Clarifying Postpartum Renal Risk After HELLP Syndrome

To the Editor:

Halimi et al.¹ used a nationwide French cohort to compare risk factors and maternal outcomes after isolated preeclampsia (iPE) and preeclampsia with HELLP syndrome (PE-HELLP). The sample size and separation of earlier and later follow-up provide valuable evidence for a rare obstetric phenotype, particularly the marked renal signal observed after PE-HELLP.

The renal interpretation warrants one qualification. Chronic Kidney Disease (CKD) was ascertained from hospital diagnostic codes or chronic dialysis, yet women with preexisting CKD were included, and the outcome models were not reported to exclude or adjust for baseline CKD. Kidney Disease: Improving Global Outcomes defines CKD by kidney abnormalities persisting for at least 3 months.² Renal dysfunction is also frequent at 6 to 8 weeks after hypertensive pregnancies and may reflect persistent postpartum injury rather than established chronic disease.³ Analyses excluding baseline CKD, using a landmark beyond 3 months, and requiring repeated CKD coding could help distinguish incident CKD from preexisting or unresolved pregnancy-associated kidney injury.

The temporal framing also deserves precision. The “first-year” Cox analysis began 6 weeks after childbirth, although thrombotic risk is highest during the initial 6 weeks and remains modestly elevated through 12 weeks.⁴ Table 2 describes events around childbirth, but whether all events between discharge and 6 weeks were captured is unclear. Reporting that interval separately—or labeling the analyzed period as 6 weeks to 1 year—would prevent the estimates from being read as covering the full postpartum year.

Finally, the proposed difference in outcome dynamics between PE-HELLP and iPE appears to rely largely on separate hazard ratios against women without PE. Differences between estimates should be tested directly rather than inferred from their individual significance.⁵ Head-to-head PE-HELLP versus iPE contrasts, an exposure-by-time interaction, and absolute event rates would clarify both statistical and clinical magnitude. These points do not diminish the study’s contribution; they would define more precisely the renal phenotype and the period in which excess risk is observed.

Disclosure

All the authors declared no competing interests.

Author Contributions

LY conceived the idea and drafted the manuscript. CH and TL critically reviewed the manuscript. YL supervised the work and critically revised the manuscript. All authors read and approved the final manuscript.