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

Abstract

Background: Acute kidney injury (AKI) 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 (CKD), and one patient having an end-stage renal disease (ESRD) 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.

Massive intraperitoneal hemorrhage in patients with COVID-19: a case series

“…Severe COVID-19 infections could also cause thrombotic microangiopathy (TMA) which is characterized by decreases in hemoglobin, increased lactate dehydrogenase (LDH), increased bilirubin, decreased haptoglobin, and appearance of schistocytes in peripheral blood smear [12]. TMA could also cause major bleeding events [13] and as the presented cases had only decreased in hemoglobin and increased LDH, this would not be the first choice underlying reason for their bleeding and even these changes could be iatrogenic due to several blood samplings.…”

Plasma Exchange in Postpartum Hemorrhage (PPH)-Associated Thrombotic Microangiopathy (TMA): A Case Report

“…The potential contribution of aHUS to obstetric renal cortical necrosis (RCN) was pointed out [ 10 ]. There are reports that some patients developed RCN and dialysis-dependent end-stage renal failure following PPH-induced AKI [ 11 , 12 ]. Supportive care has constituted the cornerstone for PPH-induced AKI, but if there is a possibility that the renal function to be recovered, special interventions such as plasma exchange and complement inhibitors should be considered [ 12 ].…”

“…There are reports that some patients developed RCN and dialysis-dependent end-stage renal failure following PPH-induced AKI [ 11 , 12 ]. Supportive care has constituted the cornerstone for PPH-induced AKI, but if there is a possibility that the renal function to be recovered, special interventions such as plasma exchange and complement inhibitors should be considered [ 12 ]. There have been reports of plasma exchange for TMA following massive bleeding because of trauma appearing to be similar to PPH-associated TMA [ 13 , 14 ].…”