Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ultrastructural changes in the visceral epithelium and proximal tubules of rats were studied by scanning and transmission electron microscopy during the onset and progression of puromycin aminonucleoside nephrosis (PAN)-induced proteinuria. These changes were compared with those that occur during a similar degree of proteinuria induced by intraperitoneal injections of albumin. With the onset of proteinuria and oliguria, PAN rats exhibit loss of podocyte pedicels and podocyte major processes, an increase in pinocytotic activity, and an accumulation of cytoplasmic vacuoles and granules of variable size, shape, and electron density. Loss of podocyte pedicels involves a gradual decrease in pedicel height beginning at the pedicel tip and progressing down the pedicel arm, formation of nublike protrusions and interpedicel microbridges (35 to 45 nm. in width and 40 to 60 nm. in length) along the pedicel's base, the merging of microbridges to form more extensive regions of interpedicel contact, and a gradual broadening and retraction of pedicels. In response to hyperalbuminemia-induced proteinuria, kidney podocytes exhibit reactions during PAN, however, the podocyte pedicels, slit pores, and major processes of rats with hyperalbuminemia-induced proteinuria remain discrete. The loss of pedicels and major processes during PAN, therefore, apparently results from the effects of puromycin aminonucleoside per se rather than from the proteinuria associated with this disease. The proximal tubules of rats with hyperalbuminemia-induced proteinurea exhibit the same characteristic changes as PAN rat proximal tubules (i.e., loss of brush border, dilated lumina, abnormally thin walls, and accumulation of periodic acid-Schiff positive electron-dense luminal casts and cytoplasmic protein absorption droplets). The significance of these ultrastructural findings during PAN and hyperalbuminemia-induced proteinurea are discussed in terms of the etiology of PAN.
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PMID:A scanning and transmission electron microscopic comparison of puromycin aminonucleoside-induced nephrosis to hyperalbuminemia-induced proteinuria with emphasis on kidney podocyte pedicel loss. 83 33

In exploratory studies aimed at elucidating CNS effects due to heavy metal toxicity, signs of compromised renal function were seen in rats. The studies reported here describe the sequential steps of the development of nephrotoxicity by trimethyltin chloride (TMT) in rats. Single doses of 12.25 mg/kg TMT administered orally to 150- to 175-g Long-Evans rats elicited overt signs of toxicity including behavioral abnormalities and marked weight loss. Concurrent with the development of these signs, nephrotoxicity was manifested as functional kidney compromise and associated histopathologic evidence of tubular damage. Pathological changes in the kidneys from treated rats were hyaline droplet inclusions, attenuated brush border, basolateral vacuolization, and eosinophilic granular casts in the proximal tubule cells. These lesions were detected as early as 2 days post-treatment and progressed with time in an orderly and sequential fashion. Renal lesions between 5 and 8 days were mild to severe cortical tubular dilatation, hydropic degeneration, and diffuse hyaline droplet deposition in the lower nephron tubules. Medullary edema and exfoliation of degenerated tubular epithelial cells with cast formation followed from 8 to 11 days. The morphological changes were accompanied by marked elevation of blood urea nitrogen, parallel with polyuria at Day 2 and oliguria by Day 14. Behavioral abnormalities as well as weight loss correlated well with the time course and severity of renal dysfunction and progression of morphological changes. A second experiment compared the effects of TMT in rats of different weights. Heavier rats were more sensitive than lighter rats to the nephrotoxic effects of TMT. These effects were independent of recognizable neurotoxic effects of TMT in the hippocampus.
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PMID:The pathogenesis of trimethyltin chloride-induced nephrotoxicity. 355 27

Acute oliguric renal failure requiring hemodialysis developed in a 59-year-old man who had myasthenia gravis. A renal biopsy on day 21 was diagnostic of tubulointerstitial nephritis. Despite regular hemodialysis, the patient died of complications 17 weeks after the onset of oliguria. At post-mortem examination, a thymoma was found, and renal histopathology indicated tubulointerstitial nephritis and concomitant generalized epimembranous and intramembranous electron-dense deposits of glomerular capillary walls. By direct immunofluorescence, immunoglobulins and C'3 were visualized in peritubular granular deposits around proximal tubules, but not on glomeruli. The renal acid-eluate contained immunoglobulins that bound to proximal tubule brush border, intracellular cytoplasmic granules, and a granular antigen probably associated with basement membrane of proximal tubule cells of normal human kidney and the patient's kidney, whereas the patient's serum apparently contained antibodies only to proximal tubule brush border. The renal eluate did not bind to normal or the patient's glomeruli, and partial elution of the patient's kidney did not expose new binding sites for the eluate. The data indicate a unique instance of tubulointerstitial nephritis caused by antibodies to multiple proximal tubule antigens apparently forming immune complexes in situ.
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PMID:Primary tubulointerstitial nephritis caused by antibodies to proximal tubular antigens. 701 72