Abstract

Chronic kidney disease can progress to end-stage chronic renal disease (ESRD), which requires the use of replacement therapy (dialysis or kidney transplant) in life-threatening conditions. In ESRD, irreversible changes in the kidneys are associated with systemic changes of proinflammatory nature and dysfunctions of internal organs, skeletal muscles, and integumentary tissues. The common components of ESRD pathogenesis, regardless of the initial nosology, are (1) local (in the kidneys) and systemic chronic low-grade inflammation (ChLGI) as a risk factor for diabetic kidney disease and its progression to ESRD, (2) inflammation of the classical type characteristic of primary and secondary autoimmune glomerulonephritis and infectious recurrent pyelonephritis, as well as immune reactions in kidney allograft rejection, and (3) chronic systemic inflammation (ChSI), pathogenetically characterized by latent microcirculatory disorders and manifestations of paracoagulation. The development of ChSI is closely associated with programmed hemodialysis in ESRD, as well as with the systemic autoimmune process. Consideration of ESRD pathogenesis from the standpoint of the theory of general pathological processes opens up the scope not only for particular but also for universal approaches to conducting pathogenetic therapies and diagnosing and predicting systemic complications in severe nephropathies.

Highlights

  • In two individuals with systemic lupus erythematosus, we found an reactivity level (RL)-5 level of systemic inflammatory response (SIR) that was uncommon for chronic disease

  • These approaches must take into account the fundamental laws, as well as the separation of the specific and the general, where the role of the general is played by general pathological processes

  • The most fundamental general pathological processes associated with the molecular mechanisms of inflammation are

Read more

Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. It is often unclear which processes these identified molecular mechanisms relate to This concerns both the accumulation of inflammatory mediators in the blood and the presence of other signs of a systemic inflammatory response (SIR). That is why “inflammation” requires classification into several independent common pathological processes to determine their common and different molecular and cellular mechanisms From these vantage points, a large group of diseases is a convenient material for describing the role of key general pathological processes associated with inflammation. We think this article could be interesting for nephrologists and specialists in related clinical disciplines, as well as pathological physiologists, general pathologists, immunologists, and other fundamental medicine and molecular biology representatives With this in mind, we outline the causes and consequences of end-stage renal disease (ESRD). This review reveals the general and distinctive molecular and cellular mechanisms of various general pathological processes of inflammation, as well as their interconnections during the development of severe renal pathology

General Characteristics of the Causes and Consequences of ESRD
Typical Low-Intensity Inflammatory Processes in CKD and ESRD
Pathogenetic Significance of ChLGI in the Onset of ESRD
General Patterns of Classic Inflammation
Typical Manifestations of Classical Inflammation in Nephrites
General Characteristics of Systemic Inflammation
Features of SIR Development in ESRD
Systemic Inflammatory Phenomena Specific to ESRD
Use of the Integral Criterion of Systemic Inflammation in ChSI
RL point
Findings
Conclusions
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call