作者: Delmar R. Finco , Scott A. Brown , Cathy A. Brown , Wayne A. Crowell , Tanya A. Cooper
DOI: 10.1111/J.1939-1676.1999.TB02204.X
关键词:
摘要: Progressive loss of nephron function may be caused by persistence factors that initiated renal disease. However, newer studies suggest damage is self-perpetuating once mass reduced to some critical level. Original theories on mechanisms self-perpetuated injury focused intraglomerular hypertension and glomerular hypertrophy, but several other have now been incriminated, including tubulointerstitial responses, proteinuria, oxidative stress. Studies dogs with surgically (remnant kidney model chronic disease) allowed investigation the self-progression theory in this species. Use eliminates pre-existing disease as a confounding factor. Data from these indicate when mild azotemia induced (plasma creatinine concentration = 2 4 mg/dL). Thus, naturally occurring disease(s), it likely before or at time most cases are diagnosed. In remnant kidneys, often occurs linear rate over time, non-linear patterns common well. The reciprocal plasma concentration, which has used monitor progression, only fair marker compared GFR. clinical results measurements should not interpreted too stringently. dogs, magnitude proteinuria (UPC ratio) was predictive decline GFR, casting doubt importance causing progression progressive increases UPC an accelerated injury. Self-perpetuation could sole mechanism diseases progress. When more information available diseases, become apparent whether initially inciting additive effect progression.