Endocrine Abstracts

Background: Primary hyperaldosteronism (PHA) typically manifests as resistant hypertension, hypokalaemia and metabolic alkalosis. We present a case of PHA who subsequently exposed type 4 renal tubular acidosis (RTA) after surgical intervention.

Case history: A 62 year old man underwent investigation for chronic resistant hypertension, which had failed to respond to titration of three antihypertensive agents including Perindopril, Amlodipine and Doxazosin. His medical history consisted of type 2 diabetes, microalbuminuria, dyslipidaemia and stage 3a chronic kidney disease (CKD). Average blood pressure recordings were typically 190/100 mm per Hg on both arms, and fundoscopy revealed hypertensive retinopathy.

Investigations: Laboratory findings showed hypokalaemia (potassium 3.4 mEq/l), alkalosis (bicarbonate 33 mmol/l) and mild hypernatraemia (sodium 147 mmol/l). CT imaging of the adrenal glands demonstrated a 17 mm left adrenal adenoma. Adrenal vein sampling lateralized aldosterone secretion, with an aldosterone: cortisol (ACR) being 53 times higher from the left adrenal gland.

Results and management: Unilateral laparoscopic adrenalectomy proceeded uneventfully. The patient was readmitted post-operatively to the High Dependency Unit (HDU) due to severe hyperkalaemia (8.0 mmol/l), this was initially attributed to an acute kidney injury (AoCKD) where the eGFR deteriorated from a pre-operative value of 45 ml/min-1 to 17 ml/min-1. This was in the context of peri-operative hypotension and ACE inhibitor therapy. The eGFR subsequently rallied to 25 ml/min-1. Post-operative renin concentration (11 mUl/l) and aldosterone concentration (<70 pmol/l) proved hyporeninaemic hypoaldosteronism (type 4 RTA). The patient was treated with sodium bicarbonate and a low potassium diet. The patient has declined fludrocortisone against medical advice.

Conclusions and points for discussion: Type 4 RTA (hyporeninaemic hypoaldosteronism) has a close relationship to diabetic patients with interstitial disease especially diabetic nephropathy [1], and mild to moderate CKD, as seen in this patient with poorly controlled type 2 diabetes (Hba1c 65) and stage 3a CKD (baseline eGFR 49). In this case, surgical removal of the source of aldosterone unmasked an underlying type 4 RTA.

Reference:

[1] Andre Gustavo P Sousa, Joae Victor de Sousa Cabral, William Batah El-Feghaly, Luisa Silva de Sousa and Adriana Bezerra Nunes.

Hyporeninemic hypoaldosteronism and diabetes mellitus: Pathophysiology assumptions, clinical aspects and implications for management.