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Amphotericin B (2.5 mg/kg, administered intravenously) increased vascular resistance (renal more than pulmonary more than systemic) and decreased glomerular filtration and urine flow 94% in 16 anesthetized female mongrel dogs. Dopamine decreased renal vascular resistance 31% in 14 dogs; when amphotericin B was given with dopamine, there was partial antagonism of amphotericin B-induced renal vasoconstriction. Saralasin partially antagonized amphotericin B-induced renal vasoconstriction in seven dogs. When amphotericin B was given during combined infusion of dopamine and saralasin in eight dogs, renal blood flow remained at initial control levels, urine flow increased above initial levels, and glomerular filtration decreased only 21% from initial values. Amphotericin B increased renal vascular resistance 296% when given alone but only 41% in dogs during injection of both dopamine and saralasin (P = 0.002). The antagonism of amphotericin B-induced renal effects by the combination of dopamine and saralasin was significant and specific for the renal vascular bed.

We describe the clinical course of a patient who developed anuria following prophylactic methicillin administration. To the best of our knowledge, this is the first report of prolonged anuria following administration of this drug. The patient's nephropathy developed as a result of routine perioperative antibiotic prophylaxis for cardiac surgery and resulted in a two-week period of complete anuria. Following discontinuation of methicillin the patient was supported throughout this period by intermittent hemodialysis and eventually had an excellent recovery of renal function without concurrent use of corticosteroids. Thus methicillin may occasionally cause severe and prolonged anuric renal failure, but maximal supportive measures, including dialysis when necessary, should nonetheless be used, since the renal failure is reversible once the antibiotic is discontinued.

The use of angiotensin-converting enzyme inhibitors as antihypertensives has increased rapidly since the introduction of captopril in 1981. Seven cases of neonatal renal failure have been reported in patients with exposure to angiotensin-converting enzyme inhibitors that continued to the time of delivery. Two cases resulted in death of the newborn; the other five patients recovered after peritoneal dialysis. Because the relative frequency of normal outcomes is unknown, these data are insufficient for incidence-rate estimates or risk/benefit analyses. However, given the potential neonatal morbidity and mortality associated with late-pregnancy exposure to angiotensin-converting enzyme inhibitors, alternative therapies in the third trimester should be given consideration. If these drugs must be used in this context, the clinician should be prepared to deal with renal failure and hypotension in the newborn. The Food and Drug Administration invites reports of adverse pregnancy outcomes associated with such exposure.

15 cases of acute renal failure following ingestion of bichloride of mercury were studied at Pahlavi medical center, university of Teheran, between 1962 and 1972. All the patients admitted suicide attempts. All had oliguria and uremia except one, in whom oliguria was moderate without azotemia. There were four deaths among the 15 patients, three of them with gastrointestinal hemorrhage; secondery infection and the prolonged acute uremia probably were the cause of death in another one. Early administration of B. A. L. and early frequent hemodialysis helps to support the patient through the period of oliguria and possibly to remove the mercury B.A.L. Complex. Although the mortality of mercury intoxication has decreased, gastrointestinal hemorrhages and secondery infections make its prognosis still unfavorable.

Severe ovarian hyperstimulation developed in a young woman during ovulation induction with human menopausal and chorionic gonadotropins. This was complicated by acute functional renal insufficiency with vascular overfilling and incipient pulmonary edema, possibly caused by indomethacine and fluid treatment. The pathogenetic mechanisms involved are discussed.

Amphotericin B causes reversible concentration-dependent loss of intracellular potassium in vitro and hyperkalemic ventricular arrhythmias in dogs. Hyperkalemic ventricular arrhythmias associated with amphotericin B infusion have not been well documented in humans. Ventricular fibrillation with progressive hyperkalemia (up to 8 to 8.4 meq/liter) occurred twice in an anuric patient during rapid infusion of high-dose amphotericin B (1.4 mg/kg over 45 min). The peak amphotericin B concentration in serum at the end of infusion was 6.7 micrograms/ml. Prolonged infusion (3 h) and concurrent hemodialysis each prevented the development of hyperkalemia and ventricular arrhythmia. In two anuric patients receiving 4-h infusions of amphotericin B during dialysis (0.7 and 1.0 mg/kg), peak amphotericin B concentrations in serum were lower, 1.6 +/- 0.1 and 2.7 +/- 0.7 micrograms/ml, respectively; serum potassium levels were maintained in the normal range; and venous access for outpatient therapy was convenient. Peak concentrations of amphotericin B in serum were also lower (1.7 +/- 0.7 micrograms/ml) in eight patients with normal renal function who received lower doses (0.7 +/- 0.2 mg/kg) over 45 min; there were only slight increases in the serum potassium level (from 3.9 +/- 0.9 to 4.4 +/- 0.6 meq/liter, P less than 0.05). We recommend that rapid infusion of amphotericin B not be used in patients with impaired potassium excretion unless accompanied by hemodialysis and careful potassium monitoring.

The effect of sodium orthovanadate (vanadate) on kidney function and hemodynamics was tested in chloralose anesthetized, fasting cats. Vanadate given i.v. caused a reversible, marked decrease in glomerular filtration rate and urine production without significantly affecting the fractional water excretion rate. In the recovery period, after administration of vanadate, urine flow and the urinary excretion rate of electrolytes were only slightly different from control values. This action of vanadate appears to be due mainly to constriction of the renal blood vessels leading to a fall in glomerular capillary pressure. Vanadate likewise caused a dose dependent decrease in arterial conductance and blood flow of other vessels in the splanchnic area, whereas the femoral and carotid arteries were reversely and less affected. The vascular effect appears to be caused by a direct action of vanadate on vascular smooth muscle, but the mechanism of action is still unsettled.

Man's ever increasing exposure to numerous drugs and chemicals, which are the results of medical and industrial progress, produces a by-product of acute toxic nephropathies. These include acute toxic renal failure, drug-induced acute oliguric renal failure, acute hemorrhagic glomerulonephritis, nephrotic syndrome, tubular disturbances and potassium deficiency. In depth information is provided for the previously mentioned disorders.

The clinical histories of two patients are presented, who both developed haemorrhagic anuria after a short course of therapy with the carbonic anhydrase inhibitor, acetazolamide (Diamox). The clinical findings, in particular the radiological changes, are illustrated in this potentially fatal condition. The therapeutic success of immediate relief of the ureteric obstruction is emphasized and it is hoped that this report will act as a reminder of the importance of this agent as a cause of anuria.

A fifty-five-year-old man was seen with anuria. Retrograde pyelograms demonstrated bilateral ureteral obstruction subsequently shown to have resulted from sloughed renal papillae. A twenty-year history of phenacetin was obtained. Treatment included bilateral ureteral intubation, then ureterotomy on one side.

A 75 year old man, treated with ajmaline, was admitted with malaise, fever, acute renal failure and cholestatic jaundice. Haemolytic anaemia and thrombocytopaenia were also found with a positive indirect Coomb's test in the presence of ajmaline. The immunological and haematological data are discussed in the light of previously published cases.

We describe an elderly man, with pre-existing renal failure and atheromatous renal artery stenosis, who developed persistent anuria due to renal artery thrombosis after acute hypotension following captopril administration. Caution should be used when captopril is first administered to patients with impaired renal function in whom renal artery stenosis is known or suspected.