Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0599766 (functional recovery)
13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 38-year-old male developed acute oliguric renal failure following repeated glue sniffing for about 8 hours. In addition, he had severe liver cell injury, mild myonecrosis and bone marrow depression indicating generalized tissue toxicity. The high urinary spot sodium during the oliguric phase and the total renal functional recovery after a period of oliguria followed by polyuria favoured a diagnosis of acute toxic tubular necrosis causing acute renal failure. Toluene which is used as the solvent is presumably the toxic agent involved in glue sniffing. It is advised that toluene inhalation be considered in the differential diagnosis of acute renal failure especially in the young. Literature on the renal toxicity of toluene is briefly reviewed.
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PMID:Oliguric acute renal failure due to glue-sniffing. Case report. 194 58

The time course for the onset of N-(3,5-dichlorophenyl)succinimide (NDPS)-induced nephrotoxicity was studied in male Sprague-Dawley rats. The ability of rats to recover from a single nephrotoxic dose (100 or 200 mg/kg) of NDPS also was examined. One hour following NDPS administration (200 mg/kg, i.p.), p-aminohippurate (PAH) accumulation by renal cortical slices was decreased 51%. Changes in renal morphology, proteinuria, hematuria, and diuresis were observed at 3 h. Renal damage at 6 h was similar to that seen at 24 h with tubular necrosis greater than that observed at 3 h and some lumina plugged with PAS+ material. Accumulation of both PAH and tetraethylammonium (TEA) by renal cortical slices was decreased; and proteinuria, hematuria, and polyuria were increased at 6 h and 24 h. Blood urea nitrogen (BUN) was not increased until 24 h. Renal function began to return to normal in rats receiving NDPS (100 mg/kg, i.p.) by 48 h, and functional recovery was complete by 168 h, although slight morphological changes were still evident. However, not all rats receiving NDPS (200 mg/kg, i.p.) recovered by 168 h, and some rats (3 of 7) died of renal failure between 96 h and 168 h. Widespread tubular necrosis and increased kidney weight were also present in this group at 168 h. Thus, NDPS-induced nephrotoxicity was evident by 1 h, established by 6 h and maximum between 24 h and 48 h. Recovery from NDPS-induced nephropathy was found to be dose-dependent, and incomplete in some animals at a dose of 200 mg/kg.
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PMID:Onset of and recovery from acute N-(3,5-dichlorophenyl)succinimide-induced nephrotoxicity in Sprague-Dawley rats. 671 May 45

To further elucidate the role of the preoptic-hypothalamic region in fluid and electrolyte balance we studied the effect of surgical preoptic-hypothalamic disconnection using either a large (preoptic-hypothalamic disconnection) or a small (medial preoptic-hypothalamic disconnection) microknife. Both the large and small cuts seemed to transect the posterior projection originating in the periventricular tissue surrounding the anteroventral third ventricle (AV3V) and extending to supraoptic nucleus, but the supraoptic-neurohypophysial pathway was severed only by the large cut. Seven-day metabolic studies showed a disruption in hydromineral balance only in large cut rats; they had increased water intake and urine volume on day 1, a near-recovery of function on days 2 and 3, and polydipsia and polyuria on days 4 to 7. There was no difference between small cut rats and sham-operated rats in metabolic measurements. The large cut rats also had sustained hypernatremia and hyperosmolality, which was enhanced after water restriction for 48 h but was not accompanied by an increase in plasma arginine vasopressin. Our data therefore suggest that the efferent fibers running caudally from the AV3V are not involved in mediation of the hydromineral regulation of the AV3V.
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PMID:Effects of large and small transections of the preoptic-hypothalamic region on hydromineral regulation in rats. 795 11

A four-month-old male Labrador retriever was presented for polyuria, polydipsia and persistent euglycaemic glucosuria. On referral, diagnostic tests demonstrated abnormal fractional excretions of electrolytes, increased urinary excretion of selected amino acids, mild renal tubular acidosis and mild proteinuria, indicating renal tubular dysfunction. Pyelonephritis was suspected and potentiated amoxycillin was administered. On re-evaluation at six months of age, the dog was no longer polyuric or polydipsic and the metabolic abnormalities associated with the tubulopathy had resolved. Transient Fanconi's syndrome has not previously been reported in small animals. This report demonstrates the potential for recovery of function in cases presenting with renal tubulopathies.
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PMID:Transient renal tubulopathy in a Labrador retriever. 1172 83