Letter to the Editor Nephron 1994:67:236 Cent Sungur Tekin Akpolat Oktay Oymak Murat Colakoglu Unal Yasavul Cetin Turgan Nephrology Unit, Hacettepe School of Medicine, Ankara, Turkey Acute Renal Failure Due to Rhabdomyolysis in a Spastic Man Dear Sir, Rhabdomyolysis is a well-known cause of acute renal failure. Renal vasoconstriction, toxic effects of myoglobin on renal tubular cells and tubular obstruction arc suggested as the probable mechanisms leading to acute re nal failure [1, 2]. The causes of acute rhabdo myolysis include a wide variety of etiologies ranging from excessive muscular activity to genetic disorders [3]. Here, we report a man with spastic cerebral palsy who developed acute renal failure after an accidental fall and vigorous attempts to attain his proper position. A 22-year-old spastic man was admitted to the emergency service after an accidental fall while alone at home. His intellectual ca- pabilitites were well-developed but there was no motor activity in his legs and he could not coordinate the motor activities of his arms. He had a neurogenic bladder but he could con trol his urination. He was alone and watching television when he fell from his wheelchair. He showed vigorous efforts to straighten up for 3 h but was unsuccessful. His initial com plaints were pain in the right thoracoabdomi nal region but he developed nausea, vomiting and decline in urine output the next day. His physical examination in the emergency unit disclosed a thin man with superficial lesions and bruising involving the upper right quad rant of the abdomen. The results of the labor atory work-up were as follows: Hb 16.5 g/dl, Htc 47%. WBC 17.2 x 10-Vmm3. Na 135 niE q/ I, K 5.8 mEq/1. BUN 63 mg/dl, creatinine 4.3 mg/dl, uric acid 11.0 mg/dl, calcium 8.6 mg/ dl. phosphorus 5.2 mg/dl, total C'PK 170.410 U/l, AST 1.963 U/l. ALT 656 U/l. alkaline phosphatase 58 U/l, GGT 8 U/l, LDH 4301 U/l, total bilirubin 0.8 mg/dl. albumin 4.2 g/dl. PT 12 s (with a control of 12.3 s), blood pH 7.36. There was slight discoloration of the urine, and urinary pH was 5. There was 60 mg/l protein excretion, urine density was 1,014. and microscopic examination revealed 5 RBC and 6 WBC per high-power field with numerous urate crystals. Urinary sodium ex cretion was measured as 79.8 niEq/l. Ultraso nographic examination showed no evidence of stones, pelvicalyceal and/or ureteral dila tation, but 2 normally sized kidneys with en hanced echogenicity and diminished visuali zation of the corticomedullary junction. The patient was admitted to the intensive care unit and was hydrated intravenously, and alkalinization of the urine was under taken. He responded promptly to this suppor tive treatment and an urine output of 3 liters day w'as achieved. His CPK. LDH and AST levels returned to normal values within 5 days. This recovery phase was not compli cated by hyperkalemia or hypercalcemia. After full recovery of his renal functions, he was discharged from the hospital. Our observations suggest that this patient developed acute renal failure due to nontrau- matic rhabdomyolysis. The reason of muscu lar breakdown w'as his struggle to straighten up and extensive muscular activity during these attempts. References 1 Honda N: Acute renal failure and rhabdo myolysis. Kidney Int 1983:23:888-898. 2 Ward MM: Eactors predictive of acute renal failure in rhabdomyolysis. Arch Intern Med 1988:148:1553-1557. 3 Gabow PA. Kaehny WD, Kelleher SD: The spectrum of rhabdomyolysis. Medicine 1982; 61:141-152. Ccm Sungur. MD PK (PO Box) 272 I R 06693 Kavaklidere-Ankara (Turkey) © 1994 S. Karger AG. Basel 0028 2766/94/ 0672 0236S5.00/0