Acute renal failure

John A Kellum; Martine Leblanc; Ramesh Venkataraman

. 2008 Sep 3;2008:2001.

Acute renal failure

John A Kellum ^1,^#, Martine Leblanc ^2,^#, Ramesh Venkataraman ^3,^#

PMCID: PMC2907962 PMID: 19445797

Abstract

Introduction

Acute renal failure is characterised by abrupt and sustained decline in glomerular filtration rate, which leads to accumulation of urea and other chemicals in the blood. The term acute kidney injury has been recently introduced to encompass a wide spectrum of acute alterations in kidney function from very mild to severe. Acute renal failure/acute kidney injury is classified according to the RIFLE criteria where a change from baseline serum creatinine or urine output determines the level of renal dysfunction.

Methods and outcomes

We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of interventions to prevent acute renal failure in people at high risk? What are the effects of treatments for critically ill people with acute renal failure? We searched: Medline, Embase, The Cochrane Library, and other important databases up to April 2007 (BMJ Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).

Results

We found 77 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.

Conclusions

In this systematic review we present information relating to the effectiveness and safety of the following interventions: albumin supplementation plus loop diuretics (intravenous), aminoglycosides, aminophylline, amphotericin B, calcium channel blockers, contrast media, dialysis membranes, dopamine, fenoldopam, loop diuretics, mannitol, N-acetylcysteine, natriuretic peptides, renal replacement therapy, sodium bicarbonate-based fluids, sodium chloride-based fluids, and theophylline.

Key Points

Acute renal failure is characterised by abrupt and sustained decline in GFR, which leads to accumulation of urea and other chemicals in the blood.

It can be classified according to a change from baseline serum creatinine or urine output, with "Risk" being defined by either a 50% increase in serum creatinine, or a urine output of less than 0.5 mL/kg/hour for at least 6 hours; and "Failure" being defined by a threefold increase in serum creatinine, or a urine output of less than 0.3 mL/kg/hour for 24 hours.

In people at high risk of developing acute renal failure, intravenous sodium chloride (0.9%) reduces incidences of acute renal failure compared with unrestricted oral fluids or 0.45% iv sodium chloride solution.

N-acetylcysteine plus intravenous fluids may reduce contrast nephropathy compared with intravenous fluids alone in people undergoing contrast nephrography, although data about prevention of renal failure are inconclusive.
Low-osmolality contrast medium is less nephrotoxic compared with high-osmolality media, and iso-osmolar contrast media may be less nephrotoxic compared with low-osmolar contrast media.
We found insufficient evidence on the effects of prophylactic renal replacement therapy.
Single-dose aminoglycosides seem as beneficial as multiple doses for treating infections, but are less nephrotoxic.
Lipid formulations of amphotericin B may cause less nephrotoxicity than standard formulations, although the evidence for this is somewhat sparse.
Mannitol, theophylline, aminophylline, fenoldopam, and calcium channel blockers do not seem useful treatments for people at high risk of acute renal failure.

In critically ill people, high-dose continuous renal replacement therapy may reduce mortality compared with low-dose, although we don't know whether continuous therapy is any more effective than intermittent renal replacement therapy.

Synthetic dialysis membranes may be associated with improved survival compared with cellulose-based membranes for treating people with acute renal failure; however, evidence is inconclusive and of variable quality.
Loop diuretics plus fluids seems to increase the risk of developing acute renal failure compared with fluids alone, both in high-risk and critically ill people, and do not seem to improve renal function or mortality compared with placebo in people with acute renal failure, but may increase the risks of ototoxicity and volume depletion.
We found no evidence that examined whether intravenous albumin supplementation improved the effects of loop diuretics, or whether continuous infusion was any more effective than bolus injection in the treatment of people critically ill with acute renal failure.

Neither natriuretic peptides nor dopamine seem beneficial in either high-risk or critically ill people, and both are associated with significant side effects.

About this condition

Definition

Acute renal failure is characterised by abrupt and sustained decline in glomerular filtration rate (GFR), which leads to accumulation of urea and other chemicals in the blood. Most studies define it biochemically as a serum creatinine of 2-3 mg/dL (200-250 µmol/L), an elevation of more than 0.5 mg/dL (45 µmol/L) over a baseline creatinine below 2 mg/dL, or a twofold increase of baseline creatinine. A recent international interdisciplinary consensus panel has classified acute renal failure (now termed acute kidney injury) according to a change from baseline serum creatinine or urine output. The three-level classification begins with "Risk" (defined by either a 50% increase in serum creatinine or a urine output of less than 0.5 mL/kg/hour for at least 6 hours), and concludes with "Failure" (defined by a threefold increase in serum creatinine or a urine output of less than 0.3 mL/kg/hour for 24 hours). Acute renal failure is usually additionally classified according to the location of the predominant primary pathology (prerenal, intrarenal, and postrenal failure). Critically ill people are clinically unstable and at imminent risk of death, which usually implies that they need to be in, or have been admitted to, the intensive care unit (ICU).

Incidence/ Prevalence

Two prospective observational studies (2576 people) found that established acute renal failure affected nearly 5% of people in hospital, and as many as 15% of critically ill people, depending on the definitions used.

Aetiology/ Risk factors

General risk factors: Risk factors for acute renal failure that are consistent across multiple causes include: age; hypovolaemia; hypotension; sepsis; pre-existing renal, hepatic, or cardiac dysfunction; diabetes mellitus; and exposure to nephrotoxins (e.g. aminoglycosides, amphotericin, immunosuppressive agents, NSAIDs, ACE inhibitors, intravenous contrast media) (see table 1 ). Risk factors/aetiology in critically ill people: Isolated episodes of acute renal failure are rarely seen in critically ill people, but are usually part of multiple organ dysfunction syndromes. Acute renal failure requiring dialysis is rarely seen in isolation (less than 5% of people). The kidneys are often the first organs to fail. In the perioperative setting, risk factors for acute renal failure include prolonged aortic clamping, emergency rather than elective surgery, and use of higher volumes (greater than 100 mL) of intravenous contrast media. One study (3695 people) using multiple logistic regression identified the following independent risk factors: baseline creatinine clearance below 47 mL/minute (OR 1.20, 95% CI 1.12 to 1.30), diabetes (OR 5.5, 95% CI 1.4 to 21.0), and a marginal effect for doses of contrast media above 100 mL (OR 1.01, 95% CI 1.00 to 1.01). Mortality of people with acute renal failure requiring dialysis was 36% while in hospital. Prerenal acute renal failure is caused by reduced blood flow to the kidney from renal artery disease, systemic hypotension, or maldistribution of blood flow. Intrarenal acute renal failure is caused by parenchymal injury (acute tubular necrosis, interstitial nephritis, embolic disease, glomerulonephritis, vasculitis, or small-vessel disease). Postrenal acute renal failure is caused by urinary tract obstruction. Observational studies (in several hundred people from Europe, North America, and West Africa with acute renal failure) found a prerenal cause in 40-80%, an intrarenal cause in 10-50%, and a postrenal cause in the remaining 10%. Prerenal acute renal failure is the most common type of acute renal failure in critically ill people. Intrarenal acute renal failure in this context is usually part of multisystem failure, most frequently due to acute tubular necrosis due to ischaemic or nephrotoxic injury, or both.

Table 1.

Selected risk factors for acute renal failure (see text).

Risk factor	Incidence of ARF	Comments
Sepsis	Unknown	Sepsis seems to be a contributing factor in as many as 43% of ARF cases
Aortic clamping	Approaches 100% when longer than 60 minutes	Refers to cross-clamping (no flow) above the renal arteries
Rhabdomyolysis	16.5%	None
Aminoglycosides	8–26%	None
Amphotericin	88% with greater than 5 g total dose	60% overall incidence of nephrotoxicity

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Prognosis

One retrospective study (1347 people with acute renal failure) found that mortality was less than 15% in people with isolated acute renal failure. One recent prospective study (more than 700 people) found that, in people with acute renal failure, overall mortality (72% in ICU v 32% in non-ICU; P = 0.001) and the need for dialysis (71% in ICU v 18% in non-ICU; P less than 0.001) were higher in an ICU than in a non-ICU setting, despite no significant difference between the groups in mean maximal serum creatinine (5.21 ± 2.34 mg/dL in ICU v 5.82 ± 3.26 mg/dL in non-ICU). One large study (more than 17,000 people admitted to Austrian ICUs) found that acute renal failure was associated with a higher than fourfold increase in mortality. Even after controlling for underlying severity of illness, mortality was still significantly higher in people with acute renal failure (62.8% in people with acute renal failure v 38.5% in people with no acute renal failure), suggesting that acute renal failure is independently responsible for increased mortality, even if dialysis is used. However, the exact mechanism that leads to increased risk of death is uncertain. A systematic review including 80 articles and a total of 15,897 people with acute renal failure from 1970-2004 found mortality unchanged at about 50%, and exceeding 30% in most studies. An observational study including 54 sites and 23 countries screened 29,269 people, and found that 1738 (5.7%) had severe acute renal failure warranting renal replacement therapy. Overall hospital mortality among people with severe acute renal failure was 60.3% (95% CI, 58.0% to 62.6%).

Aims of intervention

Prevention: To preserve renal function. Treating critically ill people: To prevent death; to prevent complications of acute renal failure (volume overload, acid-base disturbance, and electrolyte abnormalities); and to prevent the need for chronic dialysis, with minimum adverse effects.

Outcomes

Prevention: Rates of acute renal failure, nephrotoxicity, or both. Surrogate outcomes were limited to measurements of biochemical evidence of organ function (serum creatinine or creatinine clearance) after the intervention. Surrogate markers such as urine output or renal blood flow were not considered as evidence of effectiveness. Critically ill people: Rate of death; rate of renal recovery; adverse effects of treatment.

Methods

BMJ Clinical Evidence search and appraisal April 2007. The following databases were used to identify studies for this review: Medline 1966 to April 2007, Embase 1980 to April 2007, and The Cochrane Database of Systematic Reviews and Cochrane Central Register of Controlled Clinical Trials 2007, Issue 1. Additional searches were carried out using these websites: NHS Centre for Reviews and Dissemination (CRD) — for Database of Abstracts of Reviews of Effects (DARE) and Health Technology Assessment (HTA), Turning Research into Practice (TRIP), and NICE. Abstracts of the studies retrieved from the initial search were assessed by an information specialist. Selected studies were then sent to the author for additional assessment, using pre-determined criteria to identify relevant studies. Study design criteria for evaluation in this review were: published systematic reviews and RCTs in any language, at least single blinded, and containing more than 20 people, of whom more than 80% were followed up. There was no minimum length of follow-up required to include studies for the question on treating acute renal failure; there needed to be at least a 48-hour follow-up for the question pertaining to prevention. We excluded all studies described as "open", "open label", or not blinded unless blinding was impossible. In addition, we use a regular surveillance protocol to capture harms alerts from organisations such as the FDA and the UK Medicines and Healthcare products Regulatory Agency (MHRA), which are added to the review as required. We have performed a GRADE evaluation of the quality of evidence for interventions included in this review (see table ).

Table.

GRADE evaluation of interventions for acute renal failure

Important outcomes	Kidney injury, mortality, adverse effects
Number of studies (participants)	Outcome	Comparison	Type of evidence	Quality	Consistency	Directness	Effect size	GRADE	Comment
What are the effects of interventions to prevent acute renal failure in people at high risk?
31 (5146)	Kidney injury	Low-osmolality contrast media v high-osmolality contrast media	4	−1	0	0	0	Moderate	Quality point deducted for incomplete reporting of results
2 (365)	Kidney injury	Intravenous sodium chloride 0.9% v oral fluids	4	0	−1	0	0	Moderate	Consistency point deducted for conflicting results
1 (1620)	Kidney injury	Sodium chloride 0.9% v sodium chloride 0.45%	4	0	0	0	0	High
1 (45)	Kidney injury	Sodium chloride 0.45% v restricted fluids	4	−1	0	−1	0	Low	Quality points deducted for sparse data and incomplete reporting of results
1 (36)	Kidney injury	Inpatient v outpatient fluid regimens	4	−2	0	−2	0	Very low	Quality points deducted for sparse data and incomplete reporting of results. Directness points deducted for differences in amount of fluids administered and uncertainty about clinical relevance of outcome measured
17 (2201)	Kidney injury	Acetylcysteine v control in the prevention of contrast nephropathy	4	−1	0	−1	0	Low	Quality point deducted for incomplete reporting of results. Consistency point deducted for heterogeneity between RCTs and added for dose response. Directness point deducted for differences in timing and dose administration
1 (354)	Mortality	Acetylcysteine v control in the prevention of contrast nephropathy	4	0	+1	−1	0	High	Consistency point added for dose response. Directness point deducted for composite outcome
2 (337)	Kidney injury	Acetylcysteine v placebo in the prevention of perioperative acute renal failure	4	0	0	0	0	High
1 (142)	Kidney injury	Acetylcysteine v placebo in the prevention of acute renal failure after hypotension	4	−1	0	0	0	Moderate	Quality point deducted for sparse data
2 (420)	Kidney injury	Iso-osmolar contrast media v low osmolar contrast media	4	0	0	−1	0	Moderate	Directness point deducted for not using standardised volumes of contrast media or fluid regimens
4 (803)	Kidney injury	Single-dose aminoglycosides v multiple doses	4	−1	−1	0	0	Low	Quality point deducted for incomplete reporting of results. Consistency point deducted for different results for people with different disease severities
1 (119)	Kidney injury	Sodium bicarbonate v sodium chloride	4	−2	0	0	0	Low	Quality points deducted for sparse data and no intention-to-treat analysis
3 (770)	Kidney injury	Fenoldopam v placebo	4	0	0	0	0	High
3 (770)	Mortality	Fenoldopam v placebo	4	0	0	0	0	High
2 (180)	Kidney injury	Fenoldopam v dopamine	4	−2	−1	0	0	Very low	Quality points deducted for sparse data and incomplete reporting of results. Consistency point deducted for conflicting results
11 (1094)	Kidney injury	Fenoldopam v other treatments or control	4	−3	−1	−1	0	Very low	Quality points deducted for incomplete reporting of results and methodological weaknesses. Consistency point deducted for heterogeneity between RCTs. Directness point deducted for heterogenous combined control
1 (78)	Kidney injury	Mannitol plus intravenous fluids v intravenous fluids	4	−1	0	−1	0	Low	Quality point deducted for sparse data. Directness point deducted for multiple comparisons
2 (206)	Kidney injury	Renal replacement therapy (haemofiltration) v isotonic saline	4	−1	0	−2	0	Very low	Quality point deducted for methodological weaknesses. Directness points deducted for differences in treatments provided to both groups and for uncertainty about benefit
1 (114)	Mortality	Renal replacement therapy (haemofiltration) v isotonic saline	4	−2	0	−2	0	Very low	Quality points deducted for sparse data and methodological weaknessess. Directness points deducted for differences in treatments provided to both groups
7 (480)	Kidney injury	Theophylline or aminophylline v control in radiocontrast-induced nephropathy	4	−2	−1	−1	0	Very low	Quality points deducted for incomplete reporting of results and uncertainty about hydration status of people receiving radiocontrast agent and for uncertainty about heterogeneity between studies. Directness point deducted for uncertainty about clinical significance
1 (56)	Kidney injury	Theophylline v sodium chloride 0.9% after CABG	4	−1	0	0	0	Moderate	Quality point deducted for sparse data
1 (210)	Kidney injury	Calcium channel blockers v placebo in people receiving live or cadaveric kidney transplant	4	−1	0	0	0	Moderate	Quality point deducted for incomplete reporting of results
7 (349)	Kidney injury	Calcium channel blockers v no calcium channel blockers in people receiving cadaveric kidney transplant	4	−2	−1	0	0	Very Low	Quality points deducted for incomplete reporting of results and for not reporting loss to follow-up or duration. Consistency point deducted for heterogeneity between RCTs
5 (284)	Mortality	Calcium channel blockers v no calcium channel blockers in people receiving cadaveric kidney transplant	4	−2	−1	0	0	Very Low	Quality points deducted for incomplete reporting of results and for not reporting loss to follow-up or treatment duration. Consistency point deducted for heterogeneity between RCTs
at least 10 RCTs (at least 618 people)	Kidney injury	Dopamine v placebo	4	0	0	0	0	High
12 (832)	Mortality	Dopamine v placebo	4	0	0	0	0	High
3 (255)	Kidney injury	Loop diuretics v fluids alone	4	0	0	−1	0	Moderate	Directness point deducted for differences in treatment protocols
2 (202)	Mortality	Loop diuretics v fluids alone	4	0	0	−1	0	Moderate	Directness point deducted for differences in treatment protocols
2 (3067)	Kidney injury	Natriuretic peptides v placebo	4	−1	−1	−2	0	Very low	Quality point deducted for incomplete reporting of results. Consistency point deducted for conflicting results. Directness points deducted for composite outcome and for using low doses and long treatment durations
What are the effects of treatments for critically ill people with acute renal failure?
2 (531)	Mortality	High-dose continuous renal replacement therapy v low-dose continuous renal replacement therapy	4	0	0	–1	0	Moderate	Consistency point added for dose response but deducted for conflicting results. Direcntess point deducted for comparing people with different disease severities
1 (206)	Mortality	Haemofiltration v haemofiltration plus dialysis	4	0	0	0	0	High
6 (624)	Kidney injury	Renal replacement therapy (continuous) v intermittent renal haemodialysis	4	−1	0	0	0	Moderate	Quality point deducted for incomplete reporting of results
6 (624)	Mortality	Renal replacement therapy (continuous) v intermittent renal haemodialysis	4	−1	0	0	0	Moderate	Quality point deducted for incomplete reporting of results
1 (360)	Mortality	Renal replacement therapy (intermittent haemodialysis) v continuous veno-venous haemodiafiltration	4	0	0	−1	0	Moderate	Directness point deducted for uncertainty about applicability to usual practice
7 + 15 studies (1589)	Mortality	Dialysis membranes (synthetic) v cellulose-based	4	−3	−1	0	0	Very low	Quality points deducted for incomplete reporting of results, methodological weaknesses, and for including non-RCTs. Consistency point deducted for conflicting results
at least 2 RCTs (at least 422 people)	Kidney injury	Loop diuretics v control	4	−3	0	0	0	Very low	Quality points deducted for poor reporting and methodological weaknesses
5 (at least 574 people)	Mortality	Loop diuretics v control	4	−3	0	0	0	Very low	Quality points deducted for poor reporting and methodological weaknesses
10 (618) )	Kidney injury	Dopamine v placebo	4	−1	0	0	0	Moderate	Quality point deducted for inclusion of trials
1 RCT + 11 trials (832)	Mortality	Dopamine v placebo	4	−1	0	0	0	Moderate	Quality point deducted for inclusion of trials
3 (900)	Kidney injury	Natriuretic peptides v placebo	4	−1	0	0	0	Moderate	Quality point deducted for incomplete reporting of results

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Type of evidence: 4 = RCT; 2 = Observational Consistency: similarity of results across studies Directness: generalisability of population or outcomes Effect size: based on relative risk or odds ratio

Glossary

Biocompatible: Artificial materials can induce an inflammatory response. This response can be humoral (including complement) or cellular. Synthetic dialysis membranes seem to produce less of an inflammatory response in vitro and are classified as more “biocompatible”. By contrast, cellulose-based membranes seem to be less biocompatible (cause more inflammation). When cellulose-based membranes are rendered semi-synthetic by modifications or substitution of materials like acetate, they may be become more biocompatible. We found no standards by which this comparison can be made.
Cellulose-based: Dialysis membranes may be made from cellulose. “Unsubstituted” cellulose has not undergone modification to attempt to improve biocompatibility. Synthetic membranes do not use cellulose.
Continuous renal replacement therapy: Any extracorporeal blood purification treatment intended to substitute for impaired renal function over an extended period of time and applied, or aimed at being applied, for 24 hours a day.
Contrast nephropathy: Intravenous radiocontrast increases serum creatinine in some people, particularly those with underlying kidney disease. Most studies define contrast nephropathy as a small change in serum creatinine (e.g. greater than 25% increase). It is not known whether agents that reduce the risk of contrast nephropathy also reduce the risk of acute renal failure.
Early allograft dysfunction: Renal dysfunction that occurs after renal transplantation, and which is usually secondary to ischaemic injury.
Early renal dysfunction: An acute derangement in renal function that is still evolving.
Glomerular filtration rate: The rate of elaboration of protein-free plasma filtrate (ultrafiltration) across the walls of the glomerular capillaries.
High-osmolality contrast media: Contrast media with osmolality greater than 800 mOsm/L. Until recently, it was considered the standard formulation for radiological assays.
High-quality evidence: Further research is very unlikely to change our confidence in the estimate of effect.
Intermittent renal replacement therapy: Renal support that is not, nor intended to be, continuous; usually prescribed for a period of 12 hours or less.
Iso-osmolar contrast media: Contrast media that are iso-osmolar compared with plasma, and therefore of lower osmolality than “low-osmolality contrast media”.
Lipid formulations of amphotericin B: Complexes of amphotericin B and phospholipids or sterols. This reduces the toxicity of amphotericin B while preserving its antifungal activity.
Low-osmolality contrast media: Contrast media with osmolality of 600–800 mOsm/L.
Low-quality evidence: Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.
Moderate-quality evidence: Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.
Multiple organ dysfunction syndrome: A syndrome of progressive organ failure, affecting one organ after another and believed to be the result of persistent or recurrent infection or inflammation.
Nephrotoxic agents: Any agent that has the potential to produce nephrotoxicity.
Nephrotoxicity: Renal parenchymal damage manifested by a decline in glomerular filtration rate, tubular dysfunction, or both.
Oliguria: Urine output of less than 5 mL/kg daily.
Very low-quality evidence: Any estimate of effect is very uncertain.

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Contributor Information

John A Kellum, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, USA.

Martine Leblanc, Maisonneuve Rosemont Hospital, University of Montreal, Montreal, Canada.

Ramesh Venkataraman, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, USA.

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BMJ Clin Evid. 2008 Sep 3;2008:2001.

Contrast media (low-osmolality)

Summary

KIDNEY INJURY Low-osmolality contrast media compared with high-osmolality contrast media: Low-osmolality contrast media are more effective at reducing nephrotoxicity, particularly in people with underlying renal failure, but are no more effective at reducing the development of acute renal failure or the need for dialysis ( moderate-quality evidence ).

Benefits

Low-osmolality contrast media versus high-osmolality contrast media:

We found one systematic review (search date 1991, 31 RCTs, 5146 people receiving intravascularly administered iodinated contrast material) comparing low-osmolality contrast media with high-osmolality contrast media. The review found no significant difference between low-osmolality and high-osmolality contrast media in the development of acute renal failure or need for dialysis (these are rare events), but there was less nephrotoxicity with low-osmolality contrast media, measured by serum creatinine. Subgroup analysis found that low-osmolality contrast media significantly reduced the proportion of people with a rise in serum creatinine of 44 µg/L or more compared with high-osmolality contrast media in people with underlying renal failure. It found no significant difference between treatments for people without prior renal failure (prior underlying renal impairment, 8 RCTs, 1418 people: OR 0.50, 95% CI 0.36 to 0.68; no underlying renal impairment, 20 RCTs, 2865 people: OR 0.75, 95% CI 0.52 to 1.10).

Low-osmolality contrast media versus iso-osmolar contrast media:

See benefits of iso-osmolar contrast media.

Harms

Low-osmolality contrast media versus high-osmolality contrast media:

The review did not report any adverse effects.

Low-osmolality contrast media versus iso-osmolar contrast media:

See harms of iso-osmolar contrast media.

Comment

None.

Substantive changes

No new evidence

BMJ Clin Evid. 2008 Sep 3;2008:2001.

Sodium chloride-based fluids

Summary

KIDNEY INJURY Intravenous sodium chloride 0.9% compared with oral fluids: Intravenous sodium chloride seems more effective at reducing acute renal failure 48 hours after catheterisation in people having elective cardiac catheterisation, but not in people with chronic renal failure undergoing various radiological procedures ( moderate-quality evidence ). Sodium chloride 0.9% compared with sodium chloride 0.45%: Sodium chloride 0.9% infusion is more effective at reducing contrast nephropathy, particulary in women, in people with diabetes, and in people receiving more than 250 mL of contrast ( high-quality evidence ). Sodium chloride 0.45% compared with restricted fluids: Preoperative intravenous sodium chloride may be more effective at reducing kidney injury in people with moderate to severe renal insufficiency undergoing cardiac surgery. Hydration may also be more effective at reducing the proportion of people requiring postoperative dialysis ( low-quality evidence ). Inpatient compared with outpatient fluid regimens: We don't know whether inpatient intravenous fluid regimens are more effective at reducing serum creatinine levels in people with renal dysfunction having cardiac cathetherisation ( very low-quality evidence ).

Benefits

Intravenous sodium chloride 0.9% versus oral fluids:

We found one RCT (53 people having elective cardiac catheterisation with a contrast agent containing iodine), which compared intravenous sodium chloride (sodium chloride 0.9% for 24 hours at a rate of 1 mL/kg/hour begun 12 hours before catheterisation) versus unrestricted oral fluids. It found that sodium chloride hydration significantly reduced acute renal failure compared with unrestricted oral fluids within 48 hours (acute renal failure defined as increase in serum creatinine by at least 44.2 µmol/L [about 0.5 mg/dL]: 1/27 [4%] with sodium chloride intravenous v 9/26 [35%] with unrestricted oral fluids; RR 0.11, 95% CI 0.015 to 0.79). A second RCT (312 people with chronic renal failure [serum creatinine 201 ± 81 µmol/L] undergoing various radiological procedures with a non-ionic, low-osmolality contrast agent) compared four groups: oral sodium chloride 0.1 g/kg of body weight/day for 2 days before the procedure (the oral saline hydration group); intravenous 0.9% sodium chloride 15 ml/kg for 6 hours before the procedure; intravenous 0.9% sodium chloride plus theophylline 5 mg/kg orally 1 hour before the procedure; intravenous 0.9% sodium chloride plus furosemide 3 mg/kg intravenously just after the procedure.Contrast nephropathy was defined as an increase in serum creatinine of 44 µmol/L (0.5 mg/dL), and occurred in 27/312 people (9%) overall. The RCT found no significant difference in contrast nephropathy among groups (5/76 [7%] with oral sodium chloride v 4/77 [5%] with intravenous sodium chloride v 6/80 [7%] with with oral sodium chloride plus theophylline v 12/79 [15%] with intravenous sodium chloride plus furosemide; P greater than 0.05).Older RCTs compared combinations of fluids (especially sodium chloride 0.45% infusion) versus other active treatments. Comparisons between outcomes in these trials and historical untreated controls are difficult to evaluate, but suggest benefit from fluids. In certain settings, such as traumatic rhabdomyolysis, early and aggressive fluid resuscitation has had dramatic benefits compared with historical controls.

Sodium chloride 0.9% versus sodium chloride 0.45%:

We found one RCT (1620 people who had coronary angiography), which compared the effects of sodium chloride 0.9% infusion versus sodium chloride 0.45% in dextrose infusion on contrast nephropathy. Infusion solution was given the morning of the procedure for people having elective surgery, or immediately before surgery in the case of emergency surgery. Contrast nephropathy was defined as an increase in serum creatinine of more than 45 µmol/L (0.5 mg/dL) within 48 hours. The RCT found that sodium chloride 0.9% infusion significantly reduced contrast nephropathy compared with sodium chloride 0.45% in dextrose infusion (0.7% with sodium chloride 0.9% infusion v 2.0% with sodium chloride 0.45% infusion; P = 0.04). Three predefined subsets of people (women, people with diabetes, and people receiving more than 250 mL of contrast) benefited the most from sodium chloride 0.9% infusion (reduction in contrast-mediated associated nephropathy; women: reduction from 5.1% to 0.6%; P = 0.01; people with diabetes: reduction from 9.8% to 5.5%; P = 0.01; people receiving more than 250 mL of contrast: reduction from 3.0% to 0%; P = 0.01).

Sodium chloride 0.45% versus restricted fluids:

We found one RCT (45 people with chronic kidney disease undergoing cardiac surgery) which compared intravenous 0.45% sodium chloride prior to surgery versus restricted fluids.People admitted for elective open heart surgery with a quantified GFR of less than 45 mL/min were assigned using a 2:1 randomisation process, to either an intravenous infusion of 0.45% sodium chloride (1 mL/kg/hour) for 12 hours before the operation (hydration group, 30 people) or to fluid restriction (control group, 15 people). It found that kidney injury (defined as at least 25% increase in serum creatinine from baseline) developed in 9/30 (30%) people with hydration compared with 8/15 (53%) people with control (statistical analysis between groups not reported). The RCT found that hydration significantly reduced the proportion of people requiring postoperative dialysis compared with control (0/30 [0%] with hydration v 4/15 [27%] with control; P less than 0.01).

Inpatient versus outpatient fluid regimens:

We found one RCT (36 people with renal dysfunction having cardiac catheterisation), which compared an inpatient intravenous fluid regimen (sodium chloride 0.45% at 75 mL/hour iv for 12 hours before and after cardiac catheterisation) with an outpatient oral fluid regimen (1 L of clear liquids over 10 hours followed by 6 hours of iv fluids starting just before contrast exposure) for the prevention of radiocontrast-induced renal dysfunction. The predefined primary end point was the maximal change in creatinine up to 48 hours after cardiac catheterisation. The RCT found no significant differences between groups in the maximal changes in serum creatinine (0.21 ± 0.38 mg/dL [18 ± 33 µmol/L] for inpatients v 0.12 ± 0.23 mg/dL [11 ± 20 µmol/L] for outpatients; P greater than 0.05; no additional data reported). However, this study may have been underpowered to rule out clinically important differences. The outpatient group also received more fluid volume.

Sodium chloride versus sodium bicarbonate:

See benefits of sodium bicarbonate-based fluids.

Harms

The volumes of fluids recommended (e.g. 1 L) and the rates of infusion (generally less than 500 mL/hour) have little potential for harm in most people.

Intravenous sodium chloride 0.9% versus oral fluids:

The RCT (53 people having non-emergency cardiac catheterisation) comparing sodium chloride versus unrestricted oral fluids found no adverse effects with sodium chloride .The second RCT reported one person had vomiting with oral sodium chloride alone, and no other adverse effects in the other three arms.

Sodium chloride 0.9% versus sodium chloride 0.45%:

The RCT found no significant differences in cardiac or peripheral vascular complications between sodium chloride 0.9% and sodium chloride 0.45% plus dextrose (cardiac complications: 5.3% with sodium chloride 0.9% v 6.4% with sodium chloride 0.45% plus dextrose; P = 0.59; peripheral vascular complications: 1.6% with sodium chloride 0.9% v 1.5% with sodium chloride 0.45% plus dextrose; P = 0.93).

Sodium chloride 0.45% versus restricted fluids:

The RCT did not report on harms.

Inpatient versus outpatient fluid regimens:

The RCT comparing inpatient versus outpatient fluid regimen gave no information on adverse effects.

Sodium chloride versus sodium bicarbonate:

See harms of sodium bicarbonate-based fluids.

Comment

Clinical guide:

Hypovolaemia is a significant risk factor for acute renal failure. The provision of adequate maintenance fluids is considered important in preventing acute renal failure. Additional fluid loading may be useful because it assures adequate intravascular volume. It also stimulates urine output, theoretically limiting renal exposure time to higher concentrations of nephrotoxins.

Substantive changes

Sodium chloride-based fluids Two RCTs added. The first RCT (312 people) compared intravenous sodum chloride 0.9% versus oral sodium chloride in people with chronic renal failure undergoing various radiological procedures,while the second RCT (45 people) compared intravenous sodium chloride 0.45% versus fluid restriction in people with chronic kidney disease undergoing cardiac surgery.Categorisation of 'sodium chloride-based fluids' unchanged (Likely to be beneficial).

BMJ Clin Evid. 2008 Sep 3;2008:2001.

Amphotericin B (lipid formulations)

Summary

We found no direct information about the effects of amphotericin B in people with acute renal failure. NOTE Lipid formulations of amphotericin B seem to cause less nephrotoxicity compared with standard formulations, but direct comparisons of long-term safety are lacking.

Benefits

We found no systematic review and no RCTs.

Harms

We found no evidence of increased adverse effects from lipid formulations of amphotericin B. However, these formulations are still nephrotoxic and should be used with care.

Comment

A phase II trial of a lipid formulations of amphotericin B (556 people) found an incidence of renal toxicity (defined by any increase in serum creatinine) of 24% (v 60–80% with standard formulation of amphotericin B). People with baseline serum creatinine in excess of 2.5 mg/dL (221 µmol/L) on standard amphotericin B showed a significant decrease in serum creatinine when transferred to the lipid formulation (P less than 0.001). One trial found that simply infusing amphotericin B in a lipid solution designed for parenteral nutrition did not result in any benefit, and may be associated with pulmonary adverse effects.

Clinical guide:

Fluid loading can be useful in reducing the risk of acute renal failure from all nephrotoxins. Considerable variability may exist between individual lipid formulations of amphotericin B, in terms of efficacy and safety, hence the current consensus is that lipid formulations of amphotericin B are less nephrotoxic than standard formulations. It is prudent not to use any form of amphotericin B in people with or at high risk of acute renal failure, if an alternated drug treatment is available.

Substantive changes

No new evidence

BMJ Clin Evid. 2008 Sep 3;2008:2001.

N-Acetylcysteine

Summary

KIDNEY INJURY Compared with control in the prevention of contrast nephropathy: N-acetylcysteine may be more effective at reducing contrast nephropathy ( low-quality evidence ). Compared with placebo in the prevention of perioperative acute renal failure: N-acetylcysteine is no more effective at reducing the incidence of acute renal failure in people having elective aortic aneurysm surgical repair, or at reducing postoperative acute renal failure in high-risk people having elective or urgent coronary artery bypass grafts ( high-quality evidence ). Compared with placebo in the prevention of acute renal failure after hypotension: N-acetylcysteine is no more effective at reducing the incidence of acute renal failure in people with new-onset (within 12 hours) hypotension and vasopressor requirement of at least 30 minutes' duration or both ( moderate-quality evidence ). MORTALITY Compared with control in the prevention of contrast nephropathy: N-acetylcysteine is more effective at reducing the rate for a composite end point of death, acute renal failure requiring temporary renal replacement therapy, or the need for mechanical ventilation, in people undergoing primary angioplasty after acute MI (high-quality evidence).

Benefits

Acetylcysteine versus control in the prevention of contrast nephropathy:

We found seven systematic reviews (search date not reported and 2003 ) and two subsequent RCTs. The reviews had slightly different inclusion and exclusion criteria. The number of RCTs included in the reviews ranged from five to 15 RCTs. All the reviews pooled data and found benefit with acetylcysteine compared with control. Many noted significant heterogeneity between included RCTs. The largest systematic review (search date 2003) considered all RCTs that compared changes in renal function between groups receiving and not receiving N-acetylcysteine. Trials in which the control group also received active treatment were excluded, although co-intervention directed at both groups was permitted. The review included both published and unpublished RCTs. Contrast nephropathy was typically defined by an increase in serum creatinine of 0.5 mg/dL (45 µmol/L) within 24–48 hours of contrast administration. The review found that N-acetylcysteine significantly reduced the incidence of contrast nephropathy compared with control (15 RCTs, 1776 people, RR 0.65, 95% CI 0.43 to 1.00; P = 0.049; see comment below). However, there was evidence of significant heterogeneity across studies (P = 0.02). A further RCT compared standard- versus double-dose N-acetylcysteine to prevent contrast nephropathy. In total, 224 people with chronic renal insufficiency (creatinine level at least 1.5 mg/dL [135 µmol/L], creatinine clearance less than 60 mL/minute, or both), scheduled to have coronary, peripheral, or both procedures, were randomly assigned to receive 0.45% saline intravenously and N-acetylcysteine at the standard dose (600 mg orally twice daily on the day before and on the day of administration of contrast), or at a double dose (1200 mg orally twice daily on the day before and on the day of administration of contrast) with non-ionic, low-osmolality contrast dye administration. The RCT found that the double dose of N-acetylcysteine significantly reduced the proportion of people with an increase of at least 0.5 mg/dL of creatinine concentration 48 hours after the procedure compared with the standard dose (4/114 [4%] with double dose v 12/109 [11%] with standard dose; OR 0.29, 95% CI 0.09 to 0.94). The RCT found that people who received a higher volume of contrast media (at least 140 ml) benefited most from the higher dose. In a more recent large, single-centre RCT, 354 people having primary angioplasty after acute MI were randomised to three groups: standard dose N-acetylcysteine (600 mg iv bolus before primary angioplasty and 600 mg orally twice daily for the 48 hours after angioplasty; 116 people), double-dose N-acetylcysteine (1200 mg iv bolus and 1200 mg orally twice daily for the 48 hours after intervention; 119 people), and placebo (119 people). The incidence of contrast nephropathy (increase in serum creatinine of at least 25% from baseline) was 33% in control group, 15% in the standard N-acetylcysteine group, and 8% in the double-dose N-acetylcysteine group (P less than 0.001). The rate for the composite end point of death, acute renal failure requiring temporary renal replacement therapy, or the need for mechanical ventilation was 21 (18%) in the control group, eight (7%) in the standard N-acetylcysteine group, and six (5%) in the double-dose N-acetylcysteine group (P = 0.002). The subsequent RCTs (364 people,61 peopleundergoing surgery) found a similar effectiveness with N-acetylcysteine for the prevention of contrast nephropathy compared with the systematic reviews.

Acetylcysteine versus placebo in the prevention of perioperative acute renal failure:

One small RCT randomised 42 people having elective aortic aneurysm surgery to oral N-acetylcysteine (1200 mg twice daily the day before surgery and 600 mg twice daily after) or placebo. There was no significant difference in the incidence of acute renal failure (defined as an increase in serum creatinine of at least 25% from baseline) between the groups (50% with N-acetylcysteine v 27% with control; P = 0.16). Another RCT randomised 295 high-risk people having elective or urgent coronary artery bypass graft to intravenous N-acetylcysteine (2 intraoperative and 2 postoperative 600 mg doses) or placebo over 24 hours. There was no difference in the proportion of people with postoperative acute renal failure (29.7% with N-acetylcysteine v 29.0% with placebo; P = 0.89; RR 1.03, 95% CI 0.72 to 1.46).

No new evidence

BMJ Clin Evid. 2008 Sep 3;2008:2001.

Sodium bicarbonate-based fluids

Summary

KIDNEY INJURY Compared with sodium chloride: Sodium bicarbonate administered before and after contrast exposure may be more effective at reducing contrast-induced nephropathy ( low-quality evidence ).

Benefits

Sodium bicarbonate versus sodium chloride:

We found one single-centre RCT (119 people having contrast examination with stable serum creatinine levels of at least 1.1 mg/dL [97.2 µmol/L]) comparing a 154 mmol/L infusion of either sodium chloride or sodium bicarbonate, both in 5% dextrose solution. People received either sodium chloride or sodium bicarbonate solution as a bolus of 3 mL/kg an hour for 1 hour before iopamidol contrast administration, followed by an infusion of 1 mL/kg an hour for 6 hours after the procedure. Serum creatinine levels were measured at baseline and at 1 and 2 days after contrast administration. Contrast-induced nephropathy was defined as an increase of at least 25% in serum creatinine within 2 days of contrast. The RCT found that sodium bicarbonate significantly reduced contrast-induced nephropathy compared with sodium chloride (1/60 [1.7%] of people with sodium bicarbonate v 8/59 [13.6%] of people with sodium chloride; mean difference 11.9%, 95% CI 2.6% to 21.2%). Initially, 137 people had been randomised in the RCT, but 18 (13%, 9 in each group) people did not complete the study and were not included in the analysis.

Harms

Sodium bicarbonate versus sodium chloride:

The RCT gave no information on adverse effects.

Comment

The study was limited in that it was underpowered, had significant withdrawal rates in both groups, and did not perform a true intention-to-treat analysis. See comment on sodium chloride-based fluids for clinical guide.

Substantive changes

No new evidence

BMJ Clin Evid. 2008 Sep 3;2008:2001.

Fenoldopam

Summary

KIDNEY INJURY Compared with placebo: Fenoldopam is no more effective at preventing acute renal failure, or at reducing the need for dialysis in people having invasive cardiovascular procedures, in people with sepsis or in critically ill people with early acute tubular necrosis ( high-quality evidence ). Compared with dopamine: We don't know whether fenoldopam is more effective at reducing the incidence of acute renal failure ( very low-quality evidence ). Compared with other treatments or control: We don’t know whether fenoldopam is more effective at reducing the risk of acute kidney injury or the need for renal replacement therapy in people in intensive care units, or in people having major surgery (very low-quality evidence). MORTALITY Compared with placebo: Fenoldopam is no more effective at reducing mortality in people having invasive cardiovascular procedures, in people with sepsis, or in critically ill people with early acute tubular necrosis (high-quality evidence). Compared with other treatments or control: We don’t know whether fenoldopam is more effective at reducing in-hospital death in people in intensive care units, or in people having major surgery (very low-quality evidence). NOTE Fenoldopam may cause hypotension.

Benefits

Fenoldopam versus placebo:

We found seven RCTs. Four of the RCTs found some improvement in renal perfusion and creatinine clearance, but had weak methods; either they were underpowered, had differences between groups at baseline, did not compare interventions between groups directly, or did not assess valid clinical outcomes. The fifth and largest RCT (double blind, multi-centre, 315 people with creatinine clearance below 60 mL/minute having invasive cardiovascular procedures) compared intravenous fenoldopam mesylate (0.05 µg/kg/minute titrated to 0.10 µg/kg/minute) versus placebo. All people were hydrated, and treatment started 1 hour before angiography and continued for 12 hours. Contrast nephropathy was defined as an increase of 25% or more in serum creatinine level within 96 hours after the procedure. The RCT found no significant difference between fenoldopam and placebo for contrast nephropathy, 30-day mortality, dialysis, or readmission to hospital (contrast nephropathy: 34% with fenoldopam v 30% with placebo; RR 1.11, 95% CI 0.79 to 1.57; P = 0.61; 30-day mortality: 2.0% with fenoldopam v 3.8% with placebo; P = 0.50; dialysis: 2.6% with fenoldopam v 1.9% with placebo; P = 0.72; readmission to hospital: 17.6% with fenoldopam v 19.9% with placebo; P = 0.66).In a recent RCT, 300 septic people with baseline serum creatinine concentrations less than 150 µmol/L (about 1.7 mg/dL) were randomised to continuous infusion of either fenoldopam (150 people; 0.09 µg/kg/minute) or placebo (150 people). The primary outcome measure was the incidence of acute renal failure (defined as a serum creatinine concentration increase to greater than 150 µmol/L [approximately below 1.7 mg/dL]) during drug infusion. Although the incidence of acute renal failure was significantly lower in the fenoldopam group compared with the control group (29 people with fenoldopam v 51 people with control; P = 0.006), there were no differences between the groups in the incidence of severe acute renal failure or need for dialysis, or in mean survival time (creatinine greater than 300 µmol/L [about 3.3 mg/dL]; 10 with fenoldopam v 21 with control; P = 0.056; mean survival time: 47 ± 2 days with fenoldopam v 42.1 ± 2.2 days with control; P = 0.068). Another RCT randomised 155 people with early acute tubular necrosis (serum creatinine level increased to 50% greater than admission levels within 24 hours and mean arterial pressure greater than 70 mm Hg) to fenoldopam (80 people; 0.05 µg/kg/minute titrated to 0.2 µg/kg/minute) or placebo (75 people) for 72 hours. There was no significant difference between the groups in the incidence of dialysis or 21-day mortality (dialysis: 16% with fenoldopam v 25% with placebo; P = 0.163; 21-day mortality: 14% with fenoldopam v 25% with placebo; P = 0.068).

Fenoldopam versus dopamine:

Two RCTs compared fenoldopam versus low-dose dopamine in the prevention of acute renal failure. The first RCT randomised 100 critically ill adults with early renal dysfunction (intensive care unit stay less than 1 week; haemodynamic stability; and urine output 0.5 mL/kg or less over a 6-hour period, or serum creatinine concentration 1.5–3.5 mg/dL [135–315 µmol/L], or both) to dopamine (2 µg/kg/minute) or fenoldopam mesylate (0.1 µg/kg/minute) continuous infusion for 4 days. Systemic haemodynamic and renal function variables were recorded daily. The RCT found no differences between groups in heart rate, or in systolic, diastolic, or mean arterial pressure. Fenoldopam produced a more significant reduction in creatinine concentration compared with dopamine after 2, 3, and 4 days of infusion (change from baseline; at day 2: –0.32 mg/dL [–29 µmol/L] with fenoldopam v –0.03 mg/dL [–3 µmol/L] with dopamine; P = 0.047; at day 3: –0.45 mg/dL [–41 µmol/L] with fenoldopam v –0.09 mg/dL [–8 µmol/L] with dopamine; P = 0.047; at day 4: –0.041 mg/dL [–4 µmol/L] with fenoldopam v –0.09 mg/dL [–8 µmol/L] with dopamine; P = 0.02). The RCT did not evaluate clinically relevant end points such as need for dialysis, survival, or renal recovery. In the second RCT, 80 high-risk people having cardiac surgery were randomised to either fenoldopam (0.05 µg/kg/minute) or dopamine (2.5 µg/kg/minute) for a 24-hour period after the induction of anaesthesia. The RCT found no significant difference in incidence of acute renal failure between groups (17/40 [42%] with fenoldopam v 16/40 [40%] with dopamine; P = 0.9).

Renal replacement therapy (prophylactic haemofiltration/dialysis) One single-centre RCT (92 people) added comparing pre- and post-haemofiltration, post-haemofiltration, and sodium chloride, in people with baseline chronic renal dysfunction having coronary interventions with contrast.Benefits and harms data enhanced, categorisation of 'renal replacement therapy (prophylactic haemofiltration/dialysis)' changed from Unlikely to be beneficial to Unknown effectiveness.

BMJ Clin Evid. 2008 Sep 3;2008:2001.

Theophylline or aminophylline

Summary

KIDNEY INJURY Compared with control in radiocontrast-induced nephropathy: Theophylline or aminophylline may be no more effective at preventing radiocontrast-induced nephropathy in people with adequate hydration, and may attenuate the degree of increase in serum creatinine after radiocontrast administration ( very low-quality evidence ). Compared with sodium chloride 0.9% after CABG: Theophylline is no more effective at preventing renal impairment after elective CABG ( moderate-quality evidence ).

Benefits

Theophylline or aminophylline versus control in radiocontrast-induced nephropathy:

We found one systematic review (search date 2003) which included seven RCTs in which theophylline or aminophylline were used in hospitalised people receiving radiocontrast media. RCTs were included if they reported serum creatinine or creatinine clearance within 48 hours after radiocontrast exposure. However, in two RCTs, baseline serum creatinine was estimated using normal values for age, sex, and weight. The review pooled results for RCTs using theophylline or aminophylline. It found that theophylline or aminophylline significantly attenuated the increase in serum creatinine after contrast administration compared with control (7 RCTs, 480 people, difference in mean change of serum creatinine: 11.5 µmol/L [0.13 mg/dL], 95% CI 5.3 µmol/L [0.06 mg/dL] to 19.4 µmol/L [0.22 mg/dL]). The clinical effect seen from the pooled data is very small (less than 15% change from baseline), and is of unclear clinical significance. No clinically significant effects were reported. In addition, the heterogeneity of studies was not reported. In many of the RCTs included in the review, the hydration status of people receiving the radiocontrast agent was unclear. In one included RCT (80 people with pre-existent mild to moderate renal insufficiency) the GFR was preserved with hydration alone. It found that serum creatinine concentration and creatinine clearance did not change significantly with additional theophylline or placebo. Two (6%) people in the theophylline group and one (3%) in the placebo group developed acute renal failure, defined as an increase in serum creatinine of at least 0.5 mg/dL (44 µmol/L).

Theophylline versus sodium chloride 0.9% after CABG:

We found one RCT (56 people with normal renal function), which compared theophylline (a bolus of 4 mg/kg and a subsequent continuous infusion of 0.25 mg/kg/hour for up to 96 hours) versus sodium chloride 0.9% for prevention of renal impairment after elective coronary artery bypass surgery. It found no significant difference between theophylline and sodium chloride in rates of renal impairment, but the RCT may have been underpowered to detect clinically important differences (renal impairment, defined as an increase in serum creatinine of at least 0.4 mg/dL (35 µmol/L) from the baseline at day 5 after surgery: 5/28 [18%] with theophylline v 4/28 [14%] with sodium chloride; P greater than 0.05).

Harms

Theophylline or aminophylline versus control in radiocontrast-induced nephropathy:

Theophylline has a narrow therapeutic index and known adverse effects (see harms of theophyllines in review on COPD). The systematic review reported one included RCT (48 people) which had used a low dose of theophylline and had found no adverse effects in study groups. It reported no other data on adverse effects.

Theophylline versus sodium chloride 0.9% after CABG:

The RCT found no difference between the placebo and theophylline groups in the number of people whose study medication was stopped owing to presumed adverse effects. Heart rate and systolic and diastolic blood pressures were similar between the groups.

Comment

None.

Substantive changes

No new evidence

BMJ Clin Evid. 2008 Sep 3;2008:2001.

Calcium channel blockers

Summary

KIDNEY INJURY Compared with placebo in people receiving live or cadaveric kidney transplant: The calcium channel blocker isradipine is more effective at improving median serum creatinine levels at 3–12 months, but is no more effective at preventing early allograft dysfunction ( moderate-quality evidence ). Compared with no calcium channel blockers in people receiving cadaveric kidney transplant: Calcium channel blockers given in the perioperative period may be more effective at reducing post-transplant acute tubular necrosis, but not graft loss ( very low-quality evidence ). MORTALITY C ompared with no calcium channel blockers in people receiving cadaveric kidney transplant: Calcium channel blockers given in the perioperative period may be no more effective at reducing mortality (very low-quality evidence). NOTE We found no direct information assessing the effects of calcium channel blockers in preventing other forms of acute renal failure. Calcium channel blockers are associated with hypotension and bradycardia.

Benefits

Calcium channel blockers versus placebo in people receiving live or cadaveric kidney transplant:

We found one RCT, which compared isradipine versus placebo after living and cadaveric renal transplants. The RCT (210 people) found that isradipine significantly improved median serum creatinine levels at 3 and 12 months compared with placebo (3 months: 185 µmol/L [2.0 mg/dL] with isradipine v 220 µmol/L [2.4 mg/dL] with placebo; P = 0.002; 12 months: 141 µmol/L [1.4 mg/dL] with isradipine v 158 µmol/L [1.6 mg/dL] with placebo; P = 0.021). However, it found no significant difference in the incidence of early allograft dysfunction (34/98 [35%] with isradipine v 44/112 [39%] with placebo; RR 1.13, 95% CI 0.79 to 1.62) or duration (9.1 days with isradipine v 9.3 days with placebo; P value not reported).

Calcium channel blockers versus no calcium channel blockers in people receiving cadaveric kidney transplant:

We found one systematic review (search date 2005, 10 RCTs, 575 people), which compared calcium channel blockers versus no calcium channel blocker after cadaveric kidney transplantation. It included heterogeneous RCTs, in which any calcium channel blocker was given by any route before or immediately after transplant, to recipient or donor, or added to the perfusate (see comments below). Duration of follow-up, where stated, ranged from 4 weeks to 4 years. None of the included studies mentioned loses to follow-up. The review found that calcium channel blockers in the peritransplant period significantly decreased acute tubular necrosis (7 RCTs, 349 people: RR 0.57, 95% CI 0.40 to 0.82). However, it found no significant difference between treatments for graft loss, mortality, or requirement for haemodialysis postoperatively (graft loss: 6 RCTs, 347 people: RR 0.93, 95% CI 0.44 to 1.97; mortality: 5 RCTs, 284 people: RR 0.86, 95% CI: 0.16 to 4.66; postoperative haemodialysis: 4 RCTs: quantitative results not reported).

KIDNEY INJURY Compared with placebo: Atrial natriuretic peptide is no more effective at reducing dialysis-free survival in oliguric and non-oliguric people with acute renal failure, and ularitide (urodilatin) seems no more effective at reducing the need for dialysis ( moderate-quality evidence ).

Benefits

We found no systematic review, but found three RCTs. One RCT (504 people with acute tubular necrosis) found no significant difference in dialysis-free survival with atrial natriuretic peptide compared with placebo in people with acute renal failure (43% with anaritide v 47% with placebo; P = 0.35). Preplanned subgroup analysis suggested a possible benefit to people with oliguria, but lower survival rates in non-oliguric people. A second RCT (220 people) in people with oliguric acute renal failure found no improvement in dialysis-free survival with a 24-hour infusion of atrial natriuretic peptide compared with placebo. A third RCT compared ularitide (urodilatin, a natriuretic peptide with fewer systemic haemodynamic effects) in a dose-finding (ularitide 5, 20, 40, or 80 ng/kg/minute), placebo-controlled RCT (176 people). Ularitide did not significantly reduce the requirement for dialysis (people treated with dialysis: 35% with ularitide 5 ng/kg/minute v 36% with ularitide 20 ng/kg/minute v 28% with ularitide 40 ng/kg/minute v 41% with ularitide 80 ng/kg/minute v 36% with placebo; P reported as not significant, CI not reported).

Harms

One RCT found that natriuretic peptide caused significant hypotension compared with placebo (95% with natriuretic peptide v 55% with placebo; P less than 0.01). Also, atrial natriuretic peptide may be associated with a worse outcome in people with non-oliguric renal failure (dialysis-free survival in 378 non-oliguric people: 48% with anaritide v 59% with placebo; RR 0.79, 95% CI 0.64 to 0.97; P = 0.03). See harms of natriuretic peptides in high-risk people.

Comment

We found no evidence of significant improvement of acute renal failure with atrial natriuretic peptide.

Substantive changes

No new evidence

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PERMALINK

Acute renal failure

John A Kellum

Martine Leblanc

Ramesh Venkataraman

Roles

Abstract

Introduction

Methods and outcomes

Results

Conclusions

Key Points

About this condition

Definition

Incidence/ Prevalence

Aetiology/ Risk factors

Table 1.

Prognosis

Aims of intervention

Outcomes

Methods

Table.

Glossary

Disclaimer

Contributor Information

References

Contrast media (low-osmolality)

Summary

Benefits

Low-osmolality contrast media versus high-osmolality contrast media:

Low-osmolality contrast media versus iso-osmolar contrast media:

Harms

Low-osmolality contrast media versus high-osmolality contrast media:

Low-osmolality contrast media versus iso-osmolar contrast media:

Comment

Substantive changes

Sodium chloride-based fluids

Summary

Benefits

Intravenous sodium chloride 0.9% versus oral fluids:

Sodium chloride 0.9% versus sodium chloride 0.45%:

Sodium chloride 0.45% versus restricted fluids:

Inpatient versus outpatient fluid regimens:

Sodium chloride versus sodium bicarbonate:

Harms

Intravenous sodium chloride 0.9% versus oral fluids:

Sodium chloride 0.9% versus sodium chloride 0.45%:

Sodium chloride 0.45% versus restricted fluids:

Inpatient versus outpatient fluid regimens:

Sodium chloride versus sodium bicarbonate:

Comment

Clinical guide:

Substantive changes

Amphotericin B (lipid formulations)

Summary

Benefits

Harms

Comment

Clinical guide:

Substantive changes

N-Acetylcysteine

Summary

Benefits

Acetylcysteine versus control in the prevention of contrast nephropathy:

Acetylcysteine versus placebo in the prevention of perioperative acute renal failure:

Acetylcysteine versus placebo in the prevention of acute renal failure after hypotension:

Harms

Acetylcysteine versus control in the prevention of contrast nephropathy:

Acetylcysteine versus placebo in the prevention of perioperative acute renal failure:

Acetylcysteine versus placebo in the prevention of acute renal failure after hypotension:

Comment

Substantive changes

Contrast media (iso-osmolar)

Summary

Benefits

Harms

Comment

Substantive changes

Aminoglycosides (single dose)

Summary