Review Renovascular hypertension Department of nephrology R4 최소영

Renovascular hypertension(RVTH) Introduction Cause Pathophysiology Who should be screened RVHT? Diagnosis Treatment Outcome of therapy

Introduction of RVHT RVHT is an important correctable cause of secondary hypertension. Cause Atherosclerosis m/c, older Fibromuscular dysplasia, uncommon, young aged wemen Transplant RAS : 10% after KTP, usually in 1 year after surgery The frequency – variable < 1 % of mild to moderate elevations in BP 10 to 45 % of acute (even if superimposed upon a preexisting elevation in blood pressure), severe, refractory hypertension

Cause of RVHT

Pathophysiology of RVHT

AT II causes vasoconstriction of both aa and ea, with a preferential affect on the ea.  Intraglomerular pressure and GFR are maintained by AT II–mediated efferent vasoconstriction AT II ACEi,ARB intraglomerular pressure↓ GFR↓ AT II

Who should be screened RVHT? 2005 American College of Cardiology/American Heart Association (ACC/AHA) guidelines

Who should be screened RVHT?

Diagnosis of RVHT Gold standard for Diagnosis  renal arteriography Atheroembolism, Contrast induced ARF But, variety of less invasive tests have been evaluated for screening purposes. Vascular studies to evaluate renal a. MR angiography Spiral CT Doppler US Other studies Plasma renin activity Captopril renogram

Diagnosis of RVHT Doppler ultrasonography Sensitivity 85~99 %, specificity 92~97 % Advantage : both anatomic and functional assessment of the renal a. Disadvantage time-consuming, technically difficult, highly operator-dependent false-negative : accessory renal artery false-positive : coarctation of aorta

Diagnosis of RVHT Doppler ultrasonography Peak systolic renal artery velocity (Vr) Vr >180 cm/s ratio of the Vr / Vaorta ≥ 3.5  predictive of a ≥ 60% stenosis Vr in normal 120 cm/s ±12 Vaorta in normal 60 m/s ±15 Pulsus parvus et tardus Prolonged AT (> 0.07sec) RI < usually 0.56 (Normal <0.7) RI >0.8 : extremely poor outcomes after revascularization high RI may indicate irreversible intrarenal vascular disease A B

Diagnosis of RVHT MR angiography with Gadolinum Sensitivity 100 %, specificity 71 % for 50 ~75 % ASO stenosis Non-nephrotoxic Clear image of prox. Renal a, but may miss distal renal a CIx : claustrophobia, metallic implant, pacemaker or aneurysm clip GFR<30ml/min : gadolinium  nephrogenic systemic fibrosis (NSF) risk ↑ fibrosis of the skin and connective tissues prevent bending and extending joints may cause death

Diagnosis of RVHT Spiral CT (=CT angiography) sensitivity and specificity 77 and 94 % for ASO stenosis ≥50 % 28 and 99 % for fibromuscular disease 62 and 90 % for all lesions ≥70 % sCr>1.7mg/dL  accuracy is lower d/t reduced renal blood flow Contrast induced ARF

Diagnosis of RVHT Plasma renin activity Sensitivity 75~100% and specificity 60~95% In RAS, ↑renin in ischemic kidney, ↓renin in contralateral kidney Baseline PRA is elevated in only 50 to 80 % in RVHT 1 hour after administration of 25 to 50 mg of captopril  exaggerated increase in PRA. Lateralizing renal vein renin ratio (affected/contralateral) >1.5  90% predicting value for response to revascularization But false negative 50~60%, some false positive need to discontinue antihypertensive medications

Diagnosis of RVHT Captopril renogram DTPA, hippurate,MAG3 Oral captopril (25 to 50 mg) is given 1 hour before the isotope is injected positive finding Decreased relative uptake with one kidney < 40 % of total GFR. Delayed uptake on affected side Delayed washout on affected side Negative finding  essentially excludes functionally significant stenosis But limited in GFR<20ml/min, bilateral RAS

Goal of Treatment Improved blood pressure control Preservation of renal function

Treatment of RVHT Medical therapy Revascularization Percutaneous transluminal renal angioplasty with or without stent placement Surgery

Treatment of RVHT Medical therapy Antihypertensive drug ACE inhibitor or an ARB, often in combination with diuretic. CCB and βB are also effective Normalization of BP may be associated with reduced renal perfusion, pressures, and renal function may deteriorate Control of risk factors for atherosclerosis Aspirin Cessation of smoking antidyslipidemic therapy In diabetes, glycemic control  Progression of atherosclerotic stenosis may occur in one third of patients

Treatment of RVHT Revascularization therapy Indications: Uncontrolled BP despite maximal therapy Progressive rise in SCr Intolerance to ACE-I/ ARB (>30%  in SCr or severe hyperkalemia) Recurrent pulmonary edema, CHF, or volume overload Prerequisites: Experienced operator Presence of two kidneys RI < 0.80 in target kidney(s)

Treatment of RVHT Percutaneous transluminal renal angioplasty (PTRA) Young patients with fibromuscular dysplasia better outcome than atherosclerosis, ballon dilatation alone Atherosclerotic lesion: high re-stenosis rates poor outcome in bilateral RAS Complication 5~20% Hematoma, renal artery dissection, renal artery thrombosis or perforation Atheroembolic event (maybe irreversible) ARF d/t radiocontrast agent (maybe reversible) Stent migration and/or thrombosis Restenosis 14~18% Major determinant of risk : vessel size <5mm Surgical revascularization Ix multiple small renal arteries require aortic reconstruction near the renal arteries for other indications (eg, aneurysm repair or severe aortoiliac occlusive disease)

Outcome of therapy Angioplasty and STent for Renal Artery Lesions (ASTRAL) 750 patients, in the United Kingdom Changes in BP and renal function during the first year of follow-up are small, and no major differences requiring study termination CORAL trial 66 patients with creatinine<2.0 intensive medical therapy VS stent 26 with target organ injury developed (stroke, cardiac,renal events)  stent after 21mo of follow-up, no differences in BP or serum creatinine  patients with creatinine 2.0mg/dl “can be safely managed” with “intensive medical therapy.” Study to evaluate the safety and effectiveness of Palmaz balloon expandable stent In the REnal artery (ASPIRE-2) renal artery stenting for failed angioplasty 19.7% major adverse event rate during a 24-mo (in-hospital hemorrhage, stent thrombosis, or embolic events (together 2.9%), with late events including “major embolic events” (4.8%), thrombosis (0.5%), “major vascular events” (2.4%), and the need for target vessel revascularization (14.4%)  In patients with diffuse atherosclerosis, the complication rate with revascularization is relatively high. Medical therapy may be preferred.

Outcome of therapy ASN NephSAP vol7 no2 March 2008