Many types of vascular lesions can lead to renal ischemia and death of kidney tissue. The most common of these lesions are (1) atherosclerosis of the larger renal arteries, with progressive sclerotic constriction of the vessels; (2) fibromuscular hyperplasia of one or more of the large arteries, which also causes occlusion of the vessels; and (3) nephrosclerosis, caused by sclerotic lesions of the smaller arteries, arterioles, and glomeruli.

Atherosclerotic or hyperplastic lesions of the large arteries frequently affect one kidney more than the other and, therefore, cause unilaterally diminished kidney function. As discussed in Chapter 19, hypertension often occurs when the artery of one kidney is constricted while the artery of the other kidney is still normal, a condition analogous to “two-kidney” Goldblatt hypertension.

Benign nephrosclerosis, the most common form of kidney disease, is seen to at least some extent in about 70 percent of postmortem examinations in people who die after the age of 60 years. This type of vascular lesion occurs in the smaller interlobular arteries and in the afferent arterioles of the kidney. It is believed to begin with leakage of plasma through the intimal membrane of these vessels. This leakage causes fibrinoid deposits to develop in the medial layers of these vessels, followed by progressive thickening of the vessel wall that eventually constricts the vessels and, in some cases, occludes them. Because there is essentially no collateral circulation among the smaller renal arteries, occlusion of one or more of them causes destruction of a comparable number of nephrons. Therefore, much of the kidney tissue becomes replaced by small amounts of fibrous tissue. When sclerosis occurs in the glomeruli, the injury is referred to as glomerulosclerosis.

Nephrosclerosis and glomerulosclerosis occur to some extent in most people after the fourth decade of life, causing about a 10 percent decrease in the number of functional nephrons each 10 years after age 40 years (Figure 1). This loss of glomeruli and overall nephron function is reflected by a progressive decrease in both renal blood flow and GFR. Even in healthy people without underlying hypertension or diabetes, renal plasma flow and GFR decrease by 40 to 50 percent by age 80 years.

Fig1. Effect of aging on the number of functional  glomeruli.

The frequency and severity of nephrosclerosis and glomerulosclerosis are greatly increased by concurrent hypertension or diabetes mellitus. In fact, diabetes mellitus and hypertension are the two most important causes of ESRD, as discussed previously. Thus, benign nephrosclerosis in association with severe hypertension can lead to a rapidly progressing malignant nephrosclerosis. The characteristic histological features of malignant nephrosclerosis include large amounts of fibrinoid deposits in the arterioles and progressive thickening of the vessels, with severe ischemia occurring in the affected nephrons. For unknown reasons, the incidence of malignant nephrosclerosis and severe glomerulosclerosis is significantly higher in blacks than in whites of similar ages who have similar degrees of severity of hypertension or diabetes.

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مواضيع ذات صلة

Nephron Function in Chronic Kidney Disease

Vicious Cycle of Chronic Kidney Disease Leading to End-Stage Renal Disease

Intrarenal Acute Kidney Injury Caused by Abnormalities Within the Kidney

Prerenal Acute Kidney Injury Caused by Decreased Blood Flow to the Kidney

kidney Diseases

Diuretics and Their Mechanisms of Action

Conditions That Cause Large Increases in Extracellular Fluid Volume but with Normal Blood Volume

Conditions That Cause Large Increases in Blood Volume and Extracellular Fluid Volume

Integrated Responses to Changes in Sodium Intake

Role of Atrial Natriuretic Peptide in Controlling Renal Excretion

Role of Aldosterone in Controlling Renal Excretion

Role of Ang II in Controlling Renal Excretion