Adiponectin in renal disease: Relationship to phenotype and genetic variation in the gene encoding adiponectin

Stenvinkel, Peter; Marchlewska, Alicia; Pecoits‐Filho, Roberto; Heimbürger, Olof; Zhang, Zhengzhong; Hoff, Catherine M.; Holmes, C. J.; Axelsson, Jonas; Arvidsson, Sivonne; Schalling, Martin; Bárány, Peter; Lindholm, Bengt; Nordfors, Louise

doi:10.1111/j.1523-1755.2004.00370.x

Cited by 168 publications

(138 citation statements)

References 35 publications

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“…These findings indicate that adiponectin might have beneficial effects against renal dysfunction including MC disorders. In some studies, it was reported that plasma adiponectin levels were elevated in patients with CKD (Stenvinkel et al 2004, Guebre-Egziabher et al 2005. It is suggested that the elevated plasma adiponectin levels can work as a compensatory mechanism to attenuate the progression of glomerular dysfunction in the patients with CKD.…”

Section: Discussionmentioning

confidence: 99%

“…It was reported that plasma adiponectin levels are elevated when renal function is impaired -as early as CKD stage III -and particularly in proteinuric patients (Guebre-Egziabher et al 2005). Another study demonstrated that plasma adiponectin levels were markedly elevated in patients with end-stage renal disease (Stenvinkel et al 2004). It has been considered that the rise in plasma adiponectin that occurs during renal function deterioration represents an adaptive response to the altered metabolic profile associated with a high cardiovascular risk in CKD patients.…”

Section: Introductionmentioning

confidence: 99%

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Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration

Ishizawa

Dorjsuren²,

Izawa‐Ishizawa³

et al. 2009

Journal of Endocrinology

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Adiponectin, an adipocyte-derived hormone, has been involved in metabolic syndrome, a known risk factor for the development of chronic kidney disease (CKD). Recent studies have demonstrated that plasma adiponectin levels are elevated when kidney function declines in patients with CKD. Excessive mesangial cell (MC) turnover is one of the important features of CKD. The aim of the present study is to elucidate the effects of adiponectin on platelet-derived growth factor (PDGF)-induced cell migration and intracellular signaling pathways, in cultured rat MCs (RMCs). PDGF-induced RMC migration was significantly inhibited by the pretreatment of adiponectin. Adiponectin alone had no effect on RMC migration. Big mitogen-activated protein (MAP) kinase 1 (BMK1), p38 MAP kinase, and Akt were activated by PDGF stimulation in a time-and concentration-dependent manner in RMC. Adiponectin alone did not affect BMK1, p38 MAP kinase, and Akt phosphorylations in RMC. PDGF-induced BMK1 and p38 MAP kinase phosphorylations were significantly attenuated by the pretreatment of adiponectin in RMCs. On the other hand, the phosphorylation of Akt by PDGF was not diminished by the pretreatment of adiponectin. Adiponectin had no effects on PDGF-receptor autophosphorylation by PDGF. We also confirmed that PDGF-induced RMC migration was significantly suppressed by siBMK1 transfection or SB203580, a p38 MAP kinase inhibitor. From these findings, it is implied that the elevated plasma adiponectin levels in patients with CKD might play a compensatory role aimed at counteracting renal dysfunction related to MC disorders.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration

Ishizawa

Dorjsuren²,

Izawa‐Ishizawa³

et al. 2009

Journal of Endocrinology

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“…These include a benefit from the better nutritional status typically seen in obese individuals, and which provides better protein and energy reserves in the face of acute illness, and a higher muscle mass with enhanced antioxidant capacity 63 and lower circulating actin and higher plasma gelsolin levels, 71 which are associated with better outcomes. Other hypothetically beneficial characteristics of obesity include a more stable hemodynamic status with mitigation of stress responses and heightened sympathetic and renin-angiotensin activity; 72 increased production of adiponectines 73 and soluble tumor necrosis factor alfa receptors 74 by adipose tissue neutralizing the adverse effects of tumor necrosis factor alfa; enhanced binding of circulating endotoxins 75 by the characteristically higher cholesterol levels seen in obesity; and sequestration of uremic toxins by adipose tissue.…”

Section: Obesity In Patients With Advanced Kidney Disease: the Need Fmentioning

confidence: 99%

Obesity and Kidney Disease: Hidden Consequences of the Epidemic

Kövesdy¹,

Furth²,

Zoccali³

2017

Nephrol Open J

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“…[7] There was also a significant negative relationship between adiponectin and two biomarkers of inflammation, hsCRP and fibrinogen. Thus, it has been suggested that hypoadiponectinemia may also serve as a marker of increased inflammatory status in end stage renal disease (ESRD) patients in the study by Stenvinkel et al [23] Moreover, it has been established that adiponectin can accumulate in the vascular wall when the endothelial barrier is damaged. This accumulation may also contribute to hypoadiponectinemia in patients with proteinuria.…”

Section: Tablementioning

confidence: 99%

The Relationship between Adiponectin Levels and Degree of Proteinuria in Patients with Nephrotic and Non-nephrotic Proteinuria

et al. 2009

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Adipose tissue appears to be a modulator of vascular injury and systemic inflammation. The aim of this study was to establish the relationship between plasma adiponectin concentration and severity of proteinuria in patients with proteinuria. We enrolled 77 patients with nephrotic and non-nephrotic proteinuria with normal renal function along with 38 matched controls in a cross-sectional study. These patients were divided into group 1 (n = 44, non-nephrotic proteinuria, <3.5 g/day) and group 2 (n = 43, nephrotic proteinuria, >3.5 g/day) by severity of proteinuria. Circulating adiponectin and high-sensitivity C-reactive protein (hsCRP) levels were measured using commercial ELISA. HOMA index and hsCRP levels were all significantly higher in proteinuric patients than in control subjects, while plasma adiponectin levels were significantly lower (p < 0.001). When compared to patients with non-nephrotic proteinuria, patients with nephrotic proteinuria had significantly higher plasma hsCRP and HOMA index (p < 0.001). According to the multiple regression analysis, proteinuria levels were independently related to adiponectin levels. Decreases in adiponectin levels were more prominent in patients with nephrotic proteinuria than in patients with non-nephrotic proteinuria. These results show that the reduction of plasma adiponectin concentrations depend on insulin resistance and inflammation rather than directly severity of proteinuria in patients with proteinuria.

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Adiponectin in renal disease: Relationship to phenotype and genetic variation in the gene encoding adiponectin

Cited by 168 publications

References 35 publications

Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration

Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration

Obesity and Kidney Disease: Hidden Consequences of the Epidemic

The Relationship between Adiponectin Levels and Degree of Proteinuria in Patients with Nephrotic and Non-nephrotic Proteinuria

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