Renal function in diabetic nephropathy

Dabla, Pradeep Kumar

doi:10.4239/wjd.v1.i2.48

Cited by 246 publications

(181 citation statements)

References 75 publications

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“…Even minimal glomerular damage will result in a significant increase in serum Cys C and b2-MG levels, causing disease progression. 16 Some papers indicated that the great majority of diabetic patients had a significant increase in serum Cys C and b2-MG. The serum levels of both Cys C and b2-MG increased significantly in early stage of DN.…”

Section: Discussionmentioning

confidence: 99%

The role of DJ-1/Nrf2 pathway in the pathogenesis of diabetic nephropathy in rats

et al. 2015

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Diabetic nephropathy (DN) is one of the most common chronic complications of diabetes, which is associated with an increased oxidative stress induced by hyperglycemia and alterations in DJ-1/NF-E2-related factor-2 (Nrf2) pathway. In the present study, we investigated the role and the proper time nodes of DJ-1/Nrf2 pathway in the pathogenesis of DN. Diabetes mellitus (DM) model of rats was induced by intraperitoneal injection of streptozotocin (STZ) on male Sprague-Dawley (SD) rats. Then, the diabetic rats were divided into 4, 8 and 12 weeks groups. As early at 4 weeks of diabetes, renal histologic evaluation score, cystatin C (Cys C), b2-microglobulin (b2-MG) and malondialdehyde (MDA) levels were increased, and total antioxidative capacity (T-AOC) level was decreased as compared with that in the control group. The protein expressions of DJ-1, NF-E2-related factor-2 (Nrf2) and heme oxygenase-1 (HO-1) were upregulated compared with the control group from 4 weeks and further increased with the progression of DM. The protein expressions of DJ-1, Nrf2 and HO-1 in renal tissues have good line correlations with renal histologic evaluation score, respectively. Taken together, these results suggested that the activation of DJ-1/Nrf2 pathway was involved in the pathogenesis of diabetic nephropathy in rats.ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

The role of DJ-1/Nrf2 pathway in the pathogenesis of diabetic nephropathy in rats

et al. 2015

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“…38 The increase in serum creatinine, blood urea nitrogen, and protein in urine has been documented to be index of nephropathy. 40 In the present study, administration of alloxan monohydrate significantly increased the serum creatinine, blood urea 41 and concentration of protein in urine. 42 A decrease in serum nitrite concentration and increase in ratio of kidney weight/body weight has been reported to be a marker of DN.…”

Section: Discussionmentioning

confidence: 78%

Role of Brain Angiotensin (1-7) In Chronic Hyperglycaemia Induced Nephropathy in Wistar Rats

Shakya¹,

Goyal²,

Semwal³

et al. 2017

IJPER

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Objective: Ang (1-7) recognised as a biologically active component of renin angiotensin system (RAS). It has been documented that peripheral activity of Ang (1-7) gets reduced during diabetic nephropathy (DN) which is one of the most common cause of end stage renal disease. Peripheral activity of RAS is regulated by brain RAS. The purpose of present study is to investigate the role of brain angiotensin (1-7) in chronic hyperglycemia induced nephropathy in wistar rats. Material and methods: Diabetes mellitus (DM) is induced by single dose of alloxan (120 mg/kg: i.p.). The biochemical parameters related to DN was estimated using commercially available kits. Results: Diabetic rat, after 8 weeks of alloxan administration shows elevated serum creatinine, blood urea nitrogen, protein in urine, kidney weight/body weight and deceased level of serum nitrite. However, intracerebroventricular treatment with Ang (1-7) (4.8 µg/day) and valsartan (100 nmol/ day) (which do not cross blood brain barrier) alone and combination of Ang (1-7) and valsartan for 2 weeks markedly attenuated these changes and increased serum nitrite in DN induced rats. Conclusion: The finding of this study suggests that brain Ang (1-7) play a vital role in controlling the peripheral activity of RAS in diabetic nephropathy which may be due to the decreased central sympathetic outflow and peripheral activity of Ang II.

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“…A test can be done to measure the amount of urea nitrogen in the blood. In kidney disease, these substances are not excreted normally, and so they accumulate in the body, thus causing an increase in blood levels of urea [11]. The development of CRF as a consequence of diabetes mellitus was found to be related to disorders of vasodilatation and metabolic abnormalities that mediated by endothelial derived nitric oxide.…”

Section: Discussionmentioning

confidence: 99%

Chronic renal failure secondary to diabetes mellitus

Mahmoud¹,

Mahmoud²,

Fagiri³

2017

IJCRI

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International Journal of Case Reports and Images (IJCRI) is an international, peer reviewed, monthly, open access, online journal, publishing high-quality, articles in all areas of basic medical sciences and clinical specialties.Aim of IJCRI is to encourage the publication of new information by providing a platform for reporting of unique, unusual and rare cases which enhance understanding of disease process, its diagnosis, management and clinico-pathologic correlations. Diabetes mellitus is the most common cause of renal failure. Even when diabetes is controlled, the disease can lead to chronic renal failure (CRF). A patient with chronic renal failure always undergoes either dialysis or renal transplantation, which both are very expensive financially. Testing in patients with CRF typically includes a complete blood count (CBC), basic metabolic panel, and urinalysis, with calculation of renal function. Renal ultrasonography is the initial imaging modality in the diagnosis of CRF, where features of atrophied, echogenic kidneys with poor corticomedullary differentiation always observed. The aim of this case report is to focus on the role of ultrasound imaging in the workup of chronic renal failure. Case Report: A 48-year-old male, with 22 years history of type 2 diabetes mellitus complains of CRF primarily due to diabetic nephropathy, was admitted to the hospital for dialysis. The patient had been undergoing hemodialysis three times per week. On physical examination he was in a fair condition. Laboratory investigations revealed an increased level of creatinine 6.9 mg/dl (normal value <1.5 mg/dl) and blood urea nitrogen (BUN) 49 mg/dl (normal value 10-20 mg/dl) were noted. Normal levels for sodium 140 mg/dl (normal value 136-145 mg/ dl) was detected, but there was an increased level of potassium 7 mg/dl (normal value 3.5-5 mg/dl), calcium 11.9 mg/dl (normal value 9-10.5 mg/dl), and phosphorus 5.8 mg/dl (normal value 3-4.5 mg/dl). Abdominal ultrasound scanning presented sonographic features compatible with CRF as bilateral renal atrophy, poor corticomedullary differentiation, and increased renal echogenicity. Conclusion: Morphological parameters as bilateral renal size, parenchymal thickness, and renal echogenicity can influence further diagnostic and therapeutic interventions of CRF.

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Renal function in diabetic nephropathy

Cited by 246 publications

References 75 publications

The role of DJ-1/Nrf2 pathway in the pathogenesis of diabetic nephropathy in rats

The role of DJ-1/Nrf2 pathway in the pathogenesis of diabetic nephropathy in rats

Role of Brain Angiotensin (1-7) In Chronic Hyperglycaemia Induced Nephropathy in Wistar Rats

Chronic renal failure secondary to diabetes mellitus

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