However, from a physiological perspective, renin-angiotensin system (RAS) inhibitors cause a rise in creatinine owing to a reduction in intraglomerular
pressure--a 20% or less rise in creatinine is acceptable.
Bowman's capsule dilatation and edema were noted without evidence of glomerular and/or epithelial cell damage in the proximal tubules (Fig.
including increased oxidative stress, renal polyol formation, activation of PKC-mitogen-activated protein kinases, and accumulation of advanced glycation end products, as well as such hemodynamic factors as systemic hypertension and increased intraglomerular
pressure (Brownlee 2001; Jandeleit-Dahm and Cooper 2006; Schena and Gesualdo 2005; Tan et al.
A patient with unilateral total or, to a lesser extent, partial nephrectomy sustains a loss of renal mass and nephron number that leads to functional and structural adaptations of the remaining kidney, including hyperfiltration, intraglomerular
hypertension, glomerulopathy, proteinuria, and renal insufficiency.
Interestingly, 100% exhibited membranoproliferative glomerulonephritis, with immunofluorescence demonstrating subendothelial and intraglomerular
deposits of IgG, IgM, and C3.
pressure is a possible explanation for how hypertension affects the glomerular ultrastructure of the kidneys in the SHR (Martinez-Maldonado, 1987).
pressure is maintained by prostaglandin-mediated afferent vasodilatation and angiotensin II-mediated efferent vasoconstriction.
The most effective strategies for lowering intraglomerular
pressure are aggressive lowering of the BP and inhibition of the renin-angiotensin-aldosterone system (RAAS) (10).
28-31) Most frequently, AMLs occur in the kidney and comprise a variety of forms including classic angiomyolipoma, microscopic angiomyolipoma (so-called microhamartoma), intraglomerular
lesion, cystic angiomyolipoma, epithelioid angiomyolipoma, and oncocytoma-like angiomyolipoma.
Elevated glomerular filtration rate, sustained by increased intraglomerular
pressure and glomerular hypertrophy (both mediated by angiotensin II) in the initially undamaged nephrons, are implicated in the inexorably progressive renal damage.
pressure (hyperfiltration), causing stretch of the mesangial cells, produces an up-regulation of glucose transporter-1 (GLUT-1) that ultimately leads to over-expression of TGF-[beta]1 and ECM production, resulting in glomerulosclerosis (Fig.
The expansion in capsular space is probably caused by enhanced angiotensin II level leading to increased intraglomerular
pressure and filtration rate (Wolf et al.