Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 22-year-old man, had ingested more than 300 10(6) I.U. of vitamin A over a 2-year period. He presented with diffuse arthralgia, weight loss, low-grade fever, dryness and peeling of the skin, hair loss, liver enlargement with ascites and pleural effusion. He had a raised E.S.R., hypercalcemia and acute renal failure. Plasma levels of vitamin A and retinol-binding-protein were in the normal range. All symptoms disappeared after withdrawal of vitamin A except for the liver enlargement. Iliac bone biopsy showed cortical thickening, numerous resorptive lacunae and no index of bone formation. Liver biopsy showed obliteration of the space of Disse by swollen fat-storing cells (Ito cells). Tissue levels of vitamin A were very high in the liver. A second biopsy, 6 months later, showed a decrease of fat storage in the Ito cells but the development of a fibrosis.
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PMID:[A systemic-like disease: chronic vitamin A poisoning]. 371 19

A young man developed acute renal failure and hypercalcaemia following severe burns. The hypercalcaemia was initially controlled by haemodialysis, but it persisted after return of renal function. Plasma PTH was inappropriately elevated, but the nephrogenous cyclic adenosine monophosphate level was low; thus the PTH was probably not biologically active, and may have been artefactually elevated by the moderate renal impairment. Bone histology, showed a normal resorbing surface, but a zero forming surface, implying that the bone dissolution leading to hypercalcaemia resulted from a failure of bone formation. Because of widespread infection and impaired renal function, the hypercalcaemia could not be treated by corticosteroid drugs, mithramycin or phosphate, and there was no response to salmon calcitonin. He was therefore treated with intravenous sodium sulphate, which increased urinary calcium excretion and reduced the plasma calcium. Sodium sulphate still has a role in the treatment of patients with hypercalcaemia.
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PMID:Immobilization hypercalcaemia due to low bone formation and responding to intravenous sodium sulphate. 376 50

Renal impairment in sarcoidosis is unusual: cases with granulomatous interstitial nephritis (GIN) and without associated glomerular disease, nephrocalcinosis and hypercalcemia have rarely been described. We report 2 such cases, one of whom is the first patient documented as surviving following presentation in dialysis dependent renal failure. Review of the literature revealed a further 20 patients. Of the 22 patients, including our own, 3 failed to respond to treatment, all dying in acute renal failure. Relapse occurred in 4, in association with rapid reduction or early cessation of treatment. No relapse was reported later than 9 months after starting treatment with corticosteroid. The majority of patients (15/19) who responded to treatment had residual renal impairment after up to 30 months of steroid treatment.
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PMID:Renal impairment in sarcoidosis: granulomatous nephritis as an isolated cause (two case reports and review of the literature). 380 88

Increases in intracellular and mitochondrial calcium content that accompany ischemic and toxic acute renal failure have been suggested to mediate renal tubular cell injury and dysfunction, but the mechanism(s) are unknown. We studied the effects of in vivo vitamin D-induced chronic hypercalcemia on rat renal cortical brush-border and basolateral membranes and mitochondria. In the brush-border membrane, hypercalcemia caused significant decreases in alkaline phosphatase-specific activity, total phospholipid molar content, and phosphatidylserine percent molar composition and increases in the cholesterol-to-total phospholipid molar ratio and phosphatidylinositol percent molar composition. In the basolateral membrane, hypercalcemia caused significant decreases in Na+-K+-ATPase-specific activity and total phospholipid molar content and increases in the cholesterol-to-total phospholipid molar ratio and phosphatidylinositol 4,5-bisphosphate percent molar composition. In the mitochondria, hypercalcemia caused a mild increase in the mitochondrial calcium content, but no alterations in succinic dehydrogenase-specific activity, succinate-, ADP-, or uncoupler-induced respiration. Thus hypercalcemia caused alterations in brush-border and basolateral membrane enzyme activity and lipid composition, but no functional changes were detected in mitochondria. These hypercalcemia-induced plasma membrane biochemical alterations may be markers of early cell injury and suggest a role for calcium in causing or predisposing to renal tubular cell injury.
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PMID:Effects of vitamin D-induced chronic hypercalcemia on rat renal cortical plasma membranes and mitochondria. 381 41

A case is reported of amoxapine overdose followed by acute rhabdomyolysis and myoglobinuric acute renal failure. There was disseminated intravascular coagulation and later hypercalcaemia. The patient recovered.
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PMID:Acute renal failure secondary to non-traumatic rhabdomyolysis following amoxapine overdose. 386 31

In order to determine the prevalence of rhabdomyolysis-associated acute renal failure (RM-ARF) and assess the effect of oliguria on biochemical features in this condition, 127 cases of ARF seen over 18 months were reviewed. Eleven cases of RM-ARF were seen, a prevalence of 8.6% of all cases of ARF. There were ten males and one female (age range 15-72 years) with precipitating events being trauma in three, coma in two, infection in two and other causes in five. Ten had concurrent clinical or historical evidence of dehydration, two had mild hypokalemia, and one abused alcohol. Serum and urine myoglobin by radioimmunoassay were greater than 800 ng/l in all cases tested. False negative tests for urine myoglobin by o-tolidine reaction after (NH4)2SO4 extraction occurred in four cases. Despite attempted forced saline diuresis and urinary alkalinisation, seven became oliguric and required dialysis for 12-81 days. Initially (pre-dialysis) oliguric patients had significantly higher maximum serum levels of potassium, phosphate, and rate of rise of creatinine, significantly lower trough levels of calcium, and no significant difference in peak creatine phosphokinase or uric acid levels than non-oliguric patients. Two subjects developed recovery phase hypercalcemia, four required fasciotomy for compartment syndromes, three sustained permanent nerve damage, and three required limb amputation. Ten survived, with a mean creatinine clearance of 96 ml/min after nine to 30 months. RM-ARF is common, may be clinically occult and show false negative urine myoglobin tests. Hyperkalemia, hyperphosphatemia, and hypocalcemia are more common in oliguric than in non-oliguric RM-ARF, but both have a good prognosis with appropriate medical and surgical management.
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PMID:Rhabdomyolysis and acute renal failure. 386 39

By damaging cell membrane integrity, acute rhabdomyolysis leads to electrolyte shifts according to the concentration gradients and the liberation of intracellular substances. Diagnosis is confirmed by the presence of a high serum creatinkinase activity (CK) and myoglobinuria. For clinical purposes myoglobinuria is demonstrated by a blood-positive dipstick in the absence of hematuria or hemoglobinuria. Rhabdomyolysis is usually acquired and is rarely due to hereditary enzyme defects. The authors report on 61 patients admitted in the last 15 years with rhabodomyolysis. In the past 4 1/2 years the diagnosis was suggested by CK greater than 5000U/1 in 49 patients, representing 1.6% of all admissions in the departments of medicine and surgery. Originally described in crush situations, rhabdomyolysis has been observed with increasing frequency as a consequence of muscular stress and self crush due to coma or hemi- and paraplegia during the last decades. 24% of the patients with this diagnosis had had an intoxication, and in 70% there were multiple simultaneous causes. Autoimmune diseases, infections of bacterial, viral and fungal origin, endocrinopathies, and thermic and ischemic injuries can also provoke rhabdomyolysis. As a consequence of fluid shift into the damaged muscle a compartment syndrome may lead to vascular or neural defects. In 80% of cases there is initial hypocalcemia, turning later into hypercalcemia. Other frequent electrolyte disorders accompanying rhabdomyolysis are hyperkalemia, hyperphosphatemia and a widened anion gap. 6 of 13 patients showed the typical blood changes found in patients with disseminated intravascular coagulation. Acute renal failure developed in 30 patients, 15 of whom underwent dialysis or hemofiltration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute rhabdomyolysis]. 395 76

A case of hypophosphatemia-induced hypercalcemia during post-traumatic acute renal failure is described. Proposed causes for the hypophosphatemia include changes in tissue distribution of phosphate associated with hyperalimentation and phosphate losses during hemodialysis. In the absence of hyperparathyroidism the hypercalcemia as well as changes in osteoclast morphology found on bone biopsy are ascribed to a direct effect of hypophosphatemia on bone.
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PMID:Hypophosphatemia-induced hypercalcemia during acute renal failure. 667 51

In the past, patients with multiple myeloma and acute renal failure have had a poor prognosis. Few patients recovered renal function and fewer still survived for prolonged time periods. This report describes the course of 10 patients with multiple myeloma and true acute renal failure treated during the decade 1970 to 1980, and reviews recent reports concerning this association. The use of radiographic contrast agents is no longer the primary predisposing factor to acute renal failure in the myeloma population. Rather, infection, hypercalcemia, and dehydration in the presence of light chain excretion are the major conditions precipitating the renal failure. Despite severe renal failure requiring dialysis, many patients may regain good renal function. Factors associated with a good or poor prognosis in this population are reviewed. The prognosis in patients with myeloma and acute renal failure has greatly improved in recent years, and prolonged survival may occur.
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PMID:Acute renal failure in patients with multiple myeloma. 669 48

We studied six oliguric patients with rhabdomyolysis-induced acute renal failure. On admission, all had marked hyperphosphatemia and hypocalcemia associated with low levels of 1,25-dihydroxycholecalciferol [1,25(OH)2D]. During the early polyuric phase, moderate hypercalcemia was accompanied by marked elevations in plasma 1,25(OH)2D and persistent elevations in parathyroid hormone (both amino and carboxy terminals). During the late polyuric phase, the levels of serum calcium and 1,25(OH)2D reverted to normal. Thus, in rhabdomyolysis-induced acute renal failure, the hypocalcemia of the oliguric phase may be secondary to decreased synthesis of 1,25(OH)2D; severe hyperphosphatemia may also have a major role. The hypercalcemia of the polyuric phase may be partly due to increased synthesis of 1,25(OH)2D, resulting from the high parathyroid hormone levels and recovery of renal function.
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PMID:The pathophysiology of altered calcium metabolism in rhabdomyolysis-induced acute renal failure. Interactions of parathyroid hormone, 25-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol. 689 30


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