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Abstract: TH-PO237

An Interesting Presentation of Unilateral Renal Artery Stenosis

Session Information

Category: Hypertension and CVD

  • 1602 Hypertension and CVD: Clinical


  • Teh, Swee Ping, Sengkang General Hospital, Singapore, Singapore
  • Lee, Ivan Wei Zhen, Ministry of Health Holdings Pte Ltd, Singapore, Singapore
  • Chua, Jia Min, Sengkang General Hospital, Singapore, Singapore

Renal artery stenosis is uncommon, however, the prevalence increase in the presence of hypokalaemia and severe hypertension. We report a spontaneous dissection of the renal artery resulting in unilateral ischaemic nephropathy and secondary hyperaldosteronism.

Case Description

A 52-year-old Chinese Male was referred for the evaluation of hypertension and symptomatic hypokalemia (2.4mmol/L). 24-hour urine potassium (K+) was 74mmol/day suggestive of urinary loss. There was no history of diuretic use. Cortisol post 1mg ONDST was 25nmol/L, excluding Cushing’s syndrome. Serum aldosterone was elevated (29 ng/dL (<21)) and plasma renin activity was not suppressed (5.4 ng/ml/h (2.9-10.8)), suggesting secondary hyperaldosteronism. Doppler ultrasonography of the renal arteries showed an atrophied left kidney with poor visualization of the proximal segment of the left renal artery with tardus parvus waveform. CT angiography showed near complete occlusion at the origin of the dominant left renal artery with significantly reduced opacification distally and an atrophic left kidney suggesting chronic dissection with thrombosis. The right renal artery was normal. DMSA scan showed left kidney contributes to 5% and the right kidney contributes to 95% of the total kidney function. He was started on Valsartan 40mg OD and spironolactone 12.5mg OD later. His blood pressure is well controlled. Potassium supplementation was reduced from 3.6g/day to 0.6g/day while maintaining normal K+, stable serum creatinine of 119umol/L, eGFR 58ml/min/1.73m2 and urine albumin/creatinine ratio of 2.7mg/mmol.


We present an interesting case of unilateral RAS, likely from a chronic dissection of the left renal artery causing secondary hyperaldosteronism. Common etiologies of renovascular hypertension include atherosclerosis or fibromuscular dysplasia. Upon reviewing his medical history, we noted that he presented with left flank pain a year ago, and was treated for pyelonephritis. CT KUB then revealed normal-sized kidneys. We postulate that the spontaneous dissection could have happened then, resulting in left renal artery stenosis and secondary hyperaldosteronism. Initiation of RAAS blockade resulted in the reversal of the effects of hyperaldosteronism and glomerular hyperfiltration, as evidenced by the reduction in potassium supplementation, albuminuria, and BP control.