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14 Cards in this Set

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Renal System-Renovascular Disease by Leonard
Renal System-Renovascular Disease by Leonard
Benign HTN...clinical features...who gets it most?
Does not typically lead to significant renal impairment
-Often asymptomatic
-Small proportion of people with mild-moderate hypertensive disease develop renal insufficiency
-Because so many people have “benign hypertension,” if accounts for ~ 1/3 of cases of ESRD

Most prevalent in African-Americans
-Leading cause of ESRD
Benign HTN...pathology...what do the kidneys look like?
Atrophic kidneys, usually bilaterally
-Granular surface of “fixed” capsule; thinned cortex

LM: changes most prominent in subcortical area
-Varying degrees of glomerular damage: capillary walls thickened to globally sclerotic glomerulus
-Tubular atrophy (due to dysfunction of glomeruli)
Malignant Hypertension... what is it, who gets it, pathology..
-Diastolic pressures over 130 mm Hg; retinal vascular changes, papilledema, renal dysfunction

Clinical:M>W; ~ 40’s; headache, dizziness, visual disturbances; progressive renal dysfunction/failure

Pathology: Kidneys vary in size: small to large (edema)
-Cut surface is mottled red/yellow, with scattered infarcts
-Fibrinoid necrosis, marked hyaline sclerosis, hyperplastic arteritis
Renal Artery Stenosis is permanent, right? Clinical and Etiology, please.
Can be reversed with reestablishment of lumen (Surgical revascularization, angioplasty, nephrectomy)

Clinical: Mild-moderate hypertension
+/- bruit over main renal artery; Dx by imaging
-Elevation of renal vein renin from affected side

Etiology:Increased activity of Renin, angiotensin II, aldosterone
Causes: #1 – atherosclerosis; also vasculitis, fibromuscular dysplasia
What the heck is Fibromuscular Dysplasia? WHat do you see on angiogram?
Fibrosis of arterial wall with resultant stenosis
-Can affect intima, media, or and region of vessel wall from intima to adventitia
E.g., medial fibroplasia (most common; 66% of cases)

Areas of thickening (e.g., medial) alternating with areas of atrophy
-“String of beads” pattern on angiogram
Thrombotic Microangiopathies, what is it and the clinical and laboratory features
Systemic thrombus formation through small vessels (capillaries, arterioles) leading to ischemia

Clinical: Microangiopathic hemolytic anemia, thrombocytopenia, hypertension, renal failure

Laboratory: Schistocytes (fragmented RBCs) in peripheral smear
Normal coagulation times; normal or slightly elevated FSPs
Thrombotic Microangiopathies Causes
Common pathogenesis: endothelial damage with leakage of plasma proteins into subendothelial tissues; promotion thrombosis (various mechanisms)
-Both reduce vascular lumen and result in ischemia
Thrombotic Microangiopathies Morphology...what does it look like?
-Some similarity to malignancy hypertensive nephropathy
-Arteriolar fibrinoid necrosis
-Edematous expansion of arteriolar intima
-Collapsing of glomeruli, necrosis or glomerular capillary congestion
-Vascular thrombosis
So what are the two forms of Hemolytic Uremic Syndrome (HUS)?
Typical (epidemic, classic, diarrhea-positive)
-Associated most often with ingestion of food contaminated with bacteria – Shiga-like toxin

Atypical (diarrhea-negative, non-endemic)
-Inherited mutations in complement system proteins
Acquired: anti-phospholipid antibodies; associated with: pregnancy, oral contraceptives, chemotherapy, radiation therapy, autoimmune vasculitides. Occurs in Adults.
-Worse prognosis
What is the classic pentad of clinical symptoms of Thrombotic Thrombocytopenia Purpura (TTP)
-Fever
-neurologic symptoms,
-microangiopathic hemolytic anemia,
-thrombocytopenia,
-ARF
What has a decreased function, and what causes it in TTP
Usually caused by antibodies (autoimmune, drug-induced) or a genetic defect that result in decreased function of ADAMTS13
-ADAMTS13 protease normally cleaves large multimers of vWF
-Persistent very large vWF promotes platelet aggregation
Sickle cell nephropathy
Form sickle cell disease (homozygous) or trait (heterozygous)
Clinical: hematuria, diminished concentrating ability
Etiology/Pathology:
-Medullary interstitium (supplied by vasa recta) is hypertonic and relatively hypoxic: promotes sickling of RBCs with aberrant Hb
-Vascular occlusion of these vessels with hypoxic infarction of papilla and medulla – papillary necrosis
-Glomeruli are congested with sickle cells
-FSGS may develop in some
Common sources and morphologic appearance of embolic kidney disease?
Sources of emboli:
Cardiac mural thrombi (ventricular wall dyskinesia from prior MI; atrial fib)
Cardiac valvular vegetations (infected, noninfected)
Complicated atherosclerotic plaques

Responsible for majority of cases of renal infarcts
-Interlobar and arcuate arteries

-Result in wedge-shaped cortical infarcts