General Pathological Processes Research Articles

Sleep Disturbance as a Predictor of Accelerated Human Aging

Introduction. One of the main predictors of aging is sleep disturbance, the study of the role of which in the development of the accelerated aging process is recognized as an urgent problem for the medical community.The aim of the work is to analyze modern data on age-related aspects of sleep status and describe known markers of early aging associated with somnological disorders.Materials and methods. The search and selection of literary sources was carried out in the databases PubMed, eLibrary, CyberLeninka, Google Scholar. Search depth — 17 years, from 2007 to 2024. The total number of publications included in the review was 80.Results and discussion. Aging refers to a general pathological process that affects all human physiological systems. Differences between the terms biological and chronobiological age are established. The role of somnological disorders in the accelerated aging process has been determined. It has been established that as age increases, changes in the electrophysiological pattern of sleep are observed. It was found that changes in biological markers of aging are positively correlated with sleep disturbance. The importance of neuroimaging methods in determining the accelerated rate of aging in people with sleep disorders is shown.Conclusion. Sleep disturbance is defined as a significant indicator of accelerated aging of the body. Further research into changes in the structure and quality of sleep may change the understanding of the pathogenetic mechanisms of aging and contribute to the development of new diagnostic and therapeutic strategies in the field of anti-aging medicine.

Oxfendazole Nitazoxanide combination in experimental neurocysticercosis – Anti-inflammatory and cysticidal effects

Neurocysticercosis (NCC) is a parasitic infection caused by the larval stage of the pork tapeworm, Taenia solium. The complications of NCC include seizures, headaches, cognitive impairment, and focal neurological deficits. In addition to antiparasitic drugs and surgery, the management of NCC includes the use of corticosteroids to reduce inflammation and control symptoms. The traditional treatment with albendazole and praziquantel has not been altered over 30 years and present several side effects. There are other anti-helminthic drugs such as oxfendazole and nitazoxanide that may show efficacy in NCC treatment. The aim of this study was to determine the histopathologic aspects of experimental NCC after in vivo treatment with the combination of oxfendazole and nitazoxanide. Balb/c mice were infected with T. crassiceps cysticerci and divided into groups of 10 animals each that received a single dose through gavage as follows: group treated with NaCl 0.9% (control group); group treated by monotherapy of the anti-helminthic drugs, 30 mg/kg in single dose of oxfendazole (OXF) or nitazoxanide (NTZ); and groups treated with the combination of the drugs (OXF/NTZ group). Macroscopic and microscopic analysis were performed. There was greater presence of final stage cysticerci after treatment. The microscopic analysis of the general pathological processes showed that the monotherapy with all treatment groups induced higher perivasculitis than what was observed in the control group. In contrast, the combination treatment showed a lower observation of PMN and MN inflammatory infiltration in comparison to the other treatments and to the control one. These results show that indeed the association of benzimidazole derivatives which present both anti-helminthic and anti-inflammatory properties with other cysticidal drugs are beneficial for the NCC treatment in which the aim is to destroy parasite without inducing inflammatory damage in the brain tissue.

The Effect of the Toxic Dose of Baclofen on Selected Parameters of the Cardiovascular and Respiratory Systems.

The effect of the toxic dose of the muscle relaxant baclofen on the parameters of the cardiovascular and respiratory systems was studied in adult male Wistar rats (n=20). Systolic and diastolic BP, HR, and respiratory rate were measured; histological changes in the lungs 3, 4.5, and 24 h after drug administration. Baclofen was administered orally in a sublethal toxic dose of 85 mg/kg under anesthesia. Cardiac activity was analyzed using RSM physiological indicators monitoring system with MouseMonitor S (Indus Instruments) software. Histological examination was performed by light microscopy. Baclofen significantly decreased the respiratory rate and increased HR and BP. Histological examination of the lungs revealed a complex of general pathological processes, such as local circulatory disorders (venular and capillary fullness, sludge), leukocyte infiltration of the interalveolar septa and their thickening due to edema. These findings can be used to estimate the time elapsed after baclofen treatment.

THE DYNAMICS OF HISTOMORPHOLOGICAL CHANGES IN ACUTE BACLOFEN POISONING

Aim: to assess the dynamics of histolological changes in the lung under acute baclofen poisoning. Materials and methods: The study was performed on 20 male Wistar rats weighing 200-215 g and aged 20 weeks. The animals were divided into four groups (5 animals in each) – controls, group 1 (baclofen, 3h.), group 2 (baclofen, 4,5 h.) and group 3 (baclofen, 24 h.). Results: The thickness of intraalveolar septi in group 1 (baclofen, 3 h.) was considerably lower than in the group of controls. 4,5 hours after baclofen administration the thickness of intraalveolar septa was significantly higher than in group 1 (baclofen, 3 h.) and in the group of controls. 24 hours after baclofen administration the thickness of intraalveolar septa was significantly higher than in group 1 (baclofen, 3 h.) and in the group of controls. The diameter of the alveoli was considerably higher in all study groups than in the group of controls. The diameter of the alveoli 3 hours after baclofen administration was higher than 4,5 and 24 hours after baclofen administration, but the difference was not significant. Conclusion: In baclofen poisoning, a certain complex of general pathological processes in lungs develops. It includes circulatory disorders, increased vascular permeability, infiltration of intraaveolar septa. The quantitive assessment of the changes can be used to assess the severity of general pathological process in acute baclofen poisonings and to determine the exact time of the poisoning.

Atherosclerosis and Inflammation: Insights from the Theory of General Pathological Processes.

Recent advances have greatly improved our understanding of the molecular mechanisms behind atherosclerosis pathogenesis. However, there is still a need to systematize this data from a general pathology perspective, particularly with regard to atherogenesis patterns in the context of both canonical and non-classical inflammation types. In this review, we analyze various typical phenomena and outcomes of cellular pro-inflammatory stress in atherosclerosis, as well as the role of endothelial dysfunction in local and systemic manifestations of low-grade inflammation. We also present the features of immune mechanisms in the development of productive inflammation in stable and unstable plaques, along with their similarities and differences compared to canonical inflammation. There are numerous factors that act as inducers of the inflammatory process in atherosclerosis, including vascular endothelium aging, metabolic dysfunctions, autoimmune, and in some cases, infectious damage factors. Life-critical complications of atherosclerosis, such as cardiogenic shock and severe strokes, are associated with the development of acute systemic hyperinflammation. Additionally, critical atherosclerotic ischemia of the lower extremities induces paracoagulation and the development of chronic systemic inflammation. Conversely, sepsis, other critical conditions, and severe systemic chronic diseases contribute to atherogenesis. In summary, atherosclerosis can be characterized as an independent form of inflammation, sharing similarities but also having fundamental differences from low-grade inflammation and various variants of canonical inflammation (classic vasculitis).

Molecular and morphological markers of neuronal death in acute cerebrovascular accidents

Acute cerebral circulation disorder is one of the most discussed issues in modern intensive care and neurology, as it is a severe condition, leading to disability or death of the patient, in the absence of immediate medical care. This review discusses general and specific biological markers of stroke, genetic markers of stroke, and current data on their diagnostic significance. The main mechanisms of brain tissue cell death in stroke, such as apoptosis, necrosis, ferroptosis, parthanatosis, sarmoptosis, autolysis, autophagy, oncosis, excitotoxic death are analyzed; the morphological features of the observed processes and their structural manifestations are reviewed. For each type of cell death in nervous tissue, the most frequently detected molecular markers are discussed: specific kinases, Toll-like receptors in the case of apoptosis; serine-threonine protein kinases, components of the polyubiquitin system detected in necrosis; transferrin 1 receptors, typical for ferroptosis; poly(ADP-ribose)-polymerase, whose activity increases in parthanatosis; slow Wallerian degeneration protein that accumulates during sarmoptosis; and other biomarkers characteristic of both individual types of nerve cell death and general pathological processes affecting the brain.

Shock-Associated Systemic Inflammation in Amniotic Fluid Embolism, Complicated by Clinical Death.

Amniotic fluid embolism (AFE) is one of the main causes of maternal mortality in developed countries. The most critical AFE variants may be considered from the perspective of systemic inflammation (SI), a general pathological process that includes high levels of systemic inflammatory response, neuroendocrine system distress, microthrombosis, and multiple organ dysfunction syndrome (MODS). This research work aimed to characterize the dynamics of super-acute SI using four clinical case studies of patients with critical AFE. In all the cases, we examined blood coagulation parameters, plasma levels of cortisol, troponin I, myoglobin, C-reactive protein, IL-6, IL-8, IL-10, and TNF-α, and calculated the integral scores. All four patients revealed the characteristic signs of SI, including increased cytokine, myoglobin, and troponin I levels, changes in blood cortisol, and clinical manifestations of coagulopathy and MODS. At the same time, the cytokine plasma levels can be characterized not only as hypercytokinemia, and not even as a "cytokine storm", but rather as a "cytokine catastrophe" (an increase of thousands and tens of thousands of times in proinflammatory cytokine levels). AFE pathogenesis involves rapid transition from the hyperergic shock phase, with its high levels of a systemic inflammatory response over to the hypoergic shock phase, characterized by the mismatch between low systemic inflammatory response values and the patient's critical condition. In contrast to septic shock, in AFE there is a much more rapid succession of SI phases. AFE is one of the most compelling examples for studying the dynamics of super-acute SI.

Acute and Chronic Systemic Inflammation: Features and Differences in the Pathogenesis, and Integral Criteria for Verification and Differentiation.

Currently, there is rationale for separating the systemic manifestations of classical inflammation from systemic inflammation (SI) itself as an independent form of the general pathological process underlying the pathogenesis of the most severe acute and chronic diseases. With this aim in view, we used integral scales of acute and chronic SI (ChSI), including the following blood plasma parameters: interleukins 6, 8, 10; tumor necrosis factor alpha; C-reactive protein; D-dimer; cortisol; troponin I; myoglobin. The presence of multiple organ dysfunction according to the SOFA score was also taken into account. The effectiveness of the scales was tested in groups of intensive care patients during different periods of acute trauma, sepsis, and septic shock. The ChSI scale was applicable under systemic autoimmune diseases, chronic purulent infections, chronic limb threatening ischemia, and end-stage renal disease of various genesis. The number of examined patients was 764 in total. The scales allowed us to verify specific phases of acute SI and identify pathogenetic risk factors of lethal outcomes, as well as the most severe variants of the chronic pathologies course. These scales are open adaptable systems (in terms of the nomenclature and choice of indicators). They are primarily intended for scientific research. However, the SI verification methodology presented in this paper may be useful for developing advanced criteria for assessing both the typical links in the pathogenesis of many diseases and the severity of the overall condition of patients for clinical practice.

Modern aspects of burn injury immunopathogenesis and immuno-biochemical markers of wound healing (review of literature).

Burns are one of the most common traumatic injuries in the world, representing a global public health problem. Major burns (severe burn injury or burn disease) are one of the most life-threatening injuries. There is a great need to identify and monitor the development of complications (sepsis and septic shock, coagulopathy and DIC) in burned patients. The basis of the pathogenesis of burn injury, as well as any general pathological process, is an inflammatory reaction, ultimately aimed at restoring the structure and function of the damaged tissue. A feature of the inflammatory reaction in burn injury is the scale of alteration of the skin and mucous membranes. The review presents the main aspects of the burn injuries immunopathogenesis and the features of post-burn immune dysfunction, manifested by disorders in the innate and adaptive immunity systems. Attention is focused on the role in the immunopathogenesis of developing systemic and local disorders in burn injury. Also the role are discussed of a minor subpopulations of lymphocytes (Treg-, Th-17-, γδT-cells) in the immunopathogenesis and in the bacterial infection protection. The characteristics of the main immuno-biochemical markers of burn injury (cytokines and growth factors, nitric oxide, matrix metalloproteases, bacteria concentration levels) are present. The prognostic role of these biomarkers in assessing of the severity degree of patients with burn injury and wound healing processes is shown. The review has been compiled using references from major databases such as RSCI, Web of Science, PubMed, Scopus and Google Scholar (up to march 2022). After obtaining all reports from database, the papers were carefully analyzed in order to find data related to the topic of this review (60 references).

Macroporous latex biomembrane from Hancornia speciosa modulates the inflammatory process and has a debridement effect on wound healing in rats.

The angiogenic, osteogenic and anti-inflammatory activity of latex of Hancornia speciosa has been evidenced and indicates pharmacological potential with great applicability in the health area, especially in the wound healing process. The present work aimed to compare the effects of the H. speciosa macroporous latex biomembrane with saline on wound healing. Forty-three Wistar rats were submitted to excisional wound induction procedure and divided into groups according to treatment: saline (G1), and macroporous biomembrane (G2). The animals were euthanized at three, seven, 14, and 21 days after injury induction (DAI), and three animals were used for the debridement test. Morphometric, macroscopic, and microscopic analyses of general pathological processes were performed. The macroporous biomembrane minimized necrosis and inflammation during the inflammatory and proliferative phases of the healing process, confirmed by the lower intensity of the crust and the debridement effect. In addition, the wounds treated with the macroporous biomembrane presented greater contraction rates in all the experimental periods analyzed. The macroporous biomembrane presents angiogenic, anti-inflammatory and debridement effects, contributing to the healing process, and can be considered a potentially promising new biomaterial to be used as a dressing.

THE QUANTITATIVE CHARACTERISTICS OF HISTOPATHOLOGICAL CHANGES IN LUNGS IN ACUTE BACLOFEN POISONING

The aim of the study was to quantify the changes in the lungs in acute baclofen poisoning in an animal experiment. Materials and Methods: The study was performed on 20 male Wistar rats weighing 290–350 g and aged 20 weeks. The animals were divided into 4 groups. The reference group of controls included 5 intact rats. The animals of three experimental groups included 5 rats each were treated with baclofen at a dose of 85 mg/kg. The tested rats were euthanized by displacement of cervical vertebrae at 3, 4,5 and 24 hours, respectively. Lung tissue samples were examined by light microscopy using a video system at ×400 magnification. Results: The area of the intraalveolar septi 4,5 hours after baclofen administration was significantly higher than in the reference group of controls. 3 and 4,5 hours after baclofen administration an increase in the area of alveloli was observed, but the increase was insignificant and the area of alveoli returned to the initial size by the 24th hour. 3 and 4,5 hours after baclofen administration a slight decrease in the area of pulmonary parenchima was observed, which also returned to its initial size in 24 hours. The total area of pulmonary microvessels 4,5 hours after baclofen administration was significantly higher than in the control group and 3 hours after baclofen administration. The area of pulmonary microvessels 24 hours after baclofen administration was significantly higher than in the group of controls, 3 or 4,5 hours after baclofen administration. The area of edema increased and was significantly higher 24 hours after baclofen administration. In baclofen poisoning, a certain complex of general pathological processes in lungs develops. There is a circulatory disorder, increased vascular permeability, infiltration of intraaveolar septis. Conclusion: The quantitative assessment of the changes can be used to evaluate severity of general pathological process in acute baclofen poisonings and to determine the exact time of the poisonings.

Офтальмологические поражения при наследственной гиперлипидемии у декоративного домашнего кролика

In animals, as in humans, a significant part of the functional or morphological ophthalmic pathologies are associated with general or systemic diseases. Abnormalities detected during ophthalmological examination, in some cases, are symptoms of a general pathological process and can contribute to the diagnosis. The article discusses the clinical case of the eye pathological changes development in a decorative domestic rabbit (Oryctolagus cuniculus domesticus) accompanying a cholesterol metabolism hereditary disorder: chronic lipogranulomatous conjunctivitis, lipid degeneration of the cornea, massive cholesterol infiltration of the sclera fibrous stroma and eyeball posterior pole, hypertrophy of the orbit fatty cellular tissue. The observed pathological processes in the eyes and their adnexal structures were manifestated severely. The article presents MRI data and photographs of histological preparations of pathologically altered tissues. A clinical description of severe ophthalmic abnormalities in rabbit with hereditary hyperlipidemia as in our article, is not presented in the available scientific literature.

Established Liver Cell Lines: Are You Sure to Have the Right Ones?

In liver research, immortalized cell lines have assumed an important role in studying general physiological and pathological processes. However, misidentification and cross-contamination of cell lines is a widespread problem in biomedical sciences resulting in irreproducible results and false conclusions. Although the huge impact of working with wrong cell lines on life science research and publication has been well recognized, there are only limited efforts and strategies to prevent cell misidentification. This commentary provides a catalogue of the most important cell lines used in hepatology research, examples of misidentified cell lines, and short guidelines to be considered when working with continuous lines.

COVID-19-induced alopecia: a clinical case of diffuse focal alopecia in a patient with generalized pustular psoriasis after a new coronavirus infection

The clinical picture of dermatological diseases in synergy with the pandemic of coronavirus infection demonstrates various, additional, more striking features of the course of dermatoses. The proposed case of observation illustrates the development of diffuse alopecia in a patient with torpid generalized pustular psoriasis, metabolic syndrome, endocrinopathy against the background of a coronavirus infection complicated by polysegmental pneumonia.
 In the presented clinical observation, the severity of the lesion of the skin and skin appendages correlated with the severity of the course of COVID-19, which was the trigger point of the general pathological process ― immune-mediated T-cell inflammation. In the manifestation of psoriasis and its exacerbation, a significant role was played by viral load and a pronounced comorbid background ― autoimmune thyroid disease and metabolic syndrome. Thus, the severe course of COVID-19 with involvement in the pathological process of the microcirculatory bed, coagulopathy, hypoxia of hair follicles as a result, as well as the reduced estrogenic background of the sixty-one-year-old patient contributed not only to the exacerbation of psoriasis, but also led to diffuse hair loss. The degree of hair loss according to SALT criteria was 82%, which corresponded to a severe degree of lesion. The use of prolonged-acting injectable corticosteroids in the complex treatment of various forms of alopecia was an effective method of therapy in this patient, which is associated with the immunosuppressive effect of corticosteroids in autoimmune damage to hair follicles, a decrease in inflammation of the microvascular bed in various infectious and inflammatory conditions. In the presented case, the high efficiency may also have been associated with the mechanisms of reducing the damaging effect of cytokine inflammatory factors, expressed both with the existing background disease psoriasis and with coronavirus complicated infection.
 As numerous observations show, COVID-19 is a potential trigger for many dermatological conditions. Examination and treatment of patients with skin pathology infected with COVID-19 requires a systematic integrated approach.

The Possibilities of Nuclear Medicine Methods in Inflammation Diagnosis

Modern nuclear medicine is a rapidly developing field that includes various non-invasive molecular imaging techniques with the ability to examine the whole body.Inflammation is a frequent complication in surgical and traumatological practices, which is a complex, local and general pathological process that occurs in the body in response to injury. Having arisen under the influence of a damaging factor, inflammation is characterized by the development of a dynamic complex of changes. However, the search for inflammation foci of inflammation by traditional diagnostic methods in some cases is difficult even with a detailed clinical picture. In this case, nuclear medicine, which is able to visualize pathological processes, including those with a pathological increase in metabolism, may be the best option for finding the affected area.A wide variety of radiopharmaceutical drugs makes it possible to determine the localization of the inflammatory focus in a short time and with high accuracy and makes nuclear imaging methods a priority for the early diagnosis of pathophysiological reactions.This paper presents a review of domestic and foreign literature on the use of specific and nonspecific radiopharmaceuticals in the diagnosis of inflammation. Own cases is also presented.

Modern Aspects of Burn Injury Immunopathogenesis and Prognostic Immunobiochemical Markers (Mini-Review).

Burn injuries are among the most common peacetime injuries, with mortality ranging from 2.3% to 3.6%. At the same time, 85–90% of patients with burns are people of working age and children. Burn injury leads to metabolic disorders and systemic inflammatory response, inefficient energy consumption, and other physiological changes that can lead to dysfunction of organs and systems. The most formidable complication of burn injuries is sepsis mediated by multiple organ failure, the most common cause of poor prognosis in patients and has specific differences in these injuries. The purpose of this article was to dwell in detail on the most promising immunobiochemical markers of sepsis in the format of a mini-review, based on the main aspects of the immunopathogenesis of this complication. The pathogenesis of a burn injury and any general pathological process is based on an inflammatory reaction and large-scale changes in the skin and mucous membranes. This review is devoted to the progress in understanding the main aspects of the immunopathogenesis of burn lesions and the features of post-burn immune dysfunction, manifested by disorders in the innate and adaptive immunity systems. Attention is focused on the role in the immunopathogenesis of the development of systemic and local disorders in burn injury. Characterization of primary immunobiochemical markers of burn injury (cytokines, growth factors, C-reactive protein, procalcitonin, presepsin, matrix metalloproteinases, reactive oxygen species, nitric oxide, hemostasis parameters) is presented. The problem of treating burn lesions is associated with constant monitoring of the condition of patients and regular monitoring of specific immunobiochemical markers predicting sepsis for the timely initiation of a specific therapy.

Etiopathogenesis of non-exudative age-related macular degeneration (literature review)

The article presents an overview of modern publications on epidemiology, risk factors, and the main links of the etiology and pathogenesis of age-related macular degeneration (AMD). The nonexudative or “dry” form of age-related macular degeneration is a multifactorial progressive pathological process caused by hereditary predisposition, general and local disorders of lipid metabolism, negative changes in the blood supply to the eye, age-related destruction of the Bruch’s membrane and retinal pigment epithelium, the appearance of signs of local and systemic inflammation, the development of oxidative stress with the impact of toxic lipoperoxidation products on the structures of the posterior segment of the eye. Recent studies have discovered new ways of retinal pigment epithelial cell death in response to oxidative stress in AMD, in particular necroptosis, which, in addition to classical apoptosis, is considered the main mechanism of this process. It is noted that the development of AMD may be associated with an age-related decrease in the level of estrogen in women. The analysis of the data on the etiopathogenesis of age-related macular degeneration presented in the modern literature indicates the need for further research and generalization of local and general pathological processes developing in the dynamics of retinal visual function disorders by specialists of various scientific disciplines.

Acute and chronic systemic inflammation: an analysis of the phenomenological structure

The paper presents the analysis of acute and chronic variants of systemic inflammation (SI) as a general pathological process, analyzes the frequency of occurrence and severity of its main phenomena in various acute and chronic pathologies. Study goal: to carry out a comparative analysis of the phenomenological structure of acute and chronic variants of systemic inflammation in different nosologies. We examined patients with acute critical conditions of infectious and non-infectious genesis to study acute SI, and patients with autoimmune diseases, chronic organ failure and other chronic destructive diseases (18 groups of patients in total) to study chronic SI. We studied molecular markers of the following phenomena: systemic inflammatory response, systemic alteration, distress response of hypothalamic-pituitary-adrenal system, systemic microthrombosis. The results of the study showed a fundamental similarity between acute and chronic SI in terms of the phenomenological structure, which indicates the presence of a common pathogenetic mechanism at the basis of these processes. However, the scenario of SI development can differ depending on the nature, duration and intensity of the damaging factor, compensatory possibilities of the organism and the adequacy and timeliness of the pathogenetic therapy performed. In addition, the presence of individual phenomena does not always indicate the development of SI as a general pathological process.

Morphological markers of pathophysiological changes in the neuronal processes in the acute post-traumatic period of diffuse axonal injury

The purpose of the study was to establish morphological markers of pathophysiological changes in the neuronal processes of in the acute (up to 36 hours) post-traumatic period of diffuse axonal injury (DAI) for the purposes of expert practice. Histological examination of the body of corpus callosum of the corpses of 66 persons dead from DAI and of 25 persons dead from various non-violent and violent causes, excluding head trauma, was performed (control group). Morphological markers of specific pathophysiological changes in the neuronal process were established by light microscopy with the use of immunohistochemical examination in acute period DAI. Uneven contours of the processes suggested displacement of cytoskeletal elements, areas of vacuolization of the cytoplasm of the processes suggested violation of intracellular transport caused by a change of permeability with preserved integrity of the process shell without mechanical separation of the process, uneven thickness (3.9 ± 1.6 μm) of the processes, varicose and cone-shaped thickening of them was a manifestation of focal edema of the neuronal process and compression of the cytoskeleton as a result of ion-enzymatic disorders, uneven coloration, areas of fragmentary compaction of neurofilaments indicated the zones of deformation and compression of the cytoskeleton, zones of granular-lumpy decay and fibrillolysis of neurofilaments indicated destruction of the cytoskeleton. Changes in the neuronal processes are a manifestation of a polyethological general pathological process and are not a differential diagnostic criterion of DAI.

The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation.

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.