Abstract
BackgroundMonocyte chemoattractant protein-1 (MCP-1), which is up regulated in kidney diseases, is considered a marker of kidney inflammation. We examined the value of urine MCP-1 in predicting the outcome in idiopathic glomerulonephritis.MethodsBetween 1993 and 2004, 165 patients (68 females) diagnosed with idiopathic proteinuric glomerulopathy and with serum creatinine <150 µmol/L at diagnosis were selected for the study. Urine concentrations of MCP-1 were analyzed by ELISA in early morning spot urine samples collected on the day of the diagnostic kidney biopsy. The patients were followed until 2009. The progression rate to end-stage kidney disease was calculated using Kaplan–Meier survival analysis. End-stage kidney disease (ESKD) was defined as the start of kidney replacement therapy during the study follow-up time.ResultsPatients with proliferative glomerulonephritis had significantly higher urinary MCP-1 excretion levels than those with non-proliferative glomerulonephritis (p<0.001). The percentage of patients whose kidney function deteriorated significantly was 39.0% in the high MCP-1 excretion group and 29.9% in the low MCP-1 excretion group. However, after adjustment for confounding variables such as glomerular filtration rate (GFR) and proteinuria, there was no significant association between urine MCP-1 concentration and progression to ESKD, (HR = 1.75, 95% CI = 0.64–4.75, p = 0.27).ConclusionOur findings indicate that progression to end-stage kidney disease in patients with idiopathic glomerulopathies is not associated with urine MCP-1 concentrations at the time of diagnosis.
Highlights
Glomerular diseases, including idiopathic glomerulonephritis, are major causes of end-stage kidney disease (ESKD)
Urinary Monocyte chemoattractant protein-1 (MCP-1) levels were significantly higher in patients with proliferative glomerulonephritis (IgA and mesangioproliferative) than in those with non-proliferative forms of glomerulonephritis, (0.061 (IQ 0.032–0.133) mg/ mmol creatinine vs. 0.039 (IQ 0.027–0.085) mg/mmol creatinine, p = 0.049 with Bonferroni-Holm correction; (Figure 1), and both had significantly higher urine MCP-1 concentrations than healthy controls: 0.01 mg/mmol creatinine (IQ 0.008–0.023, p,0.001 with Bonferroni-Holm correction (Figure 1)
The albuminuria was significantly higher in non-proliferative glomerulonephritis than in proliferative glomerulonephritis (p = 0.002)
Summary
Glomerular diseases, including idiopathic glomerulonephritis, are major causes of end-stage kidney disease (ESKD). They are manifested with haematuria, proteinuria and declining kidney function. They are associated with inflammation and proliferation of the glomerular tissue and enhanced glomerular and interstitial production of inflammatory mediators, such as monocyte chemoattractant protein-1 (MCP-1) [1,2]. MCP-1 is produced by macrophages, vascular endothelial cells, monocytes and fibroblasts. It triggers migration and retention of monocytes and transformation of fibroblasts in the glomeruli [3,4,5]. We examined the value of urine MCP-1 in predicting the outcome in idiopathic glomerulonephritis
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
