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

The introduction of new techniques for the determination of renal parenchymal oxygenation and intrarenal microcirculation has elucidated some important aspects in the pathophysiology of acute renal failure (ARF). Data accumulated over the last decade with these techniques, together with improved morphologic evaluation of the kidney, indicate that medullary damage may play a pivotal role in various forms of acute and chronic renal hypoxic and toxic insults. The outer medulla functions normally under hypoxic conditions, as a result of limited regional oxygen supply and high oxygen consumption for urinary concentration. Outer medullary oxygenation is critically balanced by mechanisms designed to adjust oxygen demand and supply, and their insufficiency may lead to ARF with hypoxic medullary damage. In this article, we outline our current concept of the physiologic control of medullary oxygenation and review the clinical conditions that predispose to hypoxic medullary damage, including rhabdomyolysis, hypercalcemia, or the exposure to endotoxin, nonsteroidal anti-inflammatory drugs, radiologic contrast agents, cyclosporine, FK506, and amphothericin. We shall indicate a possible role for medullary oxygen insufficiency in clinical conditions known to predispose to ARF, such as preexisting renal disease, diabetes mellitus, hypertension, atherosclerosis, effective volume depletion, urinary obstruction, or aging, and suggest potential strategies to preserve medullary oxygenation and integrity.
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PMID:The role of medullary ischemia in acute renal failure. 857 90

Intensive training in a humid and warm environment can cause exertional heat stroke (ExHS) and rhabdomolysis (RBD) in military recruits. To investigate the role of vitamin D and monomeric calcitonin (CT) on the calcium metabolism in ExHS with RBD and acute renal failure (ARF), we studied 21 recruits with ExHS (mean age 21.4 years), 7 of which had ARF. Another 11 age-matched recruits with heat exhaustion (HE) and 11 healthy subjects were selected as controls. Our results showed that in 14 ExHS patients without ARF, mean serum creatinine (Cr) levels were significantly higher (151.16 vs. 106.08 mumol/l, p < 0.01), whereas serum osteocalcin (OC) levels were significantly lower (2.22 vs. 4.65 micrograms/l, p < 0.01) than in healthy controls. In 7 patients with ExHS and ARF, the mean serum Cr (774.38 vs. 105.20 mumol/l, p < 0.01), phosphorus (P) (2.26 vs. 1.26 mmol/l, p < 0.05), creatine phosphokinase (CPK) 274,143.97 vs. 85.78 IU/l, p < 0.05), intact parathyroid hormone (I-PTH) (299.81 vs. 18.66 ng/l, p < 0.05) and CT (13.58 vs. 6.63 ng/l, p < 0.01) levels on admission were significantly higher while the mean ionized calcium (iCa) levels were significantly lower than the healthy controls (0.9 vs. 1.18 mmol/l, p < 0.01). The mean serum 25-hydroxyvitamin D [25(OH)D] levels were not significantly different from healthy controls. However, mean serum 1,25-dihydroxyvitamin D [1,25(OH)2D] levels and the ratio of 1,25(OH)2D to 25(OH)D were significantly lower than healthy controls throughout the whole course of ARF. None of the 7 patients with ExHS and ARF developed hypercalcemia during the diuretic phase. Their mean serum I-PTH levels decreased significantly from 299 to 18 ng/l during the recovery phase (p < 0.05). Our study seems to suggest that the abnormal calcium metabolism in this unique patient group is in part caused by persistently decreased renal production of 1,25(OH)2D, although increased monomeric CT levels were associated with hypocalcemia. However, whether or not a causal relationship exists merits further investigation.
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PMID:A prospective study of calcium metabolism in exertional heat stroke with rhabdomyolysis and acute renal failure. 858 23

Abnormal calcium metabolism is a common complication of rhabdomyolysis -induced acute renal failure. During the oliguric phase, patients are frequently hypocalcemic. Hyperphosphatemia and skeletal resistance to parathyroid hormone are believed to be possible underlying mechanisms. In addition, there have been reports of hypercalcemia during the diuretic recovery phase after rhabdomyolysis. The pathophysiology of the hypercalcemia observed in the recovery phase is a subject of debate. Several mechanisms have been proposed, including mobilization of calcium from muscle deposits, secondary hyperparathyroidism, and elevated levels of 1,25 dihydroxyvitamin D. The authors report the case of a 30-year-old man admitted for evaluation of marked hypercalcemia (18.3 mg/dL) who was hospitalized 3 weeks earlier for acute renal failure secondary to rhabdomyolysis. Plasma parathyroid hormone and 1,25 dihydroxyvitamin D levels were suppressed during the period of maximal hypercalcemia. A technetium pyrophosphate scan demonstrated extensive deposition of calcium throughout the pelvic and lower extremity muscles. This case of delayed hypercalcemia after rhabdomyolysis supports the hypothesis that mobilization of calcium deposits from soft tissue, including muscle, is central to the pathogenesis of this syndrome.
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PMID:Case report: delayed hypercalcemia after rhabdomyolysis-induced acute renal failure. 860 49

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

Renal cell carcinoma accompanied with ossification reported in Japan is very rare. We report a case of renal cell carcinoma with ossification pathologically in a 61-year-old woman. She suddenly presented with hypercalcemia that caused acute renal failure, 6 months after the operation and died shortly thereafter. We discuss the relationship between the tumor and the hypercalcemia.
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PMID:[Renal cell carcinoma accompanied with ossification: a case report]. 871 87

Nitrogen retention of various intensity was found in 61 patients with multiple myeloma. In seven (11%) of them the disturbances of the depurative renal function manifested as acute renal failure (ARF). The syndrome was characterised in etiologic, pathogenetic, clinical, therapeutic and prognostic aspects. ARF in the study developed on the background of a light chain proteinuria in patients with hypercalcemia, dehydration, radiocontrast studies, blood loss, surgical interventions, and severe infections. Following conservative treatment, the renal function normalized in one patient, a gradual transition to chronic renal failure was observed in five patients, and lethal outcome in one patient. The average survival rate after ARF was 8 months (1-13 months).
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PMID:Acute renal failure in patients with multiple myeloma. 900 62

We reviewed the clinical features and outcome of 56 patients with myeloma and severe renal failure managed in a single institution over a 15-year period. Renal failure was recognized within 2 months of the diagnosis of myeloma in 75% of patients, and was the initial presentation of myeloma in 50%. Patients were staged by the Durie and Salmon classification. Light-chain and IgD myeloma accounted for 46% of cases, and Bence-Jones proteinuria was identified in > 90%. In 43%, a potential precipitant of renal failure was identified, usually hypercalcaemia or a non-steroidal anti-inflammatory agent. A preserved corrected calcium at presentation was characteristic (2.40 +/- 0.15 mmol/l, n = 42), even after excluding those with hypercalcaemia requiring specific intervention (n = 14, 2.76 +/- 0.51; p < 0.01): this finding in patients with unexplained acute renal failure should alert clinicians to the possibility of myeloma. Forty-seven patients (84%) required dialysis. Only seven (15%) ever regained renal function. Median survival (all patients) was 8 months. One-third died within 3 months of referral and one-third survived > 1 year. Hypoalbuminaemia and reduced platelet count at presentation were associated with reduced survival, but hypercalcaemia, infection, dialysis, (urgent or long-term), and dialysis modality were not. Chemotherapy was associated with increased survival, but progression of myeloma and infection were the two most frequent causes of death. Severe renal failure was associated with advanced myeloma stage and light-chain/IgD paraproteinaemia. Survival was related to severity of myeloma and not requirement for dialysis per se.
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PMID:Presentation and survival of patients with severe renal failure and myeloma. 953 42

A 72-year-old patient with multiple myeloma was admitted to the intensive care unit because of hypercalcemic crisis and acute renal failure. After 7 days of comprehensive therapy including diuretics steroids, calcitonin, and intermittent hemodialysis (IHD) with low-calcium dialysate, calcium still reached high levels between IHD treatments and thrombocytopenia developed after chemotherapy. CVVHDF with calcium-free bicarbonate dialysate was started. Anticoagulation with 2.2% citrate was performed in order to chelate calcium, and thus treat the hypercalcemia, and to provide regional anticoagulation, and thus reduce the risk of bleeding due to thrombocytopenia. CVVHDF with citrate anticoagulation was continued for 6 days, and standard heparin anticoagulation was started when the hypercalcemia and thrombocytopenia abated.
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PMID:Continuous venovenous hemodiafiltration (CVVHDF) with citrate anticoagulation in the treatment of a patient with acute renal failure, hypercalcemia, and thrombocytopenia. 956 11

Hypercalcaemia is a rare feature of acute lymphoblastic leukaemia (ALL) in adults, particularly of the T cell type. We report on a 24-year-old patient with T-ALL, who presented with symptoms of hypercalcaemia (vomitus, acute renal failure), bone pain, extensive osteolytic lesions and normal white cell count without circulating blasts. An increased serum tumor necrosis factor (TNF-alpha) concentration of 35 pg/ml was found; it remained elevated at 52 pg/ml four weeks later, after having achieved haematological remission. Serum concentrations of IL-1beta, IL-6 and IL-2 were within the control range. The pathophysiology of hypercalcaemia in malignancy and possible mediators of bone resorption, in particular TNF-alpha, are discussed.
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PMID:Severe hypercalcaemia and extensive osteolytic lesions in an adult patient with T cell acute lymphoblastic leukaemia. 964 32

A 20-year-old Japanese man with a hypothalamic tumor (most likely germ-cell tumor) which caused secondary hypoadrenalism, hypogonadism and diabetes insipidus developed hypercalcemia and acute renal failure. The serum levels of intact PTH (iPTH), PTH-related protein (PTH-rP), 1,25-dihydroxy vitamin D (1,25- (OH)2 D), ACTH, cortisol, gonadotropins and testosterone were decreased, but his serum levels of triiodothyronine (T3) and thyroxine (T4) were within the normal range at admission, with depressed TSH and slightly increased thyroglobulin. The hypercalcemia was refractory to extensive hydration and calcitonin, but was ameliorated by pamidronate. After irradiation of the hypothalamic tumor, panhypopituitarism gradually developed. The patient has been normocalcemic for the last 2 years and is doing well under replacement therapy with glucocorticoid, L-thyroxine, methyltestosterone and 1-desamino D arginine vasopressin (dDAVP). As to the mechanism of euthyroidism at admission, transient destructive thyroiditis associated with hypopituitarism or delayed development of hypothyroidism following the hypoadrenalism was suggested. This is the first reported case of hypercalcemia in secondary hypoadrenalism due to hypothalamic tumor. Hypercalcemia was most likely induced by increased bone resorption, which was probably elicited by the combined effects of deficient glucocorticoid and sufficient thyroid hormones in addition to hypovolemia and reduced renal calcium excretion. Furthermore, severe dehydration due to diabetes insipidus and disturbance of thirst sensation caused by the hypothalamic tumor aggravated the hypercalcemia, leading to acute renal failure.
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PMID:Hypercalcemia in an euthyroid patient with secondary hypoadrenalism and diabetes insipidus due to hypothalamic tumor. 1039 33


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