Kidney injury molecule-1 as a predicting factor for inflamed kidney, diabetic and diabetic nephropathy Egyptian patients

Ahmed, Soliman; Hamed, Manal A.

doi:10.1186/s40200-015-0131-8

Cited by 24 publications

(16 citation statements)

References 24 publications

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“…79 Previously it has been reported that KIM-1 correlate positively with the high glucose level in diabetic patients. 80 Expression of KIM-1 and NGAL reported to be increased in renal tissue of rats during DN which is consistent with the results of our present investigation. 81 Administration of LG showed significant inhibition in upregulation of diabetes-induced KIM-1 and NGAL mRNA expression, which might be due to its antihyperglycemic potential.…”

Section: Discussionsupporting

confidence: 83%

Protective effect ofL-glutamine against diabetes-induced nephropathy in experimental animal: Role of KIM-1, NGAL, TGF-β1, and collagen-1

Sadar¹,

Kaspate

Vyawahare³

2016

Renal Failure

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Diabetic nephropathy is a serious microvascular complication and one of the main causes of endstage renal disease. L-Glutamine (LG) is naturally occurring amino acids with antidiabetic and antioxidant potential. The aim of present investigation was to evaluate the potential of LG against streptozotocin (STZ)-induced diabetic nephropathy (DN) in laboratory rats. DN was induced in male Wistar rats (200-220 g) by intraperitoneal administration of STZ (55 mg/kg). Animals were treated orally with either distilled water (10 mg/kg) or LG (250, 500, and 1000 mg/kg) or Sitagliptin (5 mg/kg). Various biochemical, molecular, and histological (hematoxylin-eosin and Masson's trichrome stain) parameters were assessed. Administration of LG (500 and 1000 mg/kg) significantly inhibited (p < .05) STZ-induced alterations in serum and urine biochemistry (urine creatinine, uric acid, albumin, and BUN). It also significantly increased creatinine clearance rate. STZ induced increase in renal oxidonitrosative stress was significantly decreased (p < .05) by LG (500 and 1000 mg/kg) treatment. Upregulated renal KIM-1, NGAL, TGF-b1, and collagen-1 mRNA expression after STZ administration was significantly inhibited (p < .05) by LG (500 and 1000 mg/ kg) treatment. Correlation analysis also revealed that antidiabetic potential of LG attenuates STZinduced elevated renal KIM-1, NGAL, TGF-b1, and collagen-1 mRNA expression. Histopathological alteration induced by STZ in renal tissue was ameliorated by LG treatment. In conclusion, results of present investigation suggest that treatment with LG ameliorated STZ-induced DN via the inhibition of oxidonitrosative stress as well as downregulation of KIM-1, NGAL, TGF-b1, and collagen-1 mRNA expressions. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 83%

Protective effect ofL-glutamine against diabetes-induced nephropathy in experimental animal: Role of KIM-1, NGAL, TGF-β1, and collagen-1

Sadar¹,

Kaspate

Vyawahare³

2016

Renal Failure

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“…But these effects of high glucose were significantly blocked by KIM-1 siRNA, which was confirmed by the significantly decreased expression of the LC3-II (Fig. 3A and 3B) renal KIM-1 and urinary KIM-1 are significantly increased in DN patients [14,25]. However, whether KIM-1 plays a protective or injurious role in DN progression remain unclear.…”

Section: Effect Of Kim-1 Sirna On High Glucose-induced Autophagy and mentioning

confidence: 66%

KIM-1 Mediates High Glucose-Induced Autophagy and Apoptosis in Renal Tubular Epithelial Cells

Gou

Chen

Sheng

et al. 2016

Cell Physiol Biochem

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Background/Aim: To investigate the role of kidney injury molecular 1 (KIM-1) in high glucose-induced autophagy and apoptosis in renal tubular epithelial cells. Methods: Human renal tubular epithelial cells (HK2) were treated with normal glucose (NG, D -glucose 5.6 mmol/L), high glucose (HG, 30 mmol/L), high osmotic (HO, D-glucose 5.6 mmol/L + D-mannitol 24.4 mmol/L), HG + KIM-1 siRNA, HG + siRNA control. The expressions of KIM-1 and microtubule-associated protein 1 light chain 3II (LC3II) were measured by western blot as well as real time PCR; the number of autophagosome was detected by electron microscopy; and the level of apoptosis was analyzed by flow cytometry. Results: In the HG group, the expressions of KIM-1 and LC3II were increased markedly, which was accompanied by more autophagosome and higher level of apoptosis compared with NG group. Silencing of KIM-1 by siRNA inhibited the increases in the levels of LC3II, autophagosome and apoptosis. Conclusion: KIM-1 may mediate high glucose-induced autophagy and apoptosis in renal tubular epithelial cells.

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“…In context, KIM-1 was significantly reduced by the GLP-1 agonist, exendin-4, in rats subjected to renal ischemia/ reperfusion injury [37]. Indeed, KIM-1 has been found to be positively correlated with hyperglycemia in diabetic patients [38].…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Early Markers of Diabetic Nephropathy by Linagliptin in Fructose-Streptozotocin-Induced Type 2 Diabetic Rats

Oraby

El-Yamany

Safar

et al. 2019

Nephron

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Background: Early prediction and clinical intervention are extremely important in order to delay or hinder diabetic nephropathy (DN) progression. Objectives: This study aimed to detect early signs of DN and study the potential ameliorating effect of the dipeptidyl peptidase-4 inhibitor, linagliptin, on some early markers for DN in fructose-streptozotocin (Fr-STZ)-induced diabetic rats. Method: Fr-STZ rats were treated with either linagliptin (3 mg/kg p.o. daily), metformin (350 mg/kg p.o. daily), or their combination for 6 weeks. Results: Fr-STZ DN rats exhibited obvious tubular renal damage and glomerular podocyte injury as confirmed by renal kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and vanin-1 mRNA, as well as urinary N-acetyl-β-D-glucosaminidase elevation and nephrin mRNA suppression, associated with the appearance of marked renal interstitial fibrosis and glomerulosclerosis despite the absence of microalbuminuria. Initiation of oxidative, inflammatory, fibrotic, and apoptotic reactions was evident in the settings of renal hyperglycemia. Linagliptin significantly modulated the aforementioned renal tubular injury makers and restored glomerular nephrin expression as well as reversed renal histopathological alterations. Oxidative, inflammatory, fibrotic and apoptotic processes were also alleviated. Conclusions: This study suggests that linagliptin exerts renoprotection against early features of DN in rats probably by inhibition of high glucose-induced renal tubular and glomerular injury thereby hampering KIM-1 and NGAL as well as vanin-1 associated with renal inflammation, fibrosis and oxidative stress.

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Kidney injury molecule-1 as a predicting factor for inflamed kidney, diabetic and diabetic nephropathy Egyptian patients

Cited by 24 publications

References 24 publications

Protective effect ofL-glutamine against diabetes-induced nephropathy in experimental animal: Role of KIM-1, NGAL, TGF-β1, and collagen-1

Protective effect ofL-glutamine against diabetes-induced nephropathy in experimental animal: Role of KIM-1, NGAL, TGF-β1, and collagen-1

KIM-1 Mediates High Glucose-Induced Autophagy and Apoptosis in Renal Tubular Epithelial Cells

Amelioration of Early Markers of Diabetic Nephropathy by Linagliptin in Fructose-Streptozotocin-Induced Type 2 Diabetic Rats

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