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Objective: The purpose of this study is to emphasize the high risk of renal failure and severe morphologic changes related to prolonged prenatal exposure to indomethacin., Study Design: Referred renal specimens from six anuric neonates exposed in utero to indomethacin were studied. Clinical charts were retrospectively reviewed. Indomethacin dosages varied from 150 to 400 mg daily, and the drug was given for a 2- to 11-week period, until birth., Results: All infants died in anuria, 4 of them after 7 to 39 days on peritoneal dialysis. In 5 infants cystic dilatations of superficial nephrons were associated with ischemic changes of the deep cortex. By immunohistochemical analysis intrarenal renin content was increased in 4 of 5 patients., Conclusion: Long-term indomethacin treatment during pregnancy may lead to the development of renal failure and irreversible renal damage with cystic dilatation of developing nephrons in an exposed fetus. Prior stimulation of the renin-angiotensin system may favor this complication.

Thrombolytic agents are routinely given to patients with acute myocardial infarction, often in combination with heparin. Genitourinary hemorrhage is an uncommon adverse effect of systemic thrombolysis, and acute azotemic complications are distinctly rare. We describe a case of genitourinary hemorrhage after combined thrombolytic and antithrombotic therapy leading to acute bilateral ureteral obstruction and then briefly review renal complications of systemic thrombolysis.

A patient with myeloma nephropathy and acute, probably diclofenac-induced renal failure developed a neuroleptic malignant syndrome (NMS) during treatment with metoclopramide and neuroleptics. These drugs were withdrawn, symptomatic treatment of NMS was started and the patient was hemodialyzed because of uremia. During hemodialysis, the patient's condition improved dramatically and NMS did not recur during her further stay in the hospital. The temporal relationship between metoclopramide administration and the development of NMS, as well as the rapid reversal of NMS, suggest that NMS in this patient was caused by metoclopramide and not by neuroleptic drugs. Thus, metoclopramide should be used with caution in patients with renal failure and patients should be monitored closely for the development of neuroleptic malignant syndrome. Hemodialysis may be therapeutically effective in certain patients with metoclopramide-induced NMS.

Angiotensin-converting enzyme (ACE) inhibitors are widely used for controlling hypertension. Their use in women who are pregnant is not without risk to the fetus. We describe three infants exposed in utero to ACE inhibitors who had adverse outcomes. These cases, combined with other reports in the literature, suggest strongly that these drugs are fetotoxic. ACE inhibitor fetopathy is characterized by fetal hypotension, anuria-oligohydramnios, growth restriction, pulmonary hypoplasia, renal tubular dysplasia, and hypocalvaria. Although the true frequency of adverse fetal effects has yet to be determined, because of the debilitating and lethal nature of the fetal damage when it occurs, it is our recommendation that ACE inhibitors not be used in pregnancy, particularly in the second and third trimesters.

Post-transplantation bladder leak, a potentially serious complication, is traditionally managed by reexploration and closure, and may require percutaneous placement of a nephrostomy tube. We report intractable bladder leakage that persisted following reclosure in a patient who also had cyclosporine nephrotoxicity. The attendant oligoanuria obviated the need for nephrostomy drainage and allowed healing of the bladder leak. The patient subsequently recovered from cyclosporine injury and regained renal function.

Objective: Case reports of suspected adverse pregnancy outcomes associated with prenatal exposure to angiotensin-converting enzyme inhibitors, particularly oligohydramnios, prolonged neonatal anuria, and defects of ossification of the skull dome, prompted us to examine pregnancy outcome in a large cohort of pregnant women for whom complete drug exposure information was known., Methods: We studied the prescribed drug exposure histories and pregnancy outcomes of all women aged 15-44 years enrolled in Tennessee Medicaid who delivered a live-born or stillborn infant between January 1, 1983 and December 31, 1988., Results: Of the 106,813 women enrolled in Tennessee Medicaid who delivered either a live-born or stillborn infant during the study period, 19 were exposed to an angiotensin-converting enzyme inhibitor during pregnancy. All 19 women delivered live infants. Among the 19 newborns, one preterm infant had prolonged anuria necessitating dialysis and a second preterm infant had microcephaly and a large occipital encephalocele., Conclusions: These outcomes represent a systematic follow-up of all angiotensin-converting enzyme inhibitor-exposed pregnancies. Despite the small number of exposures, there were two outcomes previously linked to prenatal use of these drugs, suggesting that the absolute risk may be high. In light of these findings and the case reports of others, it is prudent to avoid the use of angiotensin-converting enzyme inhibitors in pregnancy.

A 65-year-old, previously healthy man developed acute renal failure, severe thrombocytopenia and hepatic icterus after a small dose of mefenamic acid (Parkemed). Drug-dependent antibodies reacting against platelets could be identified as the most probable cause for this acute and rapidly reversible disorder. A concomitant hemolytic reaction was not observed and accordingly no drug-dependent red cell antibodies could be demonstrated. The drug-specific antibodies were found only during the acute phase using the platelet immunofluorescence test and a solid-phase immunoassay but not with the monoclonal antibody specific immobilization of platelet antigens assay. After discontinuation of the drug the patient steadily improved and fully recovered until day 22 after admission and drug removal. The clinical course strongly suggests that drug-dependent antibodies against mefenamic acid and/or its metabolites reacting by immune complex mechanism were responsible not only for the thrombocytopenia but also for the renal and hepatic failure.

Herein we describe a patient with noninsulin dependent diabetes mellitus who developed acute anuric renal failure following eye surgery. This condition, ascribable to diabetic neurogenic bladder and probably to the use of anticholinergic agents, improved following placement of a urethral catheter. The physiopathological mechanisms and treatment are discussed.

A case is reported in which exposure to cocaine and indomethacin was associated with development of fetal anuria, anasarca, and neonatal gastrointestinal hemorrhage. Cocaine and indomethacin may act synergistically to adversely affect renal, cardiovascular, and platelet function. It may be prudent to obtain a drug history and urine screen for cocaine before instituting indomethacin therapy for preterm labor or polyhydramnios.

Acute renal failure is an infrequent adverse reaction following the administration of dextran-40. We report a case of anuric acute renal failure in a 59-year-old female following the administration of 90 gm of dextran-40 and radiocontrast. An increased risk secondary to radiocontrast-induced ischemia is discussed in relationship to the pathogenesis of the dextran-induced acute renal failure. In addition, plasmapheresis is demonstrated to be of potential therapeutic benefit.

In vivo use of rIL-2 autologous BMT may be the means of reproducing a kind of "adoptive immunotherapy" from grafted cells after allogeneic BMT. This approach may enhance the spontaneous generation of cytotoxic T-cells and NK cells which are presumably involved in this immunotherapy. Potential risks of such an approach would be to increase the usual toxicity of rIL-2 and to jeopardize the hemopoietic reconstitution. To determine the feasibility of this approach we have treated 19 poor prognosis patients with a succession of autologous BMT followed 78 +/- 12 days later by a continuous infusion of rIL-2. Eighteen million international units (IU) per m2 per day of Proleukine (CETUS, Amsterdam, The Netherlands) were administrated over 6 or 12 days. No patient died of the procedure. Clinical toxicity related to rIL-2 was not increased. Hemopoietic toxicity, significant both for platelets and granulocytes, was transient. Immune stimulation was dramatic for lymphocytes and subpopulations (CD3+ and NK cells) and for cytolytic functions (NK and LAK activity). This trial establishes the feasibility of administration of high doses of rIL-2, 2 months after autologous BMT. In this setting a 6 day period of continuous infusion of 18 million per m2 per day of Proleukine appears to be a regularly tolerable dosage conducting to a major immune activation and invites further studies to determine the clinical impact of such an approach.

In a female alcoholic the fatal results of an ethylene glycol intoxication is described. The alcoholic had drunk circa 200ml of ethylene glycol (freezing preventive remedy glysantin) as a substitute. Despite early beginning intensive-medical care the fatal course could not be prevented. It is referred to the therapy by means of 4-methyl pyrazol which prevents the intoxication of ethylene glycol, whereby this substance in an effective inhibitor of the alcohol dehydrogenase.

We report a case of severe ovarian hyperstimulation syndrome which developed in a patient after ovarian stimulation for in-vitro fertilization (IVF). This was complicated by prerenal oliguria due to indomethacin therapy and liver dysfunction. The pathogenetic mechanisms involved are discussed.

A sixty-year-old woman with advanced breast cancer, previously treated with cisplatin, developed an irreversible lethal renal failure with anuria, the day after 5 g/m2 bolus ifosfamide. Postrenal failure was excluded by echography. A prerenal component could have contributed to renal failure because of a transient hypotension, due to an increasing ascitis, occurring just before anuria. However, correction of the hemodynamic parameters did not improve renal function. Ifosfamide is a known nephrotoxic drug with demonstrated tubulopathies. We strongly suspect that this lethal anuria was mainly due to ifosfamide, occurring in a patient having received previous cisplatin chemotherapy and with poor kidney perfusion due to transient hypotension. We recommend careful use of ifosfamide in patients pretreated with nephrotoxic chemotherapy and inadequate renal perfusion.

A 17-year-old hairdresser developed sodium bromate poisoning after drinking a cup of hair neutralizer in a suicide attempt. She presented 1 week later with anuria, required hemodialysis for 5 days, and subsequently recovered. Sensorineural hearing loss, often a characteristic finding, was absent. Early diagnosis of bromate intoxication requires an appreciation that it commonly occurs in hairdressers, may be accompanied by deafness, and may present with insidious anuria.

The chronic use of prostaglandin synthetase inhibitors is reported in a pregnant patient with severe juvenile rheumatoid arthritis. Aspirin and indomethacin, along with corticosteroids, were required to prevent significant progression of the disease. Pregnancy was complicated by oligohydramnios and intrauterine growth retardation. The infant suffered transient anuria. The effects of prostaglandin synthetase inhibitors on renal vascular function is reviewed, and a possible association between the chronic ingestion of these drugs and compromised renal function in the newborn is pointed out.

We used the qualitative Hanssen technique in albino rats to seek morphologic demonstration of tubular obstruction in two types of acute renal failure: one induced by folic acid and another by methemoglobin. Immediately after the intravenous injection of folic acid, 250 mg/kg body weight, the animals became almost anuric. Two to three hours after the injection, sodium ferrocyanide remained within the proximal convoluted tubules. After the intravenous injection of methemoglobin, 0.5 to 1.0 g/kg body weight, the animals became oliguric but not anuric. Sodium ferrocyanide injected with methemoglobin was seen mainly in distal tubules and collecting ducts 2 to 3 hours after the injection. The degree of tubular dilatation was more marked in the former model than in the latter, in agreement with the degree of oliguria. These morphologic findings were taken to indicate that the above two types of acute renal failure were caused by tubular obstruction rather than by intrarenal vasoconstriction and subsequent cessation of glomerular filtration. (Am J Pathol 87:323-330, 1977).

A case of dobutamine overdose is presented. Due to a prescription mistake a patient with recent myocardial necrosis and acute arterial occlusion received up to 70 mcg/kg/min of dobutamine IV. This resulted in arterial hypotension, diminished vascular resistance, oliguria and signs of cutaneous and mucosal hyperemia. Interruption of the dobutamine infusion and substitution with dopamine normalised all abnormalities. The differences between the hemodynamic profiles of dobutamine and dopamine are discussed.

Infusion of 10% Dextran 40,000 (Dextran 40) solute was reported to induce acute renal failure with oligoanuria in some patients and in animals during experimental pharmacological studies. Dogs were infused daily with 40 ml.kg-1 a large volume (twice the dose intended in human clinical practice) of a 3,5% dextran 40 solute, associated with electrolytes Plasmacair After 30 days of administration, no differences in creatinine clearance and renal structures were noted between control and treated animals.

In fourteen infants, aged 9--60 days, with generalized oedema seen during a one year period the common denominator was the administration of dipyrone one to two days prior to the development of oedema. None of the other causes of oedema in early life could be incriminated in any of these babies. Pediatricians should be aware of this iatrogenic cause whenever they encounter a young infant with generalized oedema. Oedema disappeared in all the cases following discontinuation of dipyrone but anuria lasted for more than four days in one case. This stydy re-emphasizes the need to without this potentially dangerous drug, especially during the neonatal period.

Angiotensin converting-enzyme inhibitors cross the placenta and modify the maternal, foetal and utero-placental renin-angiotensin system. Eight cases of pregnancy in women taking captopril have been published, 7 other cases being reported in this review paper. There were one spontaneous and 2 therapeutic abortions, one of which disclosed a malformation of uncertain diagnosis and imputation. One intrauterine death at 28 weeks was probably due to the severity of the maternal disease. Two children born to mothers also treated with frusemide died of neonatal anuria. Delivery or caesarean section occurred before term in 8 cases, and there were 3 cases of neonatal respiratory distress with a favourable outcome. Finally, one mother gave birth at term to twins of normal weight. The cases with respiratory distress can be attributed to the mother's hypertension, to prematurity and/or to concomitant treatment with beta-blockers, while the cases with anuria seem to be due to inhibition of the effects of angiotensin on renal haemodynamics, with salt depression as a possible aggravating factor. Treatment with angiotensin converting enzyme inhibitors does not seem to warrant therapeutic abortion. However, these drugs are contra-indicated in pregnancy and should only be given to women wishing to become pregnant if they present with resistant and dangerous arterial hypertension. A programme of pharmacovigilance is being set up to follow up such pregnancies.

Oliguria in the neonate usually reflects a fall in glomerular filtration rate (GFR) secondary to prerenal disturbances such as hypovolemia, hypotension, hypoxemia and cardiac failure, or to vasoactive drugs such as indomethacin and tolazoline. The action of such drugs on renal function is reviewed, as well as the pharmacological measures that can be tried to prevent or blunt their renal side effects. The efficacy and side effects of dopamine, furosemide and mannitol, frequently used in oliguric states due to either prerenal disturbances or to vasoactive drugs, are discussed. It is concluded that available data in newborn infants do not definitely prove the efficacy of dopamine and furosemide in preventing acute renal insufficiency and that, in neonates with established oliguria, administration of mannitol, dopamine and/or furosemide can be tried, with little hope, however, of markedly improving GFR.

A 19-year-old girl was treated for a heavy mercury chloride intoxication (3 g HgCl2) with 2,3-dimercaptopropane-1-sulfonate (DMSP) and dialyses. The anuric stage lasted for 10 days. With DMSP the mercury clearance by hemodialysis was 3,5-5,0 ml/min, with BAL 0,6 ml/min. DMSP is an effective watersoluble mercury-chelator and is subjectively better tolerated and less toxic than BAL. The anuric stage was probably not shortened.