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)

Renal tubular function was examined in 5 adult patients aged 18-30 years with Bartter's syndrome associated with renal magnesium wasting and hypocalciuria. In the 3 patients studied during hypotonic saline diuresis, distal tubular fractional chloride reabsorption was lower than that reported in normal subjects. In response to a single intravenous dose of furosemide (40 mg), the increment in the excretion of sodium, chloride, and magnesium was equal to or greater than in normal subjects, while in 2 patients, in response to intravenous chlorothiazide (500 mg), the increment in sodium excretion was less than in normal subjects. Magnesium chloride infusion was undertaken in 2 patients in order to compare magnesium and calcium excretions at similar plasma magnesium levels in patients and in normal subjects. The patients exhibited magnesium wasting only at normal or low plasma magnesium levels, while calcium excretion was reduced in the patients at normal and elevated plasma magnesium levels. We conclude that in these patients the enhancement of renal magnesium reabsorption by hypomagnesemia is defective, and the hypomagnesemia is not the cause of the hypocalciuria. The tubule defect responsible for these abnormalities of magnesium and calcium excretion may be located beyond the side of action of furosemide, in the thiazide-sensitive segment of the distal convoluted tubule.
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PMID:Bartter's syndrome: evidence suggesting a distal tubular defect in a hypocalciuric variant of the syndrome. 140 4

After three weekly intraperitoneal injections of cisplatin (2.5 mg/kg body wt), male Wistar rats developed chronic hypomagnesemia, which was evident from the second week and persisted throughout the 8-week experiments. Plasma magnesium concentration was 0.69 +/- 0.01 mM in cisplatin-treated rats compared to 0.80 +/- 0.02 mM in pair-fed control rats (P less than 0.01) in the eighth week of experimentation. Despite a similar dietary magnesium intake, urinary excretion of magnesium in cisplatin-treated rats was inappropriately high, relative to the lower plasma magnesium concentration, indicating the presence of renal magnesium wasting induced by cisplatin. During the 3 weeks of cisplatin injections, metabolic balance studies indicated abnormal renal excretion and a reduction in the fractional intestinal absorption of magnesium. A compensatory period of significantly greater retention of magnesium then occurred in cisplatin-treated rats beginning in the fourth week. Clearance and recollection micropuncture studies in a separate group of rats revealed normal magnesium and calcium transport in the superficial proximal and distal nephron. Following acute MgCl2 infusion, the urinary excretion of magnesium and calcium were significantly higher in cisplatin-treated rats than in control rats; however, micropuncture studies of superficial nephrons failed to demonstrate abnormal transport of these divalent cations. It is possible, therefore, that 7 weeks of cisplatin treatment led to tubular adaptation that might have obscured the defect in magnesium reabsorption. Morphological examination indicated that pathological changes were confined to the S3 segment of proximal corticomedullary nephrons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies on the pathogenesis of cisplatin-induced hypomagnesemia in rats. 408 97

Renal calcium and magnesium handling was studied in rats with chronic thyroid hormone deficiency or excess, hyperthyroidism. Mean kidney weight of the thyroid deficient rats was 42% of age matched, euthyroid and hyperthyroid animals and glomerular filtration rate was 71% of normal. Fractional sodium excretion was consistently elevated in thyroid deficient rats (0.26%) as compared to euthyroid (0.07%) and hyperthyroid animals (0.07%). Urinary calcium excretion (0.39%) was also elevated and parallel to sodium excretion in thyroid deficiency. Despite this renal leak of sodium and calcium, thyroid deficient animals conserved magnesium much more efficiently than either euthyroid or hyperthyroid rats (5.7% vs 17.4% respectively). Plasma magnesium concentration was elevated by acute MgCl2 infusions to determine the reabsorptive capacity of magnesium. Thyroid deficient rats reabsorbed 15-30% more of the filtered magnesium at any given plasma concentration. Although these effects on electrolyte reabsorption are modest compared to the hemodynamic alterations, the data suggest that thyroid hormone has a direct effect on the tubule which if chronically absent results in subtle sodium and calcium wasting and renal retention of magnesium. Administration of thyroid hormone to euthyroid or thyroid deficient rats twenty-four hours prior to experimentation had no effect on calcium and magnesium handling.
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PMID:Effects of thyroid status on renal calcium and magnesium handling. 671 57

The clinical use of aminoglycosides often leads to renal magnesium wasting and hypomagnesemia. Of the nephron segments, both the thick ascending limb of Henle's loop and the distal tubule play significant roles in renal magnesium conservation but the distal convoluted tubule exerts the final control of urinary excretion. An immortalized mouse distal convoluted tubule (MDCT) cell line has been extensively used to study the cellular mechanisms of magnesium transport in this nephron segment. Peptide hormones, such as parathyroid hormone (PTH), glucagon, calcitonin, and arginine vasopressin (AVP) stimulate Mg2+ uptake in MDCT cells that is modulated by extracellular polyvalent cations, Ca2+ and Mg2+. The present studies determined the effect of aminoglycosides on parathyroid hormone (PTH)-mediated cAMP formation and Mg2+ uptake in MDCT cells. Gentamicin, a prototypic aminoglycoside, elicited transient increases in intracellular Ca2+ from basal levels of 102 +/- 13 nM to 713 +/- 125 nM, suggesting a receptor-mediated response. In order to determine Mg2+ transport, MDCT cells were Mg(2+)-depleted by culturing in Mg(2+)-free media for 16 h and Mg2+ uptake was measured by microfluorescence after placing the depleted cells in 1.0 mM MgCl2. The mean rate of Mg2+ uptake, d([Mg2+]i)/dt, was 138 +/- 24 nM/s in control MDCT cells. Gentamicin (50 microM) did not affect basal Mg2+ uptake (105 +/- 29 nM/s), but inhibited PTH stimulated Mg2+ entry, decreasing it from 257 +/- 36 nM/s to 108 +/- 42 nM/s. This was associated with diminished PTH-stimulated cAMP formation, from 80 +/- 2.5 to 23 +/- 1 pmol/mg protein x 5 min. Other aminoglycosides such as tobramycin, streptomycin, and neomycin also inhibited PTH-stimulated Mg2+ entry and cAMP formation. As these antibiotics are positively charged, the data suggest that aminoglycosides act through an extracellular polyvalent cation-sensing receptor present in distal convoluted tubule cells. We infer from these studies that aminoglycosides inhibit hormone-stimulated Mg2+ absorption in the distal convoluted tubule that may contribute to the renal magnesium wasting frequently observed with the clinical use of these antibiotics.
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PMID:Aminoglycosides inhibit hormone-stimulated Mg2+ uptake in mouse distal convoluted tubule cells. 1095 59

Sea star wasting disease (SSWD) describes a suite of disease signs believed to have led to catastrophic die-offs in many asteroid species, beginning in 2013. While most studies have focused on large, easily visible sea stars with widely-dispersing larvae, less information is available on the effect of this disease outbreak on smaller sea star species, such as the six-armed sea star Leptasterias spp. Unlike many larger sea stars, Leptasterias brood non-feeding young instead of broadcast-spawning planktonic larvae. Limited dispersal and thus limited gene flow may make these sea stars more vulnerable to local selective pressures, such as disease outbreaks. Here, we examined Leptasterias populations at sites along the California coast and documented abundance changes coincident with recent Pacific coast SSWD in 2014. Detection of Leptasterias in central California declined, and Leptasterias were not detected at multiple sites clustered around the San Francisco Bay outflow in the most recent surveys. Additionally, we categorized disease signs in Leptasterias in the field and laboratory, which mirrored those seen in larger sea stars in both settings. Finally, we found that magnesium chloride (MgCl2) slowed the progression of physical deterioration related to SSWD when applied to sea stars in the laboratory, suggesting that MgCl2 may prolong the survival of diseased individuals.
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PMID:Sea star wasting disease demography and etiology in the brooding sea star Leptasterias spp. 3175 76