Download Renal Vascular Diseases and more Slides Pathology in PDF only on Docsity! Scanned with CamScanner Renal Vascular Diseases
However the main diseases affecting blood vessels of the kidney are:
Benign nephrosclerosis
Malignant nephrosclerosis
Renal artery stenosis
Thrombotic microangiopathies
Thickened and hyalinized walls of the small
arteries and arterioles (hyaline
arteriolosclerosis).
resulting in ischemia.
Tubular atrophy, interstitial fibrosis
Patchy loss of glomeruli.
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Malignant Nephrosclerosis
Also called Hypertensive Emergency or Malignant Hypertension or
Accelerated Nephrosclerosis.
Malignant hypertension is extremely high blood pressure that develops
rapidly and causes organ damage (especially CNS, CVS, eye, kidney)
It usually affects younger individuals, and occurs more often in men.
The syndrome of malignant hypertension is characterized by:
Systolic pressures >200 mm Hg and diastolic pressures >120 mm Hg,
Increased intracranial pressure: papilledema, retinal hemorrhages,
headaches, nausea, vomiting, and visual impairments (scotomas or
spots before the eyes), encephalopathy
Cardiovascular abnormalities and renal failure
“Hypertensive crises” are sometimes encountered, characterized by
episodes of loss of consciousness or even convulsions.
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¢ Small, pinpoint petechial hemorrhages may appear on the cortical
surface from rupture of arterioles or glomerular capillaries, giving the
kidney a “flea-bitten” appearance.
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¢ Hyperplastic arteriolitis (onion skinning): in arteries and arterioles,
there is intimal thickening caused by a proliferation of, concentrically
arranged smooth muscle cells, together with collagen.
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QF =F
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¢ Fibrinoid necrosis of arterioles. This appears as an eosinophilic
granular change in the blood vessel wall.
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Hypertension secondary to renal artery stenosis is caused by
increased production of renin and angiotensin from the
ischemic kidney. This hypertension responds to ACE inhibitors.
The ischemic kidney is reduced in size and shows signs of
diffuse ischemic atrophy, with crowded glomeruli, atrophic
tubules, interstitial fibrosis.
The contralateral nonischemic kidney also shows signs of the
hypertension.
THROMBOTIC MICROANGIOPATHIES
Thrombosis in capillaries and arterioles throughout the body, including
kidney.
Clinically characterized by:
Microangiopathic hemolytic anemia
Thrombocytopenia
Renal failure
THROMBOTIC MICROANGIOPATHIES- TYPES
It has two forms:
1. Hemolytic-uremic syndrome (HUS)
(Endothelial activation)
2. Thrombotic thrombocytopenic purpura (TTP)
(Platelets activation)
HUS-Pathogenesis
Endothelial injury appears to be the primary cause of HUS
In typical HUS, the trigger for endothelial injury and activation is a Shiga-like toxin.
In atypical HUS the cause of the endothelial injury appears to be excessive,
inappropriate activation of complement.
The endothelial injury in HUS, causes platelet activation and thrombosis within
microvascular beds.
Reduced endothelial production of prostaglandin |2 and NO (both inhibitors of
platelet aggregation) contributes to thrombosis.
The reduction in prostaglandin I2 and NO and increased production of endothelin
may also promote vasoconstriction, aggravating the hypoperfusion of tissues.
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Thrombotic Thrombocytopenic Purpura (TTP)
TTP, which is often associated with inherited or acquired deficiencies of ADAMTS13, a
plasma metalloprotease that regulates the function of von Willebrand factor (vWF)
ADAMTS13 cleaves vWF multimers into smaller sizes.
Very large vWF multimers can bind platelet surface glycoproteins and it causes
platelets activation and microthrombi formation.
More common in women age 40 years or less.
TTP is classically manifested by fever, neurologic symptoms, microangiopathic
hemolytic anemia, thrombocytopenia, and renal failure
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Morphology—HUS & TTP
Patchy or diffuse renal cortical necrosis
The glomerular capillaries are occluded by thrombi
composed of aggregated platelets and fibrin.
Fibrinoid necrosis of arteries and arterioles
The capillary walls are thickened with luminal
narrowing
Thrombi in the glomerular capillaries
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