HTN and Renal Disease Flashcards
arterionephrosclerosis - clinical history
*long-standing HTN (“benign” hypertension)
*+/- renal insufficiency
arterionephrosclerosis - pathology
*smaller, shrunken kidneys grossly
*vascular medial wall thickening with hyaline deposits in the vascular walls
*distal ischemia results in:
-tubular atrophy
-interstitial fibrosis
-fibrosis/scarring in the glomerulus (either focal areas of scarring or global glomerulosclerosis)
hypertensive emergency - clinical history
*BP >/= 180/120 WITH evidence of end-organ damage
*more common in middle-age white males
*patients may or may not have a history of HTN
*may be associated with thrombotic microangiopathy or microangiopathic hemolytic anemia
hypertensive emergency - pathology
*gross examination shows petechial hemorrhages on the surfaces of the kidneys
*microscopically, endothelial swelling +/- complete occlusion of vessel lumen, fibrinoid necrosis of the vessel walls, RBC fragments lodged into vessel walls
*if chronic, can see “onion-skin” pattern of intimal fibrosis
hypertensive emergency - pathogenesis
*significantly increased pressure in the vessel → endothelial damage
*fibrinoid material can enter vessel walls → fibrinoid necrosis (see image)
*smooth muscle layer hyperplasia → smaller vessel lumen
*intravascular thrombosis with associated distal ischemia
*with disease in the afferent arterioles → renal ischemia → RAAS system activated → increased renin → increased blood volume → further worsened HTN
hypertensive emergency - treatment
*EMERGENCY → admit to hospital for IV anti-hypertensives (labetalol, nicardipine, sodium nitroprusside)
*lower BP gradually so that end-organs have time to auto-regulate to new pressure
*note - CKD often results, even if HTN emergency is treated
thrombotic microangiopathy (TMA) - overview
*a group of diseases characterized by microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and renal failure
*the endothelial damage → shearing of RBCs → formation of schistocytes → clots → renal failure
thrombotic microangiopathy (TMA) - pathogenesis
*many different causes (commonly associated with HUS and TTP)
*hypertensive emergency can also cause TMA
*endothelial damage that comes with HTN emergency → shearing of RBCs, creating schistocytes that can clump with fibrin & platelets and form clots
*occluded arteries → glomerulosclerosis → renal failure
thrombotic microangiopathy (TMA) - pathology
*swollen endothelium → can close off vessel walls → distal ischemia → activates RAAS system
*schistocytes in vascular walls
note - histology similar to that of hypertensive emergency
ddx for increased renin, increased aldosterone
*renal artery stenosis (RAS)
*renin-producing tumor
*hypertensive emergency
ddx for decreased renin, increased aldosterone
*Conn’s Syndrome / Primary Hyperaldosteronism
*bilateral adrenal hyperplasias
*glucocorticoid remediable hyperaldosteronism
ddx for decreased renin, decreased aldosterone
*Cushing’s Syndrome
*Liddle’s Syndrome
*SAME (Syndrome of Apparent Mineralocorticoid Excess)
*licorice ingestion
renal artery stenosis (RAS) - overview
*a narrowing of the arteries that supply blood to one or both kidneys, which prevents normal supply of oxygen to the cells → impairment of renal function
*includes RAS related to :
-ATHEROSCLEROSIS of the renal arteries (usually older age, proximal renal artery)
-fibromuscular dysplasia (usually younger age, distal renal artery)
renal artery stenosis (RAS) - clinical manifestations
*resistant hypertension
*renal failure
*acute rise in serum creatinine following administration of ACEi or ARB
*recurrent episodes of flash pulmonary edema
*RENAL ARTERY BRUITS may be heard on physical exam
renal artery stenosis (RAS) due to atherosclerosis - pathogenesis & pathology
*narrowing at the origin of the renal artery by an atheromatous plaque
*ischemic kidney becomes smaller and show signs of diffuse ischemic atrophy with crowded glomeruli, atrophic tubules, interstitial fibrosis, focal inflammatory infiltrates
renal artery stenosis (RAS) - diagnosis
*renal artery duplex (ultrasound)
*CT angiogram (gold standard)
*MR angiogram
renal artery stenosis (RAS) due to fibromuscular dysplasia
*a noninflammatory, nonatherosclerotic condition characterized by abnormal cell growth in the walls of arteries that most commonly affects the renal arteries, causing hypertension
*younger to middle aged, usually females
*commonly affects the distal 2/3 of the renal artery
*HTN responds well to revascularization
*may have family hx
*may be bilateral
*may involve other arteries (cerebral arteries common)
renal artery stenosis (RAS) due to atherosclerosis
*older adults (>50)
*evidence of other vascular disease (known PAD, CAD, history of CVA)
*other sx: headache, pulsatile tinnitus, neck pain, flank/abdominal pain
*hx of smoking, CKD common
*generally treated medically, as revascularization does not generally change outcomes
*may be bilateral
treatment of UNILATERAL renal artery stenosis (RAS)
*over time, the non-affected kidney will show signs of HTN (arterionephrosclerosis)
*treat with RAAS blockade (ACE inhibitors or ARBs) protects the good kidney
treatment of BILATERAL renal artery stenosis (RAS)
*do NOT use RAAS blockade (NO ACEi or ARBs) because these will cause renal failure
*instead, use diuretics
treatment of renal artery stenosis (RAS) due to fibromuscular dysplasia
*REVASCULARIZATION (angioplasty, stent placement)
*ACEi/ARB is first-line medical therapy
APOL1 nephropathy - overview
*APOL1 = gene that encodes apolipoprotein L1, located on chromosome 22
*G1 and G2 (i.e. 1 and 2 copies of the risk allele, respectively) are associated with earlier age and faster progression to ESRD
*almost exclusively seen in Black patients
*G1 and G2 are protective against Trypanosoma brucei, which is the parasite transmitted by the tsetse fly, that causes African sleeping sickness (trypanosomiasis)
*2-hit hypothesis where APOL1 gene variants are the first hit
APOL1 nephropathy - pathology
*solidified glomerular tufts, often with “disappearing glomeruli”
*spectrum, with increased proteinuria and nephropathy progression rate: focal global glomerulosclerosis < focal segmental glomerulosclerosis < collapsing FSGS
