Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to compare the renal effects of atrial (A-type) natriuretic peptide (ANP) on control (saline-injected) rats and rats with non-oliguric acute renal failure induced by cisplatin. The results obtained here are summarized as follows: (1) In the metabolic cage study, cisplatin-treated rats showed increases in blood urea nitrogen and serum creatinine while creatinine clearance decreased to the lowest levels on day 4. A transient increase in urinary protein was observed at day 4. (2) ANP infusion significantly increased urine flow rate (UFR), creatinine clearance (CCr), fractional excretion rates of sodium (FENa) and chloride (FECl), and urinary phosphorus and magnesium (Mg) excretions in a dose-dependent manner without affecting renal plasma flow and fractional excretion rates of potassium and urea in cisplatin-treated rats. (3) Renal effects of ANP on UFR, CCr, FENa, FECl and excretion of Mg were more pronounced in cisplatin-treated rats compared to control rats although markedly blunted responses to ANP have been reported in nephrotic patients and nephrotic animals induced by adriamycin and aminonucleoside. (4) Histological examination showed extensive necrosis of the S3 segment of the proximal tubule located in the outer stripe of the outer medulla with minimal glomerular abnormalities in the kidney of cisplatin-treated rats. In conclusion, the main mechanism of the increased renal responses to ANP is considered to be due to an increased delivery of sodium, fluid and ANP itself to the inner medullary collecting duct which is the major renal site of action of ANP under the condition of acute proximal tubular necrosis by cisplatin.
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PMID:Renal responses to atrial natriuretic peptide (ANP) in rats with non-oliguric acute renal failure induced by cisplatin. 872 36

Chelonian myxozoanosis is rarely reported and has previously not been documented to cause disease. This report describes myxozoanosis associated with significant renal disease in two Crowned River turtles (Hardella thurjii). One turtle presented with emaciation and died. The cage mate presented with emaciation and was euthanized. Histologically, renal intratubular myxozoan spores were associated with renal tubular necrosis, tubular mineralization, and chronic interstitial nephritis, with membranoproliferative and mes-angioproliferative glomerulopathy. Both turtles also had disseminated metastatic mineralization. On the basis of these findings, chronic renal insufficiency from myxozoanosis and subsequent metastatic mineralization were considered the primary problems. By light and electron microscopy, the myxozoan spores had features of the genus Myxidium. Maximum parsimony analysis of small-subunit rDNA sequences placed the turtle myxozoan basal to a clade containing Myxidium truttae and a Myxidium sp. with strong bootstrap support. This myxozoan agent appears to be a significant pathogen in H. thurjii on the basis of morphologic changes in the kidneys of in the infected turtles.
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PMID:Renal myxozoanosis in crowned river turtles Hardella thurjii: description of the putative agent Myxidium hardella n. sp. by histopathology, electron microscopy, and DNA sequencing. 1614 5