Management of diabetic nephropathy: Recent progress and future perspective

Ahmad, Jamal

doi:10.1016/j.dsx.2015.02.008

Cited by 132 publications

(108 citation statements)

References 134 publications

Supporting

Mentioning

106

Contrasting

Unclassified

Order By: Relevance

“…The chromosomal region containing the ADIPOQ Oncotarget 2 www.impactjournals.com/oncotarget gene has been reported to be one of the cardiovascular risk factors as well [18,19]. Additionally, abnormal levels of serum adiponectin have already been shown to be correlated with T2DM, insulin resistance, obesity, cardiovascular diseases and nephropathy [8,16,[20][21][22]. Reportedly, the development of microalbuminuria in T1DM cases may be predicted by high adiponectin levels [23].…”

Section: Introductionmentioning

confidence: 99%

“…Initially, altogether 174 articles were identified from the database search. During the further reviewing, 163 articles were deleted for editorials (7), on rats (6), not about DN or merely about diabetes (63), obvious irrelevancy (71), concerning the prognosis of DN (8), meta-analysis (3), and with no detailed data about genotype and allele frequencies (5). At last, 14 case-control studies with 3343 cases and 7859 controls were incorporated into the present meta-analysis [1,20,[24][25][26][27][28][29][30][31][32].…”

Section: Characteristics Of Studiesmentioning

confidence: 99%

“…DN is a multifactorial disease occurring as a result of both environmental and hereditary factors [8]. The ethnic disparity in DN development may be attributed to an important role of genetic factors; and gender has also been demonstrated to influence the predisposition of diabetic patients to developing kidney diseases, with males having a relatively higher incidence rate [8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

WITHDRAWN: Association between ADIPOQ rs2241766 polymorphism and risk of diabetic nephropathy

Zhu¹,

Zhang²,

Wang³

et al. 2017

Oncotarget

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Characteristics Of Studiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

WITHDRAWN: Association between ADIPOQ rs2241766 polymorphism and risk of diabetic nephropathy

Zhu¹,

Zhang²,

Wang³

et al. 2017

Oncotarget

View full text Add to dashboard Cite

show abstract

“…Diabetic nephropathy is progressive and irreversible and is characterised by glomerular hyperfiltration, epithelial hypertrophy, microalbuminuria, glomerulus basement membrane thickening and proteinuria and is the leading cause of end-stage renal disease worldwide (4)(5)(6)(7)(8). Intensive glycaemic control and interventions with angiotensin converting enzyme (ACE)-inhibitors are intended to delay disease progression but are not curative (9).…”

Section: Introductionmentioning

confidence: 99%

Metformin with insulin relieves oxidative stress and confers renoprotection in type 1 diabetes in vivo

Driver¹,

Hayangah²,

Nyane³

et al. 2017

J Nephropathol

View full text Add to dashboard Cite

Background: Oxidative stress and impaired antioxidant capacity in diabetes are associated with diabetic nephropathy. Metformin, as an adjunct to insulin could decrease oxidative stress and may therefore improve renal function in type 1 diabetes (T1D). Objectives: To investigate the effects of metformin as adds-on therapy to insulin on renal dysfunction in T1D. Materials and Methods: Male Sprague-Dawley rats (230-250 g) were divided into 5 groups (n =7). Rats in groups A and B were orally treated with 3.0 mL/kg body weight (BW) of distilled water, while those in groups C and D were treated with insulin (4.0 U/kg BW bid) or oral metformin (250 mg/kg BW), respectively. Group E rats were similarly treated with both metformin and insulin. Groups B-E were rendered diabetic by intraperitoneal injections of 65 mg/kg BW of streptozotocin. Fasting blood glucose concentrations and glucose tolerance tests were done. The animals were sacrificed by halothane overdose after 56 days, blood taken by cardiac puncture and kidneys excised and stored at -80°C for further analysis. Results: Untreated diabetic rats exhibited significant weight loss, increased polydipsia and polyuria, impaired glucose tolerance, electrolyte retention, reduced creatinine clearance and urea excretion and increased oxidative stress compared to controls, respectively. However, these were reversed by treatment with metformin and insulin. Conclusions: Metformin does not improve glycemic control in TID but exerts renoprotective effects by reducing oxidative stress in the presence of insulin. Metformin should therefore be considered for adjunct therapy with insulin in TID.

show abstract

“…[2][3][4] The complexity of the mechanisms involved in the pathogenesis of DN leads to the poor efficacy of the treatment with insulin combined with angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. 5,6 To better understanding of the mechanisms and pathological changes is critical for clinical treatment of this disease.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of leflunomide on renal lesions in a rat model if diabetic nephropathy

Zhang

et al. 2015

Renal Failure

View full text Add to dashboard Cite

Diabetic nephropathy is one of the most common chronic complications of diabetes with poor efficacy of clinical treatment. This study investigated the protective effects of leflunomide, a new immunosuppressant, on tubulointerstitial lesions in a rat model of diabetic nephropathy. Diabetes was induced with streptozotocin (STZ, 50 mg/kg) by intraperitoneal injection in male Wistar rats. Two weeks after STZ injection, diabetic rats were treated daily for 8 weeks with low (5 mg/kg) and high dose (10 mg/kg) of leflunomide, and benazepril hydrochloride (4 mg/kg) as a positive control. In diabetic rats, the 24-h urine volume, urine protein and microalbumin, blood creatinine and urea nitrogen significantly increased, which were attenuated by leflunomide treatment in a dose-dependent manner (all p50.05). The increase of kidney weight/body weight and the histopathological findings of tubulointerstitial lesion in diabetic rats were mitigated by leflunomide treatment. Immunohistochemistry study and real-time polymerase chain reaction results demonstrated that osteopontin (OPN), transforming growth factor beta 1 (TGF-b1), a-smooth muscle actin and CD68 expression in the renal tubulointerstitial region were significantly increased in the diabetic rats, while these increases were inhibited by leflunomide treatment. These findings suggest that leflunomide protects the kidney injury of diabetic rats might through its inhibition of OPN/TGF-b1 mediated extracellular matrix deposition and tubulointerstitial fibrosis, as well as its inhibition on tubular epithelialmyofibroblast transdifferentiation.

show abstract

Management of diabetic nephropathy: Recent progress and future perspective

Cited by 132 publications

References 134 publications

WITHDRAWN: Association between ADIPOQ rs2241766 polymorphism and risk of diabetic nephropathy

WITHDRAWN: Association between ADIPOQ rs2241766 polymorphism and risk of diabetic nephropathy

Metformin with insulin relieves oxidative stress and confers renoprotection in type 1 diabetes in vivo

Protective effects of leflunomide on renal lesions in a rat model if diabetic nephropathy

Contact Info

Product

Resources

About