This is an instance of acute peri-partum hypertension secondary to Conn’s syndrome. caesarean section, delivering a healthy baby lady. Postoperatively she received diclofenac 50 mg TDS for a total of four ABR-215062 days. Her blood pressure normalized and mother and baby were discharged home. Nine days post partum, she represented with dyspnoea, orthopnoea and central chest pain. She was hypertensive (200/110 mmHg) with moderate bilateral ankle oedema. Initial investigation revealed hypokalaemia (2.8 mmol/L) with a moderate elevation of troponin (0.09 g/L) and creatine kinase (305 U/L). Electrocardiogram showed U waves (hypokalaemia) and lateral ST HS3ST1 depressive disorder, which along with the moderate troponin rise was thought more likely from left ventricular strain rather than an acute coronary symptoms. Upper body X-ray revealed mild and cardiomegaly pulmonary congestion. CT pulmonary angiography excluded pulmonary embolism, but demonstrated interstitial cardiomegaly and oedema. Transthoracic echocardiogram uncovered light global systolic dysfunction with around still left ventricular ejection small percentage of 63%. Hypertension-induced cardiac dysfunction was diagnosed and factors behind secondary hypertension had been investigated. Renal artery phaechromocytoma and stenosis were excluded by renal Doppler ultrasound and regular plasma metanephrines respectively. Thyroid function was regular. A 24 hour urine collection showed proteinuria (0.38 g/time [<0.15]) and excluded Cushing's symptoms. Preliminary aldosterone was regular (277 mol/L [<860]) nevertheless renin was suppressed (<0.10 g/L/hr [1.10-8.6]). The individual was hypokalaemic (3.3 mmol/L) at period of testing. Aldosterone-renin proportion (ARR) was afterwards repeated and uncovered markedly raised aldosterone (2083 mol/L [<860]) and suppressed renin amounts (0.10 g/L/hr [1.10-8.6]). Resultant ARR of 20546 [<830] was in keeping with principal hyperaldosteronism. No confirmatory examining like a saline suppression check was performed. A non-contrast CT uncovered a 1.6cm correct adrenal adenoma and adrenal vein sampling verified right-sided Conn's symptoms. Initial management needed 240 mmol of intravenous potassium accompanied by dental supplementation of 198 mmol/time. Enoxaparin 40 mg daily was given for venousthromboembolism prophylaxis. After ABR-215062 careful titration she required verapamil XR 240 mg daily, prazosin 5 mg tds and hydralazine 100 mg bd until a laparoscopic right adrenalectomy was performed without complication six weeks after analysis. All antihypertensive medications and potassium health supplements ABR-215062 were ceased postoperatively. Histopathology confirmed a right adrenal adenoma. Repeat ARR, biochemistry and echocardiogram were normal and she ABR-215062 remains asymptomatic and normotensive. Conversation Main hyperaldosteronism is definitely rare and characterized by hypertension, hypokalaemia and metabolic alkalosis. In the majority of cases this is due to an adenoma of the adrenal cortex-Conn’s syndrome.1 Review of the literature, including the evaluate by Matsumoto et al.2 and subsequent reported instances, reveals 29 instances of main aldosteronism associated with pregnancy.2,9 Reported complications include intrauterine growth restriction, placental abruption, preterm labour and three cases of fetal death in utero.2, 7 Maternal complications include one statement each of cardiac failure, ABR-215062 renal failure and fatal aortic dissection.2 The majority of reported instances are associated with progressive hypertension during pregnancy (with at least six warranting urgent medical intervention).2,7,8 Six other instances were associated with masking of pre-existing hypertension during pregnancy followed by post-partum hypertension and hypokalaemia,3,5,10,11 although none as severe and acute as this patient’s presentation. In pregnancy volume expansion happens to accommodate placental perfusion. A complex interplay of hormonal mechanisms activate the renin-angiotensin-aldosterone system (RAAS) including placental oestrogen and progesterone secretion, local placental RAAS production and decreased vascular resistance.1 Plasma renin activity steadily increases from early pregnancy, reaching a peak at 20 weeks gestation with levels greater than pre-pregnancy seven-fold.12 Aldosterone amounts boost ten-fold during being pregnant, approximately tripling with the eighth week of peaking and gestation at 38 weeks.12 However, there’s a net reduction in blood pressure, minimum throughout the 28th week of gestation and time for prepregnancy amounts.