scholarly journals Stem cells: potential and challenges for kidney repair

2014 ◽  
Vol 306 (1) ◽  
pp. F12-F23 ◽  
Author(s):  
Marcela Herrera ◽  
Maria Mirotsou
Keyword(s):  
Stem Cells ◽  
Renal Damage ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Pathological Conditions ◽  
Emerging Therapies ◽  
Chronic Kidney Injury ◽  
Stage Renal Disease ◽  
End Stage

Renal damage resulting from acute and chronic kidney injury poses an important problem to public health. Currently, patients with end-stage renal disease rely solely on kidney transplantation or dialysis for survival. Emerging therapies aiming to prevent and reverse kidney damage are thus in urgent need. Although the kidney was initially thought to lack the capacity for self-repair, several studies have indicated that this might not be the case; progenitor and stem cells appear to play important roles in kidney repair under various pathological conditions. In this review, we summarize recent findings on the role of progenitor/stem cells on kidney repair as well as discuss their potential as a therapeutic approach for kidney diseases.

scholarly journals Antioxidants in Kidney Diseases: The Impact of Bardoxolone Methyl

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Jorge Rojas-Rivera ◽  
Alberto Ortiz ◽  
Jesus Egido
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
End Stage Renal Disease ◽  
Renal Damage ◽  
Kidney Diseases ◽  
New Drugs ◽  
Stage Renal Disease ◽  
End Stage ◽  
The Impact

Drugs targeting the renin-angiotensin-aldosterone system (RAAS) are the mainstay of therapy to retard the progression of proteinuric chronic kidney disease (CKD) such as diabetic nephropathy. However, diabetic nephropathy is still the first cause of end-stage renal disease. New drugs targeted to the pathogenesis and mechanisms of progression of these diseases beyond RAAS inhibition are needed. There is solid experimental evidence of a key role of oxidative stress and its interrelation with inflammation on renal damage. However, randomized and well-powered trials on these agents in CKD are scarce. We now review the biological bases of oxidative stress and its role in kidney diseases, with focus on diabetic nephropathy, as well as the role of the Keap1-Nrf2 pathway and recent clinical trials targeting this pathway with bardoxolone methyl.

scholarly journals PROTON PUMP INHIBITORS AND THE RISK OF CHRONIC KIDNEY DISEASES: A CRITICAL REVIEW

2020 ◽  
pp. 11-14
Author(s):  
SHAREEF J. ◽  
SRIDHAR S. B. ◽  
SHARIFF A.
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
End Stage Renal Disease ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Stage Renal Disease ◽  
End Stage

Proton pump inhibitors (PPIs) are most widely used medications for acid related gastrointestinal disorders. Accessible evidence based studies suggest that the increased use of PPI is linked to a greater risk of developing kidney diseases. This review aims to determine the association of kidney disease with the use of proton pump inhibitor with various study designs. PubMed, Scopus and Google Scholar databases as well as a reference list of relevant articles were systematically searched for studies by using the following search terms; ‘proton pump inhibitors’, ‘acute kidney injury’, ‘chronic kidney disease’ and ‘end stage renal disease’. Both observational and randomized controlled trials (RCTs) exploring the association of PPI use with kidney disease were eligible for inclusion. A total of 8 articles, including 9 studies (n = 794,349 participants) were identified and included in the review. Majority of the studies showed a higher risk of kidney outcomes in patients taking PPIs, with effect higher of acute kidney injury (4-to 6-fold) compared with chronic kidney disease and end stage renal disease (1.5-to 2.5-fold). However, the studies suggest that the strength of evidence is weak and could not prove causation. The risk increased considerably with the use of high dose of PPIs and prolonged duration of exposure necessitates the monitoring of renal function. Exercising vigilance in PPI use and cessation of proton pump inhibitor when there is no clear indication may be a reasonable approach to reduce the population burden of kidney diseases.

scholarly journals GLP-1 receptor agonist ameliorates obesity-induced chronic kidney injury via restoring renal lipid and energy metabolism homeostasis: revealed by metabolomics

2017 ◽  
Author(s):  
Chengshi Wang ◽  
Ling Li ◽  
Shuyun Liu ◽  
Guangneng Liao ◽  
Younan Chen ◽  
...  
Keyword(s):  
Renal Function ◽  
Energy Metabolism ◽  
High Fat Diet ◽  
Receptor Agonist ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Direct Role ◽  
Chronic Kidney Injury ◽  
Metabolomic Data

AbstractIncreasing evidence indicate that obesity is highly associated with chronic kidney disease (CKD).GLP-1 receptor (GLP-1R) agonist has shown benefits on kidney diseases, but its direct role on kidney metabolism in obesity is still not clear. This study aims to investigate the protection and metabolic modulation role of liraglutide (Lira) on kidney of obesity. Rats were induced obese by high-fat diet (HFD), and renal function and metabolism changes were evaluated by metabolomic, biological and histological methods. HFD rats exhibited metabolic disorders including elevated body weight, hyperlipidemia and impaired glucose tolerance, and remarkable renal injuries including declined renal function and inflammatory/fibrotic changes, whereas Lira significantly ameliorated these adverse effects in HFD rats. Metabolomic data showed that Lira reduced renal lipids including fatty acid residues, cholesterol, phospholipids and triglycerides, and improved mitochondria metabolites such as succinate, citrate, taurine, fumarate and NAD+ in the kidney of HDF rats. Furthermore, we revealed that Lira inhibited renal lipid accumulation by coordinating lipogenic and lipolytic signals, and rescued renal mitochondria function via Sirt1/AMPK/PGC1α pathways in HDF rats. This study suggested that Lira alleviated HFD-induced kidney injury via directly restoring renal lipid and energy metabolism, and GLP-1 receptor agonist is a promising therapy for obesity-associated CKD.

scholarly journals The Emerging Role of Innate Immunity in Chronic Kidney Diseases

2020 ◽  
Vol 21 (11) ◽  
pp. 4018
Author(s):  
Philip Chiu-Tsun Tang ◽  
Ying-Ying Zhang ◽  
Max Kam-Kwan Chan ◽  
Winson Wing-Yin Lam ◽  
Jeff Yat-Fai Chung ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Kidney Diseases ◽  
Experimental Information ◽  
Chronic Kidney Diseases ◽  
Innate Immune Signaling ◽  
Underlying Mechanisms ◽  
Stage Renal Disease ◽  
End Stage ◽  
Renal Fibrogenesis

Renal fibrosis is a common fate of chronic kidney diseases. Emerging studies suggest that unsolved inflammation will progressively transit into tissue fibrosis that finally results in an irreversible end-stage renal disease (ESRD). Renal inflammation recruits and activates immunocytes, which largely promotes tissue scarring of the diseased kidney. Importantly, studies have suggested a crucial role of innate immunity in the pathologic basis of kidney diseases. This review provides an update of both clinical and experimental information, focused on how innate immune signaling contributes to renal fibrogenesis. A better understanding of the underlying mechanisms may uncover a novel therapeutic strategy for ESRD.

scholarly journals Interleukin-22 mediated renal metabolic reprogramming via PFKFB3 to treat kidney injury

2020 ◽  
Author(s):  
Wei Chen ◽  
Yilan Shen ◽  
Jiajun Fan ◽  
Xian Zeng ◽  
Xuyao Zhang ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Kidney Damage ◽  
Metabolic Reprogramming ◽  
Protective Effects ◽  
Interleukin 22 ◽  
Renal Tubular ◽  
Stage Renal Disease ◽  
End Stage

AbstractKidney damage initiates the deteriorating metabolic states in tubule cells that lead to the development of end-stage renal disease (ESTD). Interleukin 22 (IL-22) is an effective therapeutic antidote for kidney injury via promoting kidney recovery, but little is known about the underlying molecular mechanisms. Here we first provide evidence that IL-22 attenuates kidney injury via metabolic reprogramming of renal tubular epithelial cells (TECs). Specifically, our data suggest that IL-22 regulates mitochondrial function and glycolysis in damaged TECs. Further observations indicate that IL-22 alleviates the accumulation of mitochondrial reactive oxygen species (ROS) and dysfunctional mitochondria via the induction of AMPK/AKT signaling and PFBFK3 activities. In mice, amelioration of kidney injury and necrosis and improvement of kidney functions via regulation of these metabolism relevant signaling and mitochondrial fitness of recombinant IL-22 are certificated in cisplatin induced kidney damage and diabetic nephropathy (DN) animal models. Taken together, our findings unravel new mechanistic insights into protective effects of IL-22 on kidney and highlight the therapeutic opportunities of IL-22 and the involved metabolic regulators in various kidney diseases.

scholarly journals C/EBPα deficiency in podocytes aggravates podocyte senescence and kidney injury in aging mice

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Liwen Zhang ◽  
Fangfang Zhou ◽  
Xialian Yu ◽  
Yufei Zhu ◽  
Ying Zhou ◽  
...  
Keyword(s):  
Biological Process ◽  
Critical Role ◽  
Kidney Injury ◽  
The Elderly ◽  
Chronological Aging ◽  
Tubular Cells ◽  
Complex Biological Process ◽  
Stage Renal Disease ◽  
End Stage

Abstract Kidney aging leads to an increased incidence of end-stage renal disease (ESRD) in the elderly, and aging is a complex biological process controlled by signaling pathways and transcription factors. Podocyte senescence plays a central role in injury resulting from kidney aging. Here, we demonstrated the critical role of C/EBPα in podocyte senescence and kidney aging by generating a genetically modified mouse model of chronological aging in which C/EBPα was selectively deleted in podocytes and by overexpressing C/EBPα in cultured podocytes, in which premature senescence was induced by treatment with adriamycin. Moreover, we illuminated the mechanisms by which podocyte senescence causes tubular impairment by stimulating HK-2 cells with bovine serum albumin (BSA) and chloroquine. Our findings suggest that C/EBPα knockout in podocytes aggravates podocyte senescence through the AMPK/mTOR pathway, leading to glomerulosclerosis, and that subsequent albuminuria exacerbates the epithelial–mesenchymal transdifferentiation of senescent tubular cells by suppressing autophagy. These observations highlight the importance of C/EBPα as a new potential target in kidney aging.

Monoclonal gammopathy of renal significance: when MGUS is no longer undetermined or insignificant

Blood ◽  
2012 ◽  
Vol 120 (22) ◽  
pp. 4292-4295 ◽  
Author(s):  
Nelson Leung ◽  
Frank Bridoux ◽  
Colin A. Hutchison ◽  
Samih H. Nasr ◽  
Paul Cockwell ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Kidney Transplantation ◽  
Monoclonal Gammopathy ◽  
Renal Damage ◽  
Kidney Diseases ◽  
Complete Response ◽  
Hematologic Disorder ◽  
Appropriate Therapy ◽  
Stage Renal Disease ◽  
End Stage

Abstract Multiple myeloma is the most frequent monoclonal gammopathy to involve the kidney; however, a growing number of kidney diseases associated with other monoclonal gammopathies are being recognized. Although many histopathologic patterns exist, they are all distinguished by the monoclonal immunoglobulin (or component) deposits. The hematologic disorder in these patients is more consistent with monoclonal gammopathy of undetermined significance (MGUS) than with multiple myeloma. Unfortunately, due to the limitations of the current diagnostic schema, they are frequently diagnosed as MGUS. Because treatment is not recommended for MGUS, appropriate therapy is commonly withheld. In addition to end-stage renal disease, the persistence of the monoclonal gammopathy is associated with high rates of recurrence after kidney transplantation. Preservation and restoration of kidney function are possible with successful treatment targeting the responsible clone. Achievement of hematologic complete response has been shown to prevent recurrence after kidney transplantation. There is a need for a term that properly conveys the pathologic nature of these diseases. We think the term monoclonal gammopathy of renal significance is most helpful to indicate a causal relationship between the monoclonal gammopathy and the renal damage and because the significance of the monoclonal gammopathy is no longer undetermined.

scholarly journals Roles of Inflammasomes in Inflammatory Kidney Diseases

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Jinjin Fan ◽  
Kaifeng Xie ◽  
Liqin Wang ◽  
Nuoyan Zheng ◽  
Xueqing Yu
Keyword(s):  
End Stage Renal Disease ◽  
Inflammatory Responses ◽  
Kidney Diseases ◽  
Interleukin 1 ◽  
Kidney Injury ◽  
Danger Signal ◽  
Chronic Kidney Diseases ◽  
Stage Renal Disease ◽  
End Stage ◽  
Shed Light

The immune system has a central role in eliminating detrimental factors, by frequently launching inflammatory responses towards pathogen infection and inner danger signal outbreak. Acute and chronic inflammatory responses are critical determinants for consequences of kidney diseases, in which inflammasomes were inevitably involved. Inflammasomes are closely linked to many kidney diseases such as acute kidney injury and chronic kidney diseases. Inflammasomes are macromolecules consisting of multiple proteins, and their formation initiates the cleavage of procaspase-1, resulting in the activation of gasdermin D as well as the maturation and release of interleukin-1β and IL-18, leading to pyroptosis. Here, we discuss the mechanism in which inflammasomes occur, as well as their roles in inflammatory kidney diseases, in order to shed light for discovering new therapeutical targets for the prevention and treatment of inflammatory kidney diseases and consequent end-stage renal disease.

scholarly journals A review of advances in the understanding of lupus nephritis pathogenesis as a basis for emerging therapies

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 905
Author(s):  
Susan Yung ◽  
Desmond YH Yap ◽  
Tak Mao Chan
Keyword(s):  
Lupus Nephritis ◽  
B Cell ◽  
Signaling Pathways ◽  
Lupus Erythematosus ◽  
Kidney Injury ◽  
Response To Treatment ◽  
Emerging Therapies ◽  
Specific Antigens ◽  
Stage Renal Disease ◽  
End Stage

Lupus nephritis is an important cause of both acute kidney injury and chronic kidney disease that can result in end-stage renal disease. Its pathogenic mechanisms are characterized by aberrant activation of both innate and adaptive immune responses, dysregulation of inflammatory signaling pathways, and increased cytokine production. Treatment of lupus nephritis remains a challenging issue in the management of systemic lupus erythematosus since the clinical presentation, response to treatment, and prognosis all vary considerably between patients and are influenced by ethnicity, gender, the degree of chronic kidney damage, pharmacogenomics, and non-immunological modulating factors. Elucidation of the various immunopathogenic pathways in lupus nephritis has resulted in the development of novel therapies, including biologics that target specific antigens on B lymphocytes to achieve B cell depletion, agents that modulate B cell proliferation and development, drugs that block co-stimulatory pathways, drugs that target T lymphocytes primarily, and therapies that target complement activation, signaling pathways, pro-inflammatory cytokines, and neutrophil extracellular traps. This review will discuss recent advances in the understanding of disease pathogenesis in lupus nephritis in the context of potential emerging therapies.

scholarly journals Recent Advances in Diabetic Kidney Diseases: From Kidney Injury to Kidney Fibrosis

2021 ◽  
Vol 22 (21) ◽  
pp. 11857
Author(s):  
Peir-Haur Hung ◽  
Yung-Chien Hsu ◽  
Tsung-Hsien Chen ◽  
Chun-Liang Lin
Keyword(s):  
Kidney Disease ◽  
Kidney Diseases ◽  
Epigenetic Modification ◽  
Kidney Injury ◽  
Diabetic Kidney ◽  
Kidney Fibrosis ◽  
Recent Advances ◽  
History Of ◽  
Stage Renal Disease ◽  
End Stage

Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease and end-stage renal disease. The natural history of DKD includes glomerular hyperfiltration, progressive albuminuria, declining estimated glomerular filtration rate, and, ultimately, kidney failure. It is known that DKD is associated with metabolic changes caused by hyperglycemia, resulting in glomerular hypertrophy, glomerulosclerosis, and tubulointerstitial inflammation and fibrosis. Hyperglycemia is also known to cause programmed epigenetic modification. However, the detailed mechanisms involved in the onset and progression of DKD remain elusive. In this review, we discuss recent advances regarding the pathogenic mechanisms involved in DKD.

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