Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal failure secondary to CDDP is due to acute tubular necrosis and is usually reversible. We report 4 cases of definitive renal failure secondary to administration of cisplatin (CDDP). Three women and one man, mean age 40 +/- 8 years (24 to 64 years), at onset of dialysis are reported. They had received 1 to 4 courses of CDDP for an endometrial carcinoma (n = 2), a breast carcinoma or a thymoma. The mean total dose of CDDP was 447 +/- 169 mg (160 to 900 mg). There was no additional nephrotoxic drug. Before treatment serum creatinine concentration was normal (77 +/- 7 mumol per liter) in all patients. In 2 cases dehydration (due to vomiting and use of mannitol) occurred during CDDP treatment. One patient was treated 30 days after a nephrectomy. At the onset of dialysis, renal ultrasound was normal. In 3 cases dialysis was necessary within 15 days following chemotherapy. In one case renal function deteriorated progressively to end stage renal failure 12 months after CDDP treatment. Dialysis was performed in 3 cases by hemodialysis and in one patient by peritoneal dialysis. All patients remained more than 6 months on dialysis. Three patients died from their cancer. One patient, being considered cured from his thymoma, is currently being evaluated for a kidney transplantation. Our observations outline the potential severity of CDDP nephrotoxicity. Systemic hydration with serial serum creatinine measurements are mandatory during and after CDDP administration these patients.
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PMID:[Definitive end-stage chronic kidney failure after cisplatin treatment]. 815 52

We report a 46-year-old woman who has been suffered from myasthenia gravis and underwent thymomectomy in December 1988. Her myasthenic symptoms improved by treatment with corticosteroid and azathioprine; the latter drug was administrated for more than one year. She noticed weight gain of 10 kg and edema in both legs and feet, which developed acutely in August 1994. Laboratory data showed that she suffered from nephrotic syndrome with a large amount of proteinuria (15 g/day). Renal biopsy revealed that biopsied glomeruli showed early stage of membranous nephropathy associated with acute tubular necrosis. Although therapeutic trials of steroid pulses could not eliminate proteinuria, substitution of cyclophosphamide for azathioprine brought marked improvement of the nephrotic syndrome with disappearance of the urinary protein excretion within 10 days. From reports of similar cases with myasthenia gravis in Japan and in Europe, therapeutic usage of azathioprine in patients with myasthenia gravis associated with thymoma should be cautious for appearance of nephrotic syndrome when azathioprine is continued for more than one year.
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PMID:[A post-thymomectomy case of myasthenia gravis which developed nephrotic syndrome with membranous nephropathy during azathioprine administration]. 895 54