Background/Purpose: Renal involvement in primary Sjögren’s disease (pSjD) is a well-known extraglandular manifestation with a prevalence of 5-14% in several studies. Mostly, it affects the renal tubules through tubulointerstitial nephritis, resembling lymphocytic infiltration in the exocrine glands. Distal renal tubular acidosis (RTA), rather than proximal RTA, is the most frequent tubular dysfunction in SjD. We hypothesized that RTA occurs in SjD and non-SjD sicca and will be found in those with high urinary pH, and that it will correlate with serum hypokalemia and bicarbonate.

Methods: We screened urinary and serum metabolic data from primary SjD, incomplete SjD, and healthy controls from the database maintained by Oklahoma Sjögren’s Syndrome Center of Research Translation at the Oklahoma Medical Research Foundation (OMRF). This work was part of a study approved by the Institutional Review Board of OMRF and the University of Oklahoma Health Sciences Center.

Results: We found data for urinary pH and metabolic profile in 504 pSjD, 725 incomplete Sjögren’s, and 13 healthy controls. Sixty pSjD, 115 non-Sjögren’s sicca subjects, and 2 healthy controls had a urinary pH greater than 7.5. Of these 23 SjD, 46 incomplete SjD and 1 healthy control had a pH greater than 8. Seven SjD subjects had a urinary pH of 8.5, while 2 had a pH of 9. Two each of incomplete Sjögren’s had a pH of 8.5 and 9. The 23 SjD subjects had a significantly higher alkaline pH compared to incomplete Sjögren’s (pH 8.24 ±0.275 Vs 8.06 ±0.224 respectively, p= 0.01). All the 60 pSjD or 115 non-Sjögren’s sicca subjects had a highly significant alkaline pH compared to healthy controls (p< 0.0001). However, very interestingly, there was no significant difference in bicarbonate, potassium, or chloride levels between the SjD, incomplete SjD, or the controls in subjects. Anion gap was within normal range in the SjD, non-Sjögren’s sicca, and healthy controls. While the SjD and non-Sjögren’s sicca subjects with highly alkaline urinary pH may have specific tubular defects that hinder urine acidification, the defects may not be severe enough to bring about RTA in our cohort.

Conclusion: Higher urinary pH is found in SjD compared to non-Sjögren’s sicca, and healthy controls. However, the defect in urine acidification does not appear to be related to RTA in our cohort.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/renal-tubular-acidosis-in-sjogrens-disease-and-non-sjogrens-sicca-in-an-oklahoma-cohort/