Disclosures: Olaniran reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.
March 18, 2021
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Sickle cell trait, disease linked to AKI and accelerated eGFR decline among Black patients

Disclosures: Olaniran reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.
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Among Black adults, those with sickle cell trait or disease had a higher likelihood of developing AKI compared with those who had a normal hemoglobin phenotype, according to a study.

In addition, following AKI, researchers observed patients with sickle cell trait or disease also experienced a faster decline in kidney function than those with a normal hemoglobin phenotype.

Sickle cell and AKI
Data were derived from Olaniran KO, et al. Clin J Am Soc Nephrol. 2021;doi:10.2215/CJN.06960520.

Kabir O. Olaniran, MD, of the division of nephrology in the department of internal medicine at the University of Texas Southwestern, and colleagues contended that although previous research has shown sickle cell trait is associated with eGFR decline and incident chronic kidney disease, evidence is limited regarding its potential impact on AKI risk. Similarly, the researchers noted, sickle cell disease contributes to accelerated eGFR decline and subsequent CKD, but the contribution of AKI to eGFR decline in this patient population remains understudied.

“Regardless of severity or duration, AKI has been associated with a higher risk for incident CKD and eGFR decline,” Olaniran and colleagues wrote. “Therefore, given the higher risk for eGFR decline and incident CKD in sickle cell trait/disease and the preponderance of evidence for chronic recurrent damage to the kidney medulla in sickle cell trait/disease, understanding the risks for AKI and the association between AKI and eGFR decline is important in sickle cell trait/disease.”

For the study, a hemoglobin electrophoresis test identified patients as having sickle cell trait (n = 1,279), sickle cell disease (n = 254) or normal hemoglobin phenotype (n = 8,968). Researchers compared the AKI incidence and subsequent eGFR decline between groups (mean baseline serum creatinine for all groups was 0.8 mg/dL).

AKI events were further categorized as regular AKI (defined as 1.5 times baseline serum creatinine or higher), severe (doubling of baseline serum creatinine or higher) or sustained (persisting for 72 or more hours).

During a median follow-up of 7.6 years, 796 AKI events, 466 severe AKI events and 452 sustained AKI events occurred.

When comparing patients with normal hemoglobin phenotype to those with sickle cell trait, researchers observed that risk for sustained AKI was greater for those with the trait (adjusted hazard ratio = 1.64). However, comparisons showed no associations between sickle cell trait and increased risk for AKI or severe AKI.

Sickle cell disease, on the other hand, was associated with increased risk for all three types of AKI events (HR for AKI = 2.85; HR for severe AKI = 2.38; HR for sustained AKI = 2.5).

Further results indicated that although all patients who developed AKI had a faster decline in GFR compared with pre-AKI measurements, patients with sickle cell trait and disease experienced more rapid decline than those with normal hemoglobin phenotype. The fastest decline was seen for patients with sickle cell disease (1.69 mL/min/1.73 m2 per year faster vs. 0.37 mL/min/1.73 m2 for patients with sickle cell trait).

“These findings should be investigated in prospective studies that focus on potential mechanisms and the natural history of AKI in sickle cell trait/ disease,” Olaniran and colleagues concluded. “Such studies would better inform preventive measures and interventions to attenuate AKI risk in Black patients with sickle cell trait/disease.”