Urinary tumour necrosis factor-  excretion independently correlates with clinical markers of glomerular and tubulointerstitial injury in type 2 diabetic patients

Navarro, Juan F.; Mora, Carmen; Muros, Mercedes; Garcı́a, Javier Garcı́a

doi:10.1093/ndt/gfl469

Cited by 116 publications

(110 citation statements)

References 28 publications

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“…These studies suggest a direct and independent association between the levels of this cytokine and clinical markers of glomerular and tubulointerstitial damage, with a significant rise in serum and urinary TNF-␣ as diabetic nephropathy progresses. 69,92,93 …”

Section: Tnf-␣mentioning

confidence: 99%

The Role of Inflammatory Cytokines in Diabetic Nephropathy

Navarro‐González

Mora‐Fernández

2008

Journal of the American Society of Nephrology

796

636

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Section: Tnf-␣mentioning

confidence: 99%

The Role of Inflammatory Cytokines in Diabetic Nephropathy

Navarro‐González

Mora‐Fernández

2008

Journal of the American Society of Nephrology

796

636

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“…7,16,19 -21,30 -32 Among these, the evidence for TNF-␣ as a pathogenic factor in the very early stages of DN in the experimental models of type 1 diabetes suggests that it has potential as a marker of kidney injury, as reviewed recently by Navarro et al 32 These authors also provided clinical data showing that urinary TNF-␣ was significantly and independently associated with both glomerular and tubulointerstitial lesions in type 2 diabetes 33 ; however, in our study, urinary TNF-␣ was not detectable in the majority of patients.…”

Section: Cd44mentioning

confidence: 99%

Association of Urinary Inflammatory Markers and Renal Decline in Microalbuminuric Type 1 Diabetics

Wołkow¹,

Niewczas²,

Perkins³

et al. 2008

Journal of the American Society of Nephrology

136

111

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Progressive renal function decline begins in one third of patients with microalbuminuria and type 1 diabetes. This study examined whether this decline is associated with elevated excretion of inflammatory markers in urine. Five inflammatory markers (IL-6, IL-8, monocyte chemoattractant protein-1, interferongamma-inducible protein (IP-10), and macrophage inflammatory protein-1␦) were measured in urine samples from the First Joslin Study of the Natural History of Microalbuminuria in Type 1 Diabetes, a cohort recruited in 1991. Samples were obtained from 43 participants with microalbuminuria and stable renal function (nondecliners), from 28 with microalbuminuria and early progressive renal function decline (decliners), and from 74 with normoalbuminuria and stable renal function (reference). Urinary concentrations of all five inflammatory markers were significantly higher in decliners than in nondecliners, who were similar to the reference group. Multivariate analysis revealed that those with more than two markers elevated were more than five times as likely to have early progressive decline of renal function. In contrast, serum concentrations of C-reactive protein, IL-8, and macrophage inflammatory protein-1␦ did not differ between decliners and nondecliners. These results support the hypothesis that inflammatory processes in the kidney contribute to the progression of nephropathy in patients with type 1 diabetes.

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“…In the present study, the results showed that the pro-inflammatory cytokines TNF-α, IL-1β and IL-6 were notably decreased in SIRT4-overexpressing podocytes with glucose stimulation. TNF-α plays an important role in the development and progression of diabetic nephropathy supported by the observation of increases in renal TNF-α levels in diabetic animal models and patients (37,38), indicating that increased TNF-α levels result in renal damage. Clinical studies have reported significant increases in the renal production of IL-1β and IL-6 in patients with type 2 diabetic nephropathy compared with that in diabetic patients without nephropathy, suggesting a role of IL-1β and IL-6 in the pathogenesis of diabetic nephropathy (39,40).…”

mentioning

confidence: 97%

SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis

Shi

Wang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Diabetic nephropathy is a diabetic complication associated with capillary damage and increased mortality. Sirtuin 4 (SIRT4) plays an important role in mitochondrial function and the pathogenesis of metabolic diseases, including aging kidneys. The aim of the present study was to investigate the association between SIRT4 and diabetic nephropathy in a glucose-induced mouse podocyte model. A CCK-8 assay showed that glucose simulation significantly inhibited podocyte proliferation in a time-and concentration-dependent manner. Reverse transcription-quantitative polymerase chain reaction and western blot analysis showed that the mRNA and protein levels of SIRT4 were notably decreased in a concentration-dependent manner in glucose-simulated podocytes. However, SIRT4 overexpression increased proliferation and suppressed apoptosis, which was accompanied by increases in mitochondrial membrane potential and reduced production of reactive oxygen species (ROS). Notably, SIRT4 overexpression downregulated the expression of apoptosis-related proteins NOX1, Bax and phosphorylated p38 and upregulated the expression of Bcl-2 in glucose-simulated podocytes. In addition, SIRT4 overexpression significantly attenuated the inflammatory response, indicated by reductions in the levels of TNF-α, IL-1β and IL-6. These results demonstrate for the first time that the overexpression of SIRT4 prevents glucose-induced podocyte apoptosis and ROS production and suggest that podocyte apoptosis represents an early pathological mechanism leading to diabetic nephropathy.

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Urinary tumour necrosis factor- excretion independently correlates with clinical markers of glomerular and tubulointerstitial injury in type 2 diabetic patients

Cited by 116 publications

References 28 publications

The Role of Inflammatory Cytokines in Diabetic Nephropathy

The Role of Inflammatory Cytokines in Diabetic Nephropathy

Association of Urinary Inflammatory Markers and Renal Decline in Microalbuminuric Type 1 Diabetics

SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis

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