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Published on: June 23, 2015
Selected aspects of genetic disorders in chronic kidney disease
Elżbieta Głuch1, Piotr Halicki1, Weronika Lea Śliwińska1
1Department of Internal Medicine, Nephrology and Dialysis, Military Institute of Medicine in Warsaw, Poland.
Abstract:
Chronic kidney disease (CKD) can be caused by many conditions. The most common reasons are diabetic nephropathy, hypertension - associated nephropathy, cardiovascular disease. Although there are different reasons of deterioration of kidney function, many of them have combined molecular mechanisms by modulating metabolic homeostasis, autophagy, apoptosis, oxidative stress, inflammation. The aim of this paper is to present known molecular bases of CKD development in the course of other selected diseases to research why different patients are more prone to the CKD than others with the same condition. Selected aspects of genetic conditions were conducted, such as gene polymorphism of sirtuins, APOL1 gene polymorphism, the role of reactive oxygen species. More research is needed to understand the genetics of CKD and its' affecting the process of diagnostics and treatment.
Insights
Chronic kidney disease (CKD) arises from various conditions, often sharing molecular pathways like metabolic dysregulation and inflammation. Genetic factors, including gene polymorphisms, influence individual susceptibility to CKD development.
Area of Science:
- Nephrology
- Molecular Biology
- Genetics
Background:
- Chronic kidney disease (CKD) is a significant health concern with diverse etiologies.
- Common causes include diabetic nephropathy, hypertensive nephropathy, and cardiovascular disease.
- Underlying molecular mechanisms often involve metabolic homeostasis, autophagy, apoptosis, oxidative stress, and inflammation.
Purpose of the Study:
- To elucidate the molecular underpinnings of CKD development in the context of other diseases.
- To investigate genetic factors contributing to varying patient susceptibility to CKD.
- To explore the role of specific genetic variations and reactive oxygen species in CKD pathogenesis.
Main Methods:
- Review of existing literature on molecular mechanisms of CKD.
- Analysis of genetic factors, including sirtuin gene polymorphism and APOL1 gene polymorphism.
- Examination of the role of reactive oxygen species in kidney function deterioration.
Main Results:
- Multiple conditions leading to CKD share common molecular pathways.
- Genetic variations, such as APOL1 gene polymorphism, significantly impact CKD risk.
- Oxidative stress, modulated by reactive oxygen species, is a key factor in kidney damage.
Conclusions:
- Understanding shared molecular mechanisms is crucial for comprehending CKD development.
- Genetic predisposition plays a vital role in determining individual CKD susceptibility.
- Further research into CKD genetics is essential for improving diagnostics and treatment strategies.
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