ArticleCureus2026
Do Not Dismiss Incidental Hyperkalemia in Childhood: Early Recognition of Pseudohypoaldosteronism Type II.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Persistent hyperkalemia in children warrants careful evaluation, as it may indicate an underlying renal tubular disorder. We report a case of persistent hyperkalemia in a three-year-old boy in which adenovirus infection unmasked latent pseudohypoaldosteronism type II (PHAII), allowing recognition prior to the development of hypertension. The patient presented with a nine-day history of fever. Initial laboratory tests showed hyperkalemia (5.8 mmol/L), mild hyponatremia, normal renal function, and normal anion gap (AG) metabolic acidosis (pH: 7.37; bicarbonate: 19.9 mmol/L; AG: 8.1 mmol/L). The patient was diagnosed with adenovirus infection. Although the fever and inflammatory markers improved within four days, the hyperkalemia persisted (6.2 mmol/L). At three and six weeks, serum potassium remained elevated (6.0 and 6.4 mmol/L, respectively) with normal AG metabolic acidosis (HCO₃⁻ 20.0 and 17.6 mmol/L, respectively; AG 12.8 and 11.4 mmol/L, respectively). Urinary potassium indices showed inappropriately low fractional excretion of potassium (FEK) and transtubular potassium gradient (TTKG) with normal renin-aldosterone levels. Subsequently, family history-taking identified early-onset hypertension in the child's father. Treatment with hydrochlorothiazide (HCTZ) resulted in normalization of serum potassium and correction of the metabolic acidosis. Genetic testing revealed a heterozygous
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