NephrologyTier 2Disease (DEADMAN)

Renal artery stenosis

Description

Narrowing of a renal artery -> dec perfusion -> renin release -> renovascular hypertension, and if severe or bilateral, ischaemic nephropathy

Two diseases with the same name

	Atherosclerotic (~90%)	Fibromuscular dysplasia (~10%)
Who	Older, smokers, diffuse vascular disease	Young women (15-50)
Site	Ostial and proximal third	Mid-to-distal artery, often bilateral
Angiogram	Focal or eccentric stenosis + aortic plaque	*'String of beads'* - alternating stenosis and aneurysmal dilatation
Kidney	Progressive atrophy	Often a small ipsilateral kidney
Treatment	Medical - revascularisation rarely helps	Angioplasty, usually curative
Course	Progressive, part of systemic atherosclerosis	Non-atherosclerotic, non-inflammatory

~1-5% of all hypertension; up to 15-20% of hypertension in patients over 65 with vascular disease
Present in ~25-40% of patients undergoing coronary or peripheral angiography - mostly incidental and haemodynamically insignificant
Fibromuscular dysplasia: F:M ~9:1, peak 15-50 yrs; medial fibroplasia is the commonest subtype (~80-90%)
Accounts for ~5-15% of ESKD in patients over 50

Haemodynamics - and why laterality changes everything

Unilateral stenosis
- Affected kidney: dec perfusion -> inc renin -> angiotensin II -> vasoconstriction + aldosterone
- Contralateral normal kidney pressure-natriureses, so volume stays near normal
- -> renin-dependent, angiotensin II-mediated hypertension
- ACEi/ARB works well and is safe
Bilateral stenosis, or stenosis in a single functioning kidney
- No kidney can escape -> sodium and volume retention -> volume-dependent hypertension; renin may normalise
- GFR becomes dependent on angiotensin II-mediated efferent constriction
- -> *ACEi/ARB precipitates AKI* (the classic exam finding)
- -> flash pulmonary oedema (Pickering syndrome) from impaired natriuresis

Ischaemic nephropathy

Chronic hypoperfusion -> tubulointerstitial fibrosis, glomerulosclerosis, atrophy
Cortical thinning and loss of kidney length are irreversible - so revascularising a small, scarred kidney restores nothing

Fibromuscular dysplasia

Non-atherosclerotic, non-inflammatory arterial disease; medial fibroplasia commonest
Multivessel in ~30% - carotid and vertebral (screen with CTA/MRA head and neck), mesenteric, iliac
Associated with spontaneous coronary artery dissection (SCAD), cervical artery dissection and intracranial aneurysm

Suspect renal artery stenosis when

Hypertension onset before 30 (FMD) or after 55 (atherosclerotic)
Resistant or accelerating hypertension
*Creatinine rise >30% after starting an ACEi/ARB* - the most specific clinical clue
Recurrent flash pulmonary oedema with preserved LV function
Abdominal or flank bruit (systolic-diastolic is specific but insensitive)
Asymmetric kidneys - >1.5 cm difference in length
Unexplained progressive renal impairment, especially with widespread atherosclerosis
Hypokalaemia with metabolic alkalosis (secondary hyperaldosteronism)

Imaging

Test	Notes
Duplex ultrasound	First-line, no contrast; peak systolic velocity >180-200 cm/s, renal:aortic ratio >3.5. Operator-dependent, poor in obesity and bowel gas; resistive index >0.8 predicts a poor response to revascularisation**
CT angiography	Best spatial resolution; iodinated contrast
MR angiography	No iodinated contrast; *avoid gadolinium if eGFR <30* (nephrogenic systemic fibrosis); overestimates stenosis severity
Catheter angiography	Gold standard; done when intervening. The 'string of beads' of FMD is best seen here
Captopril renography	Largely historical

A stenosis is only significant if it is >70%, or >50% with a translesional pressure gradient

Medical therapy first - in nearly everyone with atherosclerotic disease

*ASTRAL and CORAL: routine stenting adds nothing to optimal medical therapy* - no benefit for BP, renal function, cardiovascular events or mortality, and it carries procedural risk (atheroembolism, dissection, contrast nephropathy)
ACEi or ARB is the drug of choice for unilateral disease
- In bilateral disease or a single kidney: use with great caution, start low, and check creatinine at 1-2 weeks
- A creatinine rise >30% mandates stopping and reassessing
Statin (high intensity), antiplatelet, smoking cessation, glycaemic control - treat the systemic atherosclerosis
Additional agents: calcium channel blocker, diuretic, beta blocker

Revascularise (angioplasty +/- stent) only for

Recurrent flash pulmonary oedema or refractory heart failure (Pickering syndrome)
True refractory hypertension despite maximal tolerated multi-drug therapy
Rapidly deteriorating renal function, or a rise attributable to the stenosis
Stenosis in a solitary functioning kidney, or bilateral critical stenosis with AKI
Kidney length >7-8 cm and resistive index <0.8 predict a worthwhile response

Fibromuscular dysplasia

Percutaneous transluminal angioplasty, usually WITHOUT a stent - cure or marked improvement in blood pressure in the majority, especially if young with short-duration hypertension
Screen the whole arterial tree once - CTA/MRA of head, neck and abdomen (intracranial aneurysm, cervical dissection)
Antiplatelet therapy; avoid smoking; consider SCAD in any FMD patient with chest pain

Surgery

Aortorenal bypass or endarterectomy - reserved for complex anatomy, aneurysm, or failed endovascular therapy

Diffuse atherosclerosis - coronary, cerebrovascular, peripheral arterial disease, AAA
Smoking, diabetes, dyslipidaemia, older age
Flash pulmonary oedema (Pickering syndrome)
Cholesterol embolisation after angiography or anticoagulation - livedo reticularis, blue toes, eosinophilia, low complement, progressive renal failure
Fibromuscular dysplasia - carotid/vertebral FMD, spontaneous coronary artery dissection, cervical artery dissection, intracranial aneurysm
Transplant renal artery stenosis - refractory hypertension, flash pulmonary oedema, creatinine rise on ACEi in a transplant recipient
Takayasu arteritis, neurofibromatosis type 1, mid-aortic syndrome, radiation - other causes of renal artery narrowing

Atherosclerotic disease progresses: ~15-20% progress to a higher grade over 5 years, and a minority to occlusion
- Progressive cortical loss and irreversible ischaemic nephropathy if untreated
- But most incidentally found stenoses never cause a clinical problem
Prognosis is dominated by cardiovascular events, not the kidney - atherosclerotic renal artery stenosis is a marker of very high cardiovascular risk
Fibromuscular dysplasia rarely progresses to occlusion, and angioplasty gives durable benefit; cure rates are highest with short hypertension duration and younger age
Revascularisation cannot restore a kidney that has already atrophied - kidney length <7 cm or resistive index >0.8 predicts failure

Monitor

BP, eGFR, UACR; creatinine 1-2 weeks after any ACEi/ARB change
Duplex ultrasound periodically if managed medically, or after stenting (restenosis)
Cardiovascular risk factors; in FMD, one-off whole-arterial-tree imaging

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