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)

In a patient recovering from acute renal failure, hypercalcemia abruptly developed at a time when the serum creatinine level remained high (5 mg/dl) but well after the serum phosphate level had been restored to normal by oral aluminum hydroxide therapy. The renal damage had been severe, with oliguria lasting six weeks. Parathyroid hormone (PTH) immunoreactivity was measured with two different "carboxyterminal" PTH assays, giving high-normal or slightly mild renal failure could have accounted for the increased immunoreactivity. After five months of hypercalcemia, prednisone was administered and produced a prompt and sustained normalization of serum calcium. This prolonged variant of hypercalcemia after renal failure is not well recognized in the literature. The response to glucocorticoids suggests that abnormal metabolism of vitamin D or osteoclast activating factor might be involved in its genesis.
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PMID:Hypercalcemia after acute renal failure. 744 7

Acute renal failure may be caused by a failure of renal perfusion (pre-renal failure), damage to the renal parenchyma (intrinsic renal failure) or obstruction of the urinary tract (post-renal failure). Most cases of intrinsic renal failure in the newborn are due to asphyxia, often in combination with sepsis and nephrotoxic drugs. Persistent elevation of the plasma creatinine concentration above 132.5 micromol/l (1.5mg/dl) is widely accepted as a diagnostic criterion. Oliguria or anuria may occur but is not always present. Post-renal failure is diagnosed by renal ultrasonography and is treated by relief of the obstruction. Pre-renal and post-renal failure can be distinguished by an analysis of urinary indices, especially the fractional sodium excretion, and by the response to fluid replacement. The conservative management of intrinsic renal failure includes careful attention to fluid balance, maintenance of adequate nutrition and prevention or correction of hyperkalemia, acidosis and hyperphosphatemia. Severe cases may require dialysis: peritoneal dialysis is used in most cases, but extracorporeal methods, including intermittent hemodialysis, hemofiltration and hemodiafiltration, are possible. Congenital chronic renal failure, usually caused by renal dysplasia with or without obstruction, presents in a manner similar to that of acute renal failure, with a progressive deterioration of plasma biochemical values. Dialysis is rarely necessary in the newborn period. The conservative management of chronic renal failure is similar to that of acute renal failure, with particular emphasis on nutrition, control of acidosis and the prevention of renal osteodystrophy by the use of dietary phosphate binders and vitamin D analogs.
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PMID:Management of acute and chronic renal failure in the newborn. 1500 Nov 36