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Patients with hypertension-associated thrombotic microangiopathy may present with complement abnormalities.

Abstract：

:Thrombotic microangiopathy (TMA) is a pattern of endothelial damage that can be found in association with diverse clinical conditions such as malignant hypertension. Although the pathophysiological mechanisms differ, accumulating evidence links complement dysregulation to various TMA syndromes and in particular the atypical hemolytic uremic syndrome. Here, we evaluated the role of complement in nine consecutive patients with biopsy-proven renal TMA attributed to severe hypertension. Profound hematologic symptoms of TMA were uncommon. In six out of nine patients, we found mutations C3 in three, CFI in one, CD46 in one, and/or CFH in two patients either with or without the risk CFH-H3 haplotype in four patients. Elevated levels of the soluble C5b-9 and renal deposits of C3c and C5b-9 along the vasculature and/or glomerular capillary wall, confirmed complement activation in vivo. In contrast to patients without genetic defects, patients with complement defects invariably progressed to end-stage renal disease, and disease recurrence after kidney transplantation seems common. Thus, a subset of patients with hypertension-associated TMA falls within the spectrum of complement-mediated TMA, the prognosis of which is poor. Hence, testing for genetic complement abnormalities is warranted in patients with severe hypertension and TMA on renal biopsy to adopt suitable treatment options and prophylactic measures.

journal_name

Kidney Int

journal_title

Kidney international

authors

Timmermans SAMEG,Abdul-Hamid MA,Vanderlocht J,Damoiseaux JGMC,Reutelingsperger CP,van Paassen P,Limburg Renal Registry.

doi

10.1016/j.kint.2016.12.009

subject

Has Abstract

pub_date

2017-06-01 00:00:00

pages

1420-1425

issue

6

eissn

0085-2538

issn

1523-1755

pii

S0085-2538(16)30742-6

journal_volume

91

pub_type

杂志文章

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