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)

In a 33-year-old woman concurrence of a complete distal renal tubular acidosis (RTA) and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism was observed. Until recently, the rare association of RTA and hyperthyroidism had been thought to be governed by nephrocalcinosis, via hypercalcemia and hypercalciuria. However, in this case, nephrocalcinosis was not present, but there were histological signs of renal interstitial mononuclear cell infiltration, and the RTA persisted despite the resolution of the hyperthyroidism. This observation supports the idea that immunological mechanisms may relate RTA and hyperthyroidism when the latter has an autoimmune origin.
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PMID:Distal renal tubular acidosis and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism. Report of 1 case without nephrocalcinosis. 383 55

The potential toxicity of vitamin D, alpha-calcidol [1 alpha(OH)D3], and calcitriol [1,25(OH)2D3] was studied by administration of these compounds at three different doses to weanling C57BL/6J mice over a 4-week period. Drug effects on calcium were monitored by serum calcium and urine calcium/creatinine ratio determinations. Tests of renal function included serum creatinine, 24-h urine volume, urinary protein, and glucose excretion, and histological evaluation of renal tissue. At 2 weeks, serum calcium was significantly elevated in animals receiving the higher doses of alpha-calcidol (2.78 +/- 0.25 at 50 ng/kg and 3.45 +/- 0.13 at 250 ng/kg body wt vs 2.14 +/- 0.06 mmol/l in controls, respectively). A similar effect was seen in the urinary calcium/creatinine ratio but serum creatinine remained unchanged. By 4 weeks, all animals receiving alpha-calcidol had significantly higher serum calcium and urinary calcium/creatinine ratios than other groups. Severe nephrocalcinosis was observed in the high-dose alpha-calcidol group only. We conclude that alpha-calcidol is more toxic than calcitriol in the mouse and suggest that the degree of toxicity is correlated to the degree of hypercalcemia and to the vitamin D metabolite used.
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PMID:The comparative toxicity of vitamin D metabolites in the weanling mouse. 387 64

Glucocorticoids are often used to treat hypercalcemia due to vitamin D overdosage. We measured the effect of 1.5 mg/day of prednisolone on the amount of calcium deposited in the kidney of rats dosed with either 500 ng/d or 2000 ng/day of 1-alpha OHD2 or 1-alpha OHD3. The rats were given a diet containing 0.3% calcium and 0.5% phosphate. A second group of rats received 2000 ng/d of the vitamin D analogs and a diet which contained only 0.02% calcium. After 6 weeks, rats given the vitamin D analogs had two to six times more calcium in the kidney compared with the controls (0.096-0.276 mg vs. 0.240-1.064 mg). When a pharmacological dose of prednisolone was added to treatment, calcium in renal tissue increased to 0.305-3.083 mg. The urinary output of calcium seemed to be increased by prednisolone whereas the serum calcium was lowered. It appears that glucocorticoids given at the same time as vitamin D compounds increases the risk for nephrocalcinosis possibly due to increased amounts of calcium in the urine.
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PMID:The effect of prednisolone on kidney calcification in vitamin D-treated rats. 393 84

Sarcoid granulomatous nephritis was observed in 2 patients. Renal failure was present in both patients in the absence of hypercalcemia or nephrocalcinosis. Specific tubular dysfunction manifested as an acquired Fanconi syndrome in 1 patient. Steroid therapy was effective in causing regression of the renal granuloma, but there were significant interstitial changes on repeat renal biopsy which were accompanied by persistent tubular dysfunction. Sarcoid granulomatous nephritis may be a not infrequent cause of renal dysfunction in sarcoidosis.
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PMID:Granulomatous nephritis and chronic renal failure in sarcoidosis. Long-term follow-up studies in two patients. 396 56

A 26-year-old woman was admitted to the Institute of Endocrinology in Bucharest for evaluation of primary hyperparathyroidism (P-HPT). Anamnesis revealed a 10-year history of nephrolithiasis; peptic ulcer, chronic pancreatitis, cholelithiasis. Eight months previously, she had given birth to a child who had neonatal hypocalcaemic tetany. Investigations revealed the presence of moderate hypercalcaemia, hypercalciuria, hypo-phosphoremia; serum chloride level was above 100 mEq/1, and the chloride phosphate ratio was greater than 33. X-ray films of the abdomen revealed the presence of nephrolithiasis and right nephrocalcinosis. Selenium methyonine scanning, ultrasonography and computerized tomography were negative. On surgical exploration a 2-3 cm parathyroid adenoma was removed from between the trachea and the esophagus.
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PMID:Primary hyperparathyroidism. Report of a clinical case without bone lesions. 404 20

The kidneys were evaluated on [99mTc]phosphonate bone scans using 35 studies from 23 individuals with multiple myeloma; these images were compared with those from 50 controls. In each case, the kidneys could be visualized and calculation was made of the renal:skeleton ratio. Two myeloma patients showed an elevated renal:skeleton ratio. One was due to reduced vertebral uptake of [99mTc]phosphonate following therapeutic radiation. In the second case, the elevated ratio was related to renal uptake of the tracer (independent of urinary retention), and was consistent with nephrocalcinosis. No significant correlation between the renal:skeleton ratio and the degree of hypercalcemia, proteinuria, or renal impairment was found. We conclude that bone scintigraphy represents a safe, simple means of demonstrating renal presence and activity in multiple myeloma patients. However, calculation of the renal:skeleton ratio is not directly helpful in clarifying the events of calcium metabolism.
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PMID:Evaluation of renal-skeleton ratio of technetium-99m phosphonate in multiple myeloma. 405 22

Thirteen patients with hypercalcaemia due to carcinoma received inorganic phosphate, orally or intravenously, as palliative treatment for their high serum calcium levels. The serum calcium promptly fell in all patients fully treated, and there was a striking clinical improvement in most patients. The blood urea was usually unchanged or became nearer to normal, while the serum phosphate altered variably. Only two of the eight patients who were studied at necropsy had microscopical nephrocalcinosis; corneal calcification was evident in both before phosphate treatment was started.This oral inorganic phosphate (1 gramme thrice daily) is a safe and effective means of treating hypercalcaemia due to carcinoma. An intravenous infusion of 1 gramme over eight hours may sometimes be required initially for patients who are vomiting.
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PMID:Phosphate treatment of hypercalcaemia due to carcinoma. 417 70

Investigation of a patient with hypercalcaemia, hypophosphataemia, and nephrocalcinosis failed to lead to a clear diagnosis. Neither primary hyperparathyroidism nor primary incomplete renal tubular acidosis could explain all the biochemical features, and it seems that more than one fundamental abnormality may have been present.
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PMID:Hypercalcaemia, hypophosphataemia, and inability to excrete hydrogen ions. 463 53

Hypophosphatasia represents an inborn enzymatic deficiency characterized by a reduced activity of alkaline phosphatase in serum and tissue and an increased urinary excretion of phosphoethanolamine. 278 cases have been described until the end of 1980. Based on the age of manifestation and the predominant clinical findings the following classification is possible: The prenatal form (49 cases) with caput membranaceum, skeletal deformities and respiratory distress has a mortality of 100%. The early infantile form (94 cases) shows rickets-like osseous anomalies, dystrophy, craniostenosis, nephrocalcinosis, mortality amounting to 40%. Diagnostic features of the infantile-juvenile form (112 cases) are premature loss of deciduous teeth, bone deformities, rickets-like findings, and short stature. Mortality is only 1%. The adult form (23 cases) often remains undiscovered and has a good prognosis. It presents with pseudofractures and pains in the bones as chief symptoms. Heredity is autosomal recessive in all four types of hypophosphatasia. Possibly in the adult form there is an additional autosomal dominant inheritance. Alkaline phosphatase deficiency affects all tissues excepting the intestinal isoenzyme. Urinary excretion of phosphoethanolamine is elevated. Values for calcium and inorganic phosphorus in serum are usually normal or only slightly increased. Marked hypercalcemia is observed in severely diseased patients affected by the early infantile form. In these cases hypercalcemia often leads to nephrocalcinosis and renal insufficiency. Since alkaline phosphatase is equally active as pyrophosphatase, reduced phosphatase activity induces an accumulation of pyrophosphate in serum and its increased excretion in urine. The precise pathogenetic mechanisms of hypophosphatasia are still unknown. Possibly, the accumulation of pyrophosphate implies a disorder of calcification. Postnatal diagnosis is based on clinical findings in association with decreased alkaline phosphatase activity and increased phosphoethanolamine excretion. For the detection of heterozygotes additional biochemical markers should be tested. These include the determination of alkaline phosphatase in leucocytes and cultured skin fibroblasts, the calculation of tubular phosphate reabsorption and the analysis of pyrophosphate and pyrophosphatases. The difficulty in ascertaining the carrier state is that the measurement of a single parameter may give normal results.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Congenital hypophosphatasia]. 614 51

Various abnormalities of the renal tract can be detected from the renal images seen on 99Tcm methylene diphosphonate (MDP) bone scintigrams. Diffusely increased renal parenchymal activity has been associated with cytotoxic and other drug therapy, radiation nephritis, iron overload and cirrhosis. A further association--with hypercalcaemia--is reported here. In a retrospective study, 1950 bone scintigrams were reviewed and a significant relationship between high renal activity and hypercalcaemia was found. This was subsequently confirmed by a small prospective study. None of the patients whose bone scintigrams showed this association had evidence of nephrocalcinosis on X rays. It is postulated that in these hypercalcaemic patients there may be high tissue calcium in the kidneys which results in the high uptake of MDP, and it is suggested that serum calcium be measured in patients with previously unsuspected hypercalcaemia whose bone scintigrams exhibit the finding of high parenchymal renal activity.
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PMID:High renal activity on bone scintigrams. A sign of hypercalcaemia? 622 81


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