The review is devoted to one of the important problems of the clinic of internal diseases - kidney damage associated with painkillers and main non-steroidal anti-inflammatory drugs (NSAIDs). Possible variants of acute and chronic kidney damage when taking NSAIDs are considered. Acute kidney injury is a serious side effect of NSAIDs associated with suppression of the vasodilatory effects of prostaglandins, decompensation of intrarenal hemodynamics, and an acute decrease in glomerular filtration rate levels. A high risk of acute kidney injury when taking NSAIDs is observed in elderly patients with concomitant diseases and polypharmacy, as well as with an initial impairment of renal function. Taking NSAIDs can cause the development of acute interstitial nephritis in combination with podocytopathy, which is manifested by high proteinuria and nephrotic syndrome in younger patients. The mechanisms and clinical manifestations of analgesic nephropathy - chronic kidney damage leading to progressive renal failure are considered separately. The cause of the development of analgesic nephropathy may be the long-term use of combined analgesic drugs, the so-called analgesic mixtures. The erased clinical picture and the mask of chronic pyelonephritis complicate the diagnosis of this disease. Specific for this pathology is renal papillary calcification on computed tomography in combination with a history of long-term analgesic abuse. Withdrawal of anesthetic drugs can slow down the progression of the disease and the development of end-stage chronic kidney disease. The possibility of the development and progression of chronic kidney disease associated with the certain classes of NSAIDs is discussed. An algorithm for treatment of chronic pain syndrome is presented, depending on the degree of risk of kidney damage.

ATTR amyloidosis (transthyretin amyloidosis) is a progressive, fatal disease characterized by the accumulation of transthyretin amyloid mainly in the peripheral nervous system (somatic and autonomic) and heart, as well as in the kidneys, gastrointestinal tract, eyeballs, and ligaments, which impairs the normal function of organs and systems. The hereditary form of ATTR amyloidosis, or ATTRv amyloidosis, is found all over the world and is characterized by broad genetic and phenotypic heterogeneity, resulting in late diagnosis. The kidneys are a potential target organ in ATTRv amyloidosis. Clinically, nephropathy is manifested by albuminuria, proteinuria, nephrotic syndrome, or decreased renal function. A nephrologist may be involved in the diagnosis of amyloid nephropathy/ATTRv amyloidosis in a patient with symptoms of renal damage in an endemic region or with a family history of ATTRv amyloidosis, or, more difficult, in the diagnosis of a sporadic case of ATTRv amyloidosis when symptoms of nephropathy were detected in a patient in a non-endemic region without a known family history of amyloidosis. The diagnosis of amyloidosis, especially is sporadic cases, requires the nephrologist to know the specific symptoms, the so-called "red flags" of ATTR amyloidosis that allow suspecting amyloidosis, and methods to confirm the diagnosis. Kidney biopsy in the presence of nephropathy is the gold standard in the diagnosis of amyloidosis. Congo-red staining of biopsy specimens with subsequent visualization of the apple-green birefringence of congophilic masses with polarized light is crucial for histological confirmation of the diagnosis. Immunohistochemistry is used for amyloid typing. The less available method for typing is mass spectrometry of affected tissue. Detection of "red flags" of amyloidosis in a patient with nephropathy makes it possible to diagnose ATTR amyloidosis in some cases without a biopsy, by TTR gene sequencing or myocardial scintigraphy with 99mTc-pyrophosphate. After amyloidosis is diagnosed, it is necessary to conduct a detailed examination for assessing the damage to potential target organs, which requires an interdisciplinary approach. Early diagnosis and disease-modifying therapies can slow the progression of neuropathy and cardiomyopathy, and presumably nephropathy.

Health-related quality of life (QoL) is one of the main patient-reported outcomes. Monitoring QoL in patients with chronic kidney disease (CKD) can be considered one of the approaches to the implementation of the principles of personalized medicine in clinical nephrology. The review provides a brief description of the questionnaires most used to assess QoL in patients with CKD and summarizes the results of studies of factors related to QoL at predialysis stages. It is customary to distinguish sociodemographic, clinical, and psychological factors associated with health-related QoL. Being female, smoking, low levels of education and income, the presence of coronary heart or cerebrovascular diseases, depression, and anxiety were shown to be associated with a decrease in QoL of patients with predialysis CKD. As for other clinical and socio-demographic factors, the literature data are not so unambiguous. Thus, several studies have demonstrated that a decrease in glomerular filtration rate, albumin and hemoglobin levels, the presence of diabetes, and an increase in age and creatinine level negatively affect the parameters of the physical component of QoL. At the same time, a significant number of studies have not found a relationship between these variables and the parameters of the psychosocial component of QoL, which is explained by the dependence of this QoL component primarily on the characteristics of the emotional state and personality. Of the psychological factors associated with QoL in patients with CKD treated conservatively, the attention of researchers was focused mainly on the level of depression. Only a few studies have analyzed other psychological variables (personality traits, coping strategies, effects of psychosocial interventions) related to QoL in patients with predialysis CKD. Identification and systematization of potentially modifiable factors affecting patients’ QoL set the directions for the prevention and correction of reduced QoL

The aim: to study the effect of sodium profiling and ultrafiltration on the quality of life of patients on program hemodialysis. Materials and methods of research: in the process of prospective clinical research, two groups of patients with terminal stage chronic kidney disease (CKD) were formed who received therapy with program hemodialysis (HD). Group I patients (n=54) received D-treatment on regulated profiles. Patients with comparison groups received hemodialysis therapy without considering profile-treatment regimens. The study assessed: the quality of life indicators using the SF 36 questionnaire, blood pressure, and laboratory indicators. The duration of the study was 12 months. Patients received HD treatment on Gambra machines with the Exalis system connected (automatic calculation of Kt/V, blood pressure measurement). Results: it was established that the profiling of sodium and ultrafiltration (using Profiles No. 3 and No. 5) in patients on program hemodialysis was a way of stabilizing blood pressure, positive dynamics of laboratory indicators, and was accompanied by an improvement in quality of life according to the questionnaire SF 36 on the scales of physical, role, social functioning, life activity, and psychological health. At the same time, a significant improvement in the indicators occurred in group I compared to the control group by scales: VT (life activity) (64.3±2.7 vs 54.2±4.2, p=0.0001), RE (role functioning due to emotional state) (64.1±3.3 vs 52.1±2.4, p=0.0001), SF (social functioning) (70.8±3.1 vs 65.5±2.5, p=0.0001) and MH (61.8±2.3 vs 55.4±1.6, p=0.0001). With sodium profiles and ultrafiltration, patients experienced an improvement in the physical and psychological components of health at the same time, which is very important from the standpoint of a personalized approach in medicine. Conclusions. Regulation of sodium profiling and ultrafiltration in patients on pro-gram hemodialysis allows for stabilizing blood pressure, achieving positive dynamics of laboratory indicators. When profiling sodium and ultrafiltration in patients on program hemodialysis along with improvement of somatic state there is an improvement of both physical and psychological component of health.

Introduction: intradialytic hypotension (IDH) remains one of the most common and potentially lethal acute complications encountered by patients under hemodialysis. To determine the effect of intranasal DDAVP (vasopressin) on IDH incidence and the volume of normal saline required to manage hypotension in hypotension-prone patients with chronic kidney disease stage 5 receiving hemodialysis treatment (CKD 5D). Material and Methods: ten hypotension-prone CKD 5D patients were included in the study. They had experienced IDH for at least 30% of hemodialysis treatments in the preceding month. For 30 days, they received a placebo intranasal spray. For the next month, they received 2 puffs (each containing 10 μg) of vasopressin (DDAVP) 30 minutes before hemodialysis. IDH was defined as a symptomatic decrease in systolic blood pressure (BP) by more than 20 mmHg or a drop in mean arterial pressure (MAP) by more than 10 mmHg. Results: IDH was observed in 68 hemodialysis sessions in the placebo group (63.6%) and 53 sessions in the vasopressin group (49.5%) with a marginally significant difference (P =0.07). A significant difference (P =0.04) was found between the two groups regarding the decrease in systolic BP that was more pronounced in the placebo group. Mean (±SD) normal saline volume administered intravenously was significantly lower in the vasopressin group (34±67.6 mL) compared to the placebo group (77.1±89.8 mL); P<0.001. Hypertonic saline was not required in either group. Conclusion: Although no statistically significant difference was observed between the placebo and intranasal vasopressin groups in terms of IDH incidence, mean systolic BP and MAP measurements were significantly higher in the vasopressin group. Also, the vasopressin group required significantly lower volumes of intravenous normal saline to manage IDH. Although we suggest intranasal vasopressin as a possible pharmacologic treatment to prevent IDH, it must be considered that the low sample size and non-significant difference in IDH frequency made our results non-generalizable. Further studies with a larger number of observations are required to make this statement convincing.

The purpose: to study the association of hyperuricemia and renal dysfunction in convalescents of new coronavirus infection. Materials and methods: The study included 234 people who had a new coronavirus infection COVID-19 and were observed two months after convalescence. The mean age was 54.10±12.88 years. Three groups of patients were formed according to the anamnesis according to the severity of the new coronavirus infection: mild (n=108), moderate (n=112), and severe (n=14). In patients, BMI, creatinine, and uric acid levels were determined. Statistical processing of the obtained results was performed using the SPSS software package. Results: the average level of GFR was 80.34±16.66 ml/min/1.73 m2. In patients with a mild course of coronavirus infection, the average GFR was 82.52±15.78 ml/min/1.73 m2, with a moderate course - 78.33±17.69 ml/min/1.73 m2, with a severe course - 79.71±13.38 ml/min/1.73 m2. А decrease in GFR below 90 ml/min/1.73 m2 occurred in 69.3% of cases. Significant differences were obtained between the 1st and 2nd groups (p=0.046). Hyperuricemia was registered in 33.8% of cases. Moreover, in patients with a severe course of coronavirus infection, hyperuricemia was more common than in those with a mild course (64.3% vs 26.4%, p=0.0001) and those with a moderate course (64.3% vs 31.8%, p=0.002). Decreased GFR in patients with a mild form of COVID-19 is associated with the presence of hyperglycemia. In addition, an increase in BMI by 1 kg/m2 leads to a 10% reduction in the risk of developing renal dysfunction. In patients who had moderate COVID-19, a decrease in GFR was associated only with hyperuricemia. Conclusion: hyperuricemia is observed in 33.8% of patients 2 months after a new coronavirus infection. A decrease in GFR of less than 60 ml/min/1.73 m2 was observed in 10% of patients. Hyperuricemia is directly related to the severity of COVID-19 infection. The causal relationship between hyperuricemia in patients after COVID-19 and impaired renal function requires further research.

Predictor’s study of tuberculosis reactivation among patients with end-stage renal disease (ESRD) is a vital part of recent medical examination for patients who undergo substitution therapy, including candidates for kidney transplantation. In this article, for the first time on a statistically significant sample, we presented the results of studying the relationship between the main clinical and anamnestic risk factors for the development of active tuberculosis in dialysis patients. The analysis of the clinical and anamnestic characteristics of 105 patients with ESRD examined at FSBSI "Central TB Research Institute" with intoxication syndrome of unknown origin and/or newly identified changes in the organs of the chest from 2010 to 2020 was carried out. Based on the results of a comprehensive examination, 62/105 of ESRD patients (59%), were diagnosed with tuberculosis infection -respiratory diseases of non-tuberculous etiology - 43/105 people (41%). The following data were analyzed: the patient's age and sex, the patient's body mass index, the etiology of kidney disease, the presence of treatment for kidney disease before substitution therapy, nephrectomy in the anamnesis, the period of receiving primary substitution therapy, the presence of concomitant pathology, the type of concomitant pathology, tuberculosis history, the period from the onset of uremia before the development of respiratory diseases and their correlation with the etiology of the respiratory diseases, identified based on the results of examination at FSBSI "Central TB Research Institute". It was found that even though, according to various authors, previously such factors as gender, the cause of uremia, and the duration of substitution therapy were identified as predictors of the development of tuberculosis in patients on dialysis, now none of the studied signs has a statistically significant correlation with etiology of respiratory diseases in patients on dialysis. Regardless of gender, age, body mass index (BMI), the cause of renal failure, the number of concomitant diseases, and the duration of follow-up, TCKD patients remain at a high risk of developing active tuberculosis

Fibrillary glomerulonephritis (FGN) is a rare condition, characterized by the glomerular deposition of non-amyloid fibrils. Light microscopy (LM) reveals mesangial expansion with weakly eosinophilic PAS-negative and mainly Congo-negative non-argyrophilic material, or membranoproliferative pattern; and immunofluorescence (IF) demonstrates predominantly polyclonal IgG, С3 and C1q deposits. These findings, suggestive for FGN, can be confirmed by electron microscopy (EM), which shows large (diameter 16-24 nm) nonbranching randomly oriented fibrils in mesangium and along capillary walls [1]. EM was critical to establish FGN diagnosis until 2018, when a new highly specific biomarker of FGN was identified - DNAJB9, a molecule, belonging to a family of proteins that function as “co-chaperones” to heat-shock protein 70. DNAJB9 is localized in the endoplasmic reticulum in all tissues, and it is up-regulated by various inflammatory mediators. Pathogenic role of DNAJB9 in FGN remains unknown, presumably it is related to exaggeration of its physiological role as a stress molecule; anyway, co-localization of DNAJB9 with IgG and complement deposits is characteristic for FGN and not found in amyloidosis or immunotactoid glomerulopathy [1-3]. The cause of FGN is not always established, although up to 50% of patients have a history of malignancies, monoclonal gammopathy, autoimmune diseases, hepatitis C, diabetes mellitus or chronic infections [1, 4]. 52-year-old Caucasian male presented with proteinuria and arterial hypertension. 18 years ago, he underwent inguinal hernioplasty, and same time a perianal fistula was revealed. A year ago, at admission to colorectal clinic, his blood pressure was 150/90 mm Hg, and work-up found proteinuria 1.18 g/L. After fistulectomy he was referred to nephrology, his proteinutia was 2.25 g/L and accompanied by microhaematuria 10-12-20-25 RBC/hpf; his serum creatinine was 135 µmol/L, serum urea 10 mmol/L, uric acid 677 µmol/L; the rest blood chemistry and total blood count were within normal range and infectious screening was negative. ECG, plain chest X-ray, kidney and abdominal ultrasound and ECHO-CG were otherwise normal. He underwent kidney biopsy, LM found 4 totally or partially sclerosed glomeruli, the rest 11 glomeruli were enlarged, with PAS- and Congo-negative amorphous material in mesangium and along capillary walls, without hypercellularity or double-contours; mild diffuse-focal interstitial fibrosis and tubular atrophy; and normal arteries and arterioles. IF showed IgG++, С3+, κ++, λ++ staining co-localized with amorphous material. These findings were suggestive for FGN. Screening for autoimmune diseases was negative, chest and abdominal CT was otherwise normal; bone marrow biopsy did not reveal lymphoma but could not exclude plasma cell dyscrasia, however serum and urine immunochemistry did not confirm monoclonal gammopathy. Review of bone marrow biopsy excluded lymphoproliferative disorder. Review of kidney biopsy confirmed non-immune-complex diffuse glomerulopathy with mesangial and sub-endothelial PAS/Jones/Fuchsin/Congo-negative deposits and with IgG/κ/λ expression ( Figure 1 A-D and Figure 2 A-C). Immunoperoxidase immunohistochemistry with anti-DNAJB9 antibodies showed bright homogenous-granular DNAJB9+++ expression co-localized with PAS-negative glomerular deposits ( Figure 2 D), which confirmed FGN diagnosis. As the detailed work-up did not find neither malignancy, nor monoclonal gammopathy, autoimmune disease, viral hepatitis, nor diabetes mellitus, we concluded, that FGN in this particular case is associated with chronic infection due to persistent for 18 years perianal fistula. Eight months after fistulectomy our patient doing well on nephroprotective treatment only; his blood pressure is within target range, proteinuria 0.3-0.123 g/L, urine sediment is blunt, and serum creatinine 124-102-140 µmol/L. Informed consent was obtained from the individual participant included in the study. None of the authors declares a conflict of interests.

Introduction Mineral-bone disorders (MBD) and extra-bone calcification (EBC) are common and clinically significant complications in patients undergoing maintenance hemodialysis (MH) [1]. Radiological methods of visualization and echocardiography play a key role in the diagnosis of the effects of MBD and EBC outcomes [2, 3]. Case presentation Young male patient was admitted to our hospital for treatment of rough MBD and EBC due to severe tertiary hyperparathyroidism. Proteinuria was detected for the first time at the age of 14. Nephrotic syndrome was diagnosed and glucocorticosteroid (GCS) therapy was initiated. Nephrobiopsy was performed at the age of 16, but it turned on to be inconclusive and did not allow to verify the nature of kidney disease. However, the GSC therapy was continued. Over the next 10 years the patient was lost for follow-up. He sought for medical aid only at the stage of dialysis-required renal failure. Fig. 1A shows axial CT (slice at the level of the renal arteries) without contrast enhancement with widespread calcification of the small vessels in the shrunken native kidneys and calcification of the intestinal branches of the upper mesenteric artery. Fig. 1B is performed in the mode of CT volume rendering (CT VR) without contrast enhancement and demonstrates the possibility of visualizing the contours of the kidneys with massive calcification of parenchymal renal vessels. In In Fig. 1C calcified intestinal branches of the superior mesenteric artery are visible, including its terminal arched branch (ileo-colonic artery), and the calcified inferior mesenteric artery with its branches are well visible. It should be noted that the inferior artery segment is extremely difficult to visualize even when contrast-enhanced. EBC is also known as medial calcific sclerosis, is characterised by calcific deposits within the media of medium and small muscular arteries that do not cause luminal narrowing, unlike atherosclerotic deposits are located on the wall of a large and medium-sized arteries [4]. Fig. 2A shows the computed tomography finding of the patient's spine: the signs of the "Rugger Jersey spine” describes the prominent endplate densities at multiple contiguous vertebral levels to produce an alternating sclerotic-lucent-sclerotic appearance. This mimics the horizontal stripes of a rugby jersey. This term and pattern are distinctive for renal osteodystrophy [5]. On the radiograph of the wrists ( Fig. 2B) acro-osteolysis of the distal phalanges of the 1st, 2nd, 3rd fingers on both sides is determined, initial acro-osteolysis of the distal phalanges of the 4th and 5th fingers of the right hand and the 5th finger of the left hand, pronounced compaction and an increase in the volume of the soft tissues of the 1st, 2nd, 3rd fingers of the distal phalanges by the type of finger clubbing also called "drumsticks", (arrows). The cause of distal osteolysis and the formation of "drumsticks" is a trophic disorder caused by calcification of the vessels of the hands. Fig. 2B ZOOM shows the the signs of subperiosteal resorption of the radial surface of the middle phalanx of the 3rd finger of the right hand (arrow). Similar changes are observed in the patient’s 2nd and 3rd fingers of both hands and are considered characteristic of any variants of hyperparathyroidism [5]. Echocardiographic (Echo) findings are presented at Fig. 2C (apical 4-Chamber). The arrow indicates massive calcification of the fibrous annulus and mitral valve leaflets. Inclusions of calcium in the structure of the myocardium and chordal apparatus of the mitral valve are also visible. These changes caused the formation of severe mitral valve disease. The clinical consequences of severe MBD and EBC are heart failure, disorders of peripheral blood circulation and physical disability. Conclusion The presented clinical case demonstrates underestimated and neglected MBD and EBC in the young patient on MH due to unspecified nephropathy. Radiological and Echo diagnostic approaches allow to assess the prevalence of these lesions and to control the efficiency of the applied medical strategies. The Informed Consent for the publication of the personal data and images was obtained from the patient. The authors declare no conflict of interest.

Currently, thrombotic microangiopathy (TMA) is a common finding in the histological examination of kidney biopsy specimens, while verification of the nosological diagnosis is difficult due to the many etiological factors and the variety of clinical phenotypes. Today, along with primary TMAs, which include thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS), a large group of secondary TMAs associated with a variety of diseases and conditions, considered secondary HUS, is attracting more and more attention. The article presents a clinical case of the development of thrombotic microangiopathy in a 48-year-old man with a history of intravenous drug user who suffered from severe arterial hypertension for a long time. A feature of the disease was clinically - the almost complete absence of hematological manifestations with a progressive nature of nephropathy with an outcome in end-stage kidney disease, morphologically - mainly chronic changes in small extraglomerular vessels (arteries and arterioles), which led to severe ischemic damage to the glomeruli. Considering the predominantly chronic nature of the morphological manifestations of TMA, the absence of signs of acute TMA, and hematological syndrome, the patient did not undergo plasma therapy. In connection with the development of end-stage kidney disease, hemodialysis was initiated. The presented observation illustrates the complex genesis of secondary TMA in a patient with a history of drug addiction and severe arterial hypertension approaching malignant downstream. The presence in the anamnesis of such complement-activating conditions as intravenous drug use, severe arterial hypertension, as well as vaccination against a new coronavirus infection preceding the clinical manifestation, allowed us to interpret this condition as secondary HUS, which, however, does not exclude the presence of protein gene mutations, regulators of the alternative pathway of complement activation, which could act as a predisposing factor, which requires a genetic study of the complement system, since the information obtained will determine the tactics of management in case of kidney transplantation. In addition, this clinical observation demonstrates the importance of a thorough history taking in such patients, the analysis of which will help to identify complement-activating conditions and thereby accelerate the verification of the diagnosis.

The need for central venous catheters in patients on hemodialysis is very high. Even though complications of catheter implantation are rare (on average about 0.5% of cases, according to own data - 0.37%), their treatment is extremely difficult and, in most cases, requires a large surgery. We present four clinical observations. In the first case, during the puncture was damaged the left subclavian vein in the area of its fixation to the first rib and confluence with the internal jugular vein. The resulting heavy bleeding required a thoracotomy, the bleeding was stopped. The patient was discharged. In the second case, there was damage to the left common carotid artery. The defect was eliminated during the operation. The patient was discharged. In the third case, the right common carotid artery was damaged. During the first hours after the injury, the local hematoma did not grow, the condition remained stable. Four hours after physical exertion (stool), there was a rapid increase in hematoma, compression of the trachea, and suffocation. Attempts to intubate were unsuccessful. An emergency tracheostomy was performed. Despite this, the patient died. In the fourth case, the upper vena cava was damaged. In this case, the catheter was located in the projection of the right atrium on the frontal x-ray. The pleural cavity was drained. In connection with the ongoing bleeding on the pleural drainage, an emergency computer tomography was performed, where it was found that the catheter perforates the vein and was located in the pleural cavity. An emergency thoracotomy was performed, the vein defect was eliminated. The patient was discharged after long-term treatment. Thus, a series of clinical observations demonstrate that the diagnosis of severe complications of large vessel damage during the dialysis catheters implantation is difficult due to several factors: the patient's condition, anatomical features, comorbid background, and many localizations of possible damage to vessels. Complicated catheter implantation requires mandatory ultrasound control, observation in the intensive care unit, mandatory x-ray examination, and, if necessary, computer tomography for early detection of life-threatening conditions.