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Abstract: TH-PO438

Differences in Urinary Potassium and Acid-Base Handling in African American vs. Non-African American CKD Patients

Session Information

Category: CKD (Non-Dialysis)

  • 2102 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

  • Vo, Victoria Truong, University of Chicago, Chicago, Illinois, United States
  • Chawla, Saurabh, University of Chicago, Chicago, Illinois, United States
  • Menezes, Cameron J., University of Chicago, Chicago, Illinois, United States
  • Ko, Benjamin S., University of Chicago, Chicago, Illinois, United States
  • Worcester, Elaine M., University of Chicago, Chicago, Illinois, United States
  • Coe, Fredric L., University of Chicago, Chicago, Illinois, United States
  • Zisman, Anna L., University of Chicago, Chicago, Illinois, United States
Background

African American (AA) patients with chronic kidney disease (CKD) have faster progression to end stage renal disease (ESRD) than non AA CKD patients. The underlying etiology is multifactorial related to genetics (APOL1), renal disease pathology, co-morbidities or underlying physiologic differences. Physiologic differences include potassium (K+) and acid/base metabolism within the CKD population, specifically racial differences between AA and non AA patients with CKD. Correction of metabolic acidosis in CKD patients has shown to slow progression of CKD, but few studies have examined differences between acid/base metabolism in AA and non AA. No studies have examined differences in urinary K+ excretion in these populations but studies that have shown AA CKD patients maintain lower serum K+ compared to non AA CKD patients. Our object is to identify differences in K+ handing and acid/base metabolism in AA vs non AA CKD patients

Methods

We studied a cohort of 107 patients with CKD Stage 3-5 who had collected 24-hr urine and serum studies as part of routine clinical care between 2009-2018

Results

Urinary K+ excretion in AA patients was much lower (50±3 mEq and 38±5 mEq, early and late CKD respectively; p<0.05) compared to non AA patients (64±3 mEq and 77±7 mEq, early and late CKD respectively; p value <0.01). Examination of acid/base metabolism using “GI anion”, a measure of net dietary alkaline load, found late stage CKD non AA male patients had more urinary alkali excretion (71±12, p value <0.01) compared to early stage non AA patients (27±5) and all stages of AA patients (32±4 and 25±7 mEq, early and late CKD respectively). Also, within each CKD stage, protein catabolic rate (PCR) in non AA patients was much higher (1.00±0.03 and 1.03±0.07, early and late CKD respectively; p value <0.01) than AA patients (0.8±0.03 and 0.71±0.04, early and late CKD respectively).

Conclusion

AA patients with CKD handle K+ excretion and acid/base metabolism differently than non AA patients. The mechanism and impact of these racial disparities in CKD warrant further investigation.

Funding

  • NIDDK Support