Intrarenal hemodynamic abnormality in severe form of glomerulonephritis: therapeutic benefit with vasodilators

• Published in: Journal of the Medical Association of Thailand Vol. 75; no. 7; p. 375
• Main Authors: Futrakul, P, Pochanugool, C, Poshyachinda, M, Thamaree, S, Yenrudi, S, Buranasiri, K, Saleekul, P, Watana, D, Sensirivatana, R, Kingwatanakul, P
• Format: Journal Article
• Language: English
• Published: Thailand 01-07-1992
• Subjects: Adolescent; Adult; Child; Child, Preschool; Female; Glomerulonephritis - drug therapy; Glomerulonephritis - physiopathology; Glomerulonephritis, Membranoproliferative - drug therapy; Glomerulonephritis, Membranoproliferative - physiopathology; Glomerulosclerosis, Focal Segmental - drug therapy; Glomerulosclerosis, Focal Segmental - physiopathology; Hemodynamics - drug effects; Humans; Kidney - physiopathology; Male; Renal Circulation - drug effects; Vasodilator Agents - therapeutic use
• ISSN: 0125-2208

Intrarenal hemodynamic and tubular function has been assessed in 16 patients who presented clinically with hypertension, hematuria and severe renal functional impairment. Twelve of these 16 patients had histopathologic classification as DPGN (3 cases), MPGN (3 cases) and FSGS (6 cases). The initial assessment of intrarenal hemodynamics in 11 patients revealed strikingly increased afferent (RA) and efferent arterioles (RE), filtration fraction (FF), intraglomerular capillary hydrostatic pressure (PG), whereas, there was marked reduction in renal plasma flow (RPF), in ultrafiltration coefficient (KFG) and in glomerular filtration rate (GFR). Tubular transporting defect as being reflected by enhanced fractional excretions of solutes was also observed. Both enhanced TXB2 production and diminished PGI2 may be in part responsible for the marked reduction of RPF and elevated intrarenal resistance. In light of the preceding intrarenal hemodynamics alteration, therapeutic intervention with vasodilators consisting of dipyridamole, calcium channel blocker and angiotensin convertase inhibitor has been accomplished with clinical improvement in glomerular and tubular functions following the improvement in intrarenal hemodynamics. Thus, this abnormal intrarenal hemodynamics renders a supportive view of the hemodynamically mediated glomerulo-tubulo-interstitial injury to be central to the pathogenetic mechanism.