Reassessing Postpartum Kidney Risk after Preeclampsia

The population-based cohort study by Yo et al., published in JASN,1 demonstrated that pregnancies complicated by preeclampsia were followed by significantly higher hazards of severe albuminuria and reduced eGFR compared with pregnancies without preeclampsia. However, the reported absolute risks likely underestimated the true burden of early kidney injury because laboratory-defined outcomes could only be detected among women who underwent postpartum testing. Within the first postpartum year, only a minority of women underwent serum creatinine or urine albumin testing,1 restricting case identification to a selectively monitored subgroup. This limited surveillance reduces the observed absolute incidence while generating strong relative associations, indicating that the low absolute risk reflects incomplete testing rather than biologic reassurance. Another methodologic issue concerns the restrictive outcome definition, which requires severe albuminuria exceeding 300 mg/g creatinine. Excluding moderate albuminuria (30–300 mg/g creatinine) omits an earlier and reversible stage of kidney disease that is prognostically meaningful and clinically actionable. Multicenter studies have demonstrated that hypertensive disorders of pregnancy often uncover previously undiagnosed CKD when systematic evaluations are performed, much of which falls within the moderate albuminuria range.2 Consequently, the study's estimates probably underrepresented the clinically relevant spectrum of kidney injury. Beyond the definitions of ascertainment and outcomes, the observed pattern of findings is informative. Albuminuria occurred more often than sustained eGFR decline,1 suggesting early glomerular barrier and microvascular injury rather than established nephron loss. This aligns with the mechanistic evidence implicating persistent endothelial dysfunction and angiogenic imbalance after preeclampsia, which may predispose to chronic vulnerability of the kidney even in women without overt creatinine abnormalities.3,4 Creatinine-only surveillance therefore overlooks the predominant early phenotype of kidney injury. Collectively, incomplete postpartum surveillance and restrictive outcome criteria obscure a larger, preventable burden of kidney disease after preeclampsia. Structured postpartum screening that prioritizes urine albumin testing and contextualizes absolute risks based on testing frequency would better align detection strategies with both the data and the underlying vascular pathophysiology.