scholarly journals Recent Updates on Mesenchymal Stem Cell Based Therapy for Acute Renal Failure

2019 ◽  
Vol 13 (4) ◽  
pp. 189-199 ◽  
Author(s):  
Asmaa Missoum
Keyword(s):  
Stem Cells ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Epithelial Cells ◽  
Adult Stem Cells ◽  
Pathological Condition ◽  
Organ Transplant ◽  
Kidney Injury ◽  
Cell Based Therapy ◽  
Toxic Damage

Acute kidney injury, formerly known as acute renal failure, is a pathological condition in which ischemia or toxic damage contributes to the loss of renal proximal tubule epithelial cells. Pathophysiological events such as oxidative stress, mitochondrial dysfunction, and direct renal tubular epithelial cells toxicity are responsible for the progression of the disease. This devastating decline in renal function affects mostly patients in the intensive care units and requires costly and invasive treatments such as dialysis and organ transplant. Fortunately, recent therapies such as the use of mesenchymal stem cells (MSCs) were proven to be effective in ameliorating renal failure via paracrine and immunomodulatory mechanisms. These fibroblast-like adult stem cells that differentiate multilineagely can be isolated from dental pulps, umbilical cords, amniotic fluids, adipose tissues, and bone marrows. Depending on their sources, the therapeutical application of each MSC type has its own capacities, advantages, and drawbacks. The review discusses and compares the latest research studies on the use of different MSCs sources to treat renal failure. Concerns about the future clinical application of MSCs such as homing, toxicity, and the risk of immune rejection are also highlighted.

Administered mesenchymal stem cells protect against ischemic acute renal failure through differentiation-independent mechanisms

2005 ◽  
Vol 289 (1) ◽  
pp. F31-F42 ◽  
Author(s):  
Florian Tögel ◽  
Zhuma Hu ◽  
Kathleen Weiss ◽  
Jorge Isaac ◽  
Claudia Lange ◽  
...  
Keyword(s):  
Stem Cells ◽  
Renal Failure ◽  
Mesenchymal Stem Cells ◽  
Acute Renal Failure ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Clinical Problem ◽  
Cell Phenotype ◽  
Target Cells

Severe acute renal failure (ARF) remains a common, largely treatment-resistant clinical problem with disturbingly high mortality rates. Therefore, we tested whether administration of multipotent mesenchymal stem cells (MSC) to anesthetized rats with ischemia-reperfusion-induced ARF (40-min bilateral renal pedicle clamping) could improve the outcome through amelioration of inflammatory, vascular, and apoptotic/necrotic manifestations of ischemic kidney injury. Accordingly, intracarotid administration of MSC (∼ 106/animal) either immediately or 24 h after renal ischemia resulted in significantly improved renal function, higher proliferative and lower apoptotic indexes, as well as lower renal injury and unchanged leukocyte infiltration scores. Such renoprotection was not obtained with syngeneic fibroblasts. Using in vivo two-photon laser confocal microscopy, fluorescence-labeled MSC were detected early after injection in glomeruli, and low numbers attached at microvasculature sites. However, within 3 days of administration, none of the administered MSC had differentiated into a tubular or endothelial cell phenotype. At 24 h after injury, expression of proinflammatory cytokines IL-1β, TNF-α, IFN-γ, and inducible nitric oxide synthase was significantly reduced and that of anti-inflammatory IL-10 and bFGF, TGF-α, and Bcl-2 was highly upregulated in treated kidneys. We conclude that the early, highly significant renoprotection obtained with MSC is of considerable therapeutic promise for the cell-based management of clinical ARF. The beneficial effects of MSC are primarily mediated via complex paracrine actions and not by their differentiation into target cells, which, as such, appears to be a more protracted response that may become important in late-stage organ repair.

ACUTE KIDNEY INJURY IN ELDERLY PATIENTS

2019 ◽  
Vol 72 (8) ◽  
pp. 1466-1472
Author(s):  
Grażyna Kobus ◽  
Jolanta Małyszko ◽  
Hanna Bachórzewska-Gajewska
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Elderly Patients ◽  
Older Patients ◽  
Age Groups ◽  
Kidney Injury ◽  
The Elderly ◽  
Younger Patients ◽  
Common Cause

Introduction: In the elderly, impairment of kidney function occurs. Renal diseases overlap with anatomic and functional changes related to age-related involutionary processes. Mortality among patients with acute renal injury is approximately 50%, despite advances in treatment and diagnosis of AKI. The aim: To assess the incidence of acute kidney injury in elderly patients and to analyze the causes of acute renal failure depending on age. Materials and methods: A retrospective analysis included medical documentation of patients hospitalized in the Nephrology Clinic during the 6-month period. During this period 452 patients were hospitalized in the clinic. A group of 77 patients with acute renal failure as a reason for hospitalization was included in the study. Results: The prerenal form was the most common cause of AKI in both age groups. In both age groups, the most common cause was dehydration; in the group of patients up to 65 years of age, dehydration was 29.17%; in the group of people over 65 years - 43.39%. Renal replacement therapy in patients with AKI was used in 14.29% of patients. In the group of patients up to 65 years of age hemodialysis was 16.67% and above 65 years of age. -13.21% of patients. The average creatinine level in the group of younger patients at admission was 5.16 ± 3.71 mg / dl, in the group of older patients 3.14 ± 1.63 mg / dl. The size of glomerular filtration GFR in the group of younger patients at admission was 21.14 ± 19.54 ml / min, in the group of older patients 23.34 ± 13.33 ml / min. Conclusions: The main cause of acute kidney injury regardless of the age group was dehydration. Due to the high percentage of AKI in the elderly, this group requires more preventive action, not only in the hospital but also at home.

scholarly journals Human Adult Stem Cells Maintain a Constant Phenotype Profile Irrespective of Their Origin, Basal Media, and Long Term Cultures

2015 ◽  
Vol 2015 ◽  
pp. 1-29 ◽  
Author(s):  
Indumathi Somasundaram ◽  
Rashmi Mishra ◽  
Harikrishnan Radhakrishnan ◽  
Rajkumar Sankaran ◽  
Venkata Naga Srikanth Garikipati ◽  
...  
Keyword(s):  
Stem Cells ◽  
Adult Stem Cells ◽  
Expression Profiles ◽  
Subcutaneous Fat ◽  
Adult Stem Cell ◽  
Phenotypic Marker ◽  
Human Adult ◽  
Cell Based Therapy ◽  
Basal Media

The study aims to identify the phenotypic marker expressions of different human adult stem cells derived from, namely, bone marrow, subcutaneous fat, and omentum fat, cultured in different media, namely, DMEM-Low Glucose, Alpha-MEM, DMEM-F12 and DMEM-KO and under long term culture conditions (>P20). We characterized immunophenotype by using various hematopoietic, mesenchymal, endothelial markers, and cell adhesion molecules in the long term cultures (Passages-P1, P3, P5, P9, P12, P15, and P20.) Interestingly, data revealed similar marker expression profiles irrespective of source, basal media, and extensive culturing. This demonstrates that all adult stem cell sources mentioned in this study share similar phenotypic marker and all media seem appropriate for culturing these sources. However, a disparity was observed in the markers such as CD49d, CD54, CD117, CD29, and CD106, thereby warranting further research on these markers. Besides the aforesaid objective, it is understood from the study that immunophenotyping acts as a valuable tool to identify inherent property of each cell, thereby leading to a valuable cell based therapy.

Acute Renal Failure/Kidney Injury

2013 ◽  
pp. 308-317
Author(s):  
Hazel Gibson ◽  
Gloria Hook ◽  
Rosi Simpson
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Kidney Injury

scholarly journals Amniotic fluid stem cells ameliorate cisplatin-induced acute renal failure through induction of autophagy and inhibition of apoptosis

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Ekta Minocha ◽  
Rohit Anthony Sinha ◽  
Manali Jain ◽  
Chandra Prakash Chaturvedi ◽  
Soniya Nityanand
Keyword(s):  
Stem Cells ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Amniotic Fluid ◽  
Cell Types ◽  
Treated Group ◽  
Protective Role ◽  
Protective Effects ◽  
Amniotic Fluid Stem Cells

Abstract Background We have recently demonstrated that amniotic fluid stem cells (AFSC) express renal progenitor markers and can be differentiated in vitro into renal lineage cell types, viz, juxtaglomerular and renal proximal tubular epithelial-like cells. Here, we have evaluated the therapeutic efficacy of AFSC in a cisplatin-induced rat model of acute renal failure (ARF) and investigated the underlying mechanisms responsible for their renoprotective effects. Methods ARF was induced in Wistar rats by intra-peritoneal injection of cisplatin (7 mg/kg). Five days after cisplatin injection, rats were randomized into two groups and injected with either AFSC or normal saline intravenously. On days 8 and 12 after cisplatin injection, the blood biochemical parameters, histopathological changes, apoptosis and expression of pro-apoptotic, anti-apoptotic, and autophagy-related proteins in renal tissues were studied in both groups of rats. To further confirm whether the protective effects of AFSC on cisplatin-induced apoptosis were dependent on autophagy, chloroquine, an autophagy inhibitor, was administered by the intra-peritoneal route. Results Administration of AFSC in ARF rats resulted in improvement of renal function and attenuation of renal damage as reflected by significant decrease in blood urea nitrogen, serum creatinine levels, tubular cell apoptosis as assessed by Bax/Bcl2 ratio, and expression of the pro-apoptotic proteins, viz, PUMA, Bax, cleaved caspase-3, and cleaved caspase-9, as compared to the saline-treated group. Furthermore, in the AFSC-treated group as compared to the saline-treated group, there was a significant increase in the activation of autophagy as evident by increased expression of LC3-II, ATG5, ATG7, Beclin1, and phospho-AMPK levels with a concomitant decrease in phospho-p70S6K and p62 expression levels. Chloroquine administration led to significant reduction in the anti-apoptotic effects of the AFSC therapy and further deterioration in the renal structure and function caused by cisplatin. Conclusion AFSC led to amelioration of cisplatin-induced ARF which was mediated by inhibition of apoptosis and activation of autophagy. The protective effects of AFSC were blunted by chloroquine, an inhibitor of autophagy, highlighting that activation of autophagy is an important mechanism of action for the protective role of AFSC in cisplatin-induced renal injury.

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