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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Post-partum renal cortical necrosis (RCN) is a rare but devastating complication associated with severe acute kidney injury (AKI) and poor outcome. It is characterized by ischemic necrosis of the renal cortex due to vascular occlusion or hypoperfusion.
Thrombotic microangiopathy (TMA) is a pathological condition characterized by microvascular thrombosis due to deficiency of ADAMTS13 in TTP, dysregulation of the complement system in atypical uremic hemolytic syndrome (a-HUS), infection with Shiga-toxin in ST-HUS, drugs, malignancy, disseminated intravascular coagulation (DIC), pregnancy-related TMA and other causes. It is characterized by low platelet count, anemia, indices of hemolysis and organ dysfunction.
In 50% of biopsies, RCN has been associated with TMA, making the diagnosis challenging whether RCN is the cause of TMA or the impaired blood flow caused by TMA has led to ischemic lesions of the cortex.
A 35-year old Caucasian woman at 31 weeks of gestation was admitted to our hospital for pregnancy termination, due to the presence of congenital anomalies of the fetus.
Her previous medical history was unremarkable. Vaginal delivery was complicated with hemorrhage, anuria and coagulation disorders indicative of disseminated intravascular coagulation (DIC), low platelets and indices of microangiopathic hemolysis. The patient underwent evaluation with CT-angiography that revealed massive hemorrhage in uterus wall and right paracolic space. She underwent laparotomy, while she also received RBC, FFP transfusions and fibrinogen. DIC indices normalized. A CT-angiography after surgery demonstrated a non-enhancing renal cortex.
FIGURE 1: Light microscope: cortical necrosis and TMA with fibrin thrombi occluding the glomerular capillary lumina (a,b,c), the arteriolar (a, b) and the arterial (c) lumina (a: HE x200, b: masson x200, c: HE x100). Electron microscope (d): a glomerular capillary occluded by fibrin (x5000)
Patient had been anuric after surgery and consequently dialysis-dependent with no signs of recovery of renal function in the following days. On day 9 she underwent kidney biopsy. Clinical course was complicated with fever due to endometritis and on day 10 she underwent hysterectomy that revealed diffuse ischemic necrosis of endometrium, myometrium and endocervix with presence of thrombi.
ADAMTS13 was normal. C3 was low (64.5 mg/dL). C4 was normal as well as the antiphospholipide antibodies and the rest of immunological work-up.
Kidney biopsy revealed diffuse cortical necrosis with diffuse lesions of TMA and total occlusion of glomerular capillaries and arterial lumens by fibrin clots.
Treatment with eculizumab was initiated on day 20 on the grounds of TMA diagnosis and low C3. Her renal function showed partial improvement, but she has been dialysis-dependent in a twice weekly dialysis schedule, 45 days after the initiation of treatment whereas the hematological parameters are normal.
RCN is often associated with TMA. Pathologically, it’s challenging to distinguish which is the primary cause. In our patient massive hemorrhage during labor, abrupt onset of the clinical syndrome within hours after delivery, extensive lesions of cortical necrosis, indicate RCN as the primary cause. Nevertheless, a-HUS or DIC-related TMA could not be ruled out.
