Evaluating renal function during pregnancy in patients with chronic kidney disease (CKD) is an essential component of endocrine-renal-metabolic practice. In glomerular diseases such as Focal Segmental Glomerulosclerosis (FSGS), physiologic hyperfiltration in pregnancy leads to reduced serum creatinine, which may mask underlying renal deterioration or superimposed preeclampsia. As the demand for more sensitive biomarkers reflecting the renal-placental-endocrine axis increases, cystatin C has emerged as a relatively stable marker, minimally influenced by lean mass and plasma dilution, and capable of capturing both changes in glomerular filtration and endocrine-vascular dysregulation in pregnancy. Inflammatory-immune indices such as neutrophil-lymphocyte ratio (NLR) and high-sensitive C-reactive protein (hsCRP), along with microalbuminuria has also gained attention as components of an expanding endocrine-metabolic biomarker network with potential prognostic value in early disease detection.

Case report and literature review

A 37-year-old woman with biopsy-proven FSGS and stage 3a CKD was followed throughout her pregnancy. Serum creatinine decreased slightly as a physiologic adaptation, whereas cystatin C rose from 0.88 to 1.63 mg/L, and microalbuminuria increased significantly from 114.9 to 815.8 mg/L. Both NLR and hsCRP increased during the second trimester, indicating an activated inflammatory-immune state. Obstetric ultrasound revealed early-onset intrauterine growth restriction and elevated uterine artery pulsatility index. At 30+5 weeks’ gestation, the sFlt-1/PlGF ratio reached 191 - considered severely elevated and consistent with superimposed preeclampsia on underlying CKD. Due to progressive placental dysfunction, delivery was indicated at 31+5 weeks.

In pregnant women with FSGS, serum creatinine is not sufficiently sensitive for monitoring renal function. Cystatin C, microalbuminuria and other inflammatory-immune indices provide a more accurate assessment of dynamic changes within the renal-placental-endocrine axis, and closely correlate with markers of placental vascular dysfunction such as sFlt-1/PlGF. A multimarker approach offers a more comprehensive and modern endocrine-based framework for distinguishing physiologic from pathologic changes and optimizing the timing of clinical intervention.