T he diagnosis of curable, secondary causes of hypertension is a satisfying but challenging aspect, for both patient and doctor, of the clinical management of hypertension. They are probably under-recognized, and the enthusiasm to look for causes is blunted by low pickup rates in unselected patients. Young age encourages a search more because the alternative is many decades of drug treatment than because of any good evidence that prevalence of secondary hypertension varies with age.1 Plasma renin is still not a routine measurement even in the younger patient. And although there is an increasing evidence that a low plasma renin is valuable in the detection of primary aldosteronism, 2 a high plasma renin does not usually trigger investigations for renal artery stenosis. The cases we present here are not part of a formal prospective series. But they illustrate how valuable was the finding of an extremely high plasma renin, leading to re-evaluation of magnetic resonance (MR) and computed tomographic (CT) angiograms in the light of a high, rather than low prior probability. Our report is stimulated by the coincidence of 5 such patients being diagnosed within an 18-month period, and a parallel prospective study of plasma renin concentration's prediction of treatment response, which enabled us to define the threshold for an extremely high plasma renin. 3 We will discuss the significance of the log distribution of renin, of factors such as drug treatment influencing interpretation, and of reviewing reportedly normal radiology.Plasma renin concentration was measured by the Diasorin Liaison automated immunoassay analyzer.4 Intra-assay coefficients of variation were 3.7%, 2.8%, 2.0%, and 1.2% at concentrations of 15.1, 33.8, 82.2, and 258.0 mU/L, respectively. Inter-assay coefficients of variation were 5.8% and 4.9% at concentrations of 25.6 and 101.3 mU/L, respectively. The lower limit of quantitation of the assay, as specified by the manufacturer, was 2.0 mU/L. Plasma renin activity is reported for 1 patient, in whom this was measured at the referring hospital.
Patient 1A 24-year-old woman was referred in 2013 with a 2-year history of hypertension.5 Despite treatment with ramipril 5 mg daily and lercanidipine 20 mg daily, home systolic blood pressure readings often exceeded 140 mm Hg. Cardiovascular examination was normal with no abdominal bruits; ECG and echocardiogram were also normal, as were serum electrolytes and estimated glomerular filtration rate. An MR angiogram at the referring hospital noted normal renal arteries. However, her plasma renin was at least 50-fold above normal at 4220 mU/L (normal values 5.4-60), and aldosterone was 1130 pmol/L (normal values 100-450). The increase in renin was many-fold more than could be easily ascribed to treatment with an angiotensin-converting enzyme (ACE) inhibitor, and this should have reduced levels of aldosterone. On review of the MR angiogram at the Multi-Disciplinary Team meeting, no definite abnormality of the arteries was observed, but the right kidney looked hypoperf...