Correspondence

Acute Oliguria

N Engl J Med 1998; 339:201-202July 16, 1998

Article

To the Editor:

Klahr and Miller reviewed the fundamentals of acute oliguria (March 5 issue)1 and noted that “the absence of urinary output suggests that the patient has obstructive uropathy, renal cortical necrosis, or necrotizing glomerular disease.” Once complete urinary tract obstruction has been ruled out, we agree that renal cortical necrosis and necrotizing glomerular disease should be considered in the differential diagnosis of anuria, but we would add complete renal vascular occlusion and acute tubular necrosis to the list of medical causes. Although anuria not infrequently complicates renal cortical necrosis, necrotizing glomerular disease, and renal vascular occlusion, these diseases are such rare causes of acute renal failure that they account for only a small fraction of all cases of anuria. The incidence of anuria in patients with acute tubular necrosis is low,2 but because this disorder is such a common cause of acute renal failure, patients presenting with anuria are far more likely to have acute tubular necrosis than the other nonobstructive causes. In fact, one report found that in the setting of acute tubular necrosis resulting from heat stroke, four of eight patients had anuria.3

David A. Goodkin, M.D.
227 W. Janss Rd., Thousand Oaks, CA 91360

Robert G. Narins, M.D.
Henry Ford Hospital, Detroit, MI 48202

3 References

1
Klahr S, Miller SB. Acute oliguria. N Engl J Med 1998;338:671-675
Full Text | Web of Science | Medline

2
Swann RC, Merrill JP. The clinical course of acute renal failure. Medicine (Baltimore) 1953;32:215-292
CrossRef | Web of Science | Medline

3
Schrier RW, Henderson HS, Tisher CC, Tannen RL. Nephropathy associated with heat stress and exercise. Ann Intern Med 1967;67:356-376
Web of Science | Medline

To the Editor:

I take issue with the statement that “potentially nephrotoxic substances should be avoided in patients with prerenal oliguria; these include . . . general anesthetics.” With the exception of the obsolete inhaled anesthetic methoxyflurane and possibly the rarely used inhaled anesthetic enflurane, there is no documented evidence either in studies of animals or in outcome studies that general anesthetics are nephrotoxic.1,2 Numerous studies have reported that the effect of various inhaled anesthetics on glomerular filtration and renal blood flow can be depressive, but these effects are almost always related to the cardiovascular effects of the anesthetics rather than to a direct nephrotoxic effect. The use of general anesthetics should be avoided in any patient in whom it is not necessary for the performance of important diagnostic studies or surgery. However, a blanket indictment of general anesthetics in patients with acute renal failure is misleading.

Robert G. Merin, M.D.
Medical College of Georgia, Augusta, GA 30912-2700

2 References

1
Merin RG. Preservation of renal function in the perioperative period. Recent Adv Anaesth Analg 1994;18:145-158

2
Isner RJ. The kidneys and anaesthesia: renal structure and function, renal effects of anaesthetics. In: Prys-Roberts C, Brown BR Jr, eds. International practice of anaesthesia. Vol. 1. Successor to General Anaesthesia. Oxford, England: Butterworth–Heinemann, 1996:1/76/1–1/76/9.

To the Editor:

Klahr and Miller state that doxorubicin should be avoided or the dose adjusted “in proportion to the decrease in renal function.” This is seriously misleading, since doxorubicin is neither excreted nor metabolized primarily by the kidney, and dose reduction is not necessary in cases of impaired renal function.1 In hematologic practice, doxorubicin is a valuable drug in the treatment of patients with myeloma, many of whom have impaired renal function.

R.G. Dalton, M.R.C.P.
Jackie Pope, B.Sc.
Cheltenham General Hospital, Cheltenham GL53 7AN, United Kingdom

1 References

1
Bennett WM, Aronoff GR, Golper TA, Morrison G, Brater DC, Singer I. Drug prescribing in renal failure: dosing guidelines for adults. 3rd ed. Philadelphia: American College of Physicians, 1994.

Author/Editor Response

The authors reply:

To the Editor: We agree with Dr. Merin that general anesthetics are not directly nephrotoxic. However, in patients with prerenal oliguria, any agent or procedure that further compromises renal perfusion (often because of a cardiovascular effect) may precipitate the development of acute tubular necrosis.

In response to the letter of Dalton and Pope: we are aware that doxorubicin is mainly eliminated in the bile and excreted in the feces. We also found, however, that some of the major formulary information systems in the United States (Micromedex Formulary, Micromedex, Englewood, Colo.; and FormuLex, Lexi-Comp, Hudson, Ohio) still recommend dose adjustment for doxorubicin in patients with acute renal failure. When we checked the sources used by the companies, we found that in the case of doxorubicin, they are using data that are out of date. Thus, we agree that reduction of the dose of doxorubicin is not necessary in patients with impaired renal function.

Complete anuria (no urine output) is extremely unusual in the setting of acute tubular necrosis. In this setting, urinary tract obstruction is by far the most important cause of anuria. In the recently reported study of anaritide in acute tubular necrosis,1 which involved more than 500 patients, none presented with complete anuria (Allgren RL: personal communication). This, of course, may represent a study bias or indicate that complete anuria is uncommon in patients with acute tubular necrosis.

Saulo Klahr, M.D.
Steven B. Miller, M.D.
Washington University School of Medicine, St. Louis, MO 63110

1 References