A 42‐year old woman presented with profound weakness and diffuse myalgias for two weeks now admitted for severe electrolyte abnormalities including a potassium of 1.6mmol/L. The patient denied associated fever, nausea, vomiting, diarrhea, or recent illness prior to this admission. She noted recent polyuria prior to presentation, but denied dysuria or hematuria. She denied recent inhalation exposure, IV drug abuse, alcohol use, anorexia or history of bulimia. No weight changes, tremors, cold or heat intolerance were elicited from the patient’s history. On physical exam, strength in her upper and lower extremities was 3/5 bilaterally and DTRs were diminished in all four extremities. The patient’s sensation was intact in all four extremities and Babinski sign was negative bilaterally. In addition to the potassium of 1.6mmol/L, her serum chemistries were: sodium 145mmol/L, chloride 115mmol/L, CO2 17mmol/L, glucose 93mg/dL, BUN 3mg/dL, creatinine 0.7mg/dL, anion gap 13, calcium 8mmol/L, magnesium 2.4mmol/L, phosphorous 0.8mmol/L. Transtubular potassium gradient (TTKG) was calculated to be 4 suggesting renal potassium wasting. The serum toxicology screen showed a toluene level of 2.52mg/L. In the setting of hyperchloremic non‐gap metabolic acidosis and elevated toluene level, the patient’s presentation was most consistent with distal (Type 1) renal tubular acidosis (RTA) secondary to toluene inhalation.
Toluene inhalation is most common among individuals who sniff glue or paint thinner recreationally. Over 22 million Americans have used inhalants and it remains underrecognized leading many to term it “the forgotten epidemic.” It frequently presents with profound weakness, hypokalemia, volume depletion, and normal AG hyperchloremic metabolic acidosis. Since both proximal (type I) and distal (type II) RTA can present in this way, the urine pH is helpful in differentiating between them. The pathophysiology of distal RTA is marked by a decrease in net acid excretion that results in a urine pH that is persistently above 5.5, which is inappropriately high in the setting of metabolic acidosis. This differs from type I RTA that results in a urine pH that is less than 5.5. For distal RTA, the dearth of H+ ions in distal RTA can be due to a secretory or nonsecretory defect. Direct impairment of the secretory apical H+‐ATPase can occur through several acquired or inherited defects that have been discovered for similar acid‐base transporters. Nonsecretory causes include increased permeability of the apical membrane that allows back diffusion of secreted hydrogen ions, and decreased sodium reabsorption in the adjacent principal cells in the cortical collecting duct that are necessary to create a lumen‐negative electrical potential to promote the secretion of hydrogen and potassium. Causes for distal RTA include autoimmune diseases (classically Sjogren’s syndrome), sickle cell anemia, liver cirrhosis, and chronic urinary tract obstruction. In addition, therapy with lithium, amphotericin B, and zoledronic acid have been associated with distal RTA.
Toluene inhalation most commonly presents with distal (Type I) renal tubular acidosis consistenting of profound hypokalemia, normal anion gap metabolic acidosis,
To cite this abstract:Shah C, Pickrell B. Distal Renal Tubular Acidosis As a Presentation of Toluene Inhalation. Abstract published at Hospital Medicine 2014, March 24-27, Las Vegas, Nev. Abstract 616. Journal of Hospital Medicine. 2014; 9 (suppl 2). https://www.shmabstracts.com/abstract/distal-renal-tubular-acidosis-as-a-presentation-of-toluene-inhalation/. Accessed February 17, 2020.