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 Kidney organoid systems for studies of immune-mediated kidney diseases: challenges and opportunities

2021 ◽  
Author(s):  
Melissa C. Stein ◽  
Fabian Braun ◽  
Christian F. Krebs ◽  
Madeleine J. Bunders
Keyword(s):  
Kidney Diseases ◽  
Three Dimensional ◽  
Renal Tissue ◽  
Chronic Kidney Diseases ◽  
Immune Mediated ◽  
Primary Epithelial Cell ◽  
Challenges And Opportunities ◽  
Underlying Mechanisms ◽  
Global Population

AbstractAcute and chronic kidney diseases are major contributors to morbidity and mortality in the global population. Many nephropathies are considered to be immune-mediated with dysregulated immune responses playing an important role in the pathogenesis. At present, targeted approaches for many kidney diseases are still lacking, as the underlying mechanisms remain insufficiently understood. With the recent development of organoids—a three-dimensional, multicellular culture system, which recapitulates important aspects of human tissues—new opportunities to investigate interactions between renal cells and immune cells in the pathogenesis of kidney diseases arise. To date, kidney organoid systems, which reflect the structure and closer resemble critical aspects of the organ, have been established. Here, we highlight the recent advances in the development of kidney organoid models, including pluripotent stem cell-derived kidney organoids and primary epithelial cell-based tubuloids. The employment and further required advances of current organoid models are discussed to investigate the role of the immune system in renal tissue development, regeneration, and inflammation to identify targets for the development of novel therapeutic approaches of immune-mediated kidney diseases.

scholarly journals Apoptosis-Associated Speck-Like Protein Containing a CARD Deletion Ameliorates Unilateral Ureteral Obstruction Induced Renal Fibrosis and Endoplasmic Reticulum Stress in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yao Xu ◽  
Yuqing Liu ◽  
Honglei Guo ◽  
Wei Ding
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Renal Fibrosis ◽  
Interstitial Fibrosis ◽  
Pathological Feature ◽  
Ureter Obstruction ◽  
Underlying Mechanisms ◽  
Stage Renal Disease ◽  
End Stage

Inflammation might be one of the essential underlying mechanisms of renal fibrosis, which is considered a key pathological feature of end-stage renal disease and is closely associated with proteinuria and decreased renal function. Apoptosis-associated speck-like protein containing a CARD (ASC), identified as the central structure of inflammasome, is involved in the progression of interstitial fibrosis; however, its signal transduction pathways remain unclear. In the present study, we performed unilateral ureter obstruction (UUO) in both wild-type and ASC deletion mice to determine the contribution of ASC to renal fibrosis. Compared with control groups, UUO significantly induced renal fibrosis and collagen deposition, as evidenced by photomicrographs. ASC deletion attenuated renal injury, reduced cell infiltration and the release of inflammatory cytokines, protected against apoptosis, and downregulated the PRKR-like endoplasmic reticulum kinase (PERK) pathway of endoplasmic reticulum (ER) stress. Our data identify a novel role of ASC in the regulation of renal fibrosis and ER stress after UUO, strongly indicating that ASC could serve as an attractive target in the treatment of chronic kidney disease.

scholarly journals MAPK/ERK Signaling in Renal Differentiation

2019 ◽  
Author(s):  
Kristen Kurtzeborn ◽  
Hyuk Nam Kwon ◽  
Satu Kuure
Keyword(s):  
Kidney Diseases ◽  
Branching Morphogenesis ◽  
Erk Signaling ◽  
Ureteric Bud ◽  
Final Size ◽  
Chronic Kidney Diseases ◽  
Stage Renal Disease ◽  
End Stage ◽  
Erk Activity ◽  
Renal Differentiation

Congenital anomalies of the kidney and urinary tract (CAKUT) are common birth defects deriving from abnormalities in renal differentiation during embryogenesis. CAKUT is the major cause of end-stage renal disease and chronic kidney diseases in children, but its genetic causes remain largely unresolved. Here we discuss advances in the understanding of how MAPK/ERK activity contributes to the regulation of ureteric bud branching morphogenesis, which dictates the final size, shape, and nephron number of the kidney. Recent studies also demonstrate that MAPK/ERK pathway is directly involved in nephrogenesis, regulating both the maintenance and differentiation of the nephrogenic mesenchyme. Interestingly, aberrant MAPK/ERK signaling is linked to many cancers, and recent studies suggest it also plays a role in the most common pediatric renal cancer, Wilms’ tumor.

scholarly journals Chronic Kidney Disease in Community

2020 ◽  
pp. 75-78
Author(s):  
Dimitra Paikopoulou
Keyword(s):  
Kidney Disease ◽  
Kidney Diseases ◽  
The United States ◽  
World Health ◽  
Chronic Kidney Diseases ◽  
Real Increase ◽  
Stage Renal Disease ◽  
End Stage ◽  
Developed World ◽  
Esrd Patients

The world's disease profile is changing, and chronic diseases now account for the majority of global morbidity and mortality. The causes of chronic kidney diseases (CKD) reflect this change. The increase in prevalence of CKD is partly due to a real increase in its frequency (due to the increase in the average age of people surviving), better detection of CKD, but also to the increasing incidence of diabetes and hypertension among people today, not only within the developed world, but also increasingly within the emerging world. Furthermore, hypertension, smoking, hypercholesterolemia, and obesity, currently among the World Health Organization’s (WHO’s) top 10 global health risks, are strongly associated with CKD. The factors, together with increasing diabetes prevalence and an aging population, will result in significant global increases in chronic kidney diseases (CKD) end stage renal disease (ESRD) patients. There are approximately 275000 patients with ESRD in the United States and it is estimated that an additional 8 million US adults have kidney disease (defined as a glomerular filtration rate [GFR] of 60 mL/min per 1.73 m2). Because kidney disease often progresses to ESRD and its attendant complications, the identification of precursors of kidney disease is important, with the belief that interventions will prevent or delay the progression to ESRD.

scholarly journals Role of (pro)renin receptor in albumin overload-induced nephropathy in rats

2018 ◽  
Vol 315 (6) ◽  
pp. F1759-F1768 ◽  
Author(s):  
Hui Fang ◽  
Mokan Deng ◽  
Linlin Zhang ◽  
Aihua Lu ◽  
Jiahui Su ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Interstitial Fibrosis ◽  
Kidney Diseases ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Chronic Kidney Diseases ◽  
Tubular Necrosis ◽  
Intrarenal Ras ◽  
End Stage

Proteinuria is not only a common feature of chronic kidney diseases (CKD) but also an independent risk factor promoting CKD progression to end-stage renal failure. However, the underlying molecular mechanisms for protein overload-induced renal injury remain elusive. The present study examined the role of (pro)renin receptor (PRR) in pathogenesis of albumin overload (AO)-induced nephropathy and activation of the intrarenal renin-angiotensin system (RAS) in rats. Wistar rats underwent unilateral nephrectomy and were treated for 7 wk with vehicle, bovine serum albumin (5 g·kg−1·day−1via a single ip injection), alone or in conjunction with the PRR decoy inhibitor PRO20 (500 μg·kg−1·day−1via 3 sc injections). The AO rat model exhibited severe proteinuria, tubular necrosis, and interstitial fibrosis, oxidative stress, and inflammation, accompanied by elevated urinary N-acetyl-β-d-glucosaminidase activity and urinary β2-microglobulin secretion, all of which were significantly attenuated by PRO20. Urinary and renal levels of renin, angiotensinogen, and ANG II were elevated by AO and suppressed by PRO20, contrasting to largely unaltered plasma levels of the RAS parameters. The AO model also showed increased renal expression of full-length PRR and soluble PRR (sPRR) and urinary excretion of sPRR. Taken together, we conclude that PRR antagonism with PRO20 alleviates AO-induced nephropathy via inhibition of intrarenal RAS.

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 Effect of RDA Protein on Renal Function in Children with Chronic Kidney Diseases

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Afsana Khanom ◽  
Mohammed Hanif ◽  
Sabikun Naher ◽  
Sabrina Makbbul
Keyword(s):  
Renal Function ◽  
Preliminary Data ◽  
Kidney Diseases ◽  
Recommended Dietary Allowance ◽  
Total Serum ◽  
Chronic Kidney Diseases ◽  
Dietary Allowance ◽  
Increased Risk ◽  
Stage Renal Disease ◽  
End Stage

: Children with chronic kidney diseases have an increased risk of progression to end-stage renal disease, which would ultimately result in lifelong disability and shortening of lifespan. There is no effective intervention such as renal replacement therapy because of high cost and donor shortage. This study aimed to examine the effect of recommended dietary allowance (RDA) protein on chronic kidney diseases (CKD) children without dialysis to halt the progression of CKD by preventing the deterioration of the renal function. In this observational study, 30 children aged 2 - 18 years at different CKD stages without dialysis were selected as the research sample. Anthropometric measurements (namely weight and height) and laboratory assessments (namely S. creatinine. blood urea, total serum albumin, hemoglobin, serum ferritin, and CCr) were considered at the beginning of the study. Following the intervention using the RDA protein during three- and six-month periods, anthropometric and laboratory assessments were compared using the preliminary data. Weight, weight for age Z score, and body mass index (BMI) significantly increased (P < 0.05) after three and six months, compared to the preliminary data. Moreover, laboratory assessments such as Hb, S. creatinine, blood urea, and creatinine clearance rate significantly improved (P < 0.05) after three and six months of RDA protein intake without dialysis. The growth and renal function improved following the intervention with recommended dietary allowance protein in CKD children without dialysis.

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