Hyperkalemia, Metabolic Acidosis Occur at Higher eGFRs in Sickle Cell Disease
story Heading link
Kidney function thresholds for hyperkalemia and metabolic acidosis are higher in patients with sickle cell disease (SCD), even falling within the normal range, a new study finds.
Investigators studied the estimated glomerular filtration rates (eGFR) at which hyperkalemia and metabolic acidosis occurred in 733 patients with a severe SCD genotype (hemoglobin SS or Sβ0-thalassemia) and 238 patients with a moderate (hemoglobin SC or Sβ+-thalassemia) SCD genotype from 2 cohorts compared with 1333 age- and sex-matched Black patients without SCD from the National Health and Nutrition Examination Survey. The investigators calculated eGFR using the 2021 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula, which does not include a race coefficient.
Hyperkalemia (serum potassium 5 mEq/L or higher) occurred in 13% and 3% of the severe and moderate SCD group, respectively, compared with 0.3% of the control group, Santosh L. Saraf, MD, of the University of Illinois at Chicago, and colleagues reported in Kidney360. Metabolic acidosis (serum bicarbonate less than 22 mmol/L) occurred in 21% and 11% of the severe and moderate SCD group, respectively, compared with 5% of the control group.
In patients with the severe SCD genotype, the risks of hyperkalemia and metabolic acidosis increased when eGFR declined below 85 and 91 mL/min/1.73 m2, respectively, Dr Saraf’s team reported. In patients with the moderate SCD genotype, the risks of hyperkalemia and metabolic acidosis increased when eGFR declined below 52 and 102 mL/min/1.73 m2, respectively. As eGFR declined, hyperkalemia and metabolic acidosis also affected greater proportions of patients with SCD.
Individuals with sickle cell disease tend to have an elevated eGFR compared with the general population, the investigators noted.
“Our findings highlight the need for close monitoring of serum potassium and bicarbonate once the eGFR is < 120 mL/min/1.73 m2 and to consider initiating more aggressive measures once the eGFR is < 90 mL/min/1.73 m2, Dr Saraf’s team wrote. “A more stringent cutoff for kidney dysfunction (serum creatinine of > 0.9 g/dL in men and > 0.77 g/dL in women) in severe SCD genotypes has been recommended in the literature, and our data strongly supports this practice, relative to actionable decrements in tubular function.”
For patients with SCD, the investigators recommended earlier referral to a nephrologist and prevention and treatment strategies, such as dietary potassium restriction, sodium bicarbonate replacement therapy, and avoidance of nephrotoxins. They acknowledged that the study’s definition of metabolic acidosis might have included compensatory metabolic acidosis due to respiratory alkalosis, a known feature of SCD.
Disclosure: Some study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.
Reference
Saraf S, Derebail V, Zhang X, et al. Hyperkalemia and metabolic acidosis occur at higher estimated glomerular filtration rates in sickle cell disease. Kidney360. Published February 3, 2022. doi:10.34067/KID.0006802021