Hypercalcemia after acute renal failure.
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.
D000042:Absorption; D058186:Acute Kidney Injury / Q000150:complications*; D001798:Blood Proteins / Q000032:analysis; D002118:Calcium / Q000378:metabolism; D006801:Humans; D006934:Hypercalcemia / Q000188:drug therapy / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D009846:Oliguria / Q000209:etiology / Q000378:metabolism; D010281:Parathyroid Hormone / Q000097:blood; D011241:Prednisone / Q000627:therapeutic use; D012709:Serum Albumin / Q000032:analysis
D001798:Blood Proteins; D010281:Parathyroid Hormone; D012709:Serum Albumin; D002118:Calcium; D011241:Prednisone