Rare coexistence of aldosterone resistance and adrenal insufficiency in asymptomatic infant with persistent hyperkalaemia: A case report

Table 3 Causes of persistent hyperkalemia in an infant

Differential diagnosis	Description	Test findings	Treatment
Congenital adrenal hyperplasia[18]	Inherited autosomal recessive disorder affecting adrenal steroidogenesis, most commonly is 21-hydroxylase deficiency	Raised serum 17-OHP, hypocortisolism, hyperkalaemia, hyponatraemia, Short synacthen test shows adrenal insufficiency, and genetic testing to proved the specific mutated gene involved	Glucocorticoids and mineralocorticoids (to also replace concurrent mineralocorticoid deficiency)
Hypoaldosteronism[19]	Insufficient aldosterone production or action, leading to hyperkalemia and metabolic acidosis. It could coexist with other conditions such as primary adrenal insufficiency or part of RTA type 4	Hyperkalemia and metabolic acidosis. Low urine pH in RTA type 4, hypocorticolism with ACTH stimulation test proved adrenal insufficiency in Addison’s disease	Fludrocortisone, salt supplementation, management of underlying conditions
AKI[20]	KDIGO defined AKI as an increase in serum creatinine (absolute increase of ≥ 0.3 mg/dL within 48 hours or relative increase of ≥ 50% from baseline within 7 days) and reduction in urine output (urine volume less than 0.5 mL/kg/hour for at least 6 hours)	Raised serum creatinine and urea, hyperkalaemia, hyponatraemia, emerging renal biomarker to detect early AKI e.g. neutrophil gelatinase-associated lipocalin	Depending on types (e.g., hydration for pre-renal AKI, renal replacement therapy for severe acute tubular necrosis), correction of electrolyte disturbances

AKI: Acute kidney injury; RTA: Renal tubular acidosis; 17-OHP: 17-hydroxyprogesterone; KDIGO: Kidney disease: Improving global outcomes; ACTH: Adrenocorticotropic hormone.