Urinary monocyte chemotactic protein 1: marker of renal function decline in diabetic and nondiabetic proteinuric renal disease

Camilla, Roberta; Brachemi, Soumeya; Pichette, Vincent; Cartier, P; Laforest-Renald, Alexandra; MacRae, Tara; Madore, François; Troyanov, Stéphan

doi:10.5301/jn.2010.1458

Cited by 27 publications

(21 citation statements)

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“…In addition to its presence in these autoimmune diseases, CCL2 has been detected in the urine of patients with diabetic nephropathy [40] and polycystic kidney disease [41]. Recently, urinary CCL2 has been identified as a marker of renal function decline in diabetic and nondiabetic proteinuric renal disease independent from and additive to proteinuria [42]. These reports suggest that CCL2 might be associated with the pathogenesis of several kidney diseases and be a relatively stable biomarker in patient urine samples.…”

Section: Discussionmentioning

confidence: 99%

Urinary chemokine (C-C motif) ligand 2 (monocyte chemotactic protein-1) as a tubular injury marker for early detection of cisplatin-induced nephrotoxicity

Nishihara¹,

Masuda²,

Shinke³

et al. 2013

Biochemical Pharmacology

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Because of the difficulty in detecting segment-specific response in the kidney, we investigated the molecular events underlying acute kidney injury in the proximal tubules of rats with cisplatin (cis-diamminedichloroplatinum II)-induced nephrotoxicity. Microarray analysis revealed that mRNA levels of several cytokines and chemokines, such as interleukin-1beta, chemokine (C-C motif) ligand (CCL) 2, CCL20, chemokine (C-X-C motif) ligand (CXCL) 1, and CXCL10 were significantly increased after cisplatin treatment in both isolated proximal tubules and whole kidney. Interestingly, tubular CCL2 mRNA levels increased soon after cisplatin administration, whereas CCL2 mRNA levels in whole kidney first decreased and then increased. Levels of both CCL2 and kidney injury molecule-1 (KIM-1) in the whole kidney increased after cisplatin administration. Immunofluorescence analysis revealed CCL2 changes in the proximal tubular cells initially and then in the medullary interstitium. Urinary CCL2 excretion significantly increased approximately 3-fold compared with controls the day after cisplatin administration (5 mg/kg), when no changes were observed plasma creatinine and blood urea nitrogen levels. Urinary levels of KIM-1 also increased 3-fold after cisplatin administration. In addition, urinary CCL2 rather than KIM-1 increased in chronic renal failure rats after administration of low-dose cisplatin (2 mg/kg), suggesting that urinary CCL2 was selective for cisplatin-induced nephrotoxicity in renal impairment. These results indicated that the increase in cytokine and chemokine expression in renal epithelial cells might be responsible for kidney deterioration in cisplatin-induced nephrotoxicity, and that urinary CCL2 is associated with tubular injury and serves as a sensitive and noninvasive marker for the early detection of cisplatin-induced tubular injury.

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Section: Discussionmentioning

confidence: 99%

Urinary chemokine (C-C motif) ligand 2 (monocyte chemotactic protein-1) as a tubular injury marker for early detection of cisplatin-induced nephrotoxicity

Nishihara¹,

Masuda²,

Shinke³

et al. 2013

Biochemical Pharmacology

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“…In addition, blocking MCP-1 receptor suppresses inflammation and ameliorates glomerulosclerosis in DKD rodent models (27). Human studies assessing uMCP-1 have been limited by small sample size and/or lack of clinically relevant outcomes (9,10,27,28). To the best of our knowledge, this is the first study that assessed the association of uMCP-1 with meaningful renal outcomes in a large sample of patients with T2D after adjusting for additional covariates, including thiazolidinediones, which have been associated with lower plasma MCP-1 levels (29).…”

Section: Discussionmentioning

confidence: 99%

Association of Urinary Biomarkers of Inflammation, Injury, and Fibrosis with Renal Function Decline: The ACCORD Trial

Nadkarni

Rao

Ismail‐Beigi

et al. 2016

CJASN

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Background and objectives Current measures for predicting renal functional decline in patients with type 2 diabetes with preserved renal function are unsatisfactory, and multiple markers assessing various biologic axes may improve prediction. We examined the association of four biomarker-to-creatinine ratio levels (monocyte chemotactic protein-1, IL-18, kidney injury molecule-1, and YKL-40) with renal outcome.Design, setting, participants, & measurements We used a nested case-control design in the Action to Control Cardiovascular Disease Trial by matching 190 participants with $40% sustained eGFR decline over the 5-year follow-up period to 190 participants with #10% eGFR decline in a 1:1 fashion on key characteristics (age within 5 years, sex, race, baseline albumin-to-creatinine ratio within 20 mg/mg, and baseline eGFR within 10 ml/min per 1.73 m 2 ), with #10% decline. We used a Mesoscale Multiplex Platform and measured biomarkers in baseline and 24-month specimens, and we examined biomarker associations with outcome using conditional logistic regression.Results Baseline and 24-month levels of monocyte chemotactic protein-1-to-creatinine ratio levels were higher for cases versus controls. The highest quartile of baseline monocyte chemotactic protein-1-to-creatinine ratio had fivefold greater odds, and each log increment had 2.27-fold higher odds for outcome (odds ratio, 5.27; 95% confidence interval, 2.19 to 12.71 and odds ratio, 2.27; 95% confidence interval, 1.44 to 3.58, respectively). IL-18-tocreatinine ratio, kidney injury molecule-1-to-creatinine ratio, and YKL-40-to-creatinine ratio were not consistently associated with outcome. C statistic for traditional predictors of eGFR decline was 0.70, which improved significantly to 0.74 with monocyte chemotactic protein-1-to-creatinine ratio.Conclusions Urinary monocyte chemotactic protein-1-to-creatinine ratio concentrations were strongly associated with sustained renal decline in patients with type 2 diabetes with preserved renal function.

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“…TNFR1 was found to be a strong prediction of CKD progression to ESRD [ 114 ], while circulating TNFR1 and TNFR2 were found to predict stage 3 CKD in type 1 diabetes patients. Urinary MCP-1 levels were elevated for CKD patients compared to controls [ 138 ] and were found to correlate with the rate of GFR decline [ 139 ].…”

Section: Novel Promising Biomarkers Useful In Ckd Managementmentioning

confidence: 99%

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

Mihai

Codrici

Popescu

et al. 2018

Journal of Immunology Research

420

317

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Persistent, low-grade inflammation is now considered a hallmark feature of chronic kidney disease (CKD), being involved in the development of all-cause mortality of these patients. Although substantial improvements have been made in clinical care, CKD remains a major public health burden, affecting 10–15% of the population, and its prevalence is constantly growing. Due to its insidious nature, CKD is rarely diagnosed in early stages, and once developed, its progression is unfortunately irreversible. There are many factors that contribute to the setting of the inflammatory status in CKD, including increased production of proinflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, altered metabolism of adipose tissue, and last but not least, gut microbiota dysbiosis, an underestimated source of microinflammation. In this scenario, a huge step forward was made by the increasing progression of omics approaches, specially designed for identification of biomarkers useful for early diagnostic and follow-up. Recent omics advances could provide novel insights in deciphering the disease pathophysiology; thus, identification of circulating biomarker panels using state-of-the-art proteomic technologies could improve CKD early diagnosis, monitoring, and prognostics. This review aims to summarize the recent knowledge regarding the relationship between inflammation and CKD, highlighting the current proteomic approaches, as well as the inflammasomes and gut microbiota dysbiosis involvement in the setting of CKD, culminating with the troubling bidirectional connection between CKD and renal malignancy, raised on the background of an inflammatory condition.

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Urinary monocyte chemotactic protein 1: marker of renal function decline in diabetic and nondiabetic proteinuric renal disease

Cited by 27 publications

References 0 publications

Urinary chemokine (C-C motif) ligand 2 (monocyte chemotactic protein-1) as a tubular injury marker for early detection of cisplatin-induced nephrotoxicity

Urinary chemokine (C-C motif) ligand 2 (monocyte chemotactic protein-1) as a tubular injury marker for early detection of cisplatin-induced nephrotoxicity

Association of Urinary Biomarkers of Inflammation, Injury, and Fibrosis with Renal Function Decline: The ACCORD Trial

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

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