Fogo, Ch. 10 - Nephrosclerosis & Hypertension Flashcards
What is the pathophysiology that underlies renal hypertension?
Renal ischemia (due to vascular or parenchymal disease) causes upregulation of the RAAS axis (angiotensin, aldosterone)
What are the gross findings in arterionephrosclerosis?
Small kidneys, granular surface, thinned cortex. If malignant/accelerated, petechiae or frank infarcts.
What are the LM findings in “benign” arterionephrosclerosis?
Medial thickening with arteriolar hyaline deposits (composed of plasma macromolecule insudates). Can have global sclerosis or secondary FSGS.
What are the LM findings in malignant hypertension?
RBC fragments in arteriolar walls, fibrinoid necrosis and onion-skinning.
What interstitial findings are seen in hypertension?
Proportional tubulointerstitial fibrosis. In severe lesions, nephrons will be atrophic and closely spaced.
What are the IF/EM findings in arterionephrosclerosis?
IF: Nonspecific IgM/C3 in gloms. Fibrin/fibrinogen in vessels.
EM: Corrugated, wrinkled GBM. No deposits. Variable podocyte effacement.
What population is most susceptible to renal damage in hypertension? Why?
African-Americans suffer more end-organ damage, this may be due to ApoL1 alleles which are normally protective against trypanosomes. Mechanism unknown.
Recall the features of cholestol embolization.
Can be spontaneous or following endovascular procedures. Cleft-shaped spaces with mononuclear cell reaction that fibroses. Can have secondary FSGS.
Recall the clinical features of scleroderma.
Multisystem disease mostly affecting skin, GI, lung, heart, and kidney. Anti-topoisomerase/centromere/RNApol antibodies. 70% involve the kidneys.
How does renal scleroderma appear morphologically?
What are the components of scleroderma renal crisis?
Almost identical to accelerated/malignant arterionephrosclerosis (slightly larger vessels are affected)
Malignant hypertension, acute kidney injury, and infarcts.
