Renal Thrombotic Microangiopathy: A Review.

Thrombotic microangiopathy (TMA), a pathological lesion observed in a wide spectrum of diseases, is triggered by endothelial injury and/or dysfunction. Although TMA lesions are often accompanied by clinical features of microangiopathic hemolytic anemia, thrombocytopenia, and ischemic end-organ injury, renal-limited forms of TMA are not infrequently encountered in clinical practice. The presence of renal-limited manifestations can be diagnostically challenging, often delaying the initiation of targeted therapy. Prompt investigation and empirical treatment of TMA is warranted to reduce associated morbidity and mortality. Major advances have been made with respect to the pathophysiology of primary TMA entities, with the subsequent development of novel diagnostic tools and lifesaving therapies for diseases like thrombotic thrombocytopenic purpura and complement-mediated TMA. This article will review the clinical presentation and pathologic hallmarks of TMA involving the kidney, and the disease-specific mechanisms that contribute to the endothelial injury that characterizes TMA lesions. Diagnostic approach and both empirical and disease-specific treatment strategies will be discussed, along with the potential role for emerging targeted disease-specific therapies.

Association between proteinuria and placental pathology in preeclampsia: A retrospective study.

INTRODUCTION: Preeclampsia develops due to placental insufficiency and systemic proinflammatory and antiangiogenic mediator release, with ensuing systemic endothelial dysfunction. Nephrotic-range proteinuria appears to be associated with worse pregnancy outcomes. The relationship between differing degrees of proteinuria and the severity of placental alterations has not been studied. METHODS: This is a single-centre retrospective comparison of 150 singleton pregnancies complicated by preeclampsia and varying degrees of proteinuria. Maternal demographic, obstetrical and fetal outcome data were obtained from chart review. The placental histologic evaluations were performed by a placental pathologist blinded to all other clinical information. RESULTS: Preeclamptic women with massive proteinuria had evidence of more severe maternal vascular malperfusion lesions. The severity of the lesions was progressive through mild, moderate and massive proteinuria. Women with massive proteinuria had a higher incidence of renal dysfunction and severe hypertension, and had earlier preterm deliveries compared to preeclamptic women with mild and moderate proteinuria (p < 0.05). CONCLUSION: Preeclampsia with more severe proteinuria is associated with a higher prevalence of placental maternal vascular malperfusion.