Serum levels of adiponectin and leptin as biomarkers of proteinuria in lupus nephritis

Díaz-Rizo, Valeria; Bonilla-Lara, David; González-López, Laura; Sanchez-Mosco, Dalia; Fajardo-Robledo, Nicte Selene; Pérez-Guerrero, Edsaúl Emilio; Rodriguez-Jimenez, Norma Alejandra; Saldaña-Cruz, Ana Miriam; Vazquez-Villegas, Maria Luisa; Gómez-Bañuelos, Eduardo; Mercado, Mónica Vázquez-Del; Cardona-Muñoz, Ernesto Germán; Cardona-Müller, David; Trujillo, Xóchitl; Huerta, Miguel; Salazar-Páramo, Mario; Gámez-Nava, Jorge I.

doi:10.1371/journal.pone.0184056

Cited by 35 publications

(36 citation statements)

References 42 publications

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“…Correlations with disease activity are however contradictory. 85,90,[107][108][109] PBMCs of SLE patients present higher amounts of adiponectin transcript and protein as compared to HCs, but there is no correlation between adiponectin expression levels and clinical parameters or disease activity indexes. 110 Moreover, increased adiponectin levels in MRL/lpr mice do not promote disease progression.…”

Section: Tions In Addition To Its Effects On T Cells Leptin Activatmentioning

confidence: 96%

“…81 High levels of circulating leptin correlate with disease activity in SLE patients. 63,[82][83][84][85][86] Fasting decreases the production of leptin and expands the frequency of FOXP3 + regulatory (Treg) cells in SLE patients leading to a reduced disease activity. 87 However, SLE patients with reduced serum leptin have also been reported in some studies, 88,89 while others show no difference between SLE patients and HCs.…”

Section: Lupus and Sys Temi C Me Tabolis Mmentioning

confidence: 99%

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Metabolic determinants of lupus pathogenesis

Teng

Brown

Choi

et al. 2020

Immunological Reviews

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The metabolism of healthy murine and more recently human immune cells has been investigated with an increasing amount of details. These studies have revealed the challenges presented by immune cells to respond rapidly to a wide variety of triggers by adjusting the amount, type, and utilization of the nutrients they import. A concept has emerged that cellular metabolic programs regulate the size of the immune response and the plasticity of its effector functions. This has generated a lot of enthusiasm with the prediction that cellular metabolism could be manipulated to either enhance or limit an immune response. In support of this hypothesis, studies in animal models as well as human subjects have shown that the dysregulation of the immune system in autoimmune diseases is associated with a skewing of the immunometabolic programs. These studies have been mostly conducted on autoimmune CD4 + T cells, with the metabolism of other immune cells in autoimmune settings still being understudied. Here we discuss systemic metabolism as well as cellular immunometabolism as novel tools to decipher fundamental mechanisms of autoimmunity. We review the contribution of each major metabolic pathway to autoimmune diseases, with a focus on systemic lupus erythematosus (SLE), with the relevant translational opportunities, existing or predicted from results obtained with healthy immune cells. Finally, we review how targeting metabolic programs may present novel therapeutic venues. K E Y W O R D Sglucose, glutamine, lupus, metabolic inhibitors, metabolism

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Section: Tions In Addition To Its Effects On T Cells Leptin Activatmentioning

confidence: 96%

Section: Lupus and Sys Temi C Me Tabolis Mmentioning

confidence: 99%

Metabolic determinants of lupus pathogenesis

Teng

Brown

Choi

et al. 2020

Immunological Reviews

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“…Being serum creatinine a marker of renal dysfunction; this nding is relevant for hypothesise the possible role of adiponectin levels as a marker of renal dysfunction. More recently, our group has identi ed a correlation between high adiponectin levels and severity of proteinuria as well as with high creatinine levels in LN [11].…”

Section: Introductionmentioning

confidence: 99%

“…Non-traditional markers of LN include increased serum levels of some adipokines and cytokines. Some of these markers have been associated with proteinuria, decrease in glomerular ltration rate, impairment of creatinine clearance, haematuria, increase in urinary leucocytes or casts [8][9][10][11]. The macrophage migration inhibitory factor (MIF) is an interesting cytokine that modulates in ammatory response regulating T-cell proliferation [12].…”

Section: Introductionmentioning

confidence: 99%

Value of Serum Macrophage Migration Inhibitory Factor (Mif), Adiponectin, and Other Adipokines as Markers of Proteinuria and Renal Dysfunctionin Lupus Nephritis: A Cross-sectional Study.

Diaz-Rizo

et al. 2020

Preprint

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BackgroundTo date, there is controverted the association between serum macrophage migration inhibitory factor (MIF) and serum adipokines with Lupus Nephrites.ObjectiveTo investigate the value of serum MIF, leptin, adiponectin and resistin levels as markers of proteinuria and renal dysfunction in lupus nephritisMethodsDesign: cross-sectional. We included 196 Systemic Lupus Erythematosus (SLE) and 52 controls (HC). In SLE, disease activity was assessed by SLEDAI. Renal involvement was investigated by Renal-SLEDAI: a) Renal-SLE involvement (n=43) and b) Non-Renal-SLE (n=153). MIF, adiponectin, leptin and resistin levels were quantified by ELISA. We assessed correlations of MIF, adipokines and renal involvement parameters [proteinuria (g/day), serum creatinine and other]. Multivariable linear regression was used for investigating factors associated with the intensity of proteinuria. ResultsSLE patients had higher MIF (p=0.02) and adiponectin levels (p<0.001) than HC. In renal-SLE involvement there were higher adiponectin levels (19.0 vs 13.3 µg/mL, p=0.002) and resistin levels (10.7 vs 8.9 ng/mL, p=0.01), compared with non-Renal-SLE. Proteinuria correlated with high adiponectin (rs=0.19, p<0.009) and resistin levels (rs=26, p<0.001). MIF (rs=0.27, p=0.04) and resistin (rs= 0.18; p=0.02) correlated with increased creatinine. High Renal activity correlated with adiponectin (rs=0.21, p=0.004). Multiple linear regression identified that elevated adiponectin (p=0.02), younger age (p=0.04) and low MIF (p=0.02) were associated with intensity of proteinuria. Low MIF and high adiponectin levels have interaction for intensity of proteinuria (R2=0.41). ConclusionsHigh adiponectin combined with low MIF concentrations interacts for increase proteinuria in renal-SLE, and MIF and resistin levels are associated with renal dysfunction. These findings highlight the relevance of including the assessment of MIF and adipokines as clinical markers in the evaluation of LN.

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“…Among these other markers of LN are included the serum levels of adipokines and cytokines. These molecules have been associated with the parameters of renal involvement, such as proteinuria, decrease in glomerular ltration rate, impairment of creatinine clearance, haematuria, and increase in urinary leucocytes or casts [7][8][9][10]. Nevertheless, some cytokines and adipokines such as the serum levels of the macrophage migration inhibitory factor (MIF), leptin, adiponectin and resistin have been insu ciently evaluated as markers in LN.…”

Section: Introductionmentioning

confidence: 99%

Assessment of serum macrophage migration inhibitory factor (MIF), adiponectin, and other adipokines as potential markers of proteinuria and renal dysfunction in lupus nephritis. A cross-sectional study.

Gámez-Nava

Díaz-Rizo

Pérez-Guerrero

et al. 2020

Preprint

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Background To date, the association of serum macrophage migration inhibitory factor (MIF) and serum adipokines with lupus nephritis is controversial.Objective To assess the utility of serum MIF, leptin, adiponectin and resistin levels as markers of proteinuria and renal dysfunction in lupus nephritis.Methods Cross-sectional study including 196 systemic lupus erythematosus (SLE) patients and 52 healthy controls (HCs). Disease activity was assessed by Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Renal SLE involvement was investigated by renal-SLEDAI. MIF, adiponectin, leptin and resistin levels were quantified by ELISA. We assessed the correlations of quantitative variables by Spearman correlation (rs). Multivariable linear regression adjusted the variables associated with the severity of proteinuria. Results SLE patients had higher MIF (p=0.02) and adiponectin (p<0.001) than HCs. Patients with renal SLE involvement (n=43) had higher adiponectin (19.0 vs 13.3 µg/mL, p=0.002) and resistin (10.7 vs 8.9 ng/mL, p=0.01) than patients with non-renal SLE (n=153). Proteinuria correlated with high adiponectin (rs=0.19, p<0.009) and resistin (rs=26, p<0.001). MIF (rs=0.27, p=0.04). Resistin correlated with increased creatinine (rs= 0.18, p=0.02). High renal-SLEDAI correlated with adiponectin (rs=0.21, p=0.004). Multiple linear regression showed that elevated adiponectin (p=0.02), younger age (p=0.04) and low MIF (p=0.02) were associated with the severity of proteinuria. Low MIF and high adiponectin levels interacted to explain the association with the severity of proteinuria (R2=0.41).Conclusions High adiponectin combined with low MIF concentrations interact to explain the severity of proteinuria in renal SLE. These findings highlight the relevance of adiponectin, resistin and MIF as markers of LN.

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Serum levels of adiponectin and leptin as biomarkers of proteinuria in lupus nephritis

Cited by 35 publications

References 42 publications

Metabolic determinants of lupus pathogenesis

Metabolic determinants of lupus pathogenesis

Value of Serum Macrophage Migration Inhibitory Factor (Mif), Adiponectin, and Other Adipokines as Markers of Proteinuria and Renal Dysfunctionin Lupus Nephritis: A Cross-sectional Study.

Assessment of serum macrophage migration inhibitory factor (MIF), adiponectin, and other adipokines as potential markers of proteinuria and renal dysfunction in lupus nephritis. A cross-sectional study.

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