nephrosclerosis

If this happens, the condition is called malignant nephrosclerosis.

Apoptosis can be significant particularly three weeks into the course of hypertensive nephrosclerosis in this model (Figure 1).

His wife, the former Marian Bradley, died of nephrosclerosis yesterday at the same nursing home.

I should find fibrinoid changes in the renal microvasculature or early nephrosclerosis.

Mikhail Bulgakov died from nephrosclerosis (an inherited kidney disorder) on March 10, 1940.

In advanced cases of benign nephrosclerosis the glomerular tufts may become globally sclerosed.

The strain on Bulgakov leads to an intensification of his inherited disease, nephrosclerosis, and his eventual death.

These data supported the view that the Fas/FasL pathway promoted nephrosclerosis in this model.

The role of the Fas/FasL pathway in human hypertensive nephrosclerosis remains to be determined.

Recent studies have shown that apoptosis was accentuated in kidneys of S rats during development of nephrosclerosis [ 7 ] .

Benign nephrosclerosis is the renal changes occurring in the setting of benign hypertension, which is always associated with hyaline arteriolosclerosis.

Benign nephrosclerosis alone hardly ever causes severe damage to the kidney, except in susceptible populations, such as African Americans, where it may lead to uremia and death.

Hypertensive nephropathy (or "hypertensive nephrosclerosis", or "Hypertensive renal disease") is a medical condition referring to damage to the kidney due to chronic high blood pressure.

According to the Soviet medical report, Andropov suffered from several medical conditions: interstitial nephritis, nephrosclerosis, residual hypertension and diabetes, which were worsened by chronic kidney deficiency.

Hyaline arteriolosclerosis is a major morphologic characteristic of benign nephrosclerosis, in which the arteriolar narrowing causes diffuse impairment of renal blood supply, with loss of nephrons.

While end-stage renal failure represents the second most common cause of end-stage renal disease [ 2 ] , perhaps only 1 in 2,500 hypertensive patients develops clinically important hypertensive nephrosclerosis.

The blood pressure responses to dietary salt intake of the Dahl/Rapp S rat, an experimental model of hypertensive nephrosclerosis, and of the SD strain of rat have been published.

The purpose of the present study was to demonstrate the site of expression and potential functional significance of Fas and FasL in the kidneys of S rats during development of hypertensive nephrosclerosis.

In this respect, this model is very useful in understanding hypertensive nephrosclerosis that occurs in human low-renin hypertension, especially in defined, more homogeneous populations such as the black patients described by Grim and associates [ 6 ] .

While other animal models of hypertension can be employed to study the pathogenesis of hypertension, because of the rapid and reproducible development of renal failure, S rats provide a unique means to investigate the pathogenesis of hypertensive nephrosclerosis.

On a diet containing 8.0% NaCl, young Dahl/Rapp salt-sensitive (S) rats rapidly and uniformly manifest low-renin hypertension and die from hypertensive nephrosclerosis within weeks of institution of the high-salt diet [ 5 ] .