Vazoaktivní působky u chronické glomerulonefritidy
[Vasoactive factors in chronic glomerulonephritis]
Jazyk čeština Země Česko Médium print
Typ dokumentu anglický abstrakt, časopisecké články
PubMed
8998817
- MeSH
- atriální natriuretický faktor krev fyziologie MeSH
- chronická nemoc MeSH
- dospělí MeSH
- endoteliny krev fyziologie MeSH
- fyziologická adaptace MeSH
- glomerulonefritida metabolismus patofyziologie MeSH
- hodnoty glomerulární filtrace MeSH
- lidé středního věku MeSH
- lidé MeSH
- prostaglandiny fyziologie moč MeSH
- proteinurie MeSH
- renální oběh * MeSH
- renin krev fyziologie MeSH
- vazomotorický systém patofyziologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- Publikační typ
- anglický abstrakt MeSH
- časopisecké články MeSH
- Názvy látek
- atriální natriuretický faktor MeSH
- endoteliny MeSH
- prostaglandiny MeSH
- renin MeSH
BACKGROUND: The kidney damage in chronic glomerulonephritis develops not only as a result of causal immunopathological evens, but also due to chronic adaptation changes. The study was aimed at identification of active agents, which can serve as markers of proceeding adaptation changes and to determine, if these changes may be determined in patients undergoing the stage of remission of chronic glomerulonephritis. METHODS AND RESULTS: The authors determined renin activity, concentration of atrium natriuretic peptide and endothelin in plasma and elimination of some prostanoids in urine in 33 patients with chronic stabilized glomerulonephritis with normal glomerular filtration and with normal blood pressure and in 21 healthy subjects. Seventeen patients without proteinuria did not receive therapy, 16 patients with minute proteinuria received 100 mg of acetylosalicylic acid daily. In the untreated patients without proteinuria, the elimination of thromboxane in urine was significantly higher than in both other groups. The plasma level of atrium natriuretic peptide in all 33 patients was significantly lower than in the healthy persons. CONCLUSIONS: Based on this study the authors believe that adaptation changes proceed even in patients with chronic glomerulonephritis in clinical remission. The increased production of renal thromboxane, which can be successfully blocked by acetylosalicylic acid may be the marker of glomerular changes. A decreased level of atrium natriuretic peptide could reflect tubulointerstitial changes.