Halting the Progression of Chronic Nephropathy

Campbell, Ruth; Ruggenenti, Piero; Remuzzi, Giuseppe

doi:10.1097/01.asn.0000032522.29672.0a

Cited by 47 publications

(48 citation statements)

References 60 publications

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“…DN affects approximately one third of people who suffer with type 1 or type 2 diabetes [14]. Although the time of clinical debut of DN varies between patients with T1DM and T2DM, clinical and histological progressions in both conditions are quite similar [15].Changes in the filtration unit begin soon after DM onset, and take place "silently" for a long time before the appearance of the first clinical signs of the disease. In susceptible patients DN follows a well-known physiopathological course micro albuminuria is the earliest clinically detectable sign of kidney damage.…”

Section: Discussion:-mentioning

confidence: 99%

The Role of Stem Cell Injection in Amelioration of Diabetic Nephropathy in Experimentally Induced Diabetic Rats.

Fawzy¹,

Gharib²,

Shalaby³

et al. 2016

IJAR

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Background:-Stem cell therapy holds a great promise for the repair of injured tissues and organs, including the kidney.The aim of the present study was to study the effect of human adipose derived mesenchymal stem cells (HADMSCs) on experimental diabetic nephropathy (DN) in a rat model. Materials and methods:-Rats were divided into controls, DN group, early stage DN rats receiving HADMSCs and late stages DN rats received HADMSCs. The HADMSCs were injected once in rat tail vein as a single dose of 1X10 6 cells in 1 ml PBS. At the end of the experiment, each group was subjected to 24 hour urine collection for urinary albumin,urinary N-acetyl B-D glucosaminidase (NAG),creatinine clearance measurements and blood sampling through retro-orbital vein for blood glucose, serum urea, and serum creatinine estimation. This was followed by scarification of all groups to obtain the kidneys for histopathological examination and DNA extraction. Results:-HADMSCs therapy significantly improved 24 hour urine collection for urinary albumin, urinary NAG, blood glucose,serum ureaand serum creatinine levels in HADMSCs recipient rats when compared to DN group. Histopathological examination showed minimal degeneration in renal tubules and normal tufts of glomeruli after injection of HADMSCs in DN rats. Interestingly, treated rats at early DN stages showed better results than treated rats at late DN stages. Lastly, the HADMSCs were engrafted into the rat renal tissue. Conclusion:-The current study suggests that intravenous injection of HADMSCs into rats with DN improved renal function and regenerating kidney tissues. HADMSCs accomplish this function by decreasing blood glucose levels or by direct effect due to their homing into the affected kidney.Furthermore, treated rats at early DN stages showed better results than treated rats at late DN stages.

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Section: Discussion:-mentioning

confidence: 99%

The Role of Stem Cell Injection in Amelioration of Diabetic Nephropathy in Experimentally Induced Diabetic Rats.

Fawzy¹,

Gharib²,

Shalaby³

et al. 2016

IJAR

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“…Angiotensin 1-7 is known to act as a vasodepressor agent and is involved in apoptosis and growth arrest. The protein product of the c-mas gene is a receptor for angiotensin [1][2][3][4][5][6][7]. Further experimental studies show anti-inflammatory and antifibrotic effects of angiotensin 1-7.…”

Section: Generation Of Angii and Other Peptidesmentioning

confidence: 99%

“…This article highlights some of the more recent molecular insights into the complexity of the RAAS and its role in chronic renal disease. Because of space restriction, the many clinical studies that deal with the RAAS are not covered, and the reader is referred to excellent reviews (2,3).…”

mentioning

confidence: 99%

Renin-Angiotensin-Aldosterone System and Progression of Renal Disease

Rüster

Wolf

2006

Journal of the American Society of Nephrology

413

320

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Inhibition of the renin-angiotensin-aldosterone system (RAAS) is one of the most powerful maneuvers to slow progression of renal disease. Angiotensin II (AngII) has emerged in the past decade as a multifunctional cytokine that exhibits many nonhemodynamic properties, such as acting as a growth factor and profibrogenic cytokine, and even having proinflammatory properties. Many of these deleterious functions are mediated by other factors, such as TGF-␤ and chemoattractants that are induced in the kidney by AngII. Moreover, understanding of the RAAS has become much more complex in recent years with the identification of novel peptides (e.g., AngIV) that could bind to specific receptors, elucidating deleterious effects, and non-angiotensin-converting enzyme (ACE)-mediated generation of AngII. The ability of renal cells to produce AngII in a concentration that is much higher than what is found in the systemic circulation and the observation that aldosterone may be engaged directly in profibrogenic processes independent of hypertension have added to the complexity of the RAAS. Even renin has now been identified to have a "life on its own" and mediates profibrotic effects via binding to specific receptors. Finally, drugs that are used to block the RAAS, such as ACE inhibitors or certain AngII type 1 receptor antagonists, may have properties on cells independent of AngII (ACE inhibitor-mediated outside-inside signaling and peroxisome proliferatoractivated receptor-␥ stimulatory effects of certain sartanes). Although blockade of the RAAS with ACE inhibitors, AngII type 1 receptor antagonists, or the combination of both should be part of every strategy to slow progression of renal disease, a better understanding of the novel aspects of the RAAS should contribute to the development of innovative strategies not only to completely halt progression but also to induce regression of human renal disease.

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“…14,15 The angiotensin converting enzyme inhibitor and angiotensin receptor blocker are agents that block the activated RAAS. However, the effectiveness of these treatments is limited due to compensatory increases in plasma renin levels that lead to adjustments in angiotensin production and conversion.…”

Section: Introductionmentioning

confidence: 99%

Aliskiren reduced renal fibrosis in mice with chronic ischemic kidney injury—beyond the direct renin inhibition

et al. 2011

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Chronic renal ischemia leads to renal fibrosis and atrophy. Activation of the renin-angiotensin-aldosterone system is one of the main mechanisms driving chronic renal ischemic injury. The aim of the present study was to define the effect of aliskiren in chronic ischemia of the kidney. Two-kidney, one-clip mice were used to study chronic renal ischemia. Aliskiren significantly lowered the blood pressure in mice with renal artery constriction (92.1±1.1 vs. 81.0±1.8 mm Hg, Po0.05). Renin expression was significantly increased in ischemic kidneys when treated with aliskiren. In addition, (Pro)renin receptor expression was decreased by aliskiren in ischemic kidneys. Aliskiren treatment significantly increased klotho expression and reduced the expression of fibrogenic cystokines, caspase-3 and Bax in ischemic kidneys. Histological examination revealed that aliskiren significantly reduced the nephrosclerosis score (4.5±1.9 vs. 7.3±0.4, Po0.05). Immunofluorescence staining also showed that aliskiren decreased the deposition of interstitial collagen I in ischemic kidneys. In conclusion, direct renin inhibition significantly reduced renal fibrosis and apoptosis following chronic renal ischemia.

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Halting the Progression of Chronic Nephropathy

Cited by 47 publications

References 60 publications

The Role of Stem Cell Injection in Amelioration of Diabetic Nephropathy in Experimentally Induced Diabetic Rats.

The Role of Stem Cell Injection in Amelioration of Diabetic Nephropathy in Experimentally Induced Diabetic Rats.

Renin-Angiotensin-Aldosterone System and Progression of Renal Disease

Aliskiren reduced renal fibrosis in mice with chronic ischemic kidney injury—beyond the direct renin inhibition

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