Nephrosclerosis

Nephrosclerosis is an umbrella term defining changes in all compartments of the kidney, changes caused by hypertension and by ageing. Among other lesions, arteriolosclerosis and arteriole hyalinises play a major role in inducing glomerular ischaemic shrinking and sclerosis along with glomerulomegaly and focal-segmental glomerulosclerosis.

 These lesions are accompanied by tubulointerstitial inflammation and fibrosis that predict the decline of renal function. Nephrosclerosis is a major cause of renal insufficiency in blacks of African descent with a severe, early form of renovasculopathy and a rapid course to renal failure with predominant lesions of FSGS.

It seems that in blacks, separate genetic factors independently lead to vascular lesions and to hypertension with a different time-scale of their onset and of their progression, nephroangiosclerosis preceding the onset of hypertension. Conversely, true and histologically identified nephrosclerosis in white Europeans rarely leads to end-stage renal disease in the absence of malignant hypertension. Various animal models demonstrate that renal vascular lesions may exist in the absence of hypertension.

These experiments also point to a major role of angiotensin II and of a number of independent and overlapping cellular and molecular pathways in a cascade of inflammatory events that end in renal fibrosis.

Two pathophysiologic mechanisms are at work in inducing glomerular lesions and tubulointerstitial fibrosis  a loss of auto regulation of the renal blood flow caused by an arteriolohyalinosis of the glomerular afferent arteriole and ischemia that fosters the generation of hypoxia inducible-fibrosing factors. Not all antihypertensive drugs equally protect the kidney from nephrosclerosis.

Angiotensin II antagonists exert a favourable effect on hyper filtration. Conversely, dihydropyridine calcium-channel blockers and vasodilators do not withstand the derangement of renal auto regulation.

Both nephrosclerotic kidneys have the same size, which would not be the case in atherosclerotic renal disease. Reduction of the kidney is not constant. The kidney outline may be smoothly scalloped, which reflects the presence of underlying ischaemic areas.

Whereas inflammatory interstitial changes may evoke chronic pyelonephritis, the pathologist does not find inflammatory cells under the pelvic and calyceal system. The sub capsular surface is finely granular in most cases, reflecting the subcortical arteriolosclerosis.

The main branches of the renal artery may display atherosclerotic changes. Actuate and interlobular arteries show intimal thickening by my fibroblasts and dense collagen tissue. Elastic laminae are frayed and reduplicated forming concentric layers of elastic. The media is initially thicker than normal, before undergoing atrophy. The lumen is usually narrowed. It comes as no surprise that the blood flow be curtailed to some areas of the kidney tissue.

Arteriolosclerosis of the afferent arteriole is correlated with the degree of hypertension, male gender and ageing. Arteriolohyalinosis is not necessarily a feature of nephroangiosclerosis. Nevertheless, this lesion is more severe in primary hypertension. The hyaline seen on electron microscopy appears as confluent finely granular material of varying electron density. Hyalinises affects the afferent and the efferent glomerular arterioles although in the latter plasma protein infiltration is less pronounced than in the diabetic kidney.

It was long considered that glomeruli undergo progressive ischaemic changes, well described in, ending in shrinkage and obsolescence. It has since been established that the nephrosclerotic kidney displays three populations of glomeruli.

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With Regards,

David Paul

Editorial Assistant

Journal of Clinical Nephrology and Research