Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-one patients in severe diabetic coma were treated with small doses of insulin at a rate of 4.1 units per hour (total dose about 100 units per 24 hours). Using single doses of 4 to 10 units by the intravenous or intramuscular routes the fall of blood glucose was steady in all cases. In the treatment of diabetic coma this regimen of insulin administration has proved simple, safe and effective since 1946. Main dangers during recompensation of diabetic coma are: hypovolaemia with oliguria -- anuria, dysequilibrium syndrome with cerebral edema and hypokalaemia. Therefore early intensive and adequate intravenous fluid and electrolyte replacement is the most important part of treatment. Most of the cases in this study were undiagnosed diabetics (14) and elderly patients (9). Three patients older than 65 years and a 56-year old diabetic died. In this context the most important aspects of treatment to avoid death are: prevention of diabetic coma and adequate fluid and electrolyte replacement especially in geriatric patients.
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PMID:Treatment of diabetic coma with low-dose injections of insulin. 95 92

We report a patient with rhabdomyolysis secondary to hyperosmolar nonketotic diabetic coma (HNKC), who progressed to acute renal failure. A 43-year-old male with diabetes mellitus for three years was admitted to our hospital because of loss of consciousness. The laboratory findings at admission were as follows: serum glucose 1792 mg/dl, serum Na 129 mEq/1, BUN 71 mg/d1, serum creatinine 3.3 mg/d1, CPK 715 IU/1, plasma osmolality 370 mOsm/1, and negative urine ketone bodies. A diagnosis of HNKC was made. On the 2nd day, he had oliguria and the serum creatinine increased despite adequate treatment of HNKC by the administration of intravenous fluid and insulin. On the 4th day, CPK reached 47,300 IU/1, and serum myoglobin was also increased, indicating rhabdomyolysis. His renal function improved gradually and was almost normalized on the 20th day. Renal biopsy on the 23rd day showed myoglobin at the distal renal tubules, which appeared to be involved in the pathogenesis of renal failure by rhabdomyolysis. However, we found little abnormality association with diabetic nephropathy in the renal tissue. Since HNKC is known to induce acute renal failure rarely without diabetic nephropathy, these findings suggested that the acute renal failure was caused mainly by the rhabdomyolysis. Acute renal failure induced by rhabdomyolysis in patients with HNKC is rare, but fatal. The present study showed that the measurement of serum CPK and urine myoglobin was helpful for early diagnosis. Only 12 cases have been reported to have developed renal failure due to rhabdomyolysis among patients with HNKC. To our knowledge, we demonstrated for the first time that myoglobin at the distal renal tubules after renal function was normalized.
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PMID:[Rhabdomyolysis related-acute renal failure in a patient with hyperosmolar nonketotic diabetic coma (HNKC): demonstration of myoglobin casts after normalization of renal function]. 882 59