Diets with limited daily protein intake initially were proposed to improve the quality of life of patients with reduced renal function. This approach has now become a part of nephroprotective therapy. A low protein diet reduces intoxication due to protein metabolites (hydrogen, guanidines, phenol, indoxyl sulfate, microglobulin, glycation end-products, etc.) and decreases other uremic toxins excreted in urine. The diets slow the progression of uremia and delay the onset of the renal replacement therapy. A low-protein diet can be used with non-intensive dialysis for saving of residual renal function preventing complications due to uremic toxins and hyperhydration. In patients older than 75 years a low-protein diet with the addition of essential aminoacids and it’s ketoanalogues allows one to perform hemodialysis not three times a week, but once or twice. Compliant patients can continue conservative therapy, despite the extremely low values of the glomerular filtration rate. The quality of life of patients on a low-protein diet with the addition of essential aminoacids and it’s ketoanalogues is not worse than of those on dialysis. The frequency of hospitalizations due to various complications, such as problems with vascular access, is significantly less in such patients. A long-term use of a low-protein diet does not affect the nitrogen balance in patients with chronic renal failure and is very rarely complicated by protein-energy deficiency. The main causes for transferring patient on renal replacement therapy are hypehydration and hyperkalemia. A low-protein diet allows one to use different modes of hemodialysis and continuous ambulatory peritoneal dialysis. Different aspects of the use of a low-protein diet are reviewed.

In recent years, a global increase in the incidence of Chronic Kidney Disease (CKD) has been observed. This problem has both medical (high mortality from cardiovascular causes in this population) and economic (large costs of the health care system for a relatively small category of patients) character. Therefore, a search for solutions for reduction of the CKD burden is an important problem of modern nephrology. Nutritional status impairments are widespread. They are predictors of adverse outcomes in CKD. However, with early detection they can be relatively easily corrected with special diet. Variations of nutritional status impairments include both underweight and overweight. The impact of nutritional status disorders on the progression and clinical outcomes of CKD varies depending on the stage: protein-energy wasting (PEW) is an unfavorable factor and can be found in all stages of CKD. It is more common at the later stages, whereas, obesity plays a greater role in CKD progression on its early stages. However, in dialysis patients, obesity is associated with better survival (reverse epidemiology). The combination of PEW and obesity (sarcopenia-obesity complex), was found in all stages of CKD. It was suggested that in patient with normal weight or overweight, it is the loss of muscle mass and the uneven distribution of adipose tissue by the central type, adversely affect the prognosis. The nutritional status disorders are amenable to correction and their timely identification, modification of lifestyle, correction of dietary regime and ratio can ease the burden of CKD in the group of high-risk patients. However, in practice, the importance of determining and correcting nutritional status impairments is often underestimated. The purpose of this review was to identify the role of overweight and underweight in the pathogenesis and progression of CKD, to discuss the results of the recent studies on this topic and to improve understanding of the mechanisms of violation of nutritional status in CKD, which will undoubtedly contribute to the development of effective strategies for their prevention, diagnosis and treatment.

Modern achievements of interventional cardiology in treatment of coronary heart disease (CHD) have significantly increased the number of interventions with the use of contrast media (CM). Contrast-induced acute kidney injury (CIAKI) associated with CM administration is determined by increase in the serum creatinine (SCr) concentration up to 26.5 µmol/l within 48-72 hours or >1.5-fold increase in SCr concentration compared to its known or estimated level in previous 7 days. Despite toxic CM effects on the renal tubule epithelium, no safe replacement has been found yet. Treatment of existing CIAKI is complex and not very efficient. Effective therapeutic options are limited only to adequate prevention of renal injury. Without early diagnosis and prevention, CIAKI leads to higher cardiovascular morbidity, extended admission, rare but significant need of a renal replacement therapy and involves 5-fold rise of in-hospital mortality. Without effective disease management, prevention with early CIAKI risk stratification and cessation of nephrotoxic medications taken by patients are important. The significance of the problem and diagnostic limitations associated with the measurement of SCr level require the search for clinically and diagnostically significant AKI biomarkers. In terms of coronarography and percutaneous coronary interventions, several studies have been conducted to estimate the clinical and diagnostic significance of some biomarkers. Certain AKI biomarkers have proved their efficacy in several studies, but detailed studies of the effects of their combinability are necessary to improve the quality of medical care of patients after performed percutaneous coronary intervention (PCI). This article characterises and discloses prospective practical use of neutrophil gelatinase-associated lipocalin (NGAL), liver-type fatty acid binding protein (L-FABP), kidney injury molecule-1 (KIM-1), cystatin C (CysC) and interleukins-6,8,18 (IL-6,8,18) in interventional cardiology.

The aim of the study: to assess the prognostic value of interstitial fibrosis (FI) extension in kidney biopsy for achieving a renal response to therapy in myeloma cast nephropathy (MCN) patients with dialysis-dependent acute kidney injury (AKI). Materials and methods: kidney biopsy samples were retrospectively studied in 30 patients with MCN and dialysis-dependent AKI. Interstitial fibrosis and tubular atrophy (IFTA) were evaluated using semi-quantitative (standard) method. In addition, a quantitative morphometric computer-aided analysis was performed for FI. The results were compared with clinical data. Results: FI was found in kidney biopsy samples of all patients, median of its severity was 28.3% [14.5; 59]. In 12 (40%) cases the FI was graded as the 1st (mild) degree [median 21.5%; 14.5; 24.1], in 16 (53%) patients - the 2nd (moderate) degree FI was found [median 40%; 25.1; 48.2], in 2 (7%) patients 3rd (severe) degree FI was found [54.1% and 59%]. All 30 patients who were dependent on hemodialysis at the beginning of anti-myeloma treatment, 17 (57%) of them achieved myeloma response, among them 10 patients demonstrated renal response. In the absence of myeloma response, the improvement of renal function was not observed in any case. The median quantifed FI in patients with renal response was 22.9% [14.5; 39.3]; in those without improvement renal function it was 47.1% [40.8; 59], p<0.001. The FI value of 40% or higher of the total renal cortex surface makes it possible to predict a lack of improvement kidney function with a probability of 85% (95% CI), even in whose patients in whom a hematological response to anti-myeloma treatment was achieved. Conclusion: renal response in patients with MCN and dialysis-dependent acute kidney injury was observed only when the hematological response was achieved at the first anti-myeloma treatment's line. In most patients by the beginning of treatment, FI was graded as moderate. Quantifying FI in a kidney biopsy of 40% or higher before starting therapy is an unfavorable prognostic factor in the reversibility of dialysis-dependent acute kidney injury.

Introduction: the lack of data on the epidemiology of presarcopenia/sarcopenia in the Russian Federation leads to an underestimation of the role of this condition in the structure of morbidity and mortality in haemodialysis patients. The aim of the study: to evaluate the epidemiological aspects presarcopenia/sarcopenia in haemodialysis patients. Patients and methods: 317 patients (171 women and 146 men) receiving programmed bicarbonate haemodialysis for 8.2±5.1 years were examined; the average age was 57.1±11.3 years. The assessment of the presence of sarcopenia was performed using the method recommended by the European Working Group on Sarcopenia in Older People. Results: the prevalence of presarcopenia was 0.7 % (2 patients) and sarcopenia 29.6% (93 patients). The incidence of skeletal muscle mass deficiency according to muscle mass index (IMM) was 30.3% (95 patients), 153 patients (48.7%) showed a decrease in muscle strength according to dynamometry, and a low performance of skeletal muscles according to 6 minute test was determined in 134 patients (42.8%). Patients with sarcopenia were characterized by lower body mass index, muscle mass index, muscle strength according to dynamometry, and skeletal muscle performance as estimated by a 6-minute test (statistical significance p<0.001, p<0.001, p<0.001 and p<0.001 respectively), as well as higher body fat mass values (p<0.001). The duration of haemodialysis was an independent risk factor for the development of sarcopenia (χ2=22.376, p=0.0001). Similar reliable trends were identified when assessing the influence of the patient's age on the incidence of sarcopenia. Thus, it can be considered that the patient's age is an independent risk factor for the development of sarcopenia (χ2=10.545, p=0.014). Conclusion: the incidence of sarcopenia in haemodialysis patients is 29.6%. The duration of haemodialysis therapy and the age of the patient are independent risk factors for the development of sarcopenia.

Relevance: renal artery stenosis is a serious pathology leading to the loss of renal function and progression of hypertension. Objective: to evaluate the long-term clinical results of endovascular correction of renal artery stenosis (ECRAS). Materials and methods: we analyzed the long-term results of endovascular correction of renal artery stenosis (ECRAS) in 167 patients who received 205 interventions. All patients had hypertension established in accordance with WHO recommendations (1999), and chronic kidney disease (CKD) determined by glomerular filtration rate (GFR) using CKD-EPI formula. We evaluated EСRAS results at 1 and 3 years after the intervention. We have analyzed patient survival, renal artery survival (estimated by the renal artery patency before occlusion or before the development of hemodynamically significant restenosis), the functional state of kidneys (according to CKD-stage, serum creatinine level and GFR), as well as the average blood pressure (BP) and the degree of BP control before and after EСRAS. Results: survival rate of patients after ECRAS was: 1 year 99% patients, 3 years and 5 years 93% patients, and survival of renal artery: 92%, 90% and 84% respectively. Creatinine level at 1 and 3 years after EСRAS significantly decreased (p<0,001, Student's test), as did the CKD-stage at 1 and 3 years after EСRAS (p=0,001, Wilcoxon test). GFR at 1 and 3 years after EСRAS significantly increased (p<0,001, p<0,01, Student's test). The average BP and the degree of BP control at 1 and 3 years after EСSRAS also significantly decreased (p<0,001, Wilcoxon test). Conclusions: EСRAS is highly effective in restoring renal artery patency. It allows one to preserve and improve renal function, as well as more effectively control hypertension.

Aim: to evaluate the efficacy and safety of individual correction of metabolic acidosis in hemodialysis (HD) patients. Method: the study included HD patients with the duration of renal replacement therapy (RRT) of at least 3 months. Laboratory tests were performed before the second HD session of the week, at baseline, 3 months and 1 year after the study start. We adjusted the dialysate bicarbonate (Bi) gradually, no more than 1 mmol/l per month. The target blood Bi level after 3 months of correction was 22-25 mmol/l. A cohort survival and relative risk of death analysis performed 3 years after the start of the study. Results: 146 HD patients with average age 60±11 years and average RRT duration 63±53 months were included to the study. The dialysate Bi increased from the baseline 31±1 to 33±1 at month 3 and to 34±1 mmol/l at one year (p<0.001) of HD; blood Bi level increased from the baseline to month 3 and after 1 year: 20.5±1.8→21.5±1.9→22.8±2.4 mmol/l, p<0.001. Patients with low comorbidity (Charlson comorbidity index, CCI<6 points) were characterized by a higher level of blood Bi after correction in comparison with patients with a large number of complications (CCI≥6 points): 22.6±1.8 v. 21.7±1.9 mmol/l, p=0.021. Against the background of the acidosis correction there was a significant decrease in the hyperphosphatemia severity: 1.98±0.46→1.73±0.56→1.72±0.5 mmol/l from baseline values to month 3 and after 1 year, respectively (p<0.001), serum albumin increased one year after the beginning of the study (from 37.7±2.1 to 40.3±3.1 g/l, p<0.001). Patients with low blood Bi levels after correction (≤20 mmol/l) had increased risk of all-cause mortality (HR 6.98; 95%CI 2.22÷21.9) compared with those with normal level of Bi (≥22.0 mmol/l), p=0.001. Conclusion: individualization of the dialysate bicarbonate level in HD patients contributes to a reduction in the acidosis severity and decrease in the serum phosphate level as well as increase in serum albumin. In the long term, correction of acidosis leads to a mortality reduction. Patients with a complicated comorbidity are characterized by a worse response to the acidosis correction and this requires further search for effective methods of individual acid-base disorders correction of in this group.

Aim: we analyzed changes of bone mineral density (BMD) in patients with chronic kidney disease (CKD) and severe hyperparathyroidism (НPT) in the preoperative period and after parathyroidectomy (PTХ). Methods: a single-center retrospective observational study included 44 dialysis patients with HPT. All patients underwent subtotal and total PTX. BMD in the distal forearm (1/3 Radius and Radius Total), proximal femur (Femoral Neck and Total Hip) and lumbar spine (L1-L4) was determined by dual energy X-ray absorptiometry (DRA). The absolute value of the BMD (g/cm2) and the Z- and T-scores (SD) were taken into account. The stability of the BMD was determined to be within ±2%. In total 137 DRA sessions were performed (in average once a year): 78 of them were performed in preoperative period and 59 of them after the PTX. The duration of the follow up was 1-4 years. Results: during a year before PTX the average loss of BMD was 7.6±2.3%, 11.1±4.6%, 10.5±8.9%, 9.9±8.7% and 6.0±6.8%, respectively in 1/3 Radius, Radius Total, Femoral Neck, Total Hip and L1-L4. The highest prevalence of osteopenic syndrome estimated by the Z- and T-scores was recorded in the distal forearm. BMD was markedly improved in all parts of skeleton averaging 8-9% in the distal forearm and proximal femur and 5% in L1-L4 (p=0.03 and p=0.05), after two years - 4-3% и 3% respectively. An inverse relationship was established between the percentage of BDM increase after PTX and its baseline before the PTX, for Femoral Neck (p=0.009) and Total Hip (p=0.049) and a tendency for it for 1/3 Radius (p=0.077). Conclusions: there is a high prevalence of osteopenic syndrome with predominant localization in cortical bones in patients with CKD. The dynamic increase in BMD deficiency can serve as an additional argument in favor of the need to implement the PTX. PTX leads to a significant increase in BMD and reduces the incidence of osteopenic syndrome.

Background. Hemophilia A is a congenital coagulation disorder caused by a deficiency of blood coagulation factor VIII. The method of choice for renal replacement therapy ensuring vascular access and safe anticoagulant therapy during hemodialysis in patients with hemophilia A and developing renal failure have not been studied. The aim of this clinical observation is to show the peculiarities of renal replacement therapy in a patient with severe hemophilia A. Observation. A clinical case of a patient with hemophilia A is presented. The patient needed programmed hemodialysis due to chronic kidney disease. An arteriovenous fistula was originally formed as a vascular access. Hemodialysis sessions were carried out without the use of anticoagulants, using only natural hypocoagulation due to hemophilia. However, before the end of the procedure, the factor VIII concentrate was administered to prevent bleeding from punctures of arteriovenous fistula. Two years after the start of programmed hemodialysis, the patient underwent allogenic cadaveric kidney transplantation. Due to the self-cancellation of an immunosuppressive therapy, graft rejection has developed, and therefore the graft was removed a year later. Programmed dialysis was resumed. As a vascular access, a permanent tunneled catheter was used that allowed one to performe hemodialysis sessions without anticoagulant therapy using only natural hypocoagulation, and without a subsequent introduction of the factor FVIII concentrate. Conclusion. A second case of kidney transplantation in a patient with hemophilia in Russia is described. The tactics of anticoagulant therapy in hemophilia patients during hemodialysis procedures depends on the activity of the deficient factor in the blood plasma and the selected vascular access.

Atypical hemolytic uremic syndrome (aHUS) is a rare complement-mediated life-threatening disease belonging to the group of thrombotic microangiopathies (TMA). Currently, over 400 mutations in the genes encoding complement proteins are known. In 20% of cases, familial forms of aHUS are diagnosed. C3 mutations account for 4 to 10% of cases. The presented clinical observation demonstrates the development of aHUS in three family members (father and 2 children) with indications of an autosomal dominant type of disease inheritance. The clinical diagnosis was supported by the results of a genetic study of the complement system that identified the C3 complement component gene mutation (p.Ile1157Thr) in a family member (a son). The age of implementation of aHUS differed within the family members. The father has a debut of the disease at the age of 12, the children were diagnosed in their infancy (6 months for son, 7 months for daughter). In the presented observation, the peculiarity of the course of the disease in all family members was the development of the classical symptoms of aHUS without extrarenal symptoms. The severity of clinical manifestations differed among family members: the father had 3 episodes of activity of complement-mediated TMA, the daughter - 1, and the son - 5. At the same time, for father and daughter, the severity of hematological manifestations of aHUS prevailed over nephrological ones. For the son, this was observed only in the first 2 episodes. The severity of the disease was due to the severity of hemolysis over the remaining symptoms of TMA, and in subsequent relapses the severity was caused by the development of dialysis-dependent renal failure. All family members were plasma sensitive. Complement-blocking therapy (eculizumab) in children made it possible to achieve aHUS remission with complete restoration of renal function.

Patients with chronic renal failure have a higher risk of coronary heart disease than those with normal renal function. This category of patients is also more likely to have major cardiac and cerebrovascular events (MACCE), which are the main cause of death. Myocardial revascularization in patients with CKD and multivessel coronary artery disease provides better survival rates in comparison with a drug treatment. A clinical case is presented with a successful minimal invasive direct coronary artery bypass (MIDCAB) performed 5 years after kidney transplantation. A 56 years old patient underwent performed allotransplantation of cadaveric kidney on 23.04.2013. Selection according the body system ABO (identical), negative cross-sample, HLA-1 (no matches). The duration of cold ischemia was 5 hours. The graft function was primary normalized on the 26th day after surgery as revealed from the blood creatinine level. Between the years 2013 and 2018, the renal graft function was moderately reduced, although remained stable with minimal urinary syndrome. A maintenance immunosuppression was carried out with tacrolimus (in extended-release formulation capsules), metilprednisolone and azathioprine. During the last 2 years, the patient noted increased shortness of breath and chest pain at minimal physical activity. Cardiocoronarography performed in 2018 revealed an occlusion of the middle segment of left anterior descending artery (LAD), stenosis of the first diagonal branch of permanent residence less than 50%. On 15.5.2018 the MIDCAB of LAD was performed. The left internal thoracic artery was anastomosed with LAD, distal to the second DA. The postoperative period was uneventful. The time spent in ICU was 20 hours. The patient was discharged in a satisfactory condition in 7 days. Eight months after surgery the renal graft function was stable, moderately reduced. The number of published reports of successful coronary bypass surgery (even after off-pump surgery) in patients after kidney transplantation is limited.