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

The effects of calcium-gluconate infusions on renal function were studied in unanesthetised dogs. Each dog was studied during hydropenia and saline infusion. Hypercalcemia, mean serum calcium 3.85 mmol/l (hydropenia) and 3.62 mmol/l (saline infusion), increased fractional excretion of sodium (CNa/CIn), calcium (CCa/CIn), and magnesium (CMg/CIn). The increase was significantly higher in saline-expanded dogs than in hydropenic dogs. Fractional excretion of potassium (CK/CIn) was increased in hydropenia but remained unchanged in saline-expanded animals. Fractional excretion of phosphate (Cp/CIn) was not consistently changed by hypercalcemia. Fractional excretion of chloride (CCl/CIn) was markedly increased in saline-expanded dogs but was not changed in hydropenia. Urine osmolality was reduced in hydropenic dogs but unchanged in saline-expanded dogs. In hydropenic as well as in saline-expanded dogs tubular reabsorption of solute-free water (TcH2O/CIn) increased during the first hour of hypercalcemia. In hydropenic dogs hypercalcemia caused a slight but significant decrease in blood pH, standard bicarbonate, and base excess. In hydropenic as well as in saline-expanded dogs glomerular filtration rate (CIn), renal plasma flow (CPAH), and filtration fraction were unaffected.
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PMID:Renal function in hypercalcemic dogs during hydropenia and during saline infusion. 4 8

In 36 patients with neoplastic diseases 72 episodes of hypercalcaemia with serum-calcium levels greater than or equal to 2.75 mmol/l were treated (19 breast carcinoma; 9 bronchial or lung carcinoma; 5 multiple myeloma; 1 each jejunal carcinoid, malignant lymphoma, phaeochromocytoma). Cardinal symptoms were mental, neuromuscular and renal during the hypercalcaemic episodes. Mithramycin is preferred to other methods (infusion of sodium chloride and frusemide, prednisone, sodium-potassium-phosphate infusion) of treating acute or subacute hypercalcaemia. Mithramycin in a single injection of 20-25 microgram/kg body-weight intravenously is usually sufficient to counteract a hypercalcaemic phase for at least 7-10 days, often much longer. There was a highly significant fall in serum-calcium levels from two days onwards after mithramycin injection. Toxic side-effects were minimal and restricted to transitory increase in transaminase levels, initially 5-6 times normal with a maximum on the third day and normalisation on the fifth day after mithramycin administration.
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PMID:[Treatment of hypercalcaemic syndrome in tumour patients, especially with mithramycin]. 14 99

Following an intravenous loading injection of 75 U.S.P. Units of Para-Thor-Mone (Eli Lilly and Co), seven conscious, non-pregnant, non-lactating Merino ewes were infused with a maintenance dose of the hormone at a rate of 4-75 U.S.P. units/min for 2 hr. The classical hypercalcaemia and hypophosphataemia of the non-ruminant was observed, but the hypercalcaemi- was only small. Plasma potassium concentration decreases, while there were no changes in plasma sodium, chloride or mangesium. The classical phosphaturic effect of the hormone was not observed, only trace amounts of phosphate being exreted throughout the experiment. Urinary excretion of calcium and magnesium decreased, urine flow and urinary excretion of sodium, potassium, chloride, bicarbonate and urine pH increased. Glomerular filtration rate was unaffected, but renal plasma flow increased. The concentration and secretion rate of salivary phosphate increased markedly. Changes in the other important salivary electrolytes (sodium, potassium, chloride, bicarbonate and hydrogen ion) also occurred, but it was difficult to separate primary from secondary effects of the hormone. Saliva flow rate increased transiently following hormone injection, but the effect was not sustained by the maintenance infusion.
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PMID:The acute effects of intravenous infusion of parathyroid hormone on urine, plasma and saliva in the sheep. 23 58

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

1. A denervated 'auto-transplanted' dog's kidney preparation was developed to study renin release into renal plasma and lymph. The function of the 'transplant' was compared with that of its partner. In the 'basal' state it had a similar rate of plasma and urine flow, Na, Ca, Mg and Cl excretion but a lower rate of glomerular filtration and K excretion and a lower urinary osmolality. In the 'basal' state the 'transplant' did not release renin into plasma, but invariably released it into lymph. 2. Infusions of MgCl2 solutions into the renal artery which raised the renal plasma Mg concentration (PMg) by 0.1-2 m-mole.1.-1 provoked a concentration-related increase in renin release into plasma. This was due to a rise in the veno-arterial renin difference and in the renal plasma flow rate. Blood pressure and Na excretion were unaltered. 3. In other experiments, an increase in PMg of 1.5-2.5 m-mole.1.-1 was also found to increase renin release into lymph. 4. When the plasma Ca concentration was doubled by infusion of CaCl2 into one renal artery, an increase in PMg of 1.5-2.5 m-mole.1.-1 no longer increased renin release into plasma or lymph. 5. When the plasma NaCl concentration was raised by 8-15 m-mole.1.-1 by infusion of hypertonic saline into the renal artery, MgCl2 infusion failed to increase renin release until PMg was raised by more than 3 m-mole.1-1. 6. The results demonstrate that hypermagnesaemia stimulates renal renin release by a mechanism that is independent of the renal nerves, or of any changes in blood pressure or sodium excretion, but which is antagonized by concurrent hypercalcaemia or hypersalaemia. The possibility is discussed that Mg is reabsorbed from the tubular into the interstitial fluid where it antagonizes the action(s) of Ca on renin release from the juxtaglomerular cells.
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PMID:The effect of increasing the plasma magnesium concentration on renin release from the dog's kidney: interactions with calcium and sodium. 36 8

The concepts underlying the clinical use of the anion gap (AG) and those disorders associated with its alteration are reviewed. A substantial increase in the AG usually indicates the presence of a metabolic acidosis, unless large doses of certain antibiotics or sodium salts of organic acids are being used. The etiology, pathogenesis and diagnosis of high AG metabolic acidoses are discussed. Stress is placed upon the utility of the AG in defining the cause of the acidosis, and as a guide to therapy in certain organic acidoses. A decrease in the normal AG occurs in dilutional states, hypoalbuminemia, hypercalcemia, hypermagnesemia, hypernatremia, diseases associated with hyperviscosity, bromide intoxication, and in certain paraproteinemias. The important clue provided by a low or negative AG in the diagnosis of certain of these life-threatening disorders is emphasized.
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PMID:Clinical use of the anion gap. 40 25

The UBB of Notopterus notopterus is a paired structure situated between the oesophagus and sinus venosus. Both right and left lobes of the gland are enveloped by a common thick connective tissue which gets constricted between the lobes and separates them. Numerous follicles of varying sizes are encountered in each gland. In N. notopterus the effects of hypercalcaemia (caused by keeping the specimens in 0.5% of CaCl2 solution and by injecting 4000 I.U. of vitamin D2 on alternate days) on UBB has been observed. The effects of NaCl rich environment (created by keeping the fish in 0.5% NaCl solution) on this gland has also been studied. In the UBB of N. notopterus the activity of the gland is observed in terms of: 1. increase in the blood supply of the gland and the dilation of the blood vessel, 2. increase in the height of the follicular epithelium, 3. cytoplasmic hypertrophy resulting in the increase in secretory processes, 4. appearance of pseudostratified epithelium in place of single layered cuboidal follicular epithelium and 5. nuclear and cellular hypertrophy. According to these characteristics it is evident that the gland from group II shows gradual activity from the 2nd day onwards and is maximum on the 6th day. From 8th day to the close of the experiment gradual inactivity of the gland is discerned--follicles get atrophied and the cells appear in clumps. The gland from group III shows a good response to its environment and is more hypertrophied as compared to that of group II. The activity of the gland closely parallels serum sodium levels which increase up to the 8th day when UBB shows the maximum activity. The serum sodium level rises from a normal of 110 m eq/l to a peak of 180 m eq/l on 8th day. After 10 days onwards the gland shows gradual inactivity and degeneration. The serum sodium level is 130 m eq/l on 12th day. These observations support the view that the main role of UBB in N. notopterus lies in sodium metabolism and it is only partially responsible for calcium regulation.
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PMID:Ultimobranchial body of Notopterus notopterus in relation to calcium and sodium rich environments. 52 84

The present study is an investigation of the mechanism of hypercalcemia and hyperphosphatemia induced by the intravenous injection of lead acetate (Pb-Ac). A total of 118 male rats were injected with 30 mg/kg of Pb-Ac, or with 16.5 mg/kg of sodium acetate as the control. The levels of serum calcium, phosphorus and lead were then determined at various time periods after the injections. Serum calcium and phosphorus levels increased with time after Pb-Ac injection and the maximum values of calcium (17 mg%) were found after 1 h and of phosphorus (13.5 mg%) after 30 min. Both calcium and phosphorus levels reverted to the normal range after 12 h. The maximum net rates of increase of calcium and phosphorus were found immediately after Pb-Ac injection. At that time, deposition of lead at the calcifying sites of bone and incisor dentin was demonstrated by a histochemical examination. In other experiments the changes in the calcium and phosphorus contents in the medium after shaking bone powder in serum with Pb-Ac in an in vitro system were studied. It was confirmed that the calcium and phosphorus were displaced from the bone mineral, the extent of the displacement being correlated with the concentration of the Pb-Ac added to the medium, and that these displacements were very rapid reactions. These results suggest that hypercalcemia and hyperphosphatemia following Pb-Ac injection results from a direct action of lead on the bone mineral.
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PMID:Mechanism of induction of hypercalcemia and hyperphosphatemia by lead acetate in the rat. 59 44

One case of acute hypercalcaemia and two of recurrent nephrolithiasis are reported in patients who had regularly consumed large amounts of calcium carbon-ate-sodium bicarbonate powders for more than 20 years. The powders had been obtained from pharmacists unknown to the patients' medical practitioners. It is suggested that these preparations were responsible for the patient's problems, and that such powders should no longer be freely obtainable.
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PMID:Obsolete but dangerous antacid preparations. 62 56

In intact eels in sea water (SW), ovine prolactin (PRL) treatment induces hypercalcemia, but its mechanism of action, which is discussed, remains to be defined. Corpuscles of Stannius (CSt) are modified simultaneously: two cell categories then become evident. The first cell type (type 1) predominates; it has an oval shape and large granules, it shows a nuclear and nucleolar hypertrophy and a mitotic activity, and appears greatly stimulated by PRL; it may elaborate a hypocalcemic factor (hypocalcin) which would compensate for the PRL-induced hypercalcemia. A similar effect, although slightly less intense, is detected in hypophysectomized-PRL treated eels in SW. A second cell type (type 2), is more elongated, smaller in size, and has an oval nucleus and fine granules. Scarcely less active in SW, it is significantly stimulated by PRL despite an increased blood sodium and potassium level. This experiment does not help to clarify its function.
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PMID:Prolactin, hypercalcemia and corpuscles of Stannius in seawater eels. 62 14


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