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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal involvement in patients with multiple myeloma has been described as a sign of poor prognosis. The influence of renal insufficiency in the clinical patterns and in the prognosis of patients with multiple myeloma was studied retrospectively in 45 patients. Patients with renal insufficiency, at first visit, more often presented weight loss, proteinuria, hypercalcemia. The means of uricemia, ESR, were higher and the hematocritic mean was lower in patients with renal insufficiency. There was no difference in edema, arterial hypertension, fractures and bone pain. The reversibility of renal insufficiency occurred in 47% of the cases, which happened more often in the first months of the follow up. The creatinine mean was lower in patients with reversible renal insufficiency. The median survival was: patients with renal insufficiency: 11 months; patients with normal renal function: 50 months. Among patients with renal insufficiency those with recuperation of renal function showed a higher median survival (24 months) than those with irreversible renal insufficiency (1 month). The renal involvement then is frequent and often reversible. Patients with impaired renal function showed a worse prognosis; normalization of the renal function was associated with a better outcome.
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PMID:[Clinical characteristics and prognostic implications of renal involvement in multiple myeloma]. 822 May 5

Renal failure is a frequent complication in multiple myeloma and it is present in about 50% of patients with newly-diagnosed multiple myeloma. Renal failure at the time of diagnosis has earlier been associated with a bad prognosis, but a better prognostic factor is the response to chemotherapy. In general, it is important to distinguish between 1) renal insufficiency at the time of diagnosis, 2) acute renal insufficiency and 3) chronic renal insufficiency developing during the course of the disease. The patients in the first two groups are treated with intensive therapy which is long-lasting (median four to six weeks). The improved function of the kidney is correlated to an improved survival. Patients developing chronic renal insufficiency late in the course of the disease should receive palliative therapy. The most important factors that provoke acute renal insufficiency are dehydration, hypercalcaemia and/or infection, but renal insufficiency is also provoked by the use of nephrotoxic drugs, hyperuricaemia and/or hyperviscosity. Chronic renal insufficiency is provoked by deposits of light chains, infiltration by plasma cells or deposits of amyloid. The treatment consists of elimination of the provoking factors and start of chemotherapy.
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PMID:[Renal insufficiency in myelomatosis. Causes and treatment]. 825 82

A case of sarcoidosis is described which presented with hypercalcaemia and renal insufficiency. Initially, a calciol intoxication was diagnosed, because a high daily intake was suspected. However, vitamin D3 metabolites in the blood revealed normal concentrations of calcidiol, but extremely high concentrations of calcitriol. These features rejected the first diagnosis and pointed to high endogenous calcitriol production, which may take place in granulomatous diseases. This is caused by an increased 1-alpha-hydroxylation reaction in activated macrophages. Eventually, muscle biopsy revealed non-caseating granulomas, confirming the diagnosis of sarcoidosis.
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PMID:Enhanced production of calcitriol, and hypercalcaemia in a patient with sarcoidosis provoked by daily intake of calciol. 829 70

The principal pathophysiologic alteration in severe hypercalcemia accompanying hyperparathyroidism and malignancy is enhanced osteoclastic bone resorption. Hypercalcemia impairs renal mechanisms that lead to sodium and calcium excretion; PTH and PTHrP acting on renal tubules enhance further calcium reabsorption. Although rehydration is often necessary as an initial therapy of hypercalcemia, the cornerstone of therapy is to inhibit osteoclastic bone resorption. The bisphosphonates, plicamycin, gallium, and calcitonin all inhibit osteoclastic bone resorption. Calcitonin is the most rapidly acting agent. Toxicities of calcitonin are minimal, yet its therapeutic efficacy is limited by lack of potency and tachyphylaxis. The second-generation bisphosphonates such as pamidronate represent a class of compounds that are extremely effective in inhibiting the metabolic function of the osteoclast. Given in a single infusion, a significant majority of patients will have normalization of corrected serum calcium lasting, on average, 1-2 weeks. Therapeutic benefit will be of greater duration because most patients remain only minimally symptomatic until corrected serum calcium rises above 11.5 mg/dL. Side effects of low-grade fever, hypophosphatemia, hypomagnesemia, and hypocalcemia may occur. Gallium nitrate is a potent inhibitor of bone resorption and may be of increased clinical value when more efficient administration protocols can be developed. Plicamycin, available for two decades, has cumulative toxicities and is less potent than the aminobisphosphonates. Renal insufficiency often accompanies severe hypercalcemia. The nephrotoxicity of gallium nitrate and plicamycin should preclude their use when there is moderate impairment of renal function, and amino bisphosphonates become the treatment of choice in these patients. Although several authors have advocated individualized approaches to the management of hypercalcemia, the potency and duration of action of the aminobisphosphonates make them a reasonable treatment choice for most patients with symptomatic hypercalcemia. Most importantly, the most effective therapy for hypercalcemia is to recognize and treat the underlying disease. Acute primary hyperparathyroidism requires surgery. The effective treatment of hypercalcemia of malignancy allows the introduction of tumor-specific therapy, limits morbidity, and shortens and deintensifies hospitalization. At times, the most appropriate and compassionate decision (particularly in patients with malignancy who have exhausted all therapeutic options and have relentless bone pain) is to withhold therapy for hypercalcemia. Future therapies directed at the osteoclast, such as more potent later-generation bisphosphonates; inhibitors of osteoclast attachments and inhibitors of peptides, which stimulate osteoclastic bone resorption, may permit safe, easily administered, outpatient therapies that will improve the quality of life for hypercalcemic patients.
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PMID:Pathophysiology and management of severe hypercalcemia. 832 91

Multiple myeloma was diagnosed in a 69-year-old man with pathological hip fracture, who had increased plasma cells in the bone marrow, osteolytic lesions in bones, low level of monoclonal protein (IgAK) in serum and urine, and anemia, hypercalcemia and renal insufficiency. He was treated for 1 year with chemotherapy with good results. 6 months after cessation of treatment the disease relapsed with multiple extramedullary plasmacytomas in skin and subcutaneous areas, right eyebrow, right knee, sternum and right axilla, but repeated bone marrow examinations were without evidence of disease activity. Chemotherapy was resumed but the patient died 1.5 years after the relapse with severe jaundice due to multiple liver plasmacytomas and pelvic masses.
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PMID:[Relapse of multiple myeloma in extramedullary sites]. 834 1

Sarcoidosis has been associated with a wide spectrum of renal manifestations, including disordered calcium metabolism, nephrocalcinosis, nephrolithiasis, granulomatous interstitial nephritis, and glomerulonephritis. In some patients, two or more manifestations of renal sarcoidosis may coexist. The case of a young patient with sarcoidosis who presented with hypercalcemia and acute renal failure is discussed. Despite normalization of the serum calcium with intravenous fluids and corticosteroids, his renal insufficiency persisted. A diagnostic renal biopsy was performed to determine the etiology of his renal failure and was helpful in the selection of optimal medical therapy.
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PMID:The kidney in sarcoidosis. 850 10

Acute hypercalcemic crisis is the life-threatening exacerbation of an existing hypercalcemia syndrome, which is characterized by additional cerebral symptoms such as clouding of consciousness, somnolence and coma as well as rapid deterioration of renal function. Possible causes are diseases associated with severe hypercalcemia, such as malignant diseases, primary and tertiary hyperparathyroidism, vitamin D poisoning and treatment with calcium, vitamin D and calcium-containing ion exchangers in renal insufficiency. Nowadays the specific diagnosis can usually be established quickly and simply, since only in primary and tertiary hyperparathyroidism are calcium and the intact parathormone elevated. The aim of treatment is to bring about an effective reduction in serum calcium by inhibiting bone resorption and increasing calcium excretion in the urine. Today, the substances calcitonin, biphosphonate, mithramycin (plicamycin) and glucocorticoids, each with a different mode of action, are available. In patients with underlying malignant diseases these substances are used to supplement the treatment of the malignancy, while in hyperparathyroidism they are administered prior to operative parathyroidectomy.
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PMID:[Hypercalcemic crisis. Exacerbation of an existing hypercalcemia syndrome]. 865 16

Milk-alkali syndrome is characterized by progressive hypercalcemia, systemic alkalosis, and renal insufficiency. After calcium carbonate is ingested with diary products, hypercalcemia and alkalosis may develop in susceptible persons, particularly those with underlying renal insufficiency. We describe a young woman who neither drank milk nor had peptic ulcer disease, yet who ingested enough calcium carbonate to require admission to an intensive care unit for acute renal failure. Chronically bulimic, she was taking Rolaids (Warner-Lambert Co, Morris Plains, NJ), which contained calcium carbonate, and was eating yogurt daily to prevent osteoporosis. We discuss the characteristics and complex metabolic interactions of the milk-alkali syndrome, a critical but generally reversible electrolyte disorder. Early recognition of coincident hypercalcemia and alkalosis and prompt cessation of calcium carbonate ingestion are essential for successful recovery. Finally, we suggest that nephrologists should discourage patients with renal insufficiency and chronic vomiting from consuming calcium-containing antacids and excessive dietary calcium.
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PMID:Rolaids-yogurt syndrome: a 1990s version of milk-alkali syndrome. 865 5

Solitary bone plasmacytomas account for 5-7% of multiple myeloma cases and are assumed to have a fairly good prognosis, with a long duration of relapse-free survival after primary local treatment. Isolated phalanx plasmacytoma is a very rare entity, because involvement of extremities is seen in less than 1% of all solitary bone plasmacytomas, where they are usually localized centripedally, often in the axial skeleton. A 68 year old patient with a lytic lesion involving 5th phalanx was diagnosed as having a biopsy-proven solitary plasmacytoma, with a negative work-up for coexisting plasma cell dyscrasia. Three and a half months after completion of radiotherapy of the involved phalanx, the patient was readmitted with hypercalcemia, renal insufficiency and subsequently diagnosed as having atypical plasma cell infiltration of marrow, and plasmacytomas involving the right vocal cord and the premaxillary region, as well as pathological ulna fracture. Plasmacytoma of the phalanx, with extreme short duration of remission and an aggressive type of clinical relapse, is in sharp contrast with the natural stable course of a solitary plasmacytoma where the use of systemic treatment is subject to intense debate.
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PMID:Solitary phalanx plasmacytoma relapse with disseminated extramedullary plasmacytomas and myeloma after short duration of remission. 868 59

Pamidronate (APD) is a drug widely used for the treatment of hypercalcemia of malignancy. Renal impairment has been associated with the use of other bisphosphonates in humans, and nephrotoxicity has been described after APD administration in animals. We retrospectively evaluated the safety and efficacy of APD administration in 31 patients with underlying renal insufficiency who received 33 courses of APD in doses of 60-90 mg. Hypercalcemia resolved or improved in 91% of the patients and only 1 case had severe hypocalcemia. A transient deterioration in renal function was observed in 8 courses but this was unrelated to APD administration. No systemic ill effects were observed. APD appears to be a safe drug in patients with underlying renal failure.
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PMID:Safety of pamidronate in patients with renal failure and hypercalcemia. 870 58


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