Renal Tubular Acidosis Causing Acute Hypokalemic Paralysis in Systemic Lupus Erythematosus: Sjogren's Syndrome Overlap.

Mohammad Ammad Ud Din,Gaby Razzouk

doi:10.7759/cureus.7555

Abstract

Acute hypokalemic paralysis (AHP) is a reversible medical emergency either caused by excessive loss of potassium ions (K+) or increased intracellular shift of K+. Distal renal tubular acidosis (RTA) is an important differential to rule out in patients presenting with AHP. RTA is a constellation of disorders that have been associated with renal damage caused by autoimmune conditions such as systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS). Here we present a case of a 44-year-old woman with a history of SLE in the absence of kidney disease who presented with AHP and was found to have distal RTA and antibodies positive for SS concerning tubulointerstitial nephritis in the setting of SS/SLE overlap syndrome.

Highlights

Acute hypokalemic paralysis (AHP) is a potentially fatal but reversible medical condition caused by either excessive loss of potassium (K+) ions in urine in conditions like excessive diuretic use, Bartter’s syndrome, and renal tubular acidosis (RTA) or transcellular shifts of K+ seen in hypokalemic periodic paralysis (HPP) [1]
We present a case of a 44year-old female with a history of systemic lupus erythematosus (SLE) who presented with hypokalemic paralysis and was found to have distal RTA in the setting of tubulointerstitial nephritis with antibodies positive for an SLE flare as well as Sjogren's syndrome (SS), concerning for SS/SLE overlap
SLE-SS overlap syndrome has been associated with life-threatening hypokalemia previously, which may indicate that distal RTA (dRTA) is more often seen in these cases because of the concurrent SS in the setting of SLE [14]

Summary

Introduction

Acute hypokalemic paralysis (AHP) is a potentially fatal but reversible medical condition caused by either excessive loss of potassium (K+) ions in urine in conditions like excessive diuretic use, Bartter’s syndrome, and renal tubular acidosis (RTA) or transcellular shifts of K+ seen in hypokalemic periodic paralysis (HPP) [1]. A 44-year-old female with a past medical history of previously diagnosed systemic lupus erythematosus (SLE) presented after a fall because of a progressively worsening weakness of her lower extremities. She was experiencing dry mouth, fatigue, numbness/tingling, along with morning stiffness in her hands for the past month. The degree of acidosis and electrolyte imbalances was concerning for concurrent connective tissue disease and autoimmune workup revealed elevated titers of antibodies for antinuclear antibody (ANA), Sjogren's syndrome-related antigen A (SSA-A), double-stranded deoxyribonucleic (dsDNA), with normal complement (C3, C4) levels. Serum Chemistry Sodium Potassium (mEq/l) Chloride (mEq/l) Bicarbonate (mEq/l) BUN (mg/dl) Creatinine (mg/dl) Anion gap (mEq/l) BUN/Cr Phosphorus (mg/dl) Magnesium (mg/dl) Calcium (mg/dl) CK (IU/l) pH venous PCO2, Venous (mmHg) PO2, Venous (mmHg) Bicarbonate, venous (mEq/l) Base excess, venous (mEq/l) TSH (uIU/ml) Free T4 (ng/dl)

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