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)

Serum uric acid and phosphorus concentrations were determined for 27 dogs with multicentric lymphosarcoma before and after chemotherapy. Mean serum uric acid values in dogs before treatment were significantly higher (P less than 0.05) than those of a control group of healthy dogs. Serum uric acid values did not change after treatment. Of the 27 dogs, 13 had 24-hour urine collections to determine endogenous creatinine clearance and quantitation of uric acid and phosphorus excretion before and after treatment for lymphosarcoma. Mean values for 24-hour creatinine clearance before and after treatment were statistically similar in dogs with lymphosarcoma, although the values were lower than those in a normal range. Total urinary phosphorus excretions were increased significantly (P less than 0.01) after treatment without change in fractional excretion. Chemotherapeutic agents used accounted for the significant (P less than 0.05) increase in urine volume after treatment and may have affected the excretion of uric acid and phosphorus. Seemingly, dogs with uncomplicated lymphosarcoma rarely have renal dysfunction or clinically important alterations in uric acid or phosphorus excretion secondary to rapid tumor lysis. However, preexisting renal disease or systemic complications, such as hypercalcemia, may be associated with increased risk of further renal impairment during treatment.
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PMID:Uric acid and phosphorus excretion in dogs with lymphosarcoma. 375 6

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

In 42 myeloma patients our results confirm the association of light chain proteinuria and renal damage, but suggest that while the amount of light chain excreted is an important factor, only some light chains are nephrotoxic. The excretion of the proximal tubular cell lysosomal enzyme N acetyl B D glucosaminidase was a sensitive index of tubular injury, while the presence of low molecular weight proteinuria (Retinol Binding Protein and Lysozyme) was shown to indicate tubular dysfunction in a kidney sufficiently damaged to produce an impaired GFR. Isolated defects of distal tubular function (acid load response and concentrating ability) were rare. Such changes were seen mainly as part of global renal impairment and were usually associated with such specific pathophysiological conditions as plasma hyperviscosity or tubular crystal deposition. Hypercalcemia had a specific effect on the concentrating ability independent of any impairment of renal acidification.
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PMID:Tubular function in multiple myeloma. 393 70

Hypercalcaemia can be caused by many disorders, but is most commonly due to primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause vomiting, polyuria, dehydration and renal impairment, and is then an important therapeutic problem. Therapy includes treatment of the cause, such as radiotherapy for malignant disease or surgery for primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always rehydration. If the plasma calcium concentration remains high, drug treatment must be added, the most effective and reliable agent being intravenous mithramycin. Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation. Glucocorticoids are not always effective, and phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral glucocorticoids and phosphate are often effective, and can be given in combination. When primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and hypercalciuria) are probably best treated with a low calcium diet and cellulose phosphate, a regimen also effective for the hypercalcaemia of sarcoidosis.
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PMID:Hypercalcaemia. What does it signify? 394 Aug 49

In a retrospective study, hypercalcemia was found on one or more occasions in 14 of 156 patients with newly detected, still active or relapsing non-Hodgkin's lymphoma (NHL). The incidence of hypercalcemia correlated with the histological grade of malignancy: patients with high grade NHL had a hypercalcemia incidence of 23%. Half of the patients had hypercalcemia-related symptoms, and 4 of 14 had hypercalcemia-induced renal impairment. The occurrence or recurrence of hypercalcemia correlated with progression of NHL. Remission-inducing chemotherapy and symptomatic treatment of hypercalcemia corrected the serum calcium.
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PMID:[Hypercalcemia in non-Hodgkin lymphoma]. 398 84

A retrospective survey was performed on 265 patients with primary hyperparathyroidism who had received three forms of treatment on a non-randomised basis. 'Successful' surgery (normalisation of serum calcium) was carried out in 142 patients, 'unsuccessful' surgery (persistence of hypercalcaemia after neck exploration) in 33 and no surgery in 90. Patients subjected to surgery were significantly younger than patients in the unoperated group and their serum calcium values at the time of decision were approximately 10 per cent higher. The mean follow-up period was significantly longer in the operated groups. The percentages of patients who had died were similar in each group. Clinical events relating to renal stones depended on the presence or absence of calculi at the time of decision rather than on the method of treatment. At the time of follow-up the prevalence of hypertension, renal impairment and vertebral crush fractures were similar in all three groups. Forearm osteo-densitometry showed a higher bone mineral content in the 'successful' group than in the other two groups. In spite of the selection bias inherent in a study of this kind, it is clear that untreated hyperparathyroidism is compatible with long survival and a lack of demonstrable deleterious effects on kidney and bone.
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PMID:Is parathyroidectomy of benefit in primary hyperparathyroidism? 399 79

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

Mithramycin given as a single dose for the treatment of hypercalcemia has not been reported to cause renal dysfunction. A case is presented of nephrotoxicity following a single 25 micrograms/kg dose in a patient with underlying squamous cell carcinoma, obstructive uropathy, and hypercalcemia. Underlying renal impairment may magnify the nephrotoxicity of mithramycin.
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PMID:Nephrotoxicity following single dose mithramycin therapy. 622 49

We studied the effect of a transplantable Leydig-cell tumor (Rice H-500) on serum calcium, parathyroid hormone (PTH), and urinary cAMP in intact Fischer-344 rats. The tumor caused rapid and severe hypercalcemia (control = 10.5 +/- 0.1 mg/dl [mean +/- S.E.] vs. 14.6 +/- 0.9 at day 12 post tumor inoculation) without evidence of metastasis. Progressive renal impairment and death generally occurred within 15 days of tumor inoculation. Serum PTH declined from control values before hypercalcemia occurred and was significantly reduced in tumor-bearing hypercalcemic rats (mean = 60 +/- 8% of control values). Urinary cAMP excretion was increased in tumor-bearing rats (mean at day 12 post inoculation = 12.2 +/- 1.4 nmol/dl creatinine clearance vs. control = 6.2 +/- 0.2) and correlated positively with serum calcium. The Rice H-500 Leydig-cell tumor appears to secrete a humoral factor capable of causing hypercalcemia. This factor may also increase urinary cAMP excretion in a manner analogous to PTH, but it is not detected by PTH radioimmunoassay.
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PMID:Humoral hypercalcemia caused by a rat Leydig-cell tumor is associated with suppressed parathyroid hormone secretion and increased urinary cAMP excretion. 630 50


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