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Malignant Nephrosclerosis

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MASULOT, ISFAHAN B.

Disease Etiology Pathology Histologic Incidence Clinical presentation Treatment Prognosis


feature/morphology
#158  Usually arises 1. vascular damage Gross:  Malignant 1. systolic  angiotensin 75% of patients
-Malignant from preexisting to the kidneys hypertension pressures converting survive 5 years,
 Small, 
Nephrosclero essential from a variety of is relatively greater than 200 enzyme and 50% survive
pinpoint 
sis hypertension disorders uncommon, mm Hg and (ACE) with restoration
petechial
 secondary forms 2. endothelial injury occurring in diastolic inhibitors of pre-crisis
hemorrhages
of hypertension 3. increased 1% to 5% of pressures renal function
 may   Aliskiren
 glomerulonephritis permeability of the all people greater than 120
appear on  150-
 reflux small vessels to with elevated mm Hg
the cortical  300mg/day
nephropathy fibrinogen and blood pressure
surface  2. papilledema
other plasma  more often in  angiotensin
from 
proteins men and in 3. retinal receptor
rupture of 
4. focal death of cells blacks hemorrhages blockers
arterioles 
of the vascular
or  4. encephalopathy
wall
glomerular 
5. platelet deposition 5. cardiovascular
capillaries
6. fibrinoid necrosis abnormalities
of arterioles and  “flea-bitten” 
6. renal failure
small arteries appearance
7. hyperplasia of 7. scotomas or
intimal smooth spots before the
muscle of vessels eyes
8. kidneys become
markedly ischemic 8. increased
9. elevated levels of intracranial
Microscopic:
plasma renin pressure
 Fibrinoid
10. intrarenal
necrosis of 9. “Hypertensive
vasoconstriction
arterioles crises
 smudgy 
10. marked
eosinophilic 
proteinuria
appearance
 fibrin  11. microscopic or
deposition macroscopic
 intimal  hematuria
thickening of

interlobular 
arteries 
and 
arterioles
 onion-skinning
 hyperplastic
arteriolitis

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