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Complement C3a/C3aR and C5a/C5aR deposits accelerate the progression of advanced IgA nephropathy to end-stage renal disease
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Complement C3a/C3aR and C5a/C5aR deposits accelerate the progression of advanced IgA nephropathy to end-stage renal disease
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Journal Article
Complement C3a/C3aR and C5a/C5aR deposits accelerate the progression of advanced IgA nephropathy to end-stage renal disease
2024
Overview
IgA nephropathy (IgAN) is still one of the leading causes of end-stage kidney disease (ESRD), and complement system activation is a key to the pathogenesis of IgAN. The role of complement C3a/C3aR and C5a/C5aR in late stage of IgAN remains unknown. Renal specimens of 75 IgAN patients at the stage 4 CKD were stained using immunofluorescence and immunohistochemistry. The primary outcome was a composite of end-stage renal disease (ESRD) and death. Associations of complement components with baseline clinicopathological characteristics and outcomes were assessed using multivariable Cox regression and Spearman analyses. During a median follow-up of 15.0 months, 27 patients progressed to ESRD and none died. Lower eGFR [hazards ratio (HR), 0.827, 95% confidence interval (CI), 0.732–0.935;
P
= 0.002] and glomerular C3 deposition (HR, 3.179, 95% CI, 1.079–9.363;
P
= 0.036) were predictive of time to ESRD in stage 4 CKD IgAN. Higher expression of C3a (
P
= 0.010), C3aR (
P
= 0.005), C5a (
P
= 0.015), and C5aR (
P
< 0.001) was identified in ESRD group than in non-ESRD group. Glomerular C3a/C3aR and C5a/C5aR deposits were both correlated with a lower baseline eGFR, higher baseline 24 h-urinary protein (24 h-UP) and faster decline of eGFR. Besides, C3a and C5a deposits were found in patients with high S (S1) and T (T1/2) scores, respectively. Complement C3a/C3aR and C5a/C5aR in IgAN patients with stage 4 CKD may portend a faster deterioration of kidney function.
Publisher
Springer International Publishing,Springer Nature B.V
Subject
/ Antigens
/ Biopsy
/ Epidermal growth factor receptors
/ Female
/ Glomerulonephritis, IGA - complications
/ Glomerulonephritis, IGA - pathology
/ Humans
/ Kidney Failure, Chronic - etiology
/ Kidney Failure, Chronic - pathology
/ Male
/ Medicine
/ Oncology
/ Patients
/ Receptor, Anaphylatoxin C5a - analysis
/ Receptor, Anaphylatoxin C5a - metabolism
/ Receptors, Complement - analysis
/ Software
