Effects of Paricalcitol and Aliskiren Combination Therapy on Experimental Diabetic Nephropathy Model in Rats

Eren, Zehra; Günal, Mehmet Yalçın; Bakır, Elif Arı; Çoban, Jale; Çağlayan, Berrak; Ekimci, N.; Ethemoğlu, Sinem; Albayrak, Özgür; Akdeniz, Tuba; Demirel, Gülderen Yanikkaya; Kılıç, Ertuğrul; Kantarcı, Gülçin

doi:10.1159/000368471

Cited by 24 publications

(23 citation statements)

References 29 publications

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“…Furthermore, paricalcitol has been shown to attenuate contrast-induced nephropathy by suppression of renal and systemic oxidative stress. 8 Eren et al 9 also recently reported that paricalcitol improves albuminuria and intrarenal oxidative stress in diabetic rats. These findings that address the pleiotropic effects of paricalcitol and our findings suggest that paricalcitol may well have benefits in the chronic as well as acute settings.…”

Section: Discussionmentioning

confidence: 94%

“…[5][6][7] Recently, it has been shown that paricalcitol has anti-oxidant effects on renal tissue and suppresses the reninangiotensin system (RAS) in diabetic kidney. 8,9 Fryer et al 10 demonstrated that paricalcitol suppresses renal renin expression. It has also been recently reported that the combination of paricalcitol and enalapril treatment ameliorates oxidative injury by suppressing reactive oxygen species generating enzyme NADPH oxidase activity and by up regulating the antioxidant defense system in a uremic rat model of atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

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Paricalcitol may improve oxidative DNA damage on experimental amikacin-induced nephrotoxicity model

Bulut

Başbuğan

Arı³

et al. 2016

Renal Failure

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This study aimed to investigate the possible protective effect of paricalcitol on experimental amikacin-induced nephrotoxicity model in rats. Wistar albino rats (n ¼ 32) were allocated into four equal groups of eight each, the control (Group C), paricalcitol (Group P), amikacin-induced nephrotoxicity (Group A), and paricalcitol-treated amikacin-induced nephrotoxicity (Group A þ P) groups. Paricalcitol was given intra-peritoneally at a dose of 0.4 lg/kg/d for 5 consecutive days prior to induction of amikacin-induced nephrotoxicity. Intra-peritoneal amikacin (1.2 g/kg) was used to induce nephrotoxicity at day 4. Renal function parameters, oxidative stress biomarkers, oxidative DNA damage (8-hydroxy-2 0 -deoxyguanosine/deoxyguanosine ratio), kidney histology, and vascular endothelial growth factor (VEGF) immunoexpression were determined. Group A þ P had lower mean fractional sodium excretion (p < 0.001) as well as higher creatinine clearance (p ¼ 0.026) than the amikacin group (Group A). Renal tissue malondialdehyde levels (p ¼ 0.035) and serum 8-hydroxy-2 0 -deoxyguanosine/deoxyguanosine ratio (8-OHdG/dG ratio) (p < 0.001) were significantly lower; superoxide dismutase (p ¼ 0.024) and glutathione peroxidase (p ¼ 0.007) activities of renal tissue were significantly higher in group A þ P than in group A. The mean scores of tubular necrosis (p ¼ 0.024), proteinaceous casts (p ¼ 0.038), medullary congestion (p ¼ 0.035), and VEGF immunoexpression (p ¼ 0.018) were also lower in group A þ P when compared with group A. This study demonstrates the protective effect of paricalcitol in the prevention of amikacin-induced nephrotoxicity in an experimental model. Furthermore, it is the first study to demonstrate that paricalcitol improves oxidative DNA damage in an experimental acute kidney injury model. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Paricalcitol may improve oxidative DNA damage on experimental amikacin-induced nephrotoxicity model

Bulut

Başbuğan

Arı³

et al. 2016

Renal Failure

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“…[152] Low level of vitamin D are linked to diabetic nephropathy [153] Vitamin D receptor activator such as paricalcitol is found to be interesting. [154] Paricalcitol 1) Reduces proteinuria in diabetic patient [155] 2) Reconfirmed in VITAL study-albuminuria was reduced instead of proteinuria [157] 3) Combination with aliskiren can reduce progression of diabetic nephropathy [158] 4) Addition of adequate RAAS blocker is necessary 5) Calcitriol also have same effect [159] …”

Section: ] Vitamin D Receptor Activator [152-159]mentioning

confidence: 99%

Drugs for Diabetic Nephropathy- Full Review

Soni¹

2017

WJPPS

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“…klotho also exerts inhibitory action on renal fibrosis and cardio-vascular atherosclerosis in high oxidative stress conditions such as hyperglycemia and DM ( [41] showed that vitamin D/VDR signaling in podocytes plays a critical role in the kidney protection from diabetic injury and reconstitution of VDR null mice with the human VDR (hVDR) transgene in podocytes rescued the severe diabetes-related renal damage. Experimental studies showed that administration of a selective vitamin D analogue like Paricalcitol reduces albuminuria [42].…”

Section: Iron and Oxidative Stressmentioning

confidence: 99%

“…Recently a review by Mary Choi and her group [42] showed that the accumulation of damaged proteins and organelles is associated with the pathogenesis of DN. Autophagy pathway in the kidney is activated under high glucose conditions, with increased oxidative stress via free radicals in PCT cells, and in podocytes.…”

Section: Autophagymentioning

confidence: 99%

New Insights into the Interaction between Increased Iron-Deposition in the Kidney and Vitamin D/Klotho Axis in Diabetic Nephropathy

Nakhoul¹,

Dahan²,

Farber³

et al. 2016

J Clin Exp Nephrol

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Diabetic Nephropathy (DN), a chronic complication of diabetes, is characterized by glomerular hyper-trophy, albuminuria, decreased glomerular filtration rate, and renal fibrosis resulting in end stage renal disease. Diabetic Nephropathy is one of the major micro-vascular complications of long term diabetes mellitus. The pathogenesis of diabetic nephropathy is multifactorial. For many years it was consensus among scientists that hyper filtration and activation of the renin angiotensin aldosterone system is enough to develop kidney injury (diabetic nephropathy). The goal of this review is to describe new pathways involved in the pathogenesis of diabetic nephropathy. Recent studies showed that new pathways are involved. One of these pathways is the increased production of free radicals via oxidative stress due to increased iron deposition in the lysosomes of the proximal convolute tubules. The increased oxidative stress in the lysosomes of the proximal convolute tubules can down regulate Klotho Protein expression and the synthesis of active vitamin D. The decrease in Klotho, active vitamin D and his receptor can aggravate the progression of diabetic nephropathy. AGEs-induced increased oxidative stress, also activated PKC-induced increased production of cytokines, chemokine's and different inflammatory and apoptotic signals.Another pathway involved in the pathogenesis of diabetic nephropathy is the altered autophagy process via hyperglycaemia induced activation of the mTORC1 in this review we will concentrate on new data published recently on these pathways involved in the pathogenesis of diabetic nephropathy and new treatments proposed.

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Effects of Paricalcitol and Aliskiren Combination Therapy on Experimental Diabetic Nephropathy Model in Rats

Cited by 24 publications

References 29 publications

Paricalcitol may improve oxidative DNA damage on experimental amikacin-induced nephrotoxicity model

Paricalcitol may improve oxidative DNA damage on experimental amikacin-induced nephrotoxicity model

Drugs for Diabetic Nephropathy- Full Review

New Insights into the Interaction between Increased Iron-Deposition in the Kidney and Vitamin D/Klotho Axis in Diabetic Nephropathy

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