The Role of Complement Activation in Rhabdomyolysis-induced Acute Kidney Injury

Overview

Journal PLoS One

Specialties General Medicine
Science

Date 2018 Feb 22

PMID 29466390

Citations 8

Authors

Xudong Huang

Wei Zhao

Lixia Zhang

Xinjun Yang

Lihui Wang

Yunshuang Chen

Jinghua Wang

Chao Zhang

Guangli Wu

Affiliations

Soon will be listed here.

Abstract

Rhabdomyolysis (RM) may cause kidney damage and results primarily in acute kidney injury (AKI). Complement is implicated in the pathogenesis of renal diseases and ischemia-reperfusion injury (IRI), but the role of complement, especially its activation pathway(s) and its effect in RM-induced AKI, is not clear. This study established a rat model of AKI induced by RM via intramuscular treatment with glycerol. Cobra venom factor (CVF) was administered via tail vein injection to deplete complement 12 h prior to intramuscular injection of glycerol. We found that the complement components, including complement 3 (C3), C1q, MBL-A, factor B(fB), C5a, C5b-9, and CD59, were significantly increased in rat kidneys after intramuscular glycerol administration. However, the levels of serum BUN and Cr, renal tubular injury scores, and the number of TUNEL-positive cells decreased significantly in the CVF+AKI group. These results suggest that complement plays an important role in RM-induced AKI and that complement depletion may improve renal function and decrease renal tissue damage by reducing the inflammatory response and apoptosis.

Citing Articles

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