Glomerular endothelial dysfunction and hemodynamic maladjustment in vesicoureteric reflux

A structural defect of the non-vascular component of a nephron namely vesicoureteric reflex (VUR) can induce injury to the vascular component, which is reflected by the alteration in intrarenal hemodynamics. A mild alteration in intrarenal hemodynamics was observed in grades I-II VUR which revealed (a) mild reductions in renal plasma flow (RPF) 543 +/- 104 mL/min/1.73 m2; in peritubular capillary flow (PTCF) 438 +/- 103mL/min/1.73 m2; in glomerular filtration rate (GFR) 105 +/- 19 mL/min/1.73 m2 and in ultrafiltration coefficient (KFG) 0.04 +/- 0.01 mL/s/mmHg; (b) normal values of filtration fraction (FF) 0.2 +/- 0.04, of intraglomerular hydrostatic pressure (PG) 50 +/- 0.3 mmHg, and of afferent arteriolar resistance (RA) 2261 +/- 718 dyne s cm(-5); and (c) a slight elevation of efferent arteriolar resistance (RE) 3914 +/- 962 dyne s cm(-5). In contrast, a moderately severe alteration in intrarenal hemodynamics was observed in severe VUR (grades III up) which revealed greater reductions in RPF 267 +/- 114 mL/min/1.73 m2, in PTCF 195 +/- 90 mL/min/1.73 m2, in GFR 72 +/- 34 mL/min/1.73 m2 and in KFG 0.03 +/- 0.01 mL/s/mmHg; and elevation of PG 53 +/- 2 mmHg, of filtration fraction 0.27 +/- 0.07, of RA 4557 +/- 2340 dyne s cm(-5) and of RE 9417 +/- 4163 dyne s cm(-5). Such an alteration in intrarenal hemodynamics observed in severe VUR induces both intraglomerular hypertension (elevated PG) and an exaggeratedly reduced PTCF. This intrarenal hemodynamic defect is due to the glomerular endothelial dysfunction and its hemodynamic maladjustment. In accordance with the preceding information, treatment to correct the hemodynamic maladjustment is likely to improve renal function and prevent renal disease progression.