Malignant nephrosclerosis is a disease characterized by vascular damage to the kidneys that is usually caused by long-standing hypertension. Microscopically, it shows fibrinoid necrosis of arterioles, fibrin deposition, and intimal thickening of arteries and arterioles. Clinically, it presents as malignant hypertension with systolic pressures over 200 mm Hg and diastolic pressures over 120 mm Hg, as well as papilledema, retinal hemorrhages, and encephalopathy. Treatment involves controlling blood pressure with ACE inhibitors, angiotensin receptor blockers, or aliskiren. Most patients survive 5 years with treatment and restoration of renal function.
Malignant nephrosclerosis is a disease characterized by vascular damage to the kidneys that is usually caused by long-standing hypertension. Microscopically, it shows fibrinoid necrosis of arterioles, fibrin deposition, and intimal thickening of arteries and arterioles. Clinically, it presents as malignant hypertension with systolic pressures over 200 mm Hg and diastolic pressures over 120 mm Hg, as well as papilledema, retinal hemorrhages, and encephalopathy. Treatment involves controlling blood pressure with ACE inhibitors, angiotensin receptor blockers, or aliskiren. Most patients survive 5 years with treatment and restoration of renal function.
Malignant nephrosclerosis is a disease characterized by vascular damage to the kidneys that is usually caused by long-standing hypertension. Microscopically, it shows fibrinoid necrosis of arterioles, fibrin deposition, and intimal thickening of arteries and arterioles. Clinically, it presents as malignant hypertension with systolic pressures over 200 mm Hg and diastolic pressures over 120 mm Hg, as well as papilledema, retinal hemorrhages, and encephalopathy. Treatment involves controlling blood pressure with ACE inhibitors, angiotensin receptor blockers, or aliskiren. Most patients survive 5 years with treatment and restoration of renal function.
Malignant nephrosclerosis is a disease characterized by vascular damage to the kidneys that is usually caused by long-standing hypertension. Microscopically, it shows fibrinoid necrosis of arterioles, fibrin deposition, and intimal thickening of arteries and arterioles. Clinically, it presents as malignant hypertension with systolic pressures over 200 mm Hg and diastolic pressures over 120 mm Hg, as well as papilledema, retinal hemorrhages, and encephalopathy. Treatment involves controlling blood pressure with ACE inhibitors, angiotensin receptor blockers, or aliskiren. Most patients survive 5 years with treatment and restoration of renal function.
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