Systematic review: The use of diuretics and dopamine in acute renal failure: a systematic review of the evidence

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Abstract

Objective

To evaluate the impact of diuretics and dopamine for both the prevention and treatment of renal dysfunction in the acute care setting.

Study identification and selection

Studies were identified via MEDLINE, and through bibliographies of primary and review articles. Articles were then screened by the author for studies addressing the use of diuretics or dopamine in the prevention and/or treatment of renal dysfunction.

Data abstraction and literature appraisal

From individual studies, data were abstracted regarding design features, population, intervention and outcomes. Studies were graded by levels according to their design.

Results

A total of 10 studies using diuretics and 30 involving dopamine were identified. Level I evidence exists against the use of diuretics for radiocontrast-induced acute tubular necrosis, and loop diuretics given after vascular surgery. There is level II evidence that diuretics do not improve outcome in patients with established acute renal failure. Level II evidence also exists against the use of dopamine in the prevention of acute tubular necrosis in multiple subsets of patients.

Conclusions

Routine use of diuretics or dopamine for the prevention of acute renal failure cannot be justified on the basis of available evidence.

Related collections

Most cited references 56

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Effects of saline, mannitol, and furosemide to prevent acute decreases in renal function induced by radiocontrast agents.

Keith R. Solomon, Raquel Raick P. da Silva, Daniela S P Silva … (1994)

Injections of radiocontrast agents are a frequent cause of acute decreases in renal function, occurring most often in patients with chronic renal insufficiency and diabetes mellitus. We prospectively studied 78 patients with chronic renal insufficiency (mean [+/- SD] serum creatinine concentration, 2.1 +/- 0.6 mg per deciliter [186 +/- 53 mumol per liter]) who underwent cardiac angiography. The patients were randomly assigned to receive 0.45 percent saline alone for 12 hours before and 12 hours after angiography, saline plus mannitol, or saline plus furosemide. The mannitol and furosemide were given just before angiography. Serum creatinine was measured before and for 48 hours after angiography, and urine was collected for 24 hours after angiography. An acute radiocontrast-induced decrease in renal function was defined as an increase in the base-line serum creatinine concentration of at least 0.5 mg per deciliter (44 mumol per liter) within 48 hours after the injection of radiocontrast agents. Twenty of the 78 patients (26 percent) had an increase in the serum creatinine concentration of at least 0.5 mg per deciliter after angiography. Among the 28 patients in the saline group, 3 (11 percent) had such an increase in serum creatinine, as compared with 7 of 25 in the mannitol group (28 percent) and 10 of 25 in the furosemide group (40 percent) (P = 0.05). The mean increase in serum creatinine 48 hours after angiography was significantly greater in the furosemide group (P = 0.01) than in the saline group. In patients with chronic renal insufficiency who are undergoing cardiac angiography, hydration with 0.45 percent saline provides better protection against acute decreases in renal function induced by radiocontrast agents than does hydration with 0.45 percent saline plus mannitol or furosemide.

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Early renal medullary hypoxic injury from radiocontrast and indomethacin.

Samuel Heyman, Mayer Brezis, Franklin H. Epstein … (1991)

We evaluated the acute changes in cortical and outer medullary oxygen tension and the alterations in renal function and morphology within the first 90 minutes after the administration of indomethacin and iothalamate to anesthetized Sprague-Dawley rats. Both agents were found to produce marked and protracted outer medullary hypoxia averaging 12 +/- 4 and 9 +/- 2 mm Hg, respectively (mean +/- SE). Given together to salt depleted uninephrectomized rats they produced an early hypoxic injury localized selectively in the outer medulla. This lesion progressed from 3 +/- 1% of medullary thick ascending limbs (mTALs) at 15 minutes to 22 +/- 7% at 24 hours. Condensed "dark" cells were observed at 15 minutes, probably representing a type of early injury. Residual red cell mass, quantified in the outer medullary vasculature of perfusion-fixed kidneys and presumably reflecting stasis, was substantially increased in iothalamate treated rats. Red cell mass in the interbundle zone correlated with mTAL necrosis. Taken together, these results show an early period of medullary hypoxia, accompanied by a selective injury to mTALs in the central interbundle zone with apparent stasis. These findings contrast sharply with the ischemia-reflow pattern of renal damage and emphasize the important role of medullary hypoxia in the genesis of acute renal failure in this model.