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

We have developed a simplified method for performing regional citrate anticoagulation during hemodialysis. High ultrafiltration rates and specialized equipment were obviated by the use of a 1.6-mol/L trisodium citrate solution and a standard calcium-containing dialysate. Thirty-six dialyses were performed with this technique on 14 stable and 22 high bleeding risk patients. There was no significant decline in plasma-ionized calcium during citrate dialysis, ie, 3.85 +/- 0.34 mg/dL (mean +/- SE) predialysis, to 3.31 +/- 0.26 postdialysis; furthermore, no patient developed neuromuscular symptoms or evidence of cardiovascular instability from hypocalcemia. Serum sodium rose with this procedure, but not to hypernatremic levels. This method of citrate dialysis is safe and effective during continuous blood flow (double-needle) hemodialysis, and is no more difficult to perform than conventional heparin dialysis. Single-needle (reciprocating blood flow) hemodialysis was successfully performed by the additional use of a calcium-free dialysate and separate calcium chloride infusion (10% calcium chloride), but risks the production of unexpected hypercalcemia.
 ...
PMID:Regional anticoagulation: hemodialysis with hypertonic trisodium citrate. 375 75

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.
 ...
PMID:Immobilization hypercalcaemia due to low bone formation and responding to intravenous sodium sulphate. 376 50

To assess the consequences of hypercalcemia on systemic and renal hemodynamics, vasoactive hormones, and water and electrolyte excretion in intact, conscious mongrel dogs, measurements in 10 dogs receiving 100 mg/kg calcium gluconate and 10,000 U/kg vitamin D daily for 2 weeks were compared with measurements made in 10 time-control dogs not receiving calcium or vitamin D. Hypercalcemia induced by dietary supplementation with calcium and vitamin D resulted in profoundly reduced glomerular filtration rate (40 vs 78 ml/min in controls; p less than 0.005), estimated renal plasma flow (145 vs 267 ml/min in controls; p less than 0.005), and renal blood flow (254 vs 441 ml/min in controls; p less than 0.005). Renal resistance was significantly increased in the hypercalcemic dogs (0.57 +/- 0.07 vs 0.28 +/- 0.01 mm Hg/ml/min; p less than 0.005). Hypercalcemia also resulted in increased fractional excretion of water (4.8 vs 1.4% in controls; p less than 0.005), sodium (1.4 vs 0.6% in controls; p less than 0.005), calcium (1.7 vs 0.7% in controls; p less than 0.01), and magnesium (10.2 vs 4.1% in controls; p less than 0.005). Systolic blood pressure (160 vs 172 mm Hg in controls; p less than 0.05) and stroke volume were lower (0.024 vs 0.036 L/beat in controls; p less than 0.005) in hypercalcemic dogs, presumably because of the diuresis, while total peripheral resistance was higher (36 vs 31 mm Hg/L/min; p less than 0.05) in controls. Magnesium levels were significantly lower in the experimental group (1.3 vs 1.7 mg/dl in controls; p less than 0.0005). Aldosterone levels, plasma renin activity, and urinary prostaglandin excretion were not significantly affected.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Systemic and renal vascular responses to dietary calcium and vitamin D. 377 Aug 72

The renal effect of calcitonin (independent of changes due to variations in sodium excretion) was quantitated in malignancy associated hypercalcaemia. There was considerable inter- and intra-patient variability in response but this was unaffected by tumour type. Humoral hypercalcaemia tended to be resistant to control. In responsive patients the renal effects of calcitonin unlike those described in bone did not diminish with time.
 ...
PMID:Quantitation of the renal effect of calcitonin in the hypercalcaemia of malignancy. 378 Aug 23

Sodium-retaining activity of chum salmon prolactin (PRL) was examined in several euryhaline teleosts. Chum PRL was 100 times more potent than ovine PRL in maintaining plasma sodium levels in the hypophysectomized killifish, Fundulus heteroclitus, transferred from 50% seawater to fresh water. The effects of PRLs were parabolic, high doses of the hormones being less effective than low doses. When injected into seawater-adapted fry of the ayu, Plecoglossus altivelis, or into juvenile rainbow trout, Salmo gairdneri, adapted to 50% seawater, a dose-dependent increase in plasma sodium was observed. Chum PRL was 2-10 times more active than ovine PRL, and the effects in the ayu were also parabolic. An increase in plasma sodium also occurred when the PRLs were injected into the seawater-adapted eel, Anguilla japonica; the chum and ovine PRLs were equipotent, and hypercalcemia was also observed. In contrast, both chum and ovine PRLs were without effect on plasma sodium levels of chum salmon fry, either when injected into seawater-adapted fish kept in seawater or into fish subsequently transferred to fresh water. The absence of an effect of PRLs in chum salmon fry seems to be due, at least in part, to their good osmoregulatory ability during the period of seaward migration; effects of the exogenously administered PRLs may be compensated for by other hormones responsible for their hydromineral balance.
 ...
PMID:Sodium-retaining activity of chum salmon prolactin in some euryhaline teleosts. 378 Dec 35

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.
 ...
PMID:Effects of vitamin D-induced chronic hypercalcemia on rat renal cortical plasma membranes and mitochondria. 381 41

The effects of thiazide diuretics on serum phosphate concentration, renal tubular threshold for phosphate, and urinary calcium excretion in children with renal hypophosphatemic rickets were studied. There were nine controlled acute studies conducted in five patients, and, in addition, seven long-term studies of up to 26 months were performed. During the acute studies, the children continued to receive the same doses of oral calcitriol and phosphate supplementation as at home. Hydrochlorothiazide, 1.50 to 2.25 mg/kg/d, was used alone in the first four studies; hydrochlorothiazide and amiloride at a dose of 1 mg for each 5 mg of hydrochlorothiazide were used in the other five studies. Administration of the diuretics for four days gave rise to a significant increase in serum phosphate concentration from 3.1 +/- 0.4 mg/dL to 3.7 +/- 0.9 mg/dL (P less than .01) and in tubular threshold for phosphate from 1.31 +/- 0.45 mg/dL to 1.74 +/- 0.60 mg/dL (P less than .01). These changes were accompanied by significant reductions in urinary sodium excretion from 135 +/- 39 mEq/24 h during the control period to 99 +/- 42 mEq/24 h on the fourth day of therapy (P less than .05), fractional sodium excretion from 0.99% +/- 0.42% to 0.81% +/- 0.42% (P less than .05), and urinary calcium excretion from 57.3 +/- 28.9 mg/24 h to 19.0 +/- 13.1 mg/24 h (P less than .01). Fractional excretion of phosphate divided by fractional excretion of sodium after the treatment with diuretics was not significantly different from that observed at the end of the control period. Increments in serum phosphate concentrations were correlated with elevations in serum albumin concentrations (r = .739; P less than .02). As an additional index of intravascular volume contraction, the elevations in serum phosphate concentrations were correlated with the increase in BUN, (r = .793; P less than .01). The addition of amiloride in the last five studies prevented the hypokalemia and alkalosis that had complicated the administration of hydrochlorothiazide. Long-term follow-up studies for a total of 119 therapy-months on six children and one adult, who continued to receive the diuretics concomitantly with calcitriol and phosphate supplementation, showed that they were free of complications except for a transient episode of hypercalcemia and hypercalciuria in one patient. In comparison with the previous period of treatment with calcitriol and phosphate without diuretics, linear growth velocity and healing of the rickets were not changed in two children and improved in the other four after the addition of hydrochlorothiazide and amiloride.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Effects of hydrochlorothiazide and amiloride in renal hypophosphatemic rickets. 388 56

Investigations were carried out with 24 sheep divided into two groups of twelve animals. The first group were infected via the lateral recessus of the tarsal joint with 2 cm3 of a 24-hour broth culture of Corynebacterium pyogenes, and the second one were infected i/v with 3 cm3 of the same culture. The changes in the total protein, protein fractions, and blood electrolites in the blood were followed up. It was found that the infection of Corynebacterium pyogenes affected the total reactivation of the animals and led to immunobiologic reconstruction changes. There were hyperproteinemia which depended on the route of infection as well as the severity of its course, and hyperglobulinemia which was "at the expense of' blood albumin. Noticed were also hypercalcemia, hyperpotassemia, and lower sodium and phosphorus levels.
 ...
PMID:[Biochemical changes in the blood of sheep with experimental Corynebacterium infection]. 388 45

Autosomal dominant familial hypocalciuric hypercalcemia was found in a kindred with neonatal severe primary hyperparathyroidism, previously judged to be an autosomal recessive trait. Mild hypercalcemia was documented in eight members representing three generations. Mild hypercalcemia was documented at an age as early as one week. In seven adults presumed to be heterozygotes, urinary calcium levels were in the same range as for familial hypocalciuric hypercalcemia. An additional adult member (who previously underwent parathyroidectomy for neonatal severe primary hyperparathyroidism) showed an abnormality in renal clearance of calcium and sodium characteristic of combined familial hypocalciuric hypercalcemia and surgical hypoparathyroidism. Parathyroidectomy in three hypercalcemic members did not cause normocalcemia. Unlike other kindreds with familial hypocalciuric hypercalcemia in whom hypercalcemia is consistent over time and moderate in heterozygotes, this kindred was characterized by heterozygotes showing hypercalcemia that was intermittent and mild. The consanguineous parents of the two previously described severely affected neonates were judged to be heterozygotes for familial hypocalciuric hypercalcemia. In conclusion, (1) a gene presenting as familial hypocalciuric hypercalcemia can be expressed as hypercalcemia that is intermittent and very mild in heterozygotes; (2) such a gene can cause neonatal severe primary hyperparathyroidism in homozygotes.
 ...
PMID:Familial hypocalciuric hypercalcemia. Mild expression of the gene in heterozygotes and severe expression in homozygotes. 396 79

Squamous cell carcinoma of the skin is a rare complication of hidradenitis suppurativa. We treated a case of hidradenitis-associated squamous cel carcinoma with metastases to the inguinal lymph nodes. Hypercalcemia also occurred, possibly in relation to the secretion of a hormonelike substance by the tumor. Chemotherapy with bleomycin sulfate, methotrexate sodium, and cisplatin led to tumor regression and control of the hypercalcemia.
 ...
PMID:Hypercalcemia in association with cutaneous squamous cell carcinoma. Occurrence as a late complication of hidradenitis suppurativa. 397 41


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>