Renal Perfusion in Developing Focal-Segmental Glomerulosclerosis: A Hypothesis

Renal Perfusion and Nephronal Structure

“…On the contrary, the intrarenal hemodynamics characteristic of renal hypoperfusion documented in a variety of chronic glomerulonephropathies such as nephrosis associated with focal segmental glomerulosclerosis [4][5][6][7], a moderate to diffuse mesangial proliferative nephrosis [8] and membranoproliferative glomerulonephritis [9], is likely to reflect an underlying histopathological disease of the nephronal compartments such as glomerulosclerosis, tubulointerstitial fibrosis and arteriolosclerosis. Furthermore, it has been a notion that the renal perfusion has become progressively reduced as the disease severity progresses [2,6,7]. Such an interrelationship between renal perfusion and the nephronal structure has also been implicated by the morphometric analysis of the histopathology.…”

“…In this instance, there is a transient loss of anticoagulant property of the glomerular endothelial function whereas the ability to produce the vasodilators such as prostacyclin and nitric oxide appears to be well preserved. However, when the magnitude of glomerular dysfunction increases, the ability of its function to Futrakul/Yenrudi/Sensirivatana/ Kingwatanakul/Futrakul/Futrakul maintain the microcirculatory balance is lost which is reflected by the presence of progressive reduction in renal plasma flow observed in the clinical settings of steroid-resistant nephrosis [2,6]. With multiple regression analyses, the glomerular endothelial function which is reflected by the renal plasma flow and peritubular capillary blood flow correlates in a linear fashion with the glomerular filtration rate and inversely correlates with the magnitude of damage to the nephronal structure [12,15].…”

Renal Vein Thrombosis in a Severe Form of Renal Disease

“…The severe alterations of intrarenal hemodynamics and the histopathologic derangements observed in these patients suggest that damage to the glomerular endothelium and vessel wall is likely to trigger the hemostatic change with subsequent thrombosis of the renal vein [6]. It has been demonstrated that in the severe form of renal disease, the glomerular vascu lar surface becomes procoagulant due to less production of negative surface charge pro tein and upregulatcd expression of tissue fac tors involved in clot promotion [7,8].…”