• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Nephrosclerosis
 

Nephrosclerosis

on

  • 591 views

Pathologic aspects

Pathologic aspects

Statistics

Views

Total Views
591
Views on SlideShare
591
Embed Views
0

Actions

Likes
0
Downloads
14
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Nephrosclerosis Nephrosclerosis Presentation Transcript

    • Nephrosclerosis Lecture 49 Vascular Diseases
    • Types • I. Benign Nephrosclerosis • II. Malignant Nephrosclerosis
    • BENIGN NEPHROSCLEROSIS • Benign nephrosclerosis is the term used for the renal pathology associated with sclerosis (Hardening) of renal arterioles and small arteries. • The resultant effect is focal ischemia of parenchyma supplied by vessels with thickened walls and consequent narrowed lumens.
    • Benign NephrosclerosisThe parenchymal effects include • glomerulosclerosisand • chronic tubulointersititial injury, producing a reduction in functional renal mass. Hypertension and diabetes mellitus, increase the incidence and severity of the lesions.
    • Pathogenesis Two processes participate in the arterial lesions: • I. Medial and intimal thickening, as a response to hemodynamic changes, aging, genetic defects, or some combination of these. The wall of a blood vessel is composed of 3 layers: Intima, media & adventitia.
    • Pathogenesis II. Hyaline deposition in arterioles, caused partly by extravasation of plasma proteins through injured endothelium and partly by increased deposition of basement membrane matrix.
    • Gross- Morphology • The kidneys are either normal or moderately reduced in size, with average weights between 110 and 130 gm. • The cortical surfaces have a fine, even granularity that resembles grain leather. • The loss of mass is due mainly to cortical scarring and shrinking. The weight of one kidney averages about 120-150 g Size: 12x 6x3 cm.
    • Close-up of the gross appearance of the cortical surface in benign nephrosclerosis illustrating the fine, leathery granularity of the surface.
    • MICROSCOPY There is • Narrowing of the lumens of arterioles and small arteries, caused by thickening and hyalinization of the walls (hyaline arteriolosclerosis)
    • Hyaline Arteriosclerosis A fatty deposit In intima Hyaline: A glass, pink protieinacious material
    • Benign Nephrosclerosis: Hyaline Arteriolarsclerosis
    • MICROSCOPY • Corresponding to the fine surface granulations are • microscopic subcapsular scars • with sclerotic glomeruli and • tubular dropout (Foci of tubular atrophy), • alternating with better preserved parenchyma.
    • MICROSCOPY • The interlobular and arcuate arteries show a characteristic lesion that consists of • Medial hypertrophy, • Reduplication of the elastic lamina, and • Increased myofibroblastic tissue in the intima, • which combine to narrow the lumen.
    • MICROSCOPY • This change, called fibroelastic hyperplasia • often accompanies hyalin arteriolosclerosis and • increases in severity with AGEand • in the presence of HYPERTENSION.
    • Morphology cont…. There is Patchy Ischemic Atrophy, which consists of (1) Foci Of Tubular Atrophy and Interstitial Fibrosis and (2) A Variety Of Glomerular Alterations.
    • Morphology Glomerular alterations include: 1.Collapse Of The GBM, 2. Deposition Of Collagen Within The Bowman Space, 3. Periglomerular Fibrosis, and 4. Total Sclerosis Of Glomeruli.
    • Morphology • When the ischemic changes are pronounced and affect large areas of parenchyma, they can produce regional scars.
    • Clinical Features. It is unusual for uncomplicated benign nephrosclerosis to cause renal insufficiency or uremia. There are usually moderate reductions in renal blood flow, but the GFR is normal or only slightly reduced.
    • Three groups of hypertensive patients with benign nephrosclerosis are at increased risk of developing renal failure: 1. People Of African Descent, 2. People with more severe blood pressure elevations, 3. Persons with a second underlying disease, especially diabetes. In these groups renal insufficiency may supervene after prolonged benign hypertension.
    • Malignant Nephrosclerosis • Malignant nephrosclerosis is the form of Renal Disease associated with The Malignant or Accelerated Phase of HYPERTENSION.
    • Malignant Nephrosclerosis • Malignant hypertension may occasionally develop in previously normotensive individuals but often is superimposed on • Preexisting essential benign hypertension • Secondary forms of hypertension, or • An underlying chronic renal disease, particularly glomerulonephritis or reflux nephropathy Associated with vesico-ureteric reflux
    • Malignant Nephrosclerosis • It is also a frequent cause of death from uremia in individuals with scleroderma. Malignant hypertension is relatively uncommon, occurring in 1% to 5% of all people with elevated blood pressure. • In its pure form it usually affects younger individuals, and occurs more often in men and in blacks.
    • Pathogenesis- Unclear • The basis for this turn for the worse (Zawaal) in hypertensive subjects is unclear, but the following sequence of events is suggested.
    • • 1.The initial insult seems to be some form of vascular damage to the kidneys. This might result • from long-standing benign hypertension, with eventual injury to the arteriolar walls, or • 2. The initiating injury may spring de novo from arteritis, • a coagulopathy, or • some injury causing acute exacerbation of the hypertension.
    • Pathogenesis • In any case, the result is • 1. increased permeability of the small vessels to fibrinogen and other plasma proteins, • 2. endothelial injury, • 3. focal death of cells of the vascular wall, and • 4. platelet deposition.
    • Pathogenesis • This leads to the appearance of 1. Fibrinoid necrosis of arterioles and small arteries, 2. Swelling of the vascular intima, and 3. Intravascular Thrombosis.
    • Pathogenesis • Mitogenic factors from platelets (e.g., PDGF), plasma, and other cells cause hyperplasia of intimal smooth muscle of vessels, resulting in the hyperplastic arteriolosclerosis that is typical of malignant hypertension and further narrowing of the lumens. • The kidneys become markedly ischemic.
    • Pathogenesis • 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.
    • Pathogenesis • This sets up a self-perpetuating cycle in which angiotensin II causes intrarenal vasoconstriction, and the attendant renal ischemia perpetuates renin secretion.
    • Pathogenesis • Other vasoconstrictors (e.g., endothelin) and loss of vasodilators (nitric oxide) may also contribute to vasoconstriction.
    • Pathogenesis • Aldosterone levels are also elevated, and salt retention undoubtedly contributes to the elevation of blood pressure.
    • Pathogenesis • 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.
    • Gross 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.
    • Microscopy • Two histologic alterations characterize blood vessels in malignant hypertension: 1. 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.
    • Malignant Nephrosclerosis
    • Microscopy • This change represents an acute event; it may be accompanied by limited inflammatory infiltrate within the wall. • Sometimes the glomeruli become necrotic and infiltrated with neutrophils, and the glomerular capillaries may thrombose.
    • 2. 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 probably represents accumulations of proteoglycans and plasma proteins. This alteration has been referred to as onion-skinning because of its concentric appearance.
    • Malignant Nephrosclerosis
    • • The lesion, also called hyperplastic arteriolitis, correlates well with renal failure in malignant hypertension. • There may be superimposed intraluminal thrombosis. • The arteriolar and arterial lesions result in considerable narrowing of all vascular lumens, ischemic atrophy and, at times, infarction distal to the abnormal vessels.
    • Clinical Features • SP>200 mm Hg & DP>120 mm Hg, • Papilledema, • Retinal hemorrhages, • Encephalopathy, • Cardiovascular abnormalities, & • Renal failure.
    • Clinical features • Most often, the early symptoms are related to increased intracranial pressure and include • headaches, • nausea, • vomiting, and • visual impairments, particularly scotomas or spots before the eyes.
    • Clinical Features •Hypertensive crises are sometimes encountered, characterized by • episodes of loss of consciousness or even convulsions.
    • Clinical Features • At the onset of rapidly mounting blood pressure, there is marked proteinuria and microscopic or sometimes macroscopic hematuria but no significant alteration in renal function. • Soon, however, renal failure makes its appearance.
    • Treatment • The syndrome is • a true medical emergency requiring the institution of aggressive and prompt antihypertensive therapy to prevent the development of irreversible renal lesions.
    • Prognosis • Before the introduction of current antihypertensive drugs, malignant hypertension was associated with a • 50% mortality rate within 3 months of onset, progressing to 90%within a year.
    • Prognosis • At present, however, • about 75% of patients survive 5 years, and 50% survive with restoration of pre-crisis renal function.