HTN Renal Disease

How kidney disease causes hypertension

Loss of nephrons → impaired sodium excretion + RAAS activation → increased blood pressure.

How hypertension causes kidney disease

Chronic high BP → arteriolar hyalinosis, ischemia, glomerulosclerosis, tubular atrophy, interstitial fibrosis.

Histologic finding: arterionephrosclerosis

Hyaline arteriosclerosis, medial thickening, narrowed lumens, global/focal glomerulosclerosis, tubular atrophy.

Histologic finding: hypertensive emergency

Endothelial swelling, fibrinoid necrosis, RBC fragments in vessel walls, thrombi, “onion-skin” hyperplastic arteriolitis.

Histologic finding: thrombotic microangiopathy

Schistocytes lodged in vessel walls, endothelial swelling, thrombosis occluding arterioles and glomeruli.

Physical exam clues for hypertensive emergency

Papilledema, confusion, focal neurologic deficits, pulmonary edema, chest pain, oliguria.

Laboratory clues for hypertensive emergency

Proteinuria, hematuria, elevated creatinine, MAHA (schistocytes), thrombocytopenia.

End-organ damage: brain

Headache, confusion, seizures, PRES, stroke.

End-organ damage: eyes

Papilledema, flame hemorrhages, cotton-wool spots.

End-organ damage: heart

Chest pain, MI, arrhythmia, acute heart failure, pulmonary edema.

End-organ damage: kidneys

Rising creatinine, oliguria/anuria, proteinuria, hematuria.

RAAS activation in hypertensive emergency

Afferent arteriolar injury → ischemia → macula densa senses low flow → massive renin release → worsens BP.

Pathogenesis of hypertensive emergency

Extreme BP → endothelial injury → fibrinoid necrosis → thrombosis → ischemia → RAAS activation.

Definition of hypertensive emergency + tx

BP ≥180/120 with evidence of end-organ damage. Tx: Antihypertensives like labetolol, nicardipine, sodium nitroprusside

Renal artery stenosis: clinical clues

Resistant HTN, abdominal bruit, acute rise in creatinine after ACEi/ARB, flash pulmonary edema.

Renal artery stenosis: renin/aldosterone pattern

High renin + high aldosterone.

Fibromuscular dysplasia features

Young women, distal renal artery involvement, “string-of-beads,” responds well to revascularization.

Atherosclerotic renal artery stenosis features

Older adults, proximal renal artery plaque, associated with PVD/CAD, treated medically.

APOL1 nephropathy clinical pattern

Strong family historyoften black patients), progressive CKD, heavy proteinuria, seen almost exclusively in Black patients.

APOL1 nephropathy histology

Collapsing glomerulopathy, segmental/global sclerosis, prominent podocyte injury.

Thrombotic Microangiopathy (TMA) causes relevant to hypertension

Hypertensive emergency, HUS (Shiga toxin), TTP, drugs (cocaine, chemo).

HUS distinguishing features

MAHA(microangiopathic hemolytic anemia) + thrombocytopenia + AKI + Shiga toxin–positive stool.

Why hypertensive emergency causes Microangiopathic Hemolytic Anemia (MAHA)

Endothelial injury → RBC shearing → schistocytes → thrombosis → ischemia.

IV medications for hypertensive emergency

Labetalol, nicardipine, clevidipine, sodium nitroprusside.

Why BP must be lowered gradually in hypertensive emergency

Sudden drops impair autoregulation → worsen ischemia in brain, heart, kidneys.

Why CKD worsens hypertension

Reduced nephron mass → impaired sodium excretion → volume expansion → RAAS activation.

Why hypertension worsens CKD

Chronic pressure → vascular thickening → ischemia → glomerulosclerosis → progressive renal failure.

Why ACEi/ARB worsen creatinine in bilateral Renal Artery Stenosis

Efferent dilation → drop in GFR when renal perfusion already low.

Lab findings suggesting Thrombocytic Microangiopathy (TMA)

Schistocytes, thrombocytopenia, elevated LDH, low haptoglobin, AKI.

UA findings in HUS

Hemoglobin-positive dipstick with no RBCs (hemolysis), proteinuria.

Why renal biopsy is avoided in TMA

Severe HTN + thrombocytopenia → high bleeding risk.

TX for 1 sided Renal Artery Stenosis vs 2 sided (bilateral) RAS

1 Sided: use RAAS blockage (ACEi/ARBs)
2 Sided (bilateral: use diuretics, as RAAS block would cause renal failure as they are reliant on RAAS)

High Renin, High Aldosterone Differential

Renal artery stenosis, renin producing tumor, hypertensive emergency

Low renin, High aldosterone Differential

Primary hyperaldosteronism, bilateral adrenal hyperplasias, Glucocorticoid Remediable Hyperaldosteronism

Low renin, Low aldosterone Differential

Cushing sydrome, Liddle’s syndrome, Syndrome of Apparent Mineralcorticoid Excess (SAME)