RGD Reference Report - Impaired glomerular and tubular antioxidative defense mechanisms in nephrotic syndrome. - Rat Genome Database

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Impaired glomerular and tubular antioxidative defense mechanisms in nephrotic syndrome.

Authors: Granqvist, A  Nilsson, UA  Ebefors, K  Haraldsson, B  Nystrom, J 
Citation: Granqvist A, etal., Am J Physiol Renal Physiol. 2010 Oct;299(4):F898-904. doi: 10.1152/ajprenal.00124.2010. Epub 2010 Aug 4.
RGD ID: 7205671
Pubmed: PMID:20685819   (View Abstract at PubMed)
DOI: DOI:10.1152/ajprenal.00124.2010   (Journal Full-text)

The molecular mechanisms behind acquired nephrotic syndrome (NS) are still largely unknown. One possible explanation for the development of proteinuria is oxidative damage to the glomerular cells. Our hypothesis was that the oxidative defense is weakened in NS, and we focused on measurements of the oxidative-antioxidative status in the glomerular and tubular parts of the nephron. Gene expression was analyzed in renal biopsies from patients with NS. In addition, to compare the acute and chronic phases of the disease, we studied puromycin-treated rats. In the biopsy material, the expression of enzymes involved in the antioxidative defense was higher in the tubulointerstitial compartment than in the glomerular cells. Real-time PCR analysis revealed a decreased glomerular expression in nephrotic kidneys for the antioxidant enzymes catalase and glutathione peroxidase-3, and -4. The tubular gene expression was downregulated for catalase, glutathione peroxidase-3, and thioredoxin reductase-1 and -2. The altered gene expression was accompanied by increased lipid peroxidation in urine. In rats, serum concentrations of ascorbyl-free radicals, measured with electron spin resonance, were elevated in the acute phase of the disease, suggesting increased oxidative stress in the circulation. In addition, we saw an increase in the plasma antioxidant capacity combined with a decreased oxidation of proteins in sera from nephrotic rats, but not from humans. In conclusion, there is a marked downregulation of several antioxidative enzymes in nephrotic kidneys, especially in glomerular structures. Our data suggest that oxidative damage to glomerular cells may contribute significantly to the course and prognosis of nephrotic syndrome.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
nephrosis  IEP 7205671mRNA: decreased expression: glomerulusRGD 
nephrosis  ISOCAT (Homo sapiens)7205671; 7205671mRNA: decreased expression: glomerulusRGD 
nephrotic syndrome  ISOGpx1 (Rattus norvegicus)7205671; 7205671mRNA:increased expression:kidneyRGD 
nephrotic syndrome  ISOGpx3 (Rattus norvegicus)7205671; 7205671mRNA:decreased expression:kidneyRGD 
nephrotic syndrome  IEP 7205671; 7205671; 7205671mRNA:decreased expression:kidneyRGD 
nephrotic syndrome  IEP 7205671mRNA:increased expression:kidneyRGD 
nephrotic syndrome  ISOGPX3 (Homo sapiens)7205671; 7205671mRNA:decreased expression:kidneyRGD 
nephrotic syndrome  ISOGPX4 (Homo sapiens)7205671; 7205671mRNA:decreased expression:kidneyRGD 

Objects Annotated

Genes (Rattus norvegicus)
Cat  (catalase)
Gpx1  (glutathione peroxidase 1)
Gpx3  (glutathione peroxidase 3)
Gpx4  (glutathione peroxidase 4)

Genes (Mus musculus)
Cat  (catalase)
Gpx1  (glutathione peroxidase 1)
Gpx3  (glutathione peroxidase 3)
Gpx4  (glutathione peroxidase 4)

Genes (Homo sapiens)
CAT  (catalase)
GPX1  (glutathione peroxidase 1)
GPX3  (glutathione peroxidase 3)
GPX4  (glutathione peroxidase 4)


Additional Information