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Alterations in glomerular dynamics in congenital, unilateral hydronephrosis
B G Hanss1, J E Lewy, R C Vari
1Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana.
Kidney International
|July 1, 1994
Summary
Congenital hydronephrosis reduces single nephron glomerular filtration rate (SNGFR) by decreasing the ultrafiltration coefficient (Kf). Blocking angiotensin II (Ang II) and thromboxane A2 (TxA2) pathways fully restores SNGFR in rats.
Area of Science:
- Nephrology
- Renal Physiology
- Pediatric Urology
Background:
- Congenital unilateral hydronephrosis is associated with reduced glomerular filtration rate (GFR).
- Previous studies indicated that blocking the renin-angiotensin system or thromboxane A2 (TxA2) normalizes GFR in affected rats.
Purpose of the Study:
- To define the specific single nephron defect in congenital unilateral hydronephrosis.
- To evaluate the distinct roles of angiotensin II (Ang II) and TxA2 in this renal dysfunction.
Main Methods:
- Renal micropuncture experiments were conducted on hydronephrotic (HYDRO) and control (CONTROL) rats.
- HYDRO rats were treated with TxA2 receptor antagonist (SQ-29548), Ang II receptor antagonists (saralasin, DuP-753), or a combination.
- Single nephron glomerular filtration rate (SNGFR) and glomerular ultrafiltration coefficient (Kf) were measured.
Main Results:
- SNGFR was significantly reduced in HYDRO rats compared to controls.
- TxA2 blockade normalized SNGFR; Ang II receptor blockade partially restored it.
- Combined blockade of Ang II and TxA2 fully normalized SNGFR and increased Kf above control levels.
Conclusions:
- The reduction in SNGFR in congenital unilateral hydronephrosis is primarily due to a marked fall in Kf.
- Both Ang II and TxA2 contribute independently to the reduction in Kf.
- Combined blockade of Ang II and TxA2 effectively reverses the SNGFR defect in this model.