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Hemodynamic maladjustment is a unique observation in chronically severe glomerulonephritides. It is characterized by a markedly elevated efferent arteriolar resistance (RE), an elevated intraglomerular hydrostatic pressure (PG) and a markedly decreased renal plasma flow (RPF), and peritubular capillary flow (PTCF). A correction of such hemodynamic maladjustment can be accomplished by administering a combination of vasodilators (angiotensin receptor antagonist, angiotensin converting enzyme inhibitor, and calcium channel blocker) in 14 chronic glomerulonephritides with severe renal function impairment (mean serum creatinine 3.6 + 1.3 mg/dL). Doses titration aim for maximal renal perfusion effect (increased RPF, PTCF) or maximal renal function improvement (increased CCr, reduced FE Mg) usually higher than needed for maximal blood pressure reduction. Evidence of oxidative stress is also corrected with high doses of vitamins C and E. After a mean period of treatment for 13.5 months, improvements in CCr (pre Rx 22 ± 10 vs. post Rx 32 ± 13 mL/min/1.73 m2), and FE Mg (pre Rx 11.9 ± 4% vs. post Rx 10 ± 3%) were observed in conjunction with the improvement in intrarenal hemodynamics namely RPF (pre Rx 201 ± 71 vs. post Rx 288 ± 99 mL/min/1.73 m2), PTCF (pre Rx 161 ± 57 vs. post Rx 242 ± 90 mL/min/1.73 m2), PG (pre Rx 56.7 ± 0.5 vs. post Rx 51 ± 0.1 mm Hg), and RE (pre Rx 12085 ± 6503 vs. post Rx 6550 ± 1872 dyne.s.cm−5). [ABSTRACT FROM AUTHOR]

Hemodynamic maladjustment with predominant constriction at the efferent arteriole has been encountered in a variety of clinical settings of glomerulonephropathy. In essence, it induces not only intraglomerular hypertension but also exaggeratedly reduces the peritubular capillary flow, which supplies the tubulointerstitial compartment. The hemodynamic maladjustment is believed to reflect a glomerular endothelial cell dysfunction. In this regard, oxidative stress and antioxidant defect are likely responsible for the glomerular endothelial dysfunction. Improvement in renal function was accomplished following the correction of oxidant and antioxidant imbalance with antioxidant therapy and vasodilators. Following such therapy, there was a correction in hemodynamic maladjustment with a decline in intraglomerular hydrostatic pressure and an increase in renal perfusion with a subsequent increase in renal functions namely creatinine clearance, glomerular filtration rate and a decline in FEMg. [ABSTRACT FROM AUTHOR]

Enhanced tumor necrosis factor alpha associated with immunocirculatory imbalance expressed as increased ratio between proinflammatory (TNFα) and antiinflammatory (IL-10) cytokines was observed in the serum of nephrosis associated with focal segmental glomerulosclerosis. Such altered immunocirculatory balance correlated with the reduction in renal plasma flow determined by the intrarenal hemodynamic study by which it implies that a glomerular endothelial cell injury associated with impaired renal perfusion is likely to be spontaneously induced by enhanced tumor necrosis factor in the presence of inadequate release of antiinflammatory cytokine (IL-10). [ABSTRACT FROM AUTHOR]