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Five patients are described in whom only gentamicin sulfate appeared responsible for acute renal failure. Subjects received 1.2 to 2.88 gm over 12 to 18 days. All were over 45 years of age, and premorbid kidney abnormalities may have enhanced susceptibility to toxic effects of the drug. Renal failure appeared 8 to 17 days after beginning gentamicin therapy and was characterized by creatinine clearances 4 to 10 ml/min, urine to plasma creatinine ratios < 20, urinary sodium concentrations 16 to 60 mEq/ liter, proteinuria, and cylindruria. Oliguria was not observed and this feature may impair recognition of kidney damage. Clinical recovery required an average of 42 days and was complete in four of five patients. Gentamicin alone may be nephrotoxic and should be given with particular caution to the elderly and those with even mild kidney abnormalities.(Arch Intern Med 136:1101-1104, 1976)

Poisoning due to accidental or intentional ingestion of large quantities of propoxyphene hydrochloride (Darvon) has been reported 15 times.1 Many types of intoxications have been treated by dialysis, but severe propoxyphene poisoning is rare and therapeutic removal of this drug has not been studied in detail. This communication presents data on the value of osmotic diuresis, peritoneal, and hemodialysis for the therapy of propoxyphene poisoning. PATIENT SUMMARY A 17-year-old white girl was brought to the Georgetown University Hospital at 8:30 AM on May 1, 1967. She was apneic and without detectable blood pressure. She had left for school earlier in the morning and told a friend that she was going to die. It was alleged that she ingested an overdose of "pain pills" at 7:30 AM. In the emergency ward she was noted to be without vital signs; her electrocardiogram revealed an idioventricular rhythm with a ventricular rate of

A new technique for the management of intractable ascites in uremic patients, involving extracorporeal dialysis of ascitic fluid, may be applicable also for the management of ascites in the absence of renal failure.(Arch Intern Med 1981;141:1550-1551)

Streptococcal infection frequently leads to proliferative glomerulonephritis, and, on rare occasions, to renal cortical necrosis. We report a case in which post-streptococcal proliferative glomerulonephritis and renal cortical necrosis occurred concomitantly.(Arch Intern Med 137:1196-1197, 1977)

IN REPLY.— As noted by Dr Sweet, ampicillin has been implicated as a cause of acute interstitial nephritis. However, all reported patients with ampicillin-related nephropathy have exhibited one or more allergic manifestations (fever, eosinophilia, or skin rash).1-3 As stated in our report, these features were absent in all our patients.4Even though the term "nephrotubular necrosis secondary to a toxic exposure, perhaps we should have been more precise and stated that ampicillin has not been reported to cause renal tubular cell damage.Contrary to Dr Sweet's impression, there were no similarities between Beaufils et al's5 patients and ours. In fact, our patients' recovery of renal function did not parallel treatment of the infection, but rather kidney malfunction appeared after resolution of infection and during or after exposure to gentamicin.Furthermore, the patients with proliferative glomerulonephritis and visceral abscesses were described as critically ill with high fever and

IN REPLY.— Dr Sporn's well-documented recent observation of renal cortical necrosis following streptococcal infection lends support to our impression both from the older literature and from our case that such an association should be recognized. A causal connection also seems implied by the apparent absence in Dr Sporn's patient of any other known cause of cortical necrosis. Evidently the differentiation of poststreptococcal glomerulonephritis from cortical necrosis or from combined cortical necrosis with proliferative nephritis has prognostic importance and thus requires our consideration in appropriate circumstances.