Renovascular hypertension is hypertension caused by renal ischemia from partial or complete renal-artery occlusion — the most common form of secondary, potentially curable hypertension. Although renal-artery disease affects only a small fraction of hypertensives, it may underlie renal failure in 10–20% of ESRD patients.
Etiology
- Adults — atherosclerosis is the most common cause (60–80%), typically involving the proximal third of the renal artery (often an aortic plaque impinging on the ostium); fibromuscular dysplasia is second (20–40%), involving the distal segments.
- Children — fibromuscular dysplasia, vasculitis, neurofibromatosis, and neuroblastoma.
Pathophysiology
| Feature | 2-Kidney, 1-Clip (vasoconstrictor) | 1-Kidney, 1-Clip (volume) |
|---|---|---|
| Driver | RAAS activation → angiotensin II vasoconstriction | Volume expansion and sodium retention |
| Renin | ↑ in the ischemic kidney, suppressed in the normal contralateral kidney | Suppressed (feedback inhibition) |
| Treatment | ACE inhibitor/ARB, or "unclipping" | Volume management (normal angiotensin II) |
In 2K1C, the normal contralateral kidney mounts a natriuresis; in 1K1C, the absence of a normal contralateral kidney prevents that natriuresis, so volume expansion sustains the hypertension even as renin falls.
Ischemic nephropathy — hemodynamically significant RAS damages the whole parenchyma, driven more by proinflammatory mediators than by the drop in renal blood flow alone. A "critical stenosis" is 70–80% (reducing RBF >40%); beyond 80% stenosis, perfusion pressure falls below 70–80 mmHg and the kidney can no longer autoregulate. Renovascular hypertension is most likely with ≥70% stenosis (one or both arteries) or 50% stenosis with post-stenotic dilatation.
Diagnosis and Evaluation
Clinical clues that warrant evaluation: severe/refractory hypertension with grade III–IV retinopathy; abrupt-onset moderate–severe hypertension; onset before age 20 or after 50; unexplained worsening renal function on an ACE inhibitor/ARB; paradoxical worsening with diuretics; recurrent "flash" pulmonary edema; a systolic-diastolic abdominal bruit radiating to the flanks; and diffuse vascular disease/cholesterol embolisation.
- Screening (highest sensitivity/specificity): MRA, CTA, and duplex Doppler US (renal scintigraphy is no longer recommended). CTA and MRA poorly visualise the distal arterial tree. Gadolinium MRA gives both RBF and GFR but is limited by nephrogenic-systemic-fibrosis risk when GFR <30 mL/min; CTA is limited by creatinine >1.7 mg/dL; duplex US relies on a peak systolic velocity >180 cm/s (operator-dependent).
- Confirmatory: angiography (conventional and intra-arterial digital subtraction) remains the gold standard and is indicated when suspicion is high — renovascular disease can be present despite a negative screen, especially with distal/intrarenal lesions.
Fibromuscular Dysplasia
FMD typically affects younger Caucasian women and is usually bilateral, presenting with hypertension, headache, and pulsatile tinnitus.
- Medial fibroplasia — the most common type (70–80%); women 25–50; involves the distal main renal artery; unlikely to progress to occlusion or function loss (the classic "string of beads").
- Intimal fibroplasia — the most common focal type; may cause dissection, mural hematoma, and infarction; likely to progress without intervention.
- Perimedial fibroplasia — 10–25%; younger women (5–15); mid-renal artery; likely to progress.
- Medial hyperplasia — rare; likely to progress.
Surveillance is duplex ultrasound of kidney length and cortical thickness once or twice yearly.
Management
Three options control BP: medical therapy, percutaneous transluminal renal angioplasty (PTRA) ± stenting, and surgery.
- Medical therapy controls BP in >90%; ACE inhibitors/ARBs are particularly effective (the hypertension is renin-driven) but are contraindicated in bilateral RAS. Because they can drop perfusion below the critical level, monitor renal function closely.
- PTRA ± stenting — successful for FMD (restenosis up to 27%) but not for atherosclerotic RAS (the CORAL trial showed no meaningful benefit over medical therapy). For renal-function preservation, PTRA matches surgery for non-ostial lesions, but the ostial lesions that make up 80–85% of atherosclerotic RAS need stenting (plain angioplasty fails).
- Surgical revascularization — indicated for concomitant aortic aneurysm/occlusive disease, a renal-artery macroaneurysm with stenosis, malignant/accelerated hypertension refractory to medical therapy, >75% occlusion (bilateral or solitary kidney), or when PTRA is impossible. Best outcomes need a kidney >8 cm (a kidney <8 cm is end-stage), a patent distal artery with collateral filling, viability on renography, and minimal glomerulosclerosis on biopsy; severe loss (creatinine >4 mg/dL) makes recovery unlikely. With a severely diseased aorta, use a splenorenal bypass on the left or a hepatorenal bypass on the right.
- Renal denervation — endovascular radiofrequency ablation of the renal sympathetics (which run in the arterial adventitia) lowers plasma renin and raises RBF, but the SIMPLICITY trial showed it was unsuccessful for resistant hypertension.