Structural Changes That May Impair Autoregulation Of

The most characteristic glomerular lesion in patients with incipient or overt nephropathy is mesangial expansion. Biopsies from patients with hypertension and/or diabetic nephropathy have furthermore revealed arteriolar hyalinosis [71,72].

Arteriolar hyalinosis may impair the afferent arteriole capacity to constrict, and can thereby lead to enhanced transmission of the systemic BP into the glomerular capillary network, and lead to glomerular hypertension [19,73,74]. This haemodynamic alteration is associated with increase wall tension causing distension of the elastic glomerulus. Studies have shown that mechanical stretch of vascular smooth muscle cells, vascular endothelial cells and mesangial cells leads to an overproduction of extracellular matrix [75,76]. Mesangial expansion is closely associated with renal function in diabetic nephropathy [77]. This relationship probably results from the expanding mesangium compromising the structure of contiguous glomerular capillaries and from a reduction in filtration surface, which may per se lead to increased intraglomerular pressure, and creating a vicious circle.

However, impaired autoregulation have been demonstrated in remnant kidney models in rats and in humans with non-diabetic nephropathies in the absence of arteriolar hyalinosis [37,78-80]. Consequently, autoregulation can be impaired before structural changes are detectable and thereby contribute to the progression of nephropathy, by creating glomrular hypertension [16].

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