Late-Onset Hypokalemic Periodic Paralysis in an Adult Female With Type 2 Renal Tubular Acidosis: A Case Report

Proximal renal tubular acidosis (type 2 RTA) is a metabolic disorder characterized by an inability of the proximal renal tubules to reabsorb bicarbonate, resulting in excessive urinary loss of bicarbonate. In return, this causes a standard anion gap metabolic acidosis with aberrant renal acidification, culminating in excessive urinary potassium loss and hyperchloremic metabolic acidosis. Several sources can induce potassium deficiency, ranging from slight abnormalities in potassium homeostasis to catastrophic and occasionally lethal circumstances. Hypokalemic periodic paralysis (HPP) manifests with broad muscle weakness and the absence of deep tendon reflexes, with the facial, bulbar, and respiratory muscles spared, and it subsequently requires the administration of intravenous potassium chloride to address the potassium imbalance. Some patients suffering from chronic potassium shortage may have periods of weakness. The clinical symptoms of distal RTA are identical to those of attacks induced by familial hypokalemic periodic paralysis (FPP). Muscle weakness may begin slowly and worsen over 24-48 hours to flaccid quadriplegia. RTA and FPP typically spare speech, swallowing, and ocular and respiratory muscles. As a result, families with RTA children must be aware of this risk. We present a case of HPP in a female caused by type 2 RTA.

Automated summary

Proximal renal tubular acidosis (type 2 RTA) is a metabolic disorder that results in excessive urinary loss of bicarbonate and hyperchloremic metabolic acidosis. Hypokalemic periodic paralysis (HPP) is a manifestation of RTA characterized by broad muscle weakness and absent deep tendon reflexes.