Postpartum renal cortical necrosis: experience from a tertiary care center in India.

Abstract

Background: Renal cortical necrosis is a rare but severe form  of acute kidney injury (AKI), frequently seen in obstetric settings. This study examines the clinical features, laboratory trends, and renal outcomes of postpartum renal cortical necrosis.

Methods: We retrospectively reviewed the medical records of patients who developed postpartum renal cortical necrosis over two years, analyzing their clinical profiles, hematological data at various time points, and kidney outcomes, at three months postpartum.

Results: Among 88 patients with post partum AKI requiring dialysis, 25 were diagnosed with renal cortical necrosis (23 via kidney biopsy, 2 via contrast-enhanced computed tomography). The causes included puerperal sepsis (9), atypical hemolytic-uremic syndrome (aHUS) (8), placental abruption (7), postpartum hemorrhage (7), and lupus nephritis (2). All patients exhibited signs of  hemolysis, thrombocytopenia, and elevated liver enzymes immediately postpartum. Over 11.84 ± 2.76 days, the mean hemoglobin level, mean platelet count, and mean liver enzyme levels (SGPT and SGOT) improved significantly, while the mean serum creatinine level remained unchanged (p = 0.27). Of the 23 cases with a kidney biopsy, 19 had diffuse renal cortical necrosis and 4 had partial necrosis; 52.2% showed signs of thrombotic microangiopathy (TMA). Only 4 patients had partial renal recovery at discharge, with improved estimated glomerular filtration rate (eGFR) at 3 months; the remaining 21 showed no recovery. Diffuse cortical necrosis, persistent anuria, dialysis dependence at discharge, and elevated follow-up lactate dehydrogenase (LDH) and D-dimer were associated with no kidney recovery.

Conclusions: In this recent series, postpartum renal cortical necrosis is associated with microangiopathic hemolysis, thrombocytopenia, and elevated liver enzymes, with over half of biopsies showing TMA. Renal outcomes were poor. Further research is needed to explore the pathogenesis of TMA and exploring eventual genetic factors.