A hemodynamically mediated mechanism of renal disease progression in severe glomerulonephritides or nephrosis

Article type: Research Article

Authors: Futrakul, Prasit^; | Siriviriyakul, Prasong | Patumraj, Suthiluk | Bunnag, Srichitra | Kulaputana, Ornanong | Futrakul, Narisa

Affiliations: Department of Pediatrics, King Chulalongkorn Memorial Hospital, Bangkok 10330, Thailand | Department of Physiology, King Chulalongkorn Memorial Hospital, Bangkok 10330, Thailand | Department of Endocrinology, King Chulalongkorn Memorial Hospital, Bangkok 10330, Thailand

Note: [] Corresponding author. E‐mail: fmedpft@md.chula.ac.th.

Abstract: Glomerular endothelial cell (GEC) dysfunction due to oxidative stress and enhanced proinflammatory cytokines plays an important role in inducing proteinuria and procoagulant activity, namely blood hypercoagulability, hyperviscosity and local intravascular coagulation and altered hemorheology in NS. A dysfunctioning GEC releases fewer endothelium‐dependent vasodilators but produces more vasoconstrictors. Severe intrarenal hemodynamic alteration associated with hemodynamic maladjustment with preferential constriction at the efferent arteriole has been uniquely implicated in severe GN and NS‐FSGS. Such a constriction exerts three significant hemodynamic impacts. Proximal to the efferent arteriolar constriction, it induces (i) an overestimated GFR due to hyperfiltration and (ii) an elevated intraglomerular hydrostatic pressure. Distal to the efferent arteriolar constriction, it (iii) exaggeratedly reduces PTCF which correlates with the TIF.

Keywords: Renal disease, glomerulonephritides, nephrosis, hemodynamics

Journal: Clinical Hemorheology and Microcirculation, vol. 29, no. 3-4, pp. 183-187, 2003