Acute kidney injuries induced by thrombotic microangiopathy following severe hemorrhage in puerperants: a case series and literature review

Background Acute kidney injury in puerperants is generally caused by acute tubular necrosis and occasionally by thrombotic microangiopathy (TMA) following post-partum hemorrhage. However, TMA leads to worse clinical outcomes and is rarely reported in the literature. Therefore, this study aimed to evaluate the pathological mechanism behind the development of TMA in puerperants to improve the diagnosis and treatment of this condition. Methods Three patients diagnosed with severe postpartum hemorrhage and TMA from 2014 to 2017 at a nephrology center were retrospectively investigated. Results All patients had severe hemorrhage during delivery with a mean blood loss, 4.0 L (range, 2.7-5.0 L). AKI developed rapidly in these patients and was treated with hemodialysis. Following treatment, the mean volume of packed red blood cells was 2.3 L (range, 1.2-3.6 L), and the mean volume of resuscitation fluid was 3.7 L (range, 3.5-4.0 L). All patients had renal biopsy specimens with typical TMA and ATN changes on light microscopy. Two patients required a hysterectomy while another two patients received respiratory support. Only one patient received plasma exchange. None of the patients had recovered normal kidney function by the final follow-up (26-61 months), with two patients having stage 3 chronic kidney disease, and one patient having an end-stage renal disease requiring maintenance hemodialysis. Conclusion Severe postpartum hemorrhage could lead to TMA, in addition to the common finding of ATN. Renal histology revealed that poor renal outcomes could be attributed to TMA coexisting with ATN. The potential mechanism was ischemia-reperfusion, which was followed by endothelial cell injury and activation of the alternative complement pathway.