BEYOND DELIVERY: APOL1 RISK AND EARLY POST-PARTUM KIDNEY HEALTH AFTER PRE-ECLAMPSIA IN SOUTH AFRICA

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Abstract Title *

BEYOND DELIVERY: APOL1 RISK AND EARLY POST-PARTUM KIDNEY HEALTH AFTER PRE-ECLAMPSIA IN SOUTH AFRICA

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Co-author 1

Bianca Davidson bianca.davidson@uct.ac.za University of Cape Town Department Nephrology and Hypertension Cape Town South Africa *

Co-author 2

Nicola Wearne nicola.wearne@uct.ac.za University of Cape Town Department Nephrology and Hypertension Cape Town South Africa -

Co-author 3

Kate Bramham kate.bramham@kcl.ac.uk Kings College 2. Department Nephrology and Transplantation London United Kingdom -

Co-author 4

Erika Jones Erika.Jones@uct.ac.za University of Cape Town Department Nephrology and Hypertension Cape Town South Africa -

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Introduction

Africa carries one of the world’s highest burdens of pre-eclampsia. While pre-eclampsia increases long-term maternal kidney risk, the contribution of apolipoprotein L1 (APOL1) risk variants to pregnancy-related acute kidney injury (PrAKI) and early postpartum kidney outcomes in low-resource settings is unclear. This study aimed to evaluate whether the prevalence of APOL1 risk variants was associated with PrAKI and impaired kidney function at 3-month post-partum.

Methods

We conducted an observational cohort study at Groote Schuur Hospital, Cape Town, South Africa. Women with pre-eclampsia attending a dedicated post-partum hypertension service (January 2020 – September 2025) were genotyped for APOL1. APOL 1 risk alleles were classed as no APOL 1 variants (G0/G0), one APOL1 variant (low risk) (G1/G0 or G2/G0) or two APOL 1 variants (high risk) (G1/G1, or G1/2 and G2/G2). Demographics, clinical parameters and kidney survival were compared across groups.

Results

Of the 294 women tested, 217 (74%) had no risk alleles, 59 (20%) had one, and 18 (6%) had two risk variants. Mean age was 30.1±6.9 years; 16% had HIV and 3% diabetes, without statistical difference between the 3 APOL1 risk groups. Pre-existing chronic hypertension differed by APOL1 status (no risk 24%, low risk 36%, high risk 44%; p=0.047). Pre-eclampsia complications did not differ between the groups (HELLP p=0.747; abruptio p=0.737; eclampsia p=0.926). PrAKI occurred in 110/217 (51%) no-risk, 25/59 (42%) low-risk, and 8/18 (44%) high-risk groups (p=0.492). At 3 months, proportions with eGFR <90 mL/min/1.73 m² (no risk 19%, low risk 30%, high risk 29%; p=0.185) and persistent albuminuria (49%, 41%, 35%; p=0.353) were similar. However, women with any APOL1 risk allele (mono- or biallelic) had a lower mean eGFR within CKD stage 1 (p=0.030), suggesting early subclinical impact (Figure 1).

Conclusion

In this Cape Town cohort with complicated pre-eclampsia, APOL1 risk variants were not associated with PrAKI. Nonetheless, carriers exhibited lower eGFR within stage 1 CKD at 3 months, indicating potential early vulnerability. These findings support postpartum kidney surveillance, irrespective of APOL1 status, and longer follow-up and mechanistic studies in African populations.

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