and Renal Protection): A randomised placebo-controlled trial. Lancet 2011; 377: 2181–92.
10.1016/S0140-6736(11)60739-3
CAS PubMed Web of Science® Google Scholar
131Haynes R, Lewis D, Emberson J et al. Effects of lowering LDL cholesterol on progression of kidney disease. J. Am. Soc. Nephrol. 2014; 25: 1825–33.
10.1681/ASN.2013090965
CAS PubMed Web of Science® Google Scholar
132de Zeeuw D, Anzalone DA, Cain VA et al. Renal effects of atorvastatin and rosuvastatin in patients with diabetes who have progressive renal disease (PLANET I): A randomised clinical trial. Lancet Diabetes Endocrinol. 2015; 3: 181–90.
10.1016/S2213-8587(14)70246-3
CAS PubMed Web of Science® Google Scholar
133Pfeffer MA, Burdmann EA, Chen CY et al. A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease. N. Engl. J. Med. 2009; 361: 2019–32.
10.1056/NEJMoa0907845
PubMed Web of Science® Google Scholar
134Drueke TB, Locatelli F, Clyne N et al. CREATE investigators. Normalization of hemoglobin level in patients with chronic kidney disease and anemia. N. Engl. J. Med. 2006; 355: 2071–84.
10.1056/NEJMoa062276
CAS PubMed Web of Science® Google Scholar
135Singh AK, Szczech L, Tang KL et al. Correction of anemia with epoetin alfa in chronic kidney disease. N. Engl. J. Med. 2006; 355: 2085–98.
10.1056/NEJMoa065485
CAS PubMed Web of Science® Google Scholar
136Garneata L, Stancu A, Dragomir D, Stefan G, Mircescu G. Ketoanalogue-supplemented vegetarian very low-protein diet and CKD progression. J. Am. Soc. Nephrol. 2016; 27: 2164–76.
10.1681/ASN.2015040369
CAS PubMed Web of Science® Google Scholar
137Perkovic V, Heerspink HL, Chalmers J et al. Intensive glucose control improves kidney outcomes in patients with type 2 diabetes. Kidney Int. 2013; 83: 517–23.
10.1038/ki.2012.401
CAS PubMed Web of Science® Google Scholar
138Chan GC, Tang SC. Diabetic nephropathy: Landmark clinical trials and tribulations. Nephrol. Dial. Transplant. 2016; 31: 359–68.
10.1093/ndt/gfu411
CAS PubMed Web of Science® Google Scholar
139 Guideline Development Group. Clinical practice guideline on management of patients with diabetes and chronic kidney disease stage 3b or higher (eGFR <45 mL/min). Nephrol Dial Transplant. 2015; 30 (Suppl 2): ii1–ii142. https://doi.org/10.1093/ndt/gfv100.
10.1093/ndt/gfv100
PubMed Web of Science® Google Scholar
140Fried LF, Emanuele N, Zhang JH et al. Combined angiotensin inhibition for the treatment of diabetic nephropathy. N. Engl. J. Med. 2013; 369: 1892–903.
10.1056/NEJMoa1303154
CAS PubMed Web of Science® Google Scholar
141Bakris GL, Agarwal R, Chan JC et al. Mineralocorticoid receptor antagonist tolerability study–diabetic nephropathy (ARTS-DN) study group. Effect of finerenone on albuminuria in patients with diabetic nephropathy: A randomized clinical trial. JAMA 2015; 314: 884–94.
10.1001/jama.2015.10081
CAS PubMed Web of Science® Google Scholar
142Agarwal R, Brunelli SM, Williams K et al. Gadolinium-based contrast agents and nephrogenic systemic fibrosis: A systematic review and meta-analysis. Nephrol. Dial. Transplant. 2009; 24: 856–63.
10.1093/ndt/gfn593
CAS PubMed Web of Science® Google Scholar
143 Working Group of the International IgA Nephropathy Network and the Renal Pathology Society, Roberts IS, Cook HT, Troyanov S et al. The Oxford classification of IgA nephropathy: Pathology definitions, correlations, and reproducibility. Kidney Int. 2009; 76: 546–56.
10.1038/ki.2009.168
PubMed Web of Science® Google Scholar
144 Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group. KDIGO clinical practice guideline for glomerulonephritis. Kidney Int. Suppl. 2012; 2: 154–274.
Google Scholar
145Lane C, Brown M, Dunsmuir W, Kelly J, Mangos G. Can spot urine protein/creatinine ratio replace 24 h urine protein in usual clinical nephrology? Nephrology (Carlton) 2006; 11: 245–9.
10.1111/j.1440-1797.2006.00564.x
CAS PubMed Web of Science® Google Scholar
146Kusumoto S, Tanaka Y, Suzuki R et al. Monitoring of hepatitis B virus (HBV) DNA and risk of HBV reactivation in B-cell lymphoma: A prospective observational study. Clin. Infect. Dis. 2015; 61: 719–29.
10.1093/cid/civ344
CAS PubMed Web of Science® Google Scholar
147Huang H, Li X, Zhu J et al. Entecavir vs lamivudine for prevention of hepatitis B virus reactivation among patients with untreated diffuse large B-cell lymphoma receiving R-CHOP chemotherapy: A randomized clinical trial. JAMA 2014; 312: 2521–30.
10.1001/jama.2014.15704
CAS PubMed Web of Science® Google Scholar
148López-Serrano P, de la Fuente Briongos E, Alonso EC, Pérez-Calle JL, Rodríguez CF. Hepatitis B and immunosuppressive therapies for chronic inflammatory diseases: When and how to apply prophylaxis, with a special focus on corticosteroid therapy. World J Hepatol. 2015; 7: 539–47.
10.4254/wjh.v7.i3.539
PubMed Web of Science® Google Scholar
149Jiang L, Dasgupta I, Hurcombe JA, Colyer HF, Mathieson PW, Welsh GI. Levamisole in steroid-sensitive nephrotic syndrome: Usefulness in adult patients and laboratory insights into mechanisms of action via direct action on the kidney podocyte. Clin. Sci. (Lond.) 2015; 128: 883–93.
10.1042/CS20140749
CAS PubMed Web of Science® Google Scholar
150Yu CC, Fornoni A, Weins A et al. Abatacept in B7-1-positive proteinuric kidney disease. N. Engl. J. Med. 2013; 369: 2416–23.
10.1056/NEJMoa1304572
CAS PubMed Web of Science® Google Scholar
151Hofstra JM, Fervenza FC, Wetzels JF. Treatment of idiopathic membranous nephropathy. Nat. Rev. Nephrol. 2013; 9: 443–58.
10.1038/nrneph.2013.125
CAS PubMed Web of Science® Google Scholar
152Ruggenenti P, Cravedi P, Chianca A et al. Rituximab in idiopathic membranous nephropathy. J. Am. Soc. Nephrol. 2012; 23: 1416–25.
10.1681/ASN.2012020181
CAS PubMed Web of Science® Google Scholar
153Rauen T, Eitner F, Fitzner C et al. Intensive supportive care plus immunosuppression in IgA nephropathy. N. Engl. J. Med. 2015; 373: 2225–36.
10.1056/NEJMoa1415463
CAS PubMed Web of Science® Google Scholar
154Lv J, Zhang H, Wong MG et al. Effect of oral methylprednisolone on clinical outcomes in patients with IgA nephropathy: The TESTING randomized clinical trial. JAMA 2017; 318: 432–42.
10.1001/jama.2017.9362
CAS PubMed Web of Science® Google Scholar
155Lv J, Xu D, Perkovic V et al. Corticosteroid therapy in IgA nephropathy. J Am Soc Nephrol. 2012; 23: 1108–16.
10.1681/ASN.2011111112
CAS PubMed Web of Science® Google Scholar
156Tesar V, Troyanov S, Bellur S et al. Corticosteroids in IgA nephropathy: A retrospective analysis from the VALIGA study. J. Am. Soc. Nephrol. 2015; 26: 2248–58.
10.1681/ASN.2014070697
CAS PubMed Web of Science® Google Scholar
157Fellström BC, Barratt J, Cook H et al. Targeted-release budesonide versus placebo in patients with IgA nephropathy (NEFIGAN): A double-blind, randomised, placebo-controlled phase 2b trial. Lancet 2017; 389: 2117–27.
10.1016/S0140-6736(17)30550-0
PubMed Web of Science® Google Scholar
158Kang Z, Li Z, Duan C et al. Mycophenolate mofetil therapy for steroid-resistant IgA nephropathy with the nephrotic syndrome in children. Pediatr. Nephrol. 2015; 30: 1121–9.
10.1007/s00467-014-3041-y
PubMed Web of Science® Google Scholar
159Liu X, Dewei D, Sun S et al. Treatment of severe IgA nephropathy: Mycophenolate mofetil/prednisone compared to cyclophosphamide/prednisone. Int. J. Clin. Pharmacol. Ther. 2014; 52: 95–102.
10.5414/CP201887
CAS PubMed Web of Science® Google Scholar
160Tang SC, Tang AW, Wong SS, Leung JC, Ho YW, Lai KN. Long-term study of mycophenolate mofetil treatment in IgA nephropathy. Kidney Int. 2010; 77: 543–9.
10.1038/ki.2009.499
CAS PubMed Web of Science® Google Scholar
161Hogg RJ, Bay RC, Jennette JC et al. Randomized controlled trial of mycophenolate mofetil in children, adolescents, and adults with IgA nephropathy. Am. J. Kidney Dis. 2015; 66: 783–91.
10.1053/j.ajkd.2015.06.013
CAS PubMed Web of Science® Google Scholar
162Alberici F, Jayne DR. Impact of rituximab trials on the treatment of ANCA-associated vasculitis. Nephrol. Dial. Transplant. 2014; 29: 1151–9.
10.1093/ndt/gft318
CAS PubMed Web of Science® Google Scholar
163Jayne DR, Gaskin G, Rasmussen N et al. Randomized trial of plasma exchange or high-dosage methylprednisolone as adjunctive therapy for severe renal vasculitis. J. Am. Soc. Nephrol. 2007; 18: 2180–8.
10.1681/ASN.2007010090
CAS PubMed Web of Science® Google Scholar
164Chan TM. Treatment of severe lupus nephritis: The new horizon. Nat. Rev. Nephrol. 2015; 11: 46–61.
10.1038/nrneph.2014.215
CAS PubMed Web of Science® Google Scholar
165Liu Z, Zhang H, Liu Z et al. Multitarget therapy for induction treatment of lupus nephritis: A randomized trial. Ann. Intern. Med. 2015; 162: 18–26.
10.7326/M14-1030
PubMed Web of Science® Google Scholar

Citing Literature

Volume24, IssueS1

Supplement: Clinical Practice Guidelines for the Provision of Renal Services in Hong Kong. Guest Editors: Sydney Chi-Wai Tang, Andrew Kui-Man Wong, Cheuk Chun Szeto and Philip Kam-Tao Li. The Hong Kong Clinical Practice Guideline for Nephrology is jointly published by the Hong Kong College of Physicians and the Central Renal Committee of Hospital Authority of Hong Kong with the support from the Hong Kong Society of Nephrology. The publication of this Guideline as a Supplement in Nephrology is jointly funded by the Hong Kong College of Physicians and the Hong Kong Society of Nephrology

March 2019

Pages 9-26

Clinical practice guidelines for the provision of renal service in Hong Kong: General Nephrology