Hypertensive Nephrosclerosis and Renovascular Disease — Written Clinical Reasoning

Model answer — Part A: the young hypertensive with a bruit

Frame it. New severe hypertension in a non-smoking woman under 40 with a renal bruit is a secondary-hypertension trigger phenotype; the leading diagnosis is fibromuscular dysplasia of the renal artery, the dominant renovascular disease of young women in registry data [1]. Before imaging, confirm the pressure is real (standardised office or ambulatory readings), confirm adherence and doses, and send the screening bloods — electrolytes, creatinine, urinalysis and an aldosterone-renin ratio, since primary aldosteronism remains common even in the young [4].

Investigations, in sequence. Duplex ultrasound first if the local laboratory is skilled — safe, no contrast, and functionally informative — otherwise proceed straight to CT or MR angiography, which have near-catheter accuracy; in a 34-year-old needing possible surveillance, MRA avoids radiation and iodinated contrast [8]. The expected finding is a multifocal string-of-beads lesion of the mid-to-distal renal artery. Because FMD is a systemic arteriopathy, image the cervicocephalic vessels once (headache, pulsatile tinnitus and dissection risk make this part of complete care) [2].

Management. Renal FMD driving hypertension is treated with percutaneous balloon angioplasty without a stent — the meta-analysis shows high technical success with hypertension cure or improvement in a large fraction of patients, and the young with short hypertension duration do best [3]. Continue antihypertensives until the procedure, recheck pressure and renal function after it, and arrange surveillance imaging because restenosis occurs in a minority [2]. Close with what you would NOT do: apply atherosclerosis trial evidence to justify lifelong medication alone in a 34-year-old with a curable lesion [3].

Model answer — Part B: creatinine rise on ACEi with an asymmetric kidney

Interpret the rise. From 110 to 138 µmol/L is a 25% increase — inside the accepted haemodynamic range. ACE inhibition removes angiotensin-II-mediated efferent arteriolar constriction, intraglomerular pressure falls, and GFR drops modestly; a rise up to about 30% is expected pharmacology, not tubular injury, and the correct action is to continue the drug and recheck creatinine and potassium [7]. But the combination of a measurable GFR response and a 2 cm asymmetric kidney raises haemodynamically significant renal artery stenosis — and a rise beyond about 30%, or rapidly progressive decline, would suggest bilateral disease or a stenosed single functioning kidney [7].

Further assessment. Confirm true resistant hypertension if pressure remains uncontrolled (ambulatory readings, adherence, diuretic in the regimen), quantify baseline renal damage (repeat lengths, cortical thickness, proteinuria), and obtain anatomic imaging — duplex where skilled, CTA if GFR permits, otherwise MRA — rather than a captopril renogram, whose accuracy collapses with impaired GFR and asymmetry [8].

The stenting position. If imaging confirms atherosclerotic stenosis, the default is optimal medical therapy, not a stent: CORAL showed stenting added nothing to OMT for cardiovascular/renal events, mortality or pressure control, and ASTRAL showed no renal-function benefit with real periprocedural harm [5] [6]. His OMT is the CORAL package — continue the ACE inhibitor with monitoring, add a calcium-channel blocker and thiazide-like diuretic to target, plus high-intensity statin, antiplatelet and smoking cessation for the systemic atheroma that actually threatens him [5]. Reserve revascularisation for the defined subsets — recurrent flash pulmonary oedema, bilateral tight stenosis or a single functioning kidney with declining GFR — and say so explicitly, because that is where the marks live [7].