Abstract: SA-PO350

Apolipoprotein L1 Variants and the Prevalence of JC Polyoma Virus in Black South Africans with Hypertensive CKD

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 301 CKD: Risk Factors for Incidence and Progression

Authors

  • Nqebelele, Nolubabalo Unati, University of the Witwatersrand, Gardenview, South Africa
  • Dickens, Caroline, University of the Witwatersrand, Gardenview, South Africa
  • Dix-peek, Therese, University of the Witwatersrand, Gardenview, South Africa
  • Duarte, Raquel, University of the Witwatersrand, Gardenview, South Africa
  • Naicker, Saraladevi, University of the Witwatersrand, Gardenview, South Africa
Background

Variants in the apolipoprotein 1 (APOL1) gene associate with higher rates of nondiabetic nephropathy in black patients. First-degree relatives of African Americans with nondiabetic nephropathy with two APOL1 risk variants had lower rates of kidney disease if they also had JC viruria. We aimed to determine the association of APOL1 risk variants with renal traits and the prevalence of polyomavirus infection in black South Africans with hypertensive chronic kidney disease (CKD).

Methods

Black South Africans with hypertensive CKD (CKD patients) and their first-degree relatives were recruited. Controls were healthy black South Africans. Informed consent was obtained in 166 participants. Using restriction fragment length polymorphism, custom designed primers were used to genotype G1: rs60910145 and rs73885319 and G2: rs71785313 APOL1 risk variants. Viral DNA was extracted from urine using Maxwell® system protocols. Viral-loads were determined by quantitative qPCR using genesig® JCV and BKV standard kits.

Results

CKD patients had advanced kidney disease with a median eGFR of 7 IQR (4-13), both controls and relatives had normal renal function; median eGFR of 121 (98-130) and 124 (93-144) respectively, with eGFR measured in mL/min/1.73m2.
APOL1 high-risk alleles were absent in 50% of CKD patients, 41% of controls and 52% of relatives. Two APOL1 risk alleles were present in 10% of CKD patients, 8.6% of controls and in 6% of relatives. In CKD patients, there was no difference in blood pressure, eGFR, proteinuria based on any allele combination.
The overall prevalence of JCV was 21% compared to 6% for BKV, with coinfection present in four participants. JCV was present in only 3% CKD patients compared to 39% of controls and 21% of relatives; P < 0.0001, Fisher’s exact test. None of the CKD patients had evidence of BKV. There was no difference in mean log10 viral load JCV between CKD patients and controls (P = 0.2644), between CKD patients and their relatives (P = 0.3074) or between controls and relatives (P= 0.7073), t test.

Conclusion

Apolipoproprotein L1 risk variants are infrequent in black South Africans with hypertensive CKD. There was a higher prevalence of JCV infection in black South Africans with normal renal function. JC virus seems to protect against development of kidney disease.