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Abstract: TH-PO394

An Unusual Case of Metabolic Acidosis

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Le, Theresa T., LSU Health New Orleans, New Orleans, Louisiana, United States
  • Do, Tammy Nguyen, LSU Health New Orleans, New Orleans, Louisiana, United States
  • Wall, Norman, LSU Health New Orleans, New Orleans, Louisiana, United States
  • Mohandas, Rajesh, LSU Health New Orleans, New Orleans, Louisiana, United States

Metabolic acidosis is common in hospitalized patients, and more than half the patients admitted to intensive care units have metabolic acidosis. The cause of acidosis is usually apparent from the clinical setting, but in rare instances, a methodical workup is needed to decipher the underlying cause. We present an unusual cause of metabolic acidosis.

Case Description

A 40 yr. woman with Mitochondrial Encephalomyopathy with Lactic Acidosis and Stroke-like episodes (MELAS), presented with sudden worsening of chronic right-sided weakness. An initial work up ruled out acute stroke, and patient was started on intravenous L-Arginine for MELAS. On day five, she developed acute encephalopathy and severe acidosis (Figure-1). The severe non-gap metabolic acidosis was thought to be from L-arginine. Following discontinuation of IV L-arginine and initiation of bicarbonate supplementation, the patient’s acidosis improved rapidly.


Metabolic acidosis has been reported with prolonged use of L-arginine, particularly in high doses. The mechanisms by which L-arginine causes metabolic acidosis remains unclear. While arginine is administered as arginine hydrochloride, the number of protons added is not significant enough to cause severe acidosis. Although the urine anion gap was negative in our patient, possibly due to exogenous bicarbonate, the urine osmolar gap indicated a renal tubular acidosis. This was confirmed by generalized aminoaciduria and low levels of directly measured ammonia. There was no evidence of phosphaturia or hypophosphatemia. Interestingly, in the isolated perfused tubule exposure to L-arginine causes inhibition of bicarbonate reabsorption in the proximal tubules. Metabolic acidosis could augment L-arginine absorption in the intestine worsening acidosis. Our case highlights that L-arginine can be an unusual cause of severe metabolic acidosis. The physiology underlying this clinical observation requires further studies.