Kidney Failure Stem Cell Treatment

Kidney Failure Stem Cell Therapy

Stem Cell Treatments for Kidney Failure are now available at SIRM

Renal failure or kidney failure (formerly called renal insufficiency) describes a medical condition in which the kidneys fail to adequately filter toxins and waste products from the blood. Two forms:

  • acute (acute kidney injury)
  • chronic (chronic kidney disease)
  • a number of other diseases or health problems may cause either form of renal failure to occur.

Renal failure is described as a decrease in glomerular filtration rate. Biochemically, renal failure is typically detected by an elevated serum creatinine level.

Problems frequently encountered in kidney malfunction include abnormal fluid levels in the body, deranged acid levels, abnormal levels of potassium, calcium, phosphate, and (in the longer term) anemia as well as delayed healing in broken bones. Depending on the cause, hematuria (blood loss in the urine) and proteinuria (protein loss in the urine) may occur. Long-term kidney problems have significant repercussions on other diseases, such as cardiovascular disease.Kidney Failure Stem Cell Treatment

 

 

 

 

 

 

 

Stem Cell Treatments for Kidney Failure at SIRM

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Related Articles CRISPR/Cas9-mediated mutation of PHEX in rabbit recapitulates human X-linked hypophosphatemia (XLH). Hum Mol Genet. 2016 Jul 01;25(13):2661-2671 Authors: Sui T, Yuan L, Liu H, Chen M, Deng J, Wang Y, Li Z, Lai L Abstract X-linked hypophosphatemia (XLH) is the most common cause of inheritable rickets, with an incidence of 1/20 000 in humans. Inactivation or mutation of the gene PHEX, a phosphate-regulating endopeptidase, leads to hypophosphatemia and defective bone mineralization in XLH patients. Presently, there is no adequate animal model for safety assessments of physiotherapies and drug screening for XLH rickets. In this study, an XLH model was generated via PHEX gene knockout (KO) through coinjection of clustered regularly interspaced short palindromic repeats (CRISPR)-associated protein 9 (Cas9)/sgRNA mRNA into rabbit zygotes. The typical phenotypes of growth retardation, hypophosphatemia, elevated serum FGF23 and bone mineralization were observed in the PHEX KO rabbits but not in normal controls. In summary, for the first time, we have successfully obtained PHEX KO rabbits and recapitulated human XLH using the CRISPR/Cas9 system. This novel XLH rabbit model could be utilized as a drug screening model for XLH prevention and preclinical therapy. PMID: 27126636 [PubMed - indexed for MEDLINE]
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Related Articles An in vitro model of renal inflammation after ischemic oxidative stress injury: nephroprotective effects of a hyaluronan ester with butyric acid on mesangial cells. J Inflamm Res. 2017;10:135-142 Authors: Baraldi O, Bianchi F, Menghi V, Angeletti A, Croci Chiocchini AL, Cappuccilli M, Aiello V, Comai G, La Manna G Abstract BACKGROUND: Acute kidney injury, known as a major trigger for organ fibrosis and independent predictor of chronic kidney disease, is characterized by mesangial cell proliferation, inflammation and unbalance between biosynthesis and degradation of extracellular matrix. Therapeutic approaches targeting the inhibition of mesangial cell proliferation and matrix expansion may represent a promising opportunity for the treatment of kidney injury. An ester of hyaluronic acid and butyric acid (HB) has shown vasculogenic and regenerative properties in renal ischemic-damaged tissues, resulting in enhanced function recovery and minor degree of inflammation in vivo. This study evaluated the effect of HB treatment in mesangial cell cultures exposed to H2O2-induced oxidative stress. MATERIALS AND METHODS: Lactate dehydrogenase release and caspase-3 activation were measured using mesangial cells prepared from rat kidneys to assess necrosis and apoptosis. Akt and p38 phosphorylation was analyzed to identify the possible mechanism underlying cell response to HB treatment. The relative expressions of matrix metallopeptidase 9 (MPP-9) and collagen type 1 alpha genes were also analyzed by quantitative real-time polymerase chain reaction. Cell proliferation rate and viability were measured using thiazolyl blue assay and flow cytometry analysis of cell cycle with propidium iodide. RESULTS: HB treatment promoted apoptosis of mesangial cells after H2O2-induced damage, decreased cellular proliferation and activated p38 pathway, increasing expression of its target gene MPP-9. CONCLUSION: This in vitro model shows that HB treatment seems to redirect mesangial cells toward apoptosis after oxidative damage and to reduce cell proliferation through p38 MAPK pathway activation and upregulation of MPP-9 gene expression involved in mesangial matrix remodeling. PMID: 28932127 [PubMed]
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Related Articles Endothelial progenitor cells at the interface of chronic kidney disease: from biology to therapeutic advancement. Curr Med Chem. 2017 Sep 20;: Authors: Coppolino G, Cernaro V, Placida G, Leonardi G, Basile G, Bolignano D Abstract The 'epidemic' diffusion of chronic kidney disease (CKD) needs the development of new therapeutic approaches to slow down the progression to end-stage renal disease. Endothelial Progenitor Cells (EPCs) are promising tools for the treatment of many human diseases as they promote the repair of damaged tissues. They were also suggested as therapy to repair renal tissue after an injury. Strategies using EPCs to induce a reparative process with functional restoring of a diseased kidney or to delay CKD are of two types: direct stem cells infusion or stimulating endogenous release of EPCs. Extensive and targeted controlled clinical trials should be encouraged by the data to date available from pre-clinical and clinical models of EPCs mobilization during CKD. PMID: 28933292 [PubMed - as supplied by publisher]
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