ACE inhibitors/ARBs contribute to efferent arteriolar dilatation and reduction in intraglomerular
pressure by causing an increase in kinins and also glomerular hypertrophy and fibrosis9.
Smoking has been recognized as an independent risk factor for CKD, and smoking might result in intraglomerular
hypertension, vascular damage, or glomerulosclerosis via multiple complex interactions of nonhemodynamic (angiotensin II, transforming growth factor-[beta]1, endothelin-1) and hemodynamic factors (Orth and Hallan 2008).
hydraulic pressure or glomerular filtration barrier impairment might cause glomerular/overload proteinuria .
Caption: Figure 3: Glomerulus showing intraglomerular
Caption: FIGURE 1: ((a), (b)) Unremarkable glomeruli with acute tubular injury with scattered inflammatory cells and intratubular granular-pigmented cast and (c) Prussian blue stain highlighting the intratubular and intraglomerular
A transplant biopsy showed diffuse tubular necrosis and tubular and intraglomerular
crystal deposits that obstructed capillaries and were suggestive of FOS nephropathy.
These results provide confirmatory evidence that ACE inhibitors are able to prevent the intraglomerular
vascular action that resulted from renal hypertension and glomerular hyperfiltration more effectively than other antihypertensives .
An interesting study using computer-aided reconstruction of three-dimensional images in patients with diabetic nephropathy demonstrated that these abnormal vessels are anastomosed to lobular structure of the intraglomerular
capillary network and that the distal end of the vessels is anastomosed to the peritubular capillary .
They decrease systemic vascular resistance in congestive heart failure; enhance insulin sensitivity in Type 2 diabetes; enhance renal blood flow in renal insufficiency; enhance diminished intraglomerular
pressures in diabetic nephropathy, and enhance coronary blood flow in ischemic heart disease, thus, providing distinct benefits on concomitant conditions.
Another possible mechanism is the hemodynamic effect of ET-1, which in conjunction with other vasoactive factors lead to an increase in intraglomerular
capillary pressure which increases glomerular permeability and thus leads to increased filtration of proteins [18, 19].
Entre las hipotesis que explicarian tal proteinuria se describe el aumento de la filtracion glomerular, la alteracion de la presion intraglomerular
con dano de la barrera glomerular y la reduccion de la reabsorcion tubular (7).
Both these groups of drugs reduce intraglomerular
pressure, lower systemic arterial BP, reduce proteinuria and, thus, delay the disease progression.