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)

A proposed role for the hypothesized toxohormone/s (Vasopressin, Prostaglandin E2 and TNF-Cachectin) in the development and maintenance of cancer cachexia was investigated in rats bearing the Walker 256 carcinosarcoma. Elevated levels of arginine vasopressin and prostaglandin E2 in the plasma and urine were associated with reduced hepatic ketogenesis, fatty acid oxidation and increased fatty acid esterification. The oxidation of branched chain amino acids by the muscle tissue of tumour bearing rats was increased and attributed to the enhanced activity of muscle branched chain keto-acid dehydrogenase. Concerted actions by the triology of factors (AVP, PGE2, Cachectin-TNF) are proposed to instigate a sequence of reactivities that lead to the clinical symptoms of muscle and adipose tissue wasting, together with the negative nitrogen balance characteristic of the cachectic state.
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PMID:Tentative identification of the toxohormones of cancer cachexia: roles of vasopressin, prostaglandin E2 and cachectin-TNF. 235 26

Urinary concentrating defects and renal salt wasting have been described in the hyperbilirubinemic Gunn strain strain of rat. Homozygous animals demonstrate significant reductions in renal medullary urea and sodium ion concentrations. These observations are consistent with possible bilirubin associated disorders in the transepithelial transport of water and solute. To test this hypothesis, measurements of active sodium transport and passive water and urea fluxes were made in hemibladders isolated from the Dominican toad, Bufo marinus. Tissues were exposed to amphibian bicarbonate Ringer's solution containing 0.1 mM bilirubin with 0.05% bovine serum albumin (BSA) or BSA alone. Vasopressin-stimulated sodium transport, as reflected by short circuit current (SCC), was inhibited by 18 +/- 6% in the presence of bilirubin (N = 10; P less than 0.02). Cyclic AMP (p-Cl-phenylthio cAMP 10(-5) M) stimulated SCC was inhibited to a similar degree in the presence of bilirubin. The inhibition was noted only when bilirubin was in the serosal bath, and it could be abolished with BSA 0.5%. Bilirubin had no effect on the increase in SCC induced by higher concentrations of cyclic AMP (10(-4) M), aldosterone, or amphotericin B. Furthermore, bilirubin had no effect on the hydro-osmotic response to vasopressin and vasopressin-induced changes in urea permeability. These findings show that short-term exposure to bilirubin exerts a tissue-specific effect on the vasopressin-stimulated active transport of sodium but has no effect on the vasopressin-induced fluxes of water and urea.
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PMID:Effects of bilirubin on transepithelial transport of sodium, water, and urea. 298 53

Although cisplatin nephrotoxicity is well documented, renal sodium wasting has rarely been reported. Seven of seventy patients treated with cisplatin over 18 months developed salt-wasting nephropathy and orthostatic hypotension. All patients presented 2 to 4 months after starting cisplatin with severe orthostatic hypotension (mean orthostatic change in blood pressure, -37 +/- 8 mm Hg) without preceding extrarenal volume loss or diuretic use. Urinary sodium concentration was 85 to 145 mmol/L, fractional excretion of sodium was 1.0% to 8.0%, and urinary osmolar concentration was 340 to 619 mmol/kg, while orthostatic hypotension was present. Six patients were hyponatremic (116 to 137 mmol/L). Serum creatinine and urea levels were elevated in five patients but fell after rehydration. Vasopressin averaged 5.4 pg/mL (2.1 to 12.7 pg/mL) (n = 5) and was suppressed with hydration (mean, 2.5 pg/mL, 1.5 to 4.3 pg/mL). Plasma renin activity was undetectable in two patients and low in three patients, and aldosterone was low in six patients despite clinical volume depletion. Cisplatin may produce renal salt wasting causing symptomatic orthostatic hypotension and hyponatremia associated with abnormalities of the renin-aldosterone system.
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PMID:Renal salt wasting in patients treated with cisplatin. 333 11