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

Abstract

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.

Beyond the Nephron: Exploring Systemic Implications of Renal Tubular Acidosis

“…Hypokalemia is one common disturbance that can lead to neuromuscular symptoms like muscle weakness, cramps, and fatigue; hypokalemia is also a common risk for developing arrhythmias, as potassium affects the membrane potential in cardiac cells. One rare disorder associated with hypokalemia in RTA is Hypokalemic Periodic Paralysis (HPP); this disorder is characterized by episodic muscle weakness that can lead to periodic paralysis, hypo or areflexia, and myopathy [19]. Calcium is another electrolyte affected in RTA, which is hyper-excreted in the kidneys and leads to hypocalcemia.…”