Vitamin D in diabetic nephropathy

Attur, Ravindra Prabhu; Saraf, Karan

doi:10.4103/jpgm.jpgm_311_17

Cited by 8 publications

(8 citation statements)

References 14 publications

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“…[9] Since ACR considered as an early predictor marker for nephropathy, and VD has a role in proteinuria homeostasis. [27] Therefore, suggesting that, VD deficiency associated with nephropathy in T2DM patients. Furthermore, these findings have been reinforced by the negative association between VD level and duration of DM.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D deficiency increases risk of nephropathy and cardiovascular diseases in Type 2 diabetes mellitus patients

et al. 2019

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Background: Vitamin D (VD) deficiency is associated with insulin function and secretion. It is linked with diabetes mellitus (DM) progression, and complications were also recorded. Therefore, the current study aimed to investigate serum VD level in Type 2 DM (T2DM) patients and its association with diabetic nephropathy and cardiovascular diseases (CVD). Materials and Methods: In this cross-sectional study, 205 patients with Type 2 diabetes age ranged from 39 to 75 years old were enrolled. Serum VD, high-sensitivity C-reactive protein (hs-CRP), and hemoglobin A1c (HbA1c) were measured. In addition, urinary albumin:creatinine ratio (ACR) was estimated. Results: Patients with Type 2 diabetes had a 78.5% VD level <30 ng/m. ACR and hs-CRP levels were significantly increased in patients with diabetes with VD <30 ng/m ( P = 0.011 and P = 0.008, respectively). Female had significantly lower VD level than male P < 0.001. Patients exposed to sunlight had significantly higher VD level and lower hs-CRP levels compared with less-exposed, P value (0.001 and <0.001), respectively. Exercise significantly increased VD and decreased ACR levels in DM patients, P value (0.046 and 0.002), respectively. VD was positively associated with age ( r = 0.355 P = 0.040) and negatively correlate with BMI ( r = −0.502 P = 0.009), duration of disease ( r = −0.498 P = 0.003), ACR ( r = −0.384 P = 0.015), and HbA1c ( r = −0.327 P = 0.032). Conclusion: The evidence from this study suggest that patients with Type 2 diabetes with VD deficiency are at higher risk for developing CVD and nephropathy.

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Section: Discussionmentioning

confidence: 99%

Vitamin D deficiency increases risk of nephropathy and cardiovascular diseases in Type 2 diabetes mellitus patients

et al. 2019

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“…VD has calciotropic and pleiotropic effects mediated through VDR expressed in kidneys, including podocytes, intestine, bones, parathyroid glands, pancreatic beta cells, monocytes, and T-cells [ 37 ]. It is reported that VD can inhibit JAK/STAT signaling in hepatocytes and T cells [ 23 , 24 ].…”

Section: Discussionmentioning

confidence: 99%

Vitamin D protects glomerular mesangial cells from high glucose-induced injury by repressing JAK/STAT signaling

et al. 2021

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Aim High glucose (HG) induces the production of transforming growth factor (TGF)-β and reactive oxygen species, which further activates JAK/STAT signaling and promotes the synthesis of matrix proteins, contributes to the pathophysiological processes of diabetic nephropathy. This study aims to investigate the protection role of vitamin D (VD) in the kidney in high glucose condition. Methods Rat glomerular mesangial cells were cultured in high glucose medium, with or without VD or VD receptor (VDR) siRNAs treatment. The levels of TGF-β and fibronectin were detected by qRT-PCR, immunoblotting and enzyme-linked immunosorbent assay (ELISA). The levels of phosphorylated JAK2, STAT1 and STAT3, and JAK/STAT signaling downstream genes were examined by immunoblotting and qRT-PCR. Results In rat glomerular mesangial cells, VD treatment can repress the tyrosine phosphorylation of JAK2, STAT1 and STAT3. VD inhibited TGF-β and fibronectin expression which was rescued by vitamin d receptor (VDR) siRNA and STATs inhibitor perficitinib. The JAK/STAT signaling downstream protein coding genes including SOCS1, SOCS3 and type IV collagen were repressed by VD. Meanwhile, the expression of non-coding RNAs such as miR-181a, miR-181b, was repressed by VD, and the expression of miR-34a and Let-7b was upregulated by VD. Conclusion Vitamin D (VD) treatment inhibits the function of HG on fibronectin production through regulating JAK/STAT pathway. These results provide direct evidences that VD protects glomerular mesangial cells from high glucose-induced injury through repressing JAK/STAT signaling, which has the potential for clinical DN treatment.

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“…Calcitriol3 negatively regulates renin angiotensin aldosterone coordination, through its suppression of TGF -β, macrophage permeation, and transcription factor nuclear factor-κb activity. Vitamin D has anti-inflammatory and antifibrotic activity [38] . In 2017, Zeng X. et al investigated consequence of vitamin D on a rat model of DM and created that calcitrioli and VD3 could diminish the expression of CD68, MCP-1 and TGF-B1 and attenuated macrophages infiltration in tissues.…”

Section: Discussionmentioning

confidence: 99%

Effect of Low and High Doses of Vitamin D on Sreptozotocin-induced Diabetic Nephropathy in Adult Male Albino Rats: Histological and Immunohistochemical Sudy

Mohamady

Mostafa²,

Mohamed³

2019

Egyptian Journal of Histology

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Background: Diabetic nephropathy is an important instigate of persistent kidney ailment problem and irrevocably renal catastrophe. Vitamin D (VD) insufficiency is documented as a worldwide health delinquent and lately pondered as a conscientious factor in the onset and progression of diabetes mellitus (DM). Aim: This research paper was premeditated to explore the probable upshot of low and high doses of vitamin D on a rat model of diabetic nephropathy. Material and Methods: Forty adult male albino rats were segregated into four groups: Group I (control group). Group II (the diabetic nephropathy group): given streptozotocin intraperitoneal. Group III (the low dose VD group): rats were given streptozotocin then vitamin D orally as 8000 IU/kg/day. Group IV (the high dose VD group): rats were given streptozotocin then vitamin D orally as 20,000 IU/kg/day. After complete12 weeks from the beginning of the experiment, rats were sacrificed. Kidney specimens were handled and assayed by histological and Immunohistochemical procedures. Results: The diabetic nephr0pathy group revealed distortion of glomeruli, tubular distortion. mononuclear permeation and epithelial desquamation. Congested dilated glomeruli, peritubular blood vessels and interstitial outpouring of blood were also noticed. EM examination of proximal and distal c0nv0luted tubules exhibited multiple vacuoles. thickening of basement membrane and destructed mitochondria were also seen. Group III showed improvement of these changes and Group IV showed amelioration of most of these changes. Conclusion: High dose of vitamin D ameliorates experimentally induced diabetic nephropathy.

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Vitamin D in diabetic nephropathy

Cited by 8 publications

References 14 publications

Vitamin D deficiency increases risk of nephropathy and cardiovascular diseases in Type 2 diabetes mellitus patients

Vitamin D deficiency increases risk of nephropathy and cardiovascular diseases in Type 2 diabetes mellitus patients

Vitamin D protects glomerular mesangial cells from high glucose-induced injury by repressing JAK/STAT signaling

Effect of Low and High Doses of Vitamin D on Sreptozotocin-induced Diabetic Nephropathy in Adult Male Albino Rats: Histological and Immunohistochemical Sudy

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