Diseases of Blood Vessels

Nearly all diseases of the kidney involve the renal blood vessels secondarily. Systemic vascular diseases, such as various

Figure 20-47Myeloma kidney. Note the angulated and tubular casts with macrophages, including multinucleate cells, engulfing them.

Figure 20-48Close-up of the gross appearance of the cortical surface in benign nephrosclerosis illustrating the fine, leathery granularity of the surface.

Figure 20-49Hyaline arteriolosclerosis. High-power view of two arterioles with hyaline deposition, marked thickening of the walls, and a narrowed lumen. (Courtesy of Dr. M.A.

Venkatachalam, Department of Pathology, University of Texas Health Sciences Center, San Antonio, TX.)

TABLE 20-12-- Types of Hypertension

Primary or Essential Hypertension

Secondary Hypertension

Renal

••Acute glomerulonephritis

••Chronic renal disease

••Renal artery stenosis

••Renal vasculitis

••Renin-producing tumors

Endocrine

••Adrenocortical hyperfunction (Cushing syndrome)

••Oral contraceptives

••Pheochromocytoma

••Acromegaly

••Myxedema

••Thyrotoxicosis (systolic hypertension)

Vascular

••Coarctation of aorta

••Polyarteritis nodosa

••Aortic insufficiency (systolic hypertension)

Neurogenic

••Psychogenic

••Increased intracranial pressure

••Polyneuritis, bulbar poliomyelitis, others

hyperplastic arteriolosclerosis that is typical of malignant hypertension and further narrowing of the lumens. The kidneys become markedly ischemic. With severe involvement of the renal

afferent arterioles, the renin-angiotensin system receives a powerful stimulus; indeed, patients with malignant hypertension have markedly elevated levels of plasma renin. This then sets up

a self-perpetuating cycle in which angiotensin II causes intrarenal vasoconstriction, and the attendant renal ischemia perpetuates renin secretion. Other vasoconstrictors (e.g., endothelin)

and loss of vasodilators (nitric oxide) may also contribute to vasoconstriction. Aldosterone levels are also elevated, and salt retention undoubtedly contributes to the elevation of blood

pressure. The consequences of the markedly elevated blood pressure on the blood vessels throughout the body are known as malignant arteriosclerosis, and the renal disorder is malignant

nephrosclerosis.

Morphology.

On gross inspection, the kidney size depends on the duration and severity of the hypertensive disease. Small, pinpoint petechial hemorrhages may appear on the cortical surface from

rupture of arterioles or glomerular capillaries, giving the kidney a peculiar "flea-bitten" appearance.

Two histologic alterations characterize blood vessels in malignant hypertension ( Fig. 20-50 ):

• Fibrinoid necrosis of arterioles.This appears as an eosinophilic granular change in the blood vessel wall, which stains positively for fibrin by histochemical or

immunofluorescence techniques. This change represents an acute event, and it may be accompanied by limited inflammatory infiltrate within the wall. However, usually this

pattern of necrosis is not accompanied by prominent inflammation.

• In the interlobular arteries and arterioles, there is intimal thickening caused by a proliferation of elongated, concentrically arranged smooth muscle cells, together with fine

concentric layering of collagen and accumulation of pale staining material that likely represents accumulations of proteoglycans and plasma proteins. This alteration has been

referred to as onion-skinningbecause of its concentric appearance. The lesion, also called hyperplastic arteriolitis, correlates well with renal failure in malignant hypertension.

Sometimes the glomeruli become necrotic and infiltrated with neutrophils, and the glomerular capillaries may thrombose. The arteriolar and arterial lesions result in considerable

narrowing of all vascular lumens, with ischemic atrophy and, at times, infarction distal to the abnormal vessels.

Figure 20-50Malignant hypertension. A, Fibrinoid necrosis of afferent arteriole (PAS stain). B, Hyperplastic arteriolitis (onion-skin lesion). (Courtesy of Dr. H. Rennke, Brigham and

Women's Hospital, Boston, MA.)

Figure 20-51Fibromuscular dysplasia of the renal artery, medial type (elastic tissue stain). The medium shows marked fibrous thickening, and the lumen is stenotic. (Courtesy of Dr.

Seymour Rosen, Beth Israel Hospital, Boston, MA.)

Figure 20-52Fibrin stain showing platelet-fibrin thrombi (red) in the glomerular capillaries, characteristic of microangiopathic disorders.

Figure 20-53Atheroemboli with typical cholesterol clefts in an interlobar artery.

Figure 20-54Diffuse cortical necrosis. The pale ischemic necrotic areas are confined to the cortex and columns of Bertin.

Figure 20-55Obstructive lesions of the urinary tract.

Figure 20-56Hydronephrosis of the kidney, with marked dilation of the pelvis and calyces and thinning of the renal parenchyma.

TABLE 20-13-- Prevalence of Various Types of Renal Stones

Date: 2016-04-22; view: 797