Effects of Renal Mass Reduction and Method of Reduction in the Polycystic Rats.
- Author:
Beom Soo KIM
1
;
Chang Hee HAN
;
Sung Hak KANG
Author Information
1. Department of Urology, College of Medicine, The Catholic University of Korea, Seoul, Korea. urodr@cmc.cuk.ac.kr
- Publication Type:Original Article
- Keywords:
APDKD;
Nephrectomy;
Renal infarction
- MeSH:
Animals;
Blood Pressure;
Glomerular Filtration Rate;
Humans;
Infarction;
Kidney;
Nephrectomy;
Polycystic Kidney, Autosomal Dominant;
Proteinuria;
Rats*;
Rats, Sprague-Dawley;
Renal Artery;
Renal Plasma Flow;
Vascular Resistance
- From:Korean Journal of Urology
2001;42(10):1038-1043
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Nephrectomy or decortication is used to relieve pain in clinical autosomal dominant polycystic kidney disease (ADPKD). We evaluated the renal adaptation to unilateral nephrectomy, and segmental renal artery infarction in APDKD rats. MATERIALS AND METHODS: At 6 weeks of age, cystic Han: Sprague-Dawley (SPRD) rats and unaffected controls were subjected to renal mass reduction by uninephrectomy, by infarction of half of each kidney or sham operation. Most groups were followed up to the age of 20 weeks, with serial measurements of blood pressure and proteinuria. At 20 weeks, glomerular filtration rate (GFR) and renal plasma flow (RPF) rate were measured. Similar studies to 12 weeks of age were performed in additional groups of control and cystic rats with either sham operation or half renal infarction. RESULTS: In the uninephrectomized control rats, the values for systemic blood pressure and proteinuria increased, but not significantly. Renal compensatory hyperfiltration and hyperperfusion were observed. GFR and RPF exceeded those seen in sham operated rats (p< 0.05). In infarcted control rats showed significantly increased values for blood pressure and proteinuria and a marked reduction in GFR and RPF (p< 0.05). In the uninephrectomized cystic rats, at baseline, increased values for blood pressure and proteinuria, and a significant reduction in GFR and RPF were observed (p< 0.05). In infarcted cystic rats, at baseline, significant increased values for blood pressure and proteinuria were observed. And there was a marked reduction in GFR and RPF associated with a significant increase in renal vascular resistance (p<0.05). However, in both cystic groups, no compensatory hyperfiltration or hyperperfusion was observed after renal mass reduction. CONCLUSIONS: APDKD is vulnerable state to additional renal injury. When treatment is required for patients with symptomatic APDKD, clinical need to conserve renal function should be considered, especially such as cyst marsupialization.
