Vol 88, No 6 (2016)

Articles
Chronic kidney disease and atrial fibrillation as components of the cardiorenal continuum
Mukhin N.A., Glybochko P.V., Svistunov A.A., Fomin V.V., Kiyakbaev G.G.
Abstract
The paper discusses the present-day idea on a relationship between atrial fibrillation and chronic kidney disease, the specific features of therapeutic policy, and the place of antithrombotic therapy in particular. Based on the results of population-based studies, the authors set forth the specific features of cardiac arrhythmias concurrent with kidney injury, as well as promising directions to optimize management schemes for this category of patients.
Terapevticheskii arkhiv. 2016;88(6):4-8
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Prognostic value of acute kidney injury in patients with community-acquired pneumonia
Serov V.A., Shutov A.M., Kuzovenkova M.Y., Ivanova Y.V., Serova D.V.
Abstract
Aim. To investigate the incidence, severity, and prognostic value of acute kidney injury (AKI) in patients with community-acquired pneumonia (CAP). Subjects and methods. A total of 293 CAP patients (185 men and 108 women; mean age 54.3±17.1 years) were examined. AKI was diagnosed and classified in accordance with the 2012 KDIGO guidelines. Results. On admission, the serum concentration of creatinine averaged 104.5±73.3 µmol/l. AKI was diagnosed in 83 (28.3%) patients with CAP. Hospital-acquired AKI was found in 25 (8.5%) patients, which amounted to 30.1% of all the AKI cases. The disease severity according to both the CURB-65 scale and the CRB-65 scale, which neglect blood urea nitrogen concentrations, was higher than that in patients with CAP associated with AKI (1.4±1.0 versus 0.4±0.6 scores; respectively; р<0.0001 and 0.8±0.7 versus 0.3±0.5 scores, respectively р<0.0001). The disease ended in a fatal outcome in 16 (5.5%) patients. The mortality in the presence of AKI was higher: 9 (10.1%) patients died in the AKI-complicated CAP group; that in the absence of AKI was 7 (5.2%; χ2=4.78; р=0.03), the odds ratio for death in the patients with CAP associated with AKI was 3.4; 95% confidence interval, 2.27 to 17.46. Multivariate logistic regression analysis revealed that the occurrence of AKI was independently influenced by age (р<0.001), systolic and diastolic blood pressures (p=0.01 and p=0.01, respectively), and a history of urinary tract diseases (p=0.04) and diabetes mellitus (p<0.001). Conclusion. AKI complicates CAP in 28.3% of cases and increases mortality in patients with CAP. The predictors of AKI in CAP patients are old age, hemodynamic disorders, diabetes mellitus, and prior urinary tract diseases.
Terapevticheskii arkhiv. 2016;88(6):9-13
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Acute kidney injury and tubular biomarkers after hematopoietic stem cell transplantation
Dobronravov V.A., Smirnov K.A., Afanasiev B.V., Galkina O.V., Smirnov A.V.
Abstract
Aim. To determine the value of molecular biomarkers (BMs) associated with tubular epithelial damage in developing and predicting acute kidney injury (AKI) after hematopoietic stem cell transplantation (HSCT). Subjects and methods. The open-label observational prospective study enrolled 90 patients (46 males and 44 females) who had undergone HSCT. The concentrations of BMs (calbindin, clusterin, interleukin-18 (IL-18), kidney injury molecules-1 (KIM-1), glutathione S-transferase-π (GST-π), and monocyte chemoattractant protein-1 (MCP-1) were measured in urinary samples 7 days before HSCT (week 0) and at weeks 1, 2, 3, 4, and 5. Main clinical parameters were simultaneously monitored. AKI was diagnosed and stratified according to the Kidney Disease Improving Global Outcomes (KDIGO) guidelines. Results. At weeks 1, 2, 3, 4, and 5 after HSCT, the proportion of AKI cases was 7.8, 8.9, 12.5, 27.3, and 35.9%, respectively. The elevated urinary levels of BMs (above the median) were found to be substantially more common than AKI cases. The urinary excretion of the majority of BMs dramatically increased in the early HSCT period. The median number of simultaneously elevated BMs was 3 (2; 5) during the entire follow-up period. Clusterin, MCP-1 and KIM-1 positively and significantly correlated with serum creatinine at the week following the determination of BMs in the multivariate linear regression models adjusted for other confounders. The higher urinary KIM-1 and/or MCP-1 excretion regardless of other clinical indicators was associated with the higher relative risk (RR) of AKI, which increased by 2.3 times with a rise in one of these indicators and by 3.4 times with a rise in both indicators. Conclusion. Multiple renal toxic effects after HSCT result in a substantial and simultaneous elevation of urinary excretion of BMs for tubular damage. Among the BMs studied, KIM-1 and MCP-1 seem to be the most suitable molecules for assessing the risk of AKI in this cohort of patient within the predictive diagnostic approach.
Terapevticheskii arkhiv. 2016;88(6):14-20
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Impact of anemia correction on the production of the circulating morphogenetic protein α-Klotho in patients with Stages 3B—4 chronic kidney disease: A new direction of cardionephroprotection
Milovanov Y.S., Mukhin N.A., Kozlovskaya L.V., Milovanova S.Y., Markina M.M.
Abstract
Aim. To investigate the impact of anemia correction with erythropoiesis stimulants on the serum level of the circulating morphogenetic protein α-Klotho in patients with Stages 3B—4 chronic kidney disease (CKD). Subjects and methods. 64 patients aged 42±8 years with Stages 3B—4 nondiabetic CKD were examined and divided into 2 groups: 1) 32 patients with anemia (the target hemoglobin levels could be achieved and kept with erythropoietin and iron saccharate in 20 patients (Group A) and those could not be done in 12 patients (Group 1B). A control group (Group 2) consisted of 32 non-anemic patients matched for gender, age, and degree of a glomerular filtration rate (GFR) reduction. Along with iron exchange indicators, the time course of changes in serum Klotho levels were examined in all the 64 patients during screening and one year after the end of the study. For correction of anemia, 32 patients with this condition (Groups 1A and 1B) took short-acting epoetin (hypodermic recormon 2,000 IU thrice per week + iron (intravenous venofer 5 ml of 100 mg once per week)) under control of hemoglobin levels and serum transferrin iron and ferritin saturation. After achieving the target hemoglobin level of 110-120 g/l, for its keeping, all the patients received, instead of short-acting epoetin, long-acting hypodermic darbepoetin-α 1.5 µg once every 2 months and intravenous iron saccharate 100 mg once every 2 weeks. Results. Among the 32 anemic patients in Group 1, 20 (63%) (Group 1 A) could achieve the target hemoglobin level (110—120 g/l) and maintain it within this range, by performing therapy with epoitin-β + iron saccharate; anemia (the hemoglobin level of <110 g/l) persisted in 12 (37%) patients (Group 1B) despite the fact that epoetin and iron saccharate had been administered. Group 1A was noted to have an increase in α-Klotho concentrations by an average of 100±11.6-pg/ml as compared to Group 1B (by only 72±4.2 pg/ml). At the same time, the α-Klotho levels in the control group by the end of the follow-up decreased by an average of 210±12.9 pg/ml as compared to the prescreening value. There was a direct correlation between hemoglobin and serum ferritin concentrations and iron ferritin saturation percentage and α-Klotho levels. It was ascertained that the hemoglobin concentration of ≥110 g/l with a sensitivity of 89% and a specificity of 75% could predict higher serum α-Klotho levels in CKD. The same patients were found to have an inverse relationship between the serum level of α-Klotho and the risk of cardiovascular events. Conclusion. The serum level of the protein Klotho is not only a marker for the severity of CKD and its complications (anemia, left ventricular hypertrophy, and heart failure), but also a pathogenetic factor of CKD progression. Anemia correction with erythropoiesis stimulants has been shown to enhance the renal and extrarenal production of α-Klotho.
Terapevticheskii arkhiv. 2016;88(6):21-25
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The role of chronic kidney disease in assessing the risk of the poor course of hospital ST-segment elevation myocardial infarction
Karetnikova V.N., Kalaeva V.V., Evseeva M.V., Osokina A.V., Kashtalap V.V., Gruzdeva O.V., Shafranskaya K.S., Zykov M.V., Barbarash O.L.
Abstract
Aim. To evaluate the prognostic impact of chronic kidney disease (CKD) during hospital stay in patients with ST-segment elevation myocardial infarction (STEMI) and to specify factors showing a negative impact of CKD. Subjects and methods. 954 patients with STEMI were examined. The diagnosis of CKD was verified in 338 (35.4%). In all the patients, glomerular filtration rate (GFR) was calculated using the CKD-EPI formula with regard to serum creatinine levels on admission and before discharge (on days 10—12). In the patients who had undergone X-ray contrast intervention, serum creatinine levels were additionally determined on days 2—3 of this procedure in order to identify contrast-induced nephropathy (CIN). Cardiovascular events were assessed in the hospital period. Results. Endovascular interventions into the coronary vessels were made much more rarely in the patients with CHD; but CIN cases were twice more commonly recorded. Nonfatal cardiovascular events were 1.5 times more frequently observed in the CKD patients in the hospital period. The odds of fatal outcomes in both the total sample of STEMI patients and in those with CKD increased by 3.5 and 3.1 times, respectively, in the over 60 age group and by 7.9 and 5.8 times in the presence of Killip Classes II—IV clinically relevant acute heart failure (AHF). In the total sample, the independent predictors for a fatal outcome were a decreased admission GFR less than 60 ml/min/1.73 m2, CIN, and Killip II—IV AHF. The hospital nonfatal complications were also associated with a decreased admission GFR less than 60 ml/min/1.73 m2. Conclusion. The independent predictor of a poor hospital period of STEMI, including fatal outcomes, was a decreased admission GFR less than 60 ml/min/1.73 m2; the presence of CKD was of no independent value.
Terapevticheskii arkhiv. 2016;88(6):26-32
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Risk factors for pulmonary hypertension at the predialysis stage of chronic kidney disease
Rudenko T.E., Vasilyeva M.P., Solomakhina N.I., Kutyrina I.M.
Abstract
Aim. To investigate the incidence and risk factors of pulmonary hypertension (PH) in patients with chronic kidney disease (CKD). Subjects and methods. 86 patients (53% men, 47% women; mean age, 45±13 years) with nondiabetic CKD were examined. According to the magnitude of glomerular filtration rate (GFR) decrease, all the patients were divided into 3 groups: 1) 33 patients with a GFR of 89—45 ml/min; 2) 33 with a GFR of 44—15 ml/min; 3) 20 with a GFR of <15 ml/min who were treated with hemodialysis. A control group consisted of 20 individuals with preserved kidney function (a GFR of >90 ml/min). Physical examination and transthoracic echocardiography were performed in all the patients. The serum concentrations of N-terminal pro-B-type natriuretic peptide (NT-proBNT) and cystatin C were determined. Results. PH was detected in 21 (24.4%) of the 86 patients with CKD. As CKD progressed, its prevalence in Groups 1, 2, and 3 increased, amounting to 18.2, 24.2, and 35%, respectively. The most predictably significant risk factors for PH were hypertension (ρ=0.35; р=0.001) and kidney dysfunction (creatinine (ρ=0.23; р=0.02). Elevated pulmonary artery systolic pressure (PASP) correlated with right ventricular (RV) dimension index (ρ=0.45; р<0.0001), right atrial volume index (ρ=0.3; р=0.02), left atrial volume index (ρ=0.3; р=0.009), and left ventricular mass index (ρ=0.35; р=0.03). In all the patients with CKD in the presence of PH, the NT-proBNP level was significantly higher than in its absence: 37.43 (5.83; 59.84) and 8.54 (5.1; 20.43) fmol/ml, respectively (р=0.01). Positive correlations were found between the level of cystatin C and the presence of PH (ρ=0.32; р=0.003). Analysis of the ROC curve (AUC=0.718; р=0.03) in the predialysis-stage CKD groups (n=66) revealed that the cystatin C level of > 1045 ng/ml with a sensitivity of 71% and a specificity of 60% suggested that PH was present. Multivariate analysis showed that the factors correlating with the presence of PH were NT-proBNP (β=0.34; р=0.008) and RV dimension index (β=0.3; р=0.002). Conclusion. EchoCG reveals PH in almost 25% of the patients with CKD, which occurs at its predialysis stage. Elevated PASP is associated with myocardial structural changes. Traditional risk factors (hypertension) and diminished kidney function affect the development of PH.
Terapevticheskii arkhiv. 2016;88(6):33-39
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The concurrence of kidney and liver dysfunctions in decompensated heart failure
Villevalde S.V., Kobalava Z.D., Solovyeva A.Е., Moiseev V.S.
Abstract
Aim. To study the incidence, pattern, and predictive factors of concurrent kidney and liver dysfunctions in patients with decompensated heart failure (HF). Subjects and methods. The kidney and liver function indicators were estimated in 322 patients aged 69.5±10.6 years with decompensated HF (hypertension in 87%, myocardial infarction in 57%, atrial fibrillation in 65%, chronic kidney disease in 39%, type 2 diabetes in 42%, a left ventricular ejection fraction (EF) of 38±13%, EF <35% 39%, NYHA Functional Class IV in 56%). Cardiohepatic syndrome (CHS) was diagnosed if at least one indicator of liver function was increased; acute kidney injury (AKI) was diagnosed using the KDIGO criteria. Results. AKI and CHS had been previously diagnosed in 60 (18.6%) and 274 (85.1%) patients, respectively. Among the patients with signs of kidney and/or liver dysfunction, the incidence of isolated CHS, concurrent AKI and CHS, and isolated AKI was 78.4, 20.1, and 1.5%, respectively. The patients with concurrent kidney and liver dysfunctions were observed to have more profound systemic hemodynamic changes (hypoperfusion and congestion). The risk of concurrent AKI and CHS increased glomerular filtration rate (GFR) <45 ml/min/1.73 m2, admission systolic blood pressure <110 mm Hg, needs for vasopressors, hydropericardium, and EF <35%. The concurrence of AKI and CHS was associated with longer hospital stay (15.7±6.5 and 13.5±4.8 days, respectively; p<0.05). Conclusion. The incidence of concurrent AKI and CHS in patients with decompensated HF is 20.1%. Concurrent kidney and liver dysfunctions is associated with more obvious signs of hypoperfusion and congestion and characterized by worse prognosis.
Terapevticheskii arkhiv. 2016;88(6):40-44
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Clinical value of TNF, IL-6, and IL-10 gene polymorphic markers in chronic glomerulonephritis
Kamyshova E.S., Shvetsov M.Y., Kutyrina I.M., Burdennyi A.M., Zheng A., Nosikov V.V., Bobkova I.N.
Abstract
Aim. To study the association of the polymorphic markers (PMs) G(-238)A of the TNF gene, G(–174)C of the IL-6 gene, and G(–1082)A of the IL-10 gene with the clinical characteristics of chronic glomerulonephritis (CGN) and a response to immunosuppressive therapy (IST). Subjects and methods. Clinical syndromes at the time of diagnosis, the morphological types of nephritis, and a response to IST were analyzed in relation to the carriage of the examined PMs of the TNF, IL-6, and IL-10 genes in 102 patients with CGN. Results. No association was found between the PM G(-238)A of the TNF gene and the clinical features of CGN. The carriers of the C allele of the PM G(-174) C of the IL-6 gene versus the homozygous individuals were observed to have more frequently kidney dysfunction at the time of diagnosis (р=0.014). Hypertension was more common in the carriers of the AA genotype of the PM G(-1082)A of the IL-10 gene (p=0.023); moreover, they tended to have a more frequent concurrence of nephrotic syndrome and hypertension (p=0.082). Analysis of the distribution of the morphological types of CGN disclosed that the proliferative variants were more common in the patients with the GG genotype (the TNF gene) as compared to the A allele carriers (p=0.067); and the nonproliferative forms were in the individuals homozygous for GG (the IL-6 gene) as compared to the C allele carriers (p=0.067). Examination of an IST response showed that a complete response at 12 months of treatment occurred more frequently in the carriers of the C allele of the IL-6 gene (p=0.045) and in those of the GG genotypes of the IL-10 gene (p=0.030). Conclusion. There was an association of the PMs G(–174)C of the IL-6 gene and G(–1082)A of the IL-10 gene with the clinical features of CGN and a response to IST.
Terapevticheskii arkhiv. 2016;88(6):45-50
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Serum calgranulin C is a highly sensitive autoinflammation activity indicator in patients with familial periodic fevers
Bogdanova M.V., Rameev V.V., Kozlovskaya L.V., Fedorov E.S., Salugina S.O.
Abstract
Aim. To determine the possibility of using the serum proinflammatory calcium-binding protein, or calgranulin C (S100A12), to assess activity and therapeutic efficiency in patients with periodic disease (PD) and other familial periodic fevers (FPFs). Subjects and methods. Thirty-five patients with PD and other FPDs, which were verified by molecular genetic study, were examined. In accordance with the disease activity, the patients were divided into 2 groups. The investigators determined the concentration of S100A12 by solid-phase enzyme immunoassay and that of other acute-phase inflammatory markers (erythrocyte sedimentation rate (ERT), neutrophil counts, and fibrinogen and C-reactive protein (CRP) concentrations). Results. The serum concentration of S100A12 in the stage of disease activity was 466.7 (265.22—851.7) ng/ml, which was significantly higher than in remission (244.29 (118.93—409.85) ng/ml (p=0.000002). The highest S100A12 concentrations were noted in the patients with PD; these were 758.95 (434.80—1035.95) ng/ml; the S100A12 level in the majority of PD patients even during remission remained moderately higher. An investigation of the relationship of A100A12 to genetic variants found no differences between the patients homozygous for M694V and those with other genotypes (p=0.37). Estimation of the time course of therapy-induced changes in the serum S100A12 concentration revealed its considerable reduction (р=0.0018). However, normalization of S100A12 levels was not achieved in PD. The remaining increased S100A12 concentration in these patients may be suggestive of the activity of PD despite the absence of its clinical manifestations. S100A12 as a highly sensitive marker allows more exact evaluation of the anti-inflammatory effect of therapy. The S100A12 identification of the subclinical activity of autoinflammatory diseases made all the more important since traditional inflammatory markers, such as ERT, CRP, fibrinogen, and leukocyte counts, are less sensitive for these purposes. In our study, these markers were within the reference range in remission. No differences were found in the S100A12 levels between the groups with and without amyloidosis (p=0.62). Conclusion. S100A12 is a highly sensitive marker for the activity of autoinflammatory diseases and the efficiency of their therapy. The serum level of S100A12 in PD may be used to diagnose the subclinical activity of inflammation, which is of importance in monitoring the risk of amyloidosis.
Terapevticheskii arkhiv. 2016;88(6):58-64
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Examination of skin autofluorescence for the determination of glycation end-products in patients on chronic hemodialysis
Golubev R.V., Papayan G.V., Glazunova A.A., Korosteleva N.Y., Petrishchev N.N., Smirnov A.V.
Abstract
Aim. To assess the results of determination of glycation end-products (GEPs) by skin autofluorescence (AF) in patients on chronic hemodialysis (HD). Subjects and methods. A device made in Russia was used to estimate skin AF intensity in 40 apparently healthy individuals and in 76 patients treated with chronic HD. While analyzing the findings, comparisons were made in both groups; a relationship between skin AF intensity and clinical and laboratory parameters was also investigated in patients on HD. Results. The intensity of AF in the patients treated with chronic HD proved to be significantly higher than that in the control group. There was a direct correlation of the intensity of AF with age in both groups and that with the duration of dialysis treatment in patients on HD. In patients with coronary heart disease, the intensity of AF was significantly higher than in those without this condition. The intensity of AF directly correlated with the Charlson comorbidity index in the patients on HD. There were no correlations of skin AF intensity with main generally detected laboratory blood indicators, body mass index, and the nature of drug therapy in the patients on HD. Conclusion. Tissue GEP levels may serve as a cumulative index of metabolic stress in HD patients. The determination of GEP by measuring the intensity of skin AF may be used to assess prognosis in patients treated with chronic HD.
Terapevticheskii arkhiv. 2016;88(6):65-72
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Resistant cytomegalovirus infection in related donor kidney allograft recipients
Goryainov V.A., Kaabak M.M., Babenko N.N., Platova E.N., Aganesov A.G., Morozova M.M., Panin V.V.
Abstract
Aim. To clarify whether cytomegalovirus (CMV) infection can affect the results of living related donor kidney transplantation. Subjects and methods. A study group included 17 (7.27%) patients (10 men and 7 women; 8 children and 9 adults) aged 3 to 51 years who had developed resistant CMV infection. For comparative analysis, a control group was formed from 113 patients (61 men and 52 women; 40 children and 73 adults) aged 1 to 61 years, whose CMV polymerase chain reaction (PCR) had always been negative, i.e. CMV DNA was absent. The duration of CMV infection episodes was 44 to 232 days. Results. The patients were given valganciclovir in a dose of 450 mg/day. CMV PCR was negative in all the patients at the end of therapy. None of the patients died; one graft was lost. In the control (negative CMV PCR) group, 6 grafts were lost in 113 patients lost and 4 patients died. Statistical analysis showed that the results of related donor kidney transplantation were virtually equal. Conclusion. Suppression of resistant CMV infection can be achieved with the longer use of valganciclovir or its higher dose. CMV infection fails to affect the results of related donor kidney transplantation.
Terapevticheskii arkhiv. 2016;88(6):73-76
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Incomplete thrombotic microangiopathy as a variant of hemolytic-uremic syndrome
Kozlovskaya N.L., Chebotareva N.V., Nikogosova A.D., Demyanova K.A., Varshavsky V.A., Roshchupkina S.V.
Abstract
The described case illustrates difficulties in diagnosing atypical hemolytic-uremic syndrome (aHUS) in incomplete thrombotic microangiopathy (TMA) in the absence of thrombocytopenia, one of the signs of the classic triad of aHUS, which has resulted in the delayed verification of its diagnosis and in progressive kidney injury. The paper discusses the need to carry out kidney biopsy and to include sHUS in both the presence of a complete set of symptoms of this disease and in the absence of one of them into a range of diagnostic search.
Terapevticheskii arkhiv. 2016;88(6):77-79
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Secondary monoclonal gammopathy after bone marrow autotransplantation as a cause of worse renal function in light chain immunoglobulin deposition disease
Rekhtina I.G., Mendeleeva L.P., Stolyarevich E.S., Galtseva I.V., Povilaitite P.E., Biryukova L.S.
Abstract
The paper describes a clinical case of a female woman with nephropathy due to light chain deposition disease caused by secretion of κ Bence-Jones protein. Complete immunochemical remission was achieved after induction therapy using a bortezomib + cyclophosphamide + dexamethasone regimen. Renal function remained unchanged (glomerular filtration rate 16 ml/min), there was a reduction in proteinuria from 5.8 to 2.6 g/day. High-dose melphalan (200 mg/m2) chemotherapy with peripheral blood stem cell autotransplantation was performed as consolidation of remission. A year posttransplantation, there was no secretion of κ light chains; however, monoclonal IgG lambda emerged in a quantity of 3.2 g/l. At the same period, nephrotic syndrome became progressive (daily proteinuria 12 g) and dialysis-dependent renal failure developed. A repeat renal biopsy specimen revealed changes, suggesting that there was a decrease in renal deposits of κ light chains. Simultaneously with this, the obvious negative trend as progressive nephrosclerosis and fixation of IgG and λ light chains in the glomeruli (in the sclerotic areas) cause IgGλ monoclonal protein to be involved in the genesis of further kidney injury. Attention is also paid to different characteristics of capillary wall deposits by density (according to the electron microscopic findings), which may point to their different qualitative composition and possibly different formation duration. Papaprotein Gλ disappeared after a year without therapy, suggesting its reactivity. The findings confirm that worse renal function is caused by the action of paraprotein Gλ due to secondary (after autologous hematopoietic stem cells transplantation) monoclonal gammopathy.
Terapevticheskii arkhiv. 2016;88(6):80-83
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Diabetes mellitus and chronic kidney disease: Possibilities of prediction, early diagnosis, and nephroprotection in the 21st century
Shestakova M.V.
Abstract
The review gives data on the prognostic value of genetic markers when analyzing the risk of chronic kidney disease in diabetes mellitus, those on new possibilities of early diagnosis of diabetic nephropathy using urinary biomarkers (nephrinuria, podocinuria) and proteomic urinalysis at the stage of normoalbuminuria. The interpretation of the index microalbuminuria in type 2 diabetes is critically analyzed. The nephroprotective properties of novel classes of glucose-lowering drugs, such as incretins and gliflozins, are considered.
Terapevticheskii arkhiv. 2016;88(6):84-88
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Idiopathic membranous nephropathy: Evolution in understanding the problem
Bobkova I.N., Kakhsurueva P.A., Stavrovskaya E.V.
Abstract
The review highlights the evolution of ideas on the mechanisms responsible for the development of membranous nephropathy (MN), glomerulopathy that is the most common cause of nephrotic syndrome in adults. Primary emphasis is placed on the primary form of MN. The important step to understanding the nature of this clinical and morphological form of glomerulonephritis is to create its animal model (Heymann nephritis), then to decipher the mechanisms of immune complex damage (complement activation, a role of cellular immunity), and to identify autoantigens responsible for the development of idiopathic MN in man (podocyte neutral endopeptidase, transmembrane M-type phospholipase A2 receptor, thrombospondin type-1 domain-containing 7A. The findings constituted the basis for developing current methods for the diagnosis and treatment of MN, including the pathogenetically sound inhibition of autoantibody production, as well as a molecular orientation effect on podocyte dysfunction.
Terapevticheskii arkhiv. 2016;88(6):89-94
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Difficulties in correcting hyperphosphatemia in patients with chronic renal failure. A place of noncalcium-containing phosphate-binding drugs
Milovanov Y.S., Fomin V.V., Milovanova L.Y.
Abstract
The review considers the current views of the mechanisms of hyperphosphatemia in patients with chronic renal failure. It shows indications for the use of different classes of phosphate-binding drugs to correct hyperphosphatemia.
Terapevticheskii arkhiv. 2016;88(6):95-100
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The efficiency of antiviral therapy in patients with chronic hepatitis C infected with hepatitis C virus recombinants
Yushchuk N.D., Znoyko O.O., Dudina K.R., Kozina A.N., Kalininа O.V.
Abstract
The review gives the data available in the literature on the efficiency of treatment in patients with chronic hepatitis C infected with hepatitis C virus (HCV) recombinants, by applying various antiviral therapy regimens. The low efficiency of treatment with pegylated interferons (PEG IFN) + ribavirin (RIB) and sofosburin (SOF) + RIB in this patient group (a sustained virologic response was achieved in 22 and 30.7%, respectively) compared with the efficiency of treatment (87—97 and 83—97%, respectively) in patients infected with HCV genotype 2 does not allow the 2015 EASL HCV genotype 2 treatment regimens to be used in such patients. In this connection, subtyping genotype 2 isolates by NS5B sequencing should be introduced into clinical laboratory practice to successfully detect recombinant HCVs and to enhance the efficiency of antiviral therapy.
Terapevticheskii arkhiv. 2016;88(6):101-105
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