Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the role of parathyroid hormone (PTH) and(or) an intrinsic renal tubular reabsorptive defect for phosphate in mice with hereditary hypophosphatemic rickets, we performed clearance and micropuncture studies in hypophosphatemic mutants and nonaffected littermate controls. Increased fractional excretion of phosphate in mutants (47.2+/-4 vs. 30.8+/-2% in controls) was associated with reduced fractional and absolute reabsorption in the proximal convoluted tubule and more distal sites. Acute thyropara-thyroidectomy (TPTX) increased phosphate reabsorption in both mutants and controls with a fall in fractional phosphate excretion to congruent with7.5% in both groups indicating that PTH modified the degree of phosphaturia in the intact mutants. Absolute reabsorption in the proximal tubule and beyond remained reduced in the mutants, however, possibly because of the reduced filtered load. Serum PTH levels were the same in intact mutants and normals as was renal cortical adenylate cyclase activity both before and after PTH stimulation. To evaluate the possibility that the phosphate wasting was caused by an intrinsic tubular defect that was masked by TPTX, glomerular fluid phosphate concentration was raised by phosphate infusion in TPTX mutants to levels approaching those of control mice. Phosphate excretion rose markedly and fractional reabsorption fell, but there was no change in absolute phosphate reabsorption in either the proximal tubule or beyond, indicating a persistent reabsorptive defect in the absence of PTH. We conclude that hereditary hypophosphatemia in the mouse is associated with a renal tubular defect in phosphate reabsorption, which is independent of PTH and therefore represents a specific intrinsic abnormality of phosphate transport.
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PMID:Evidence for an intrinsic renal tubular defect in mice with genetic hypophosphatemic rickets. 22 35

In the thyroparathyroidectomized (TPTX) rat, fasting increased urinary phosphorus excretion by decreasing the tubular reabsorption of P1 (TRP) and resulted in hypophosphatemia. The administration of either sucrose or NaHCO3 prevented the metabolic acidosis associated with fasting and decreased the phosphaturia, indicating that the phosphaturia in fasting is in part due to metabolic acidosis. In rats on partial reduction of P1 intake selectively, the phosphaturic response to parathyroid hormone (PTH) was completely suppressed. On the other hand, the fasting rat partially retained the phosphaturic response to PTH, although dietary P1 intake was totally absent. These findings suggest that the renal P1 wasting in fasting may take place by dual mechanisms: a) the PTH-independent decrease in TRP, and b) an inability to totally suppress the response to PTH. Cyclic AMP generation in response to PTH, determined both in vivo and in vitro, was not measurably altered in fasting. However, the phosphaturic response to cyclic AMP was decreased in fasting, suggesting that the mechanism of partial resistance to PTH is probably not at but after cyclic AMP generation.
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PMID:Effect of fasting on tubular phosphorus reabsorption. 22 13

The pathogenesis of the association of medullary sponge kidney and hyperparathyroidism from parathyroid adenoma remains obscure. This unusual case of medullary sponge kidney and secondary hyperparathyroidism due to renal-leak hypercalciuria gives insight into a possible mechanism for the occurrence of medullary sponge kidney with parathyroid adenoma. Suppressible hyperparathyroidism due to renal calcium wasting could represent an intermediate stage in the development of unsuppressible parathyroid hormone secretion. Thus, parathyroid adenoma occurring with medullary sponge kidney may represent a consequence of disordered renal calcium excretion rather than a primary abnormality.
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PMID:Medullary sponge kidney and renal-leak hypercalciuria. A link to the development of parathyroid adenoma? 43 Jun 89

A 57-year-old male developed hypomagnesemia, hypokalemia and hypocalcemia during the course of repeated gentamicin therapy. Renal wasting of magnesium and potassium was demonstrated. Associated endocrine abnormalities included decreased level of serum immunoreactive parathyroid hormone and increased levels of plasma renin and aldosterone. Our findings are compared to those previously reported by other investigators.
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PMID:Symptomatic hypomagnesemia associated with gentamicin therapy. 45 Jan 67

Porcine thyrocalcitonin (TCT) given intramuscularly at a dose of 2-3 MRC units/kg body weight induces a renal bicarbonate wasting probably at the level of the proximal tubule. This effect is found in normal children as well as in patients with renal tubular acidosis and with vitamin D deficiency. The mechanism by which TCT acts on the acidification mechanism is probably independent of parathyroid hormone (PTH) because the effect could also be obtained in hypoparathyroid patients.
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PMID:Effect of thyrocalcitonin on renal reabsorption of bicarbonate. 53 80

A proximal renal tubular acidosis (RTA) is the mechanism underlying the systemic acidosis found in vitamin D deficiency rickets. Acidotic subjects have high levels of PTH. In non-acidotic subjects proximal bicarbonate wasting can be induced by exogenous PTH injection. Carbonic anhydrase activity is not involved in this process. Calcium infusion is able to suppress both the spontaneous and the PTH-induced bicarbonate leak. The development of RTA in vitamin D deficiency is related to a particular equilibrium between two antagonizing factors at tubular level, parathyroid hormone and calcium.
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PMID:Proximal renal tubular acidosis in vitamin D deficiency rickets. 81 Jan 89

Seventeen patients with malignant disease developed a complex metabolic syndrome of 2-8 weeks' duration characterized by hypocalcemia, hypomagnesemia and hypokalemia following administration of the aminoglycoside group of antibiotics. Gentamicin, Tobramycin, Amikacin, and Sisomicin were all involved. Other features noted were hypoalbuminemia, hypophosphatemia, and hypouricemia. Low immunoreactive parathyroid hormone (i-PTH) levels in the presence of hypocalcemia and absence of hyperplastic changes in the parathyroid gland examined at postmortem confirmed a diagnosis of hypoparathyroidism. Immunoreactive calcitonin levels (i-CT) were not elevated. Renal tubular wasting of potassium and magnesium was documented in six patients and excessive urinary loss of sodium, phosphate, and uric acid was noticed. Twelve patients died before recovering from the metabolic stress and five patients developed progressive renal impairment. A possible potentiating action of chemotherapeutic agents, especially Adriamycin, is suggested.
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PMID:Hypocalcemia with hypoparathyroidism and renal tubular dysfunction associated with aminoglycoside therapy. 85 39

Two patients developed severe hypomagnesemia, hypocalcemia, and hypokalemia as a result of renal wasting of magnesium and potassium shortly after being treated with large doses of gentamicin. When therapy with gentamicin was discontinued renal loss of magnesium and potassium ceased, and serum calcium, magnesium, and potassium returned toward normal. Serum immunoreactive parathyroid hormone levels were inappropriately low during the episodes of hypocalcemia. Both patients represent examples of hypomagnesemic hypocalcemia induced by inappropriate magnesuria, possibly caused by gentamicin. These observations suggest that serum calcium, magnesium, and potassium should be monitored during gentamicin therapy.
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PMID:Hypomagnesemic hypocalcemia secondary to renal magnesium wasting. 113 60

A group of six patients with hypomagnesemia (serum magnesium less than or equal to 0.5 mmol/L), previously given treatment with cisplatin for ovarian or testicular cancer, received calcitriol at a dose of 0.5 to 1.0 microgram/day for a period of 4 weeks to determine whether treatment with this vitamin D metabolite could improve their hypomagnesemia. In response to treatment, the serum magnesium concentration fell progressively in association with a rise in serum and urinary calcium levels and a decrease in parathyroid hormone level. In a single previous report, active vitamin D metabolites markedly improved renal magnesium wasting. However, in the present study, increases in serum and urinary calcium levels and suppression of parathyroid hormone, factors known to decrease magnesium reabsorption, presumably overwhelmed any direct effect calcitriol may have had to enhance magnesium reabsorption, so that the net effect was a marked exacerbation of the renal magnesium wasting.
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PMID:Chronic hypomagnesemia caused by cisplatin: effect of calcitriol. 198 6

Magnesium is the fourth most abundant cation in the human body and the second most common cation in the intracellular fluid. The abundance and distribution of this divalent cation implies an essential role of magnesium in intracellular metabolism. Although no single homeostatic control has been demonstrated for magnesium, the cellular availability of this cation is closely regulated by the gastrointestinal tract, kidney and bone. The purpose of this review is to survey some of the events involved in renal magnesium handling. The excretory side of magnesium balance involves appropriate changes in renal magnesium handling. Present evidence suggests that the renal handling of magnesium is normally a filtration-reabsorption process. Experimental support for secretion remains unconvincing. Renal magnesium reabsorption has distinctive features when compared with that of sodium and calcium. The concentration of magnesium in the proximal tubule rises 1.5 times greater than the glomerular filtrate. Some 20-30% of the filtered magnesium is reabsorbed in the proximal tubule compared to the fractional absorption of sodium or calcium of 50-60%. Although the fractional reabsorption of magnesium is only half that of sodium, it changes in parallel with that of sodium in response to changes in extracellular fluid volume. The major portion of filtered magnesium (some 65%) is reabsorbed in the loop of Henle, mainly in the thick ascending limb. Recent evidence suggests that magnesium reabsorption in the ascending limb may be voltage-dependent and secondary to active sodium chloride reabsorption. Evidence also suggests an important competition between magnesium and calcium for transport at the basolateral surface of the ascending limb cell. The loop of Henle appears to be the major nephron site where magnesium reabsorption is controlled. The principal factors which alter magnesium reabsorption in the loop include parathyroid hormone, changes in plasma magnesium and calcium concentration and the loop diuretics. About 10% of the filtered magnesium is delivered into the distal nephron where only a small fraction of the filtered magnesium is reabsorbed and the transport capacity is readily exceeded with increased magnesium delivery. A number of drugs have been shown to alter magnesium handling; these include antibiotics such as gentamicin, antineoplastic agents such as cisplatin and immunological suppressive drugs such as cyclosporin. The cellular alterations of these diverse drugs leading to renal magnesium wasting are not well understood.
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PMID:Renal handling of magnesium: drug and hormone interactions. 354 13


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