scholarly journals The Role of Wnt Signalling in Chronic Kidney Disease (CKD)

Genes ◽  
2020 ◽  
Vol 11 (5) ◽  
pp. 496
Author(s):  
Soniya A. Malik ◽  
Kavindiya Modarage ◽  
Paraskevi Goggolidou
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Planar Cell Polarity ◽  
Molecular Mechanisms ◽  
Kidney Diseases ◽  
Wnt Signalling ◽  
Kidney Damage ◽  
Current Evidence ◽  
Disease Manifestation

Chronic kidney disease (CKD) encompasses a group of diverse diseases that are associated with accumulating kidney damage and a decline in glomerular filtration rate (GFR). These conditions can be of an acquired or genetic nature and, in many cases, interactions between genetics and the environment also play a role in disease manifestation and severity. In this review, we focus on genetically inherited chronic kidney diseases and dissect the links between canonical and non-canonical Wnt signalling, and this umbrella of conditions that result in kidney damage. Most of the current evidence on the role of Wnt signalling in CKD is gathered from studies in polycystic kidney disease (PKD) and nephronophthisis (NPHP) and reveals the involvement of β-catenin. Nevertheless, recent findings have also linked planar cell polarity (PCP) signalling to CKD, with further studies being required to fully understand the links and molecular mechanisms.

scholarly journals Novel biomarkers in kidney disease: roles for cilia, Wnt signalling and ATMIN in polycystic kidney disease

2016 ◽  
Vol 44 (6) ◽  
pp. 1745-1751 ◽  
Author(s):  
Paraskevi Goggolidou ◽  
Patricia D. Wilson
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Diseases ◽  
Wnt Signalling ◽  
Therapeutic Interventions ◽  
The Novel ◽  
Kidney Dialysis ◽  
Novel Biomarkers ◽  
Canonical Wnt

Biomarkers, the measurable indicators of biological conditions, are fast becoming a popular approach in providing information to track disease processes that could lead to novel therapeutic interventions for chronic conditions. Inherited, chronic kidney disease affects millions of people worldwide and although pharmacological treatments exist for some conditions, there are still patients whose only option is kidney dialysis and kidney transplantation. In the past 10 years, certain chronic kidney diseases have been reclassified as ciliopathies. Cilia in the kidney are antenna-like, sensory organelles that are required for signal transduction. One of the signalling pathways that requires the primary cilium in the kidney is Wnt signalling and it has three components such as canonical Wnt, non-canonical Wnt/planar cell olarity (PCP) and non-canonical Wnt/Ca2+ signalling. Identification of the novel role of ATM INteractor (ATMIN) as an effector molecule in the non-canonical Wnt/PCP pathway has intrigued us to investigate its potential role in chronic kidney disease. ATMIN could thus be an important biomarker in disease prognosis and treatment that might lighten the burden of chronic kidney disease and also affect on its progression.

scholarly journals Kidney Cancer and Chronic Kidney Disease: Too Close for Comfort

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1761
Author(s):  
Pedro Caetano Pinto ◽  
Cindy Rönnau ◽  
Martin Burchardt ◽  
Ingmar Wolff
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Cancer ◽  
Molecular Mechanisms ◽  
Kidney Diseases ◽  
Management Strategies ◽  
Renal Physiology ◽  
Biological Traits ◽  
Cellular Phenotypes

Kidney cancer and chronic kidney disease are two renal pathologies with very different clinical management strategies and therapeutical options. Nonetheless, the cellular and molecular mechanisms underlying both conditions are closely related. Renal physiology is adapted to operate with a limited oxygen supply, making the kidney remarkably equipped to respond to hypoxia. This tightly regulated response mechanism is at the heart of kidney cancer, leading to the onset of malignant cellular phenotypes. Although elusive, the role of hypoxia in chronic kidney diseases is emerging as related to fibrosis, a pivotal factor in decaying renal function. The present review offers a perspective on the common biological traits shared between kidney cancer and chronic kidney disease and the available and prospective therapies for both conditions.

scholarly journals GENETIC KIDNEY DISEASES AS AN UNDERECOGNIZED CAUSE OF CHRONIC KIDNEY DISEASE: THE KEY ROLE OF INTERNATIONAL REGISTRY REPORTS

2021 ◽  
Author(s):  
Roser Torra ◽  
Mónica Furlano ◽  
Alberto Ortiz ◽  
Elisabet Ars
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Diseases ◽  
Unknown Etiology ◽  
Correct Treatment ◽  
Monogenic Diseases ◽  
High Prevalence ◽  
Incorrect Diagnosis ◽  
Kidney Replacement Therapy

Abstract Inherited kidney diseases (IKDs) are among the leading causes of early-onset chronic kidney disease (CKD) and are responsible for at least 10–15% of cases of kidney replacement therapy (KRT) in adults. Pediatric nephrologists are very aware of the high prevalence of IKDs among their patients, but this is not the case for adult nephrologists. Recent publications have demonstrated that monogenic diseases account for a significant percentage of adult cases of CKD. A substantial number of these patients have received a non-specific/incorrect diagnosis or a diagnosis of CKD of unknown etiology, which precludes correct treatment, follow-up and genetic counseling. There are a number of reasons why genetic kidney diseases are difficult to diagnose in adulthood: a) adult nephrologists, in general, are not knowledgeable about IKDs, b) existence of atypical phenotypes, c) genetic testing is not universally available, d) family history is not always available or may be negative, e) lack of knowledge of various genotype–phenotype relationships, f) conflicting interpretation of the pathogenicity of many sequence variants.

scholarly journals The renal microcirculation in chronic kidney disease: novel diagnostic methods and therapeutic perspectives

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shulin Li ◽  
Fei Wang ◽  
Dong Sun
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Fibrosis ◽  
Molecular Mechanisms ◽  
Leukocyte Adhesion ◽  
Diagnostic Methods ◽  
Mesenchymal Transition ◽  
Microvascular Injury ◽  
Renal Microcirculation

AbstractChronic kidney disease (CKD) affects 8–16% of the population worldwide and is characterized by fibrotic processes. Understanding the cellular and molecular mechanisms underpinning renal fibrosis is critical to the development of new therapeutics. Microvascular injury is considered an important contributor to renal progressive diseases. Vascular endothelium plays a significant role in responding to physical and chemical signals by generating factors that help maintain normal vascular tone, inhibit leukocyte adhesion and platelet aggregation, and suppress smooth muscle cell proliferation. Loss of the rich capillary network results in endothelial dysfunction, hypoxia, and inflammatory and oxidative effects and further leads to the imbalance of pro- and antiangiogenic factors, endothelial cell apoptosis and endothelial-mesenchymal transition. New techniques, including both invasive and noninvasive techniques, offer multiple methods to observe and monitor renal microcirculation and guide targeted therapeutic strategies. A better understanding of the role of endothelium in CKD will help in the development of effective interventions for renal microcirculation improvement. This review focuses on the role of microvascular injury in CKD, the methods to detect microvessels and the novel treatments to ameliorate renal fibrosis.

scholarly journals Role of interactive survey in early diagnosis of chronic kidney diseases

2021 ◽  
Vol 38 (6) ◽  
pp. 74-82
Author(s):  
Ekaterina Alekseevna Burtseva ◽  
Vitaly Yurievich Mishlanov ◽  
Anna Vladimirovna Anikeeva ◽  
Victoria Ivanovna Selezneva ◽  
Ekaterina Petrovna Koshurnikova ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Early Diagnosis ◽  
Comparative Study ◽  
High Efficiency ◽  
Kidney Diseases ◽  
Kidney Damage ◽  
Control Group ◽  
Low Sensitivity ◽  
Healthy Persons

Objective. To conduct a comparative study of the prevalence of specific symptoms in patients with kidney damage using the automated program "Electronic Polyclinic" to optimize the algorithm for early diagnosis of chronic kidney disease. Materials and methods. 18 patients of the therapeutic unit with kidney lesions, confirmed by laboratory and instrumental studies, as well as 7 healthy persons were examined. The main problems of patients were identified by the method of interactive questioning with the help of the program "Electronic Polyclinic". Further, a statistical analysis of the data and a comparative study with the control group of healthy persons were carried out using STATISTICA 12.0 program. Results. The main symptoms of kidney damage were reliably determined and a low sensitivity of individual symptoms in the diagnosis, in contrast to the syndromic approach, was revealed. It showed that in 100 % of cases the automated program "Electronic Polyclinic" detected the syndromes, that indicates its high efficiency. An algorithm for early diagnosis of chronic kidney disease was proposed, which consists in an initial interactive survey followed by examination formulated by the computer program. Conclusions. The method of interactive survey using the automated program "Electronic Polyclinic" allows you to effectively identify the syndromes of kidney damage, makes a preliminary diagnosis and draws up a plan of examination for further confirmation of the diagnosis. Symptomatic diagnosis has a number of disadvantages including low sensitivity and specificity, so it yields to syndromic diagnosis.

scholarly journals Use of Lipid-Modifying Agents for the Treatment of Glomerular Diseases

2021 ◽  
Vol 11 (8) ◽  
pp. 820
Author(s):  
Mengyuan Ge ◽  
Sandra Merscher ◽  
Alessia Fornoni
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Recent Progress ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Glomerular Diseases ◽  
Intracellular Lipids ◽  
Lipid Modifying Agents ◽  
Made In

Although dyslipidemia is associated with chronic kidney disease (CKD), it is more common in nephrotic syndrome (NS), and guidelines for the management of hyperlipidemia in NS are largely opinion-based. In addition to the role of circulating lipids, an increasing number of studies suggest that intrarenal lipids contribute to the progression of glomerular diseases, indicating that proteinuric kidney diseases may be a form of “fatty kidney disease” and that reducing intracellular lipids could represent a new therapeutic approach to slow the progression of CKD. In this review, we summarize recent progress made in the utilization of lipid-modifying agents to lower renal parenchymal lipid accumulation and to prevent or reduce kidney injury. The agents mentioned in this review are categorized according to their specific targets, but they may also regulate other lipid-relevant pathways.

scholarly journals The role of metabolic acidosis in chronic kidney diseases

2010 ◽  
Vol 4 (3) ◽  
pp. 367-372
Author(s):  
James C. M. Chan
Keyword(s):  
Chronic Kidney Disease ◽  
Metabolic Acidosis ◽  
Kidney Disease ◽  
Kidney Diseases ◽  
Original Research ◽  
Due Diligence ◽  
Acid Base ◽  
Chronic Kidney Diseases ◽  
Balance Development

Abstract Background and objectives: This review focuses on three areas, basic acid-base physiology especially concerning hydrogen ion balance, development of acidosis in chronic kidney disease (CKD), and the consequences of acidosis. We highlight what is well established, what is less certain, and what is unknown. Method and results: The literature on acidosis in CKD were searched from 2004 to 2010 utilizing PubMed, Google Scholar, and Ovid to augment the classic work on acid base physiology over the past three decades. The original research in endogenous acid production and net acid excretion were reviewed. Touching upon the development of metabolic acidosis in CKD, we focused on the consequences of chronic metabolic acidosis on growth and other important variables. Finally, we recognize the significant issue of patients’ medical non-compliance and presented treatment strategy to counter this problem. Conclusion: The correction of acidosis in chronic kidney disease needs no advocacy. The case is made conclusively. Patient non-compliance because of the medication that needs to be taken several times a day is a problem, requiring due diligence.

scholarly journals Hyperuricemia and Progression of Chronic Kidney Disease: A Review from Physiology and Pathogenesis to the Role of Urate-Lowering Therapy

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1674
Author(s):  
Tao Han Lee ◽  
Jia-Jin Chen ◽  
Chao-Yi Wu ◽  
Chih-Wei Yang ◽  
Huang-Yu Yang
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
Disease Progression ◽  
Reciprocal Relationship ◽  
Current Evidence ◽  
Renal Disease Progression ◽  
Lowering Therapy ◽  
The Relationship

The relationship between hyperuricemia, gout, and renal disease has been investigated for several years. From the beginning, kidney disease has been considered a complication of gout; however, the viewpoints changed, claiming that hypertension and elevated uric acid (UA) levels are caused by decreased urate excretion in patients with renal impairment. To date, several examples of evidence support the role of hyperuricemia in cardiovascular or renal diseases. Several mechanisms have been identified that explain the relationship between hyperuricemia and chronic kidney disease, including the crystal effect, renin–angiotensin–aldosterone system activation, nitric oxide synthesis inhibition, and intracellular oxidative stress stimulation, and urate-lowering therapy (ULT) has been proven to reduce renal disease progression in the past few years. In this comprehensive review, the source and physiology of UA are introduced, and the mechanisms that explain the reciprocal relationship between hyperuricemia and kidney disease are reviewed. Lastly, current evidence supporting the use of ULT to postpone renal disease progression in patients with hyperuricemia and gout are summarized.

COLONIC MICROBIOTA AND CHRONIC KIDNEY DISEASES INTESTINAL MICROBIOTA AND CHRONIC KIDNEY DISEASE. PART II

2019 ◽  
Vol 23 (1) ◽  
pp. 18-31 ◽  
Author(s):  
B. G. Lukichev ◽  
A. Sh. Rumyantsev ◽  
I. Yu. Panina ◽  
V. Akimenko
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Intestinal Microbiota ◽  
Kidney Diseases ◽  
Biologically Active ◽  
Chronic Kidney Diseases ◽  
Mechanical Removal ◽  
Starting Point ◽  
Active Substances

Interest in studying the role of the gastrointestinal tract in maintaining homeostasis in chronic kidney disease is a traditional one. It served, in particular, as a starting point for the creation of enterosorbents. However, if earlier the main attention was paid to the mechanical removal of a number of potentially dangerous biologically active substances, recently an intestinal microbiota has become an object of interest. The first part of the review of the literature on this topic is devoted to questions of terminology, the normal physiology of the colon microbiota. A detailed description of dysbiosis is given. The features of the main groups of microorganisms are reflected. The hypothetical and confirmed interrelations of the intestine-kidney axis are presented. The pathogenetic mechanisms of the influence of colon dysbiosis on the processes of local and systemic inflammation are discussed. The influence of dysbiosis on the state of the kidney parenchyma and its participation in the progression of CKD are debated.

Semicarbazide-sensitive amine oxidase and kidney disease

2013 ◽  
Vol 305 (12) ◽  
pp. F1637-F1644 ◽  
Author(s):  
May Y. W. Wong ◽  
Sonia Saad ◽  
Carol Pollock ◽  
Muh Geot Wong
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Fibrosis ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Amine Oxidase ◽  
Tubular Atrophy ◽  
Progression Of Renal Disease ◽  
Protein Enzyme

With better understanding of the molecular mechanisms underpinning chronic kidney disease, the roles of inflammation and fibrosis are becoming increasingly inseparable. The progression of renal disease is characterized by pathomorphological changes that consist of early inflammatory responses followed by tubulointerstitial fibrosis, tubular atrophy, and glomerular and vascular sclerosis. Currently available therapies that reduce hypertension, proteinuria, hyperglycemia, and interruption of the renin-angiotensin-aldosterone system are at best only partially effective. Hence, there remains a need to explore agents targeting nonrenin-angiotensin-aldosterone system pathways. In this review, we discuss mechanistic aspects in the physiological and pathological role of semicarbazide-sensitive amine oxidase, a protein enzyme involved in cellular trafficking and inflammation, with respect to the kidney. We explore the evidence for the use of semicarbazide-sensitive amine oxidase inhibitors as potential agents in renal fibrosis to delay the onset and progression of chronic kidney disease.

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