Fleuria Meibody1, Matthieu Jamme2, Vassilis Tsatsaris3, François Provot4,5, Jérôme Lambert6, Véronique Frémeaux-Bacchi7, Anne-Sophie Ducloy-Bouthors8, Mercédès Jourdain9, Yahsou Delmas5,10, Pierre Perez1,5, Julien Darmian11, Alain Wynckel12, Jean-Michel Rebibou13, Paul Coppo5,14, Cédric Rafat2, Eric Rondeau2,5, Luc Frimat1, Alexandre Hertig2. 1. Department of Nephrology and Kidney Transplantation, University Hospital of Nancy, Vandoeuvre-les-Nancy, France. 2. Sorbonne Université, Urgences Néphrologiques et Transplantation Rénale, Assistance Publique-Hôpital de Paris (APHP), Hôpital Tenon, Paris, France. 3. APHP, Department of Obstetrics and Gynecology, Port-Royal Maternity, University Hospital Center Cochin Broca Hôtel Dieu, Groupe Hospitalier Universitaire Ouest, Paris, France. 4. Department of Nephrology, Transplantation, Dialysis and Apheresis, Claude-Huriez Hospital, CHRU de Lille, Lille, France. 5. French Reference Center for Thrombotic Microangiopathies, APHP, Hôpital Saint-Antoine, Paris, France. 6. Biostatistics Department, Saint Louis Teaching Hospital, APHP, Paris, France. 7. INSERM UMRS-1138, Cordeliers Research Center, Complement and Diseases Team, Paris, France. 8. Department of Anesthesia and Intensive Care, Jeanne-de-Flandre Hospital, CHRU de Lille, Lille, France. 9. Intensive Care Unit, Pôle de Réanimation, University of Lille, CHU Lille, U1190, Lille, France. 10. Department of Nephrology Transplantation-Dialysis, Centre Hospitalier Universitaire de Bordeaux, Bordeaux, France. 11. Department of Intensive Care, Centre Hospitalier Régional Metz-Thionville, Ars-Laquenexy, France. 12. Department of Nephrology, Centre Hospitalier Universitaire, Reims, France. 13. Department of Nephrology, Dijon University Hospital, Dijon, France. 14. Sorbonne Université, Hematology, APHP, Hôpital Saint-Antoine, Paris, France.
Abstract
BACKGROUND: Among the severe complications of preeclampsia (PE), acute kidney injury (AKI) is problematic if features of thrombotic microangiopathy (TMA) are present. Although a haemolysis enzyme liver low-platelets syndrome is considerably more frequent, it is vital to rule out a flare of atypical haemolytic and uraemic syndrome (aHUS). Our objective was to improve differential diagnosis procedures in post-partum AKI. METHODS: A total of 105 cases of post-partum AKI, admitted to nine different regional French intensive care units from 2011 to 2015, were analysed. Analysis included initial and final diagnosis, renal features, haemostasis and TMA parameters, with particular focus on the dynamics of each component within the first days following delivery. A classification and regression tree (CART) was used to construct a diagnostic algorithm. RESULTS: AKI was attributed to severe PE (n = 40), post-partum haemorrhage (n = 33, including 13 renal cortical necrosis) and 'primary' TMA (n = 14, including 10 aHUS and 4 thrombotic thrombocytopenic purpura). Congruence between initial and final diagnosis was low (63%). The dynamics of haemoglobin, haptoglobin and liver enzymes were poorly discriminant. In contrast, the dynamic pattern of platelets was statistically different between primary TMA-related AKI and other groups. CART analysis independently highlighted the usefulness of platelet trajectory in the diagnostic algorithm. Limitations of this study include that only the most severe cases were included in this retrospective study, and the circumstantial complexity is high. CONCLUSION: Trajectory of platelet count between admission and Day 3 helps to guide therapeutic decisions in cases of TMA-associated post-partum AKI. Our study also strongly suggests that during the post-partum period, there may be a risk of transient, slowly recovering TMA in cases of severe endothelial injury in women without a genetic mutation known to induce aHUS.
BACKGROUND: Among the severe complications of preeclampsia (PE), acute kidney injury (AKI) is problematic if features of thrombotic microangiopathy (TMA) are present. Although a haemolysis enzyme liver low-platelets syndrome is considerably more frequent, it is vital to rule out a flare of atypical haemolytic and uraemic syndrome (aHUS). Our objective was to improve differential diagnosis procedures in post-partum AKI. METHODS: A total of 105 cases of post-partum AKI, admitted to nine different regional French intensive care units from 2011 to 2015, were analysed. Analysis included initial and final diagnosis, renal features, haemostasis and TMA parameters, with particular focus on the dynamics of each component within the first days following delivery. A classification and regression tree (CART) was used to construct a diagnostic algorithm. RESULTS: AKI was attributed to severe PE (n = 40), post-partum haemorrhage (n = 33, including 13 renal cortical necrosis) and 'primary' TMA (n = 14, including 10 aHUS and 4 thrombotic thrombocytopenic purpura). Congruence between initial and final diagnosis was low (63%). The dynamics of haemoglobin, haptoglobin and liver enzymes were poorly discriminant. In contrast, the dynamic pattern of platelets was statistically different between primary TMA-related AKI and other groups. CART analysis independently highlighted the usefulness of platelet trajectory in the diagnostic algorithm. Limitations of this study include that only the most severe cases were included in this retrospective study, and the circumstantial complexity is high. CONCLUSION: Trajectory of platelet count between admission and Day 3 helps to guide therapeutic decisions in cases of TMA-associated post-partum AKI. Our study also strongly suggests that during the post-partum period, there may be a risk of transient, slowly recovering TMA in cases of severe endothelial injury in women without a genetic mutation known to induce aHUS.
Authors: Jamie Szczepanski; Shauna-Kay Spencer; Ashley Griffin; Teylor Bowles; Jan Michael Williams; Patrick B Kyle; John Polk Dumas; Sarah Araji; Kedra Wallace Journal: Biol Sex Differ Date: 2020-09-24 Impact factor: 5.027