Renal Cortical Necrosis in Pregnancy: A Rare Yet Critical Condition with Varied Pathogenic Mechanisms

Introduction: Renal cortical necrosis (RCN) is a form of severe AKI characterized by ischemic necrosis of the renal cortex, resulting from severely diminished renal arterial perfusion involving vascular spasm and intravascular thrombosis. RCN is an uncommon entity, with a higher incidence in developing countries. We report two cases of RCN in the postpartum setting, each diagnosed differently, with two different pathogenetic mechanisms Case Description: Case 1: 40-year-old female who had an uneventful dilation and evacuation (D&E) for fetal anomaly presented with weakness and decreased urination for 1 week. Labs revealed a creatinine (Cr) of 20 mg/dl, BUN of 115 mg/dl, UA revealed 30 mg/dL of protein, 1 RBC/hpf. CT abdomen/pelvis (CTAP) did not reveal obstruction. Patient underwent repeat D&E for retained products. After no improvement in kidney function, she was initiated on hemodialysis (HD). Serologic workup was negative. Renal biopsy revealed severe thrombotic microangiopathy (TMA) involving glomeruli, arterioles and arteries extensively, together with diffuse acute tubular necrosis, suggestive of cortical infarction. Given concern for a complement-mediated process in the setting of profound TMA, she received Eculizumab empirically and was evaluated for atypical hemolytic-uremic syndrome. Functional and genetic complement testing was negative. After 6 weeks, patient remains HD dependent, however with improved urine output. Case 2: 39-year-old female presented for induction of labor and subsequently had a cesarean section complicated by severe postpartum hemorrhage and shock requiring 5 Units PRBCs, 3 Units of FFP due to DIC and coagulopathy. She developed anuric AKI with a Cr of 4.8 mg/dl. CTAP revealed reverse cortical rim sign consistent with RCN. HD was initiated given worsening volume status and electrolyte abnormalities. Patient remains HD dependent. Discussion: RCN is a rare but devastating cause of obstetrical AKI, often resulting in poor outcomes. The mechanisms can include severe hypoperfusion and vascular endothelial injury. These cases illustrate the different pathogenetic mechanisms of RCN in obstetric AKI and its possible diagnosis by imaging and kidney biopsy. Work up for an underlying cause including complement testing may be indicated in some cases and may affect management.