Pub Date : 2023-06-07DOI: 10.36485/1561-6274-2023-27-2-98-101
O. D. Yagmurov, V. D. Isakov
The structure of the detected kidney pathology was studied according to the results of a forensic medical examination of corpses in the St. Petersburg Bureau of Forensic Medical Examination (BSME) in 2020–2021. As a result of the research, it turned out that out of the total number of all corpses that were sent by the investigative bodies for forensic medical examination to the St. Petersburg Bureau of Forensic Medical Examination over the years, kidney pathology amounted to 0.7 %. The most frequent (67 %) renal pathology leading to death were malignant kidney diseases. In the group of malignant kidney diseases, the age of the deceased was in the range of 40–90 years (with a pronounced peak of 80–90 years). The age of the majority of those who died from non-malignant kidney diseases was 50-90 years (with a pronounced peak of 80-90 years). Gender differences in the causes of death in the groups of malignant and non-malignant kidney diseases have not been established.
{"title":"The structure of detected kidney diseases based on the results of forensic medical examination of corpses","authors":"O. D. Yagmurov, V. D. Isakov","doi":"10.36485/1561-6274-2023-27-2-98-101","DOIUrl":"https://doi.org/10.36485/1561-6274-2023-27-2-98-101","url":null,"abstract":"The structure of the detected kidney pathology was studied according to the results of a forensic medical examination of corpses in the St. Petersburg Bureau of Forensic Medical Examination (BSME) in 2020–2021. As a result of the research, it turned out that out of the total number of all corpses that were sent by the investigative bodies for forensic medical examination to the St. Petersburg Bureau of Forensic Medical Examination over the years, kidney pathology amounted to 0.7 %. The most frequent (67 %) renal pathology leading to death were malignant kidney diseases. In the group of malignant kidney diseases, the age of the deceased was in the range of 40–90 years (with a pronounced peak of 80–90 years). The age of the majority of those who died from non-malignant kidney diseases was 50-90 years (with a pronounced peak of 80-90 years). Gender differences in the causes of death in the groups of malignant and non-malignant kidney diseases have not been established.","PeriodicalId":19089,"journal":{"name":"Nephrology (Saint-Petersburg)","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83560811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-07DOI: 10.36485/1561-6274-2023-27-2-72-77
D. Chemodanova, A. Vinogradov, V. Сao, T. Krasnova, N. Chebotareva
BACKGROUND. In the mechanisms of immune inflammation in chronic glomerulonephritis (CGN), activation of T-cells plays an important role. The role of Th1 and Th2 cells in the pathogenesis of some forms of CGN has been well studied, while the activation of Th17 cells in CGN has been only evaluated in isolated studies. THE AIM: to evaluate the value of determining the level of IL-17 in urine and blood serum in chronic glomerulonephritis.PATIENTS AND METHODS. Adult patients with active CGN (N=40) were recruited aged from 18 to 75 years. Ten patients had focal segmental glomerulosclerosis, 6 had membranoproliferative glomerulonephritis, 15 had IgA nephropathy, and 9 had membranous nephropathy at histological examination. The control group included 10 healthy subjects. The IL-17A levels in the urine and blood serum were determined by enzyme-linked immunosorbent assay (ELISA). The IL17A levels in the urine were calculated as the ratio to urinary creatinine. The levels of IL-17 in urine and blood serum were compared with the indicators of proteinuria, albumin, creatinine, serum sodium, also the severity of hypertension, edema and daily sodium excretion.RESULTS. The results of our study showed a significantly higher concentration of IL-17 in urine in patients with a marked decrease in renal function. Also, the levels of IL-17 in urine directly correlated with serum sodium and inversely correlated with eGFR. We also found an association between increase levels of IL-17 in urine with arterial hypertension and the severity of edema. There were no significant correlations of IL-17 in blood serum and other laboratory indicators of nephritis activity.CONCLUSION. Patients with CGN have increase levels of IL-17 in the urine compared to healthy subjects. A more significant increase of IL-17 in urine is observed in patients with high clinical activity of HCG. IL-17A may participate in the mechanisms of sodium retention, the development of hypertension and edema in patients with nephrotic syndrome.
{"title":"The concentration of interleukin-17 in the blood and urine of patients with chronic glomerulonephritis with nephrotic syndrome","authors":"D. Chemodanova, A. Vinogradov, V. Сao, T. Krasnova, N. Chebotareva","doi":"10.36485/1561-6274-2023-27-2-72-77","DOIUrl":"https://doi.org/10.36485/1561-6274-2023-27-2-72-77","url":null,"abstract":"BACKGROUND. In the mechanisms of immune inflammation in chronic glomerulonephritis (CGN), activation of T-cells plays an important role. The role of Th1 and Th2 cells in the pathogenesis of some forms of CGN has been well studied, while the activation of Th17 cells in CGN has been only evaluated in isolated studies. THE AIM: to evaluate the value of determining the level of IL-17 in urine and blood serum in chronic glomerulonephritis.PATIENTS AND METHODS. Adult patients with active CGN (N=40) were recruited aged from 18 to 75 years. Ten patients had focal segmental glomerulosclerosis, 6 had membranoproliferative glomerulonephritis, 15 had IgA nephropathy, and 9 had membranous nephropathy at histological examination. The control group included 10 healthy subjects. The IL-17A levels in the urine and blood serum were determined by enzyme-linked immunosorbent assay (ELISA). The IL17A levels in the urine were calculated as the ratio to urinary creatinine. The levels of IL-17 in urine and blood serum were compared with the indicators of proteinuria, albumin, creatinine, serum sodium, also the severity of hypertension, edema and daily sodium excretion.RESULTS. The results of our study showed a significantly higher concentration of IL-17 in urine in patients with a marked decrease in renal function. Also, the levels of IL-17 in urine directly correlated with serum sodium and inversely correlated with eGFR. We also found an association between increase levels of IL-17 in urine with arterial hypertension and the severity of edema. There were no significant correlations of IL-17 in blood serum and other laboratory indicators of nephritis activity.CONCLUSION. Patients with CGN have increase levels of IL-17 in the urine compared to healthy subjects. A more significant increase of IL-17 in urine is observed in patients with high clinical activity of HCG. IL-17A may participate in the mechanisms of sodium retention, the development of hypertension and edema in patients with nephrotic syndrome.","PeriodicalId":19089,"journal":{"name":"Nephrology (Saint-Petersburg)","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87618621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-06DOI: 10.36485/1561-6274-2023-27-2-29-38
F. Yusupov, A. Yuldashev
In physiological states, the nervous system and kidneys interact with each other to maintain normal homeostasis in the body. However, pathological conditions such as hypertension, pathology of the kidney itself, both acute and chronic, disrupt this interaction. In acute kidney injury (AKI of various etiologies) and chronic kidney disease (CKD), damaged kidneys can have a significant impact on the function of the central nervous system. CKD is an independent risk factor for the development of cerebrovascular diseases and cognitive impairment due to many factors, including the retention of uremic toxins and phosphates, have been proposed as CKD-specific factors responsible for structural and functional cerebral changes in patients with CKD, however, additional studies are needed to determine the exact pathogenesis. Our review is devoted to the interaction of the kidney and the nervous system in physiological conditions and pathophysiological conditions, we are trying to reveal in detail the mechanisms of dysfunction of the nervous system in kidney pathologies.
{"title":"Nervous system and kidneys. Cross-mechanisms of interaction in normal and pathological conditions","authors":"F. Yusupov, A. Yuldashev","doi":"10.36485/1561-6274-2023-27-2-29-38","DOIUrl":"https://doi.org/10.36485/1561-6274-2023-27-2-29-38","url":null,"abstract":"In physiological states, the nervous system and kidneys interact with each other to maintain normal homeostasis in the body. However, pathological conditions such as hypertension, pathology of the kidney itself, both acute and chronic, disrupt this interaction. In acute kidney injury (AKI of various etiologies) and chronic kidney disease (CKD), damaged kidneys can have a significant impact on the function of the central nervous system. CKD is an independent risk factor for the development of cerebrovascular diseases and cognitive impairment due to many factors, including the retention of uremic toxins and phosphates, have been proposed as CKD-specific factors responsible for structural and functional cerebral changes in patients with CKD, however, additional studies are needed to determine the exact pathogenesis. Our review is devoted to the interaction of the kidney and the nervous system in physiological conditions and pathophysiological conditions, we are trying to reveal in detail the mechanisms of dysfunction of the nervous system in kidney pathologies.","PeriodicalId":19089,"journal":{"name":"Nephrology (Saint-Petersburg)","volume":"152 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79582582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-08DOI: 10.36485/1561-6274-2023-27-1-108-114
S. L. Morozov, V. Dlin
The concept of focal segmental glomerulosclerosis in clinical practice is used to describe both a separate disease and morphological characteristics of secondary kidney damage. Most often, focal segmental glomerulosclerosis occurs as a result of the course of primary glomerulonephritis and is the cause of the development of nephrotic syndrome. A feature of the course of nephrotic syndrome in focal segmental glomerulosclerosis is a longer response to steroid therapy, or the formation of dependence/resistance to glucocorticosteroids. Despite the development of scientific progress, the problem of focal segmental glomerulosclerosis in primary glomerulonephritis is still relevant. Understanding the mechanisms of podocyte damage and disease progression is important not only for basic research, but also for everyday clinical practice.
{"title":"The problem of focal-segmental glomerulosclerosis in primary glomerulonephritis","authors":"S. L. Morozov, V. Dlin","doi":"10.36485/1561-6274-2023-27-1-108-114","DOIUrl":"https://doi.org/10.36485/1561-6274-2023-27-1-108-114","url":null,"abstract":" The concept of focal segmental glomerulosclerosis in clinical practice is used to describe both a separate disease and morphological characteristics of secondary kidney damage. Most often, focal segmental glomerulosclerosis occurs as a result of the course of primary glomerulonephritis and is the cause of the development of nephrotic syndrome. A feature of the course of nephrotic syndrome in focal segmental glomerulosclerosis is a longer response to steroid therapy, or the formation of dependence/resistance to glucocorticosteroids. Despite the development of scientific progress, the problem of focal segmental glomerulosclerosis in primary glomerulonephritis is still relevant. Understanding the mechanisms of podocyte damage and disease progression is important not only for basic research, but also for everyday clinical practice.","PeriodicalId":19089,"journal":{"name":"Nephrology (Saint-Petersburg)","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82106823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-08DOI: 10.36485/1561-6274-2023-27-1-86-91
A. Mambetova, M. H. Hutueva, I. K. Thabisimova
BACKGROUND. Chronic kidney disease (CKD) is a common pathology influencing mortality risk in the world population. Calcification of aorta and heart structures (valves, coronary arteries) is a risk factor for cardiovascular complications. The influence of cytokines, integrin proinflammatory indices, acute phase proteins and other inflammatory factors on the risk of extravasal calcification is promising. THE AIM: to study the effect of cytokines, integrative proinflammatory indices, acute phase proteins and other inflammatory factors on the risk of extra-osseous calcification. PATIENTS AND METHODS. A one-stage, cohort study of 85 patients with CKD 5D treated with programmed hemodialysis was conducted. General clinical examination was carried out according to the protocol. Blood levels of C-reactive protein (CRP) were determined by immunoturbodimetry. A Glasgow Prognostic Score (GPS) risk index for systemic inflammation was calculated using CRP and plasma albumin concentrations. Interleukin-6 (IL-6), interleukin-3 (IL-3) were assessed by enzyme immunoassay. Blood leukocyte shift index (BLI) was calculated. Echocardioscopy was performed using Doppler mode. The presence of cardiac valve calcification (CAC) was registered, its severity was assessed. To estimate the abdominal aortic calcification, the abdominal radiography was carried out in the left lateral projection. The severity of manifestations of aortic calcification was assessed using the L.I. Kauppilla Calcification Scale. Statistical analysis was performed using STATISTICA 12.6. toolkit (StatSoft, USA). RESULTS. Systemic inflammatory factors negatively affected the severity of cardiovascular calcification. An increased GPS value was found to correlate with the severity of CAC and CSA. In the case of calcification severity analysis considering IL-3 and IL-6 values, it was also shown that high levels of these pro-inflammatory cytokines are associated with severe manifestations of anterior aortic wall calcification and aortic calcification at the L3 level. Inclusion of ISLC in the analysis had no effect on the severity of calcification of the aortic wall and no effect on the intensity of cardiac valve calcification in general, the aortic valve and the mitral valve in particular.
{"title":"Systemic inflammation factors influence on the risk of detecting signs of cardiovascular calcification in a patient with stage 5D chronic kidney disease","authors":"A. Mambetova, M. H. Hutueva, I. K. Thabisimova","doi":"10.36485/1561-6274-2023-27-1-86-91","DOIUrl":"https://doi.org/10.36485/1561-6274-2023-27-1-86-91","url":null,"abstract":" BACKGROUND. Chronic kidney disease (CKD) is a common pathology influencing mortality risk in the world population. Calcification of aorta and heart structures (valves, coronary arteries) is a risk factor for cardiovascular complications. The influence of cytokines, integrin proinflammatory indices, acute phase proteins and other inflammatory factors on the risk of extravasal calcification is promising. THE AIM: to study the effect of cytokines, integrative proinflammatory indices, acute phase proteins and other inflammatory factors on the risk of extra-osseous calcification. PATIENTS AND METHODS. A one-stage, cohort study of 85 patients with CKD 5D treated with programmed hemodialysis was conducted. General clinical examination was carried out according to the protocol. Blood levels of C-reactive protein (CRP) were determined by immunoturbodimetry. A Glasgow Prognostic Score (GPS) risk index for systemic inflammation was calculated using CRP and plasma albumin concentrations. Interleukin-6 (IL-6), interleukin-3 (IL-3) were assessed by enzyme immunoassay. Blood leukocyte shift index (BLI) was calculated. Echocardioscopy was performed using Doppler mode. The presence of cardiac valve calcification (CAC) was registered, its severity was assessed. To estimate the abdominal aortic calcification, the abdominal radiography was carried out in the left lateral projection. The severity of manifestations of aortic calcification was assessed using the L.I. Kauppilla Calcification Scale. Statistical analysis was performed using STATISTICA 12.6. toolkit (StatSoft, USA). RESULTS. Systemic inflammatory factors negatively affected the severity of cardiovascular calcification. An increased GPS value was found to correlate with the severity of CAC and CSA. In the case of calcification severity analysis considering IL-3 and IL-6 values, it was also shown that high levels of these pro-inflammatory cytokines are associated with severe manifestations of anterior aortic wall calcification and aortic calcification at the L3 level. Inclusion of ISLC in the analysis had no effect on the severity of calcification of the aortic wall and no effect on the intensity of cardiac valve calcification in general, the aortic valve and the mitral valve in particular.","PeriodicalId":19089,"journal":{"name":"Nephrology (Saint-Petersburg)","volume":"40 4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89605071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-08DOI: 10.36485/1561-6274-2023-27-1-92-101
N. Savenkova, D. Ivanov, O. V. Lubimova, V. N. Barsukova, E. A. Pankov, E. Fedotova, E. Dmitrieva
This article presents the features of atypical haemolytic-uremic syndrome (ORPHA 544472) in children. Atypical haemolytic-uremic syndrome (aHUS) is defined by a triad: haemolytic anaemia, thrombocytopenia and acute kidney injury in pediatric and adult patients. The OMIM catalogue presents the phenotypic series of aHUS with mutations of the C3, CFB, CFH, CFHR1, CFHR3, DGKE, MCP, THBD genes. Atypical haemolytic-uremic syndrome is often associated with gene mutations in proteins and activators that regulate complement. We report the case of a girl who had a manifestation of aHUS at 8 years 5 months of age and a severe relapse at 8 years 10 months of age. The relapse was characterised by manifestations of haemolytic anaemia, thrombocytopenia, acute renal damage, severe arterial hypertension, high lactate dehydrogenase and membrane attack complex levels and low C3 component. After 5 courses of haemodialysis, 3 haemodiafiltration, diuresis increased and biochemical parameters improved. We presented with ASUS in a child associated with a p.Cys1101Tyr C3 gene mutation. We used a complement inhibitor, Elizaria®, a biosimilar to the original drug eculizumab, to treat a child with atypical haemolytic-uremic syndrome due to the C3 gene mutation. The complement system inhibitor therapy with Elizaria preserved the health and life of a sick girl with a severe relapse of aHUS.
{"title":"The use of the drug Elizaria – a biosimilar of the original eculizumab in atypical hemolytic-uremic syndrome due to mutation of the С3 gene in children: clinical observation and literature review","authors":"N. Savenkova, D. Ivanov, O. V. Lubimova, V. N. Barsukova, E. A. Pankov, E. Fedotova, E. Dmitrieva","doi":"10.36485/1561-6274-2023-27-1-92-101","DOIUrl":"https://doi.org/10.36485/1561-6274-2023-27-1-92-101","url":null,"abstract":" This article presents the features of atypical haemolytic-uremic syndrome (ORPHA 544472) in children. Atypical haemolytic-uremic syndrome (aHUS) is defined by a triad: haemolytic anaemia, thrombocytopenia and acute kidney injury in pediatric and adult patients. The OMIM catalogue presents the phenotypic series of aHUS with mutations of the C3, CFB, CFH, CFHR1, CFHR3, DGKE, MCP, THBD genes. Atypical haemolytic-uremic syndrome is often associated with gene mutations in proteins and activators that regulate complement. We report the case of a girl who had a manifestation of aHUS at 8 years 5 months of age and a severe relapse at 8 years 10 months of age. The relapse was characterised by manifestations of haemolytic anaemia, thrombocytopenia, acute renal damage, severe arterial hypertension, high lactate dehydrogenase and membrane attack complex levels and low C3 component. After 5 courses of haemodialysis, 3 haemodiafiltration, diuresis increased and biochemical parameters improved. We presented with ASUS in a child associated with a p.Cys1101Tyr C3 gene mutation. We used a complement inhibitor, Elizaria®, a biosimilar to the original drug eculizumab, to treat a child with atypical haemolytic-uremic syndrome due to the C3 gene mutation. The complement system inhibitor therapy with Elizaria preserved the health and life of a sick girl with a severe relapse of aHUS.","PeriodicalId":19089,"journal":{"name":"Nephrology (Saint-Petersburg)","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89435725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-08DOI: 10.36485/1561-6274-2023-27-1-102-107
K. S. Suprunovich, I. Paltyshev, A. Zakharenko, V. Dobronravov
The risk of acute kidney injury (AKI) in cancer patients is much higher than in the general population. Common causes of AKI in this group of patients are toxicity of chemotherapy com ponents and water-electrolyte imbalances. The risks of AKI increase significantly if the patient has a history of chronic kidney disease of any etiology. Risk assessment and correction, prevention and treatment of acute and chronic renal dysfunction are the standard tasks of onconephrology The clinical case of acute kidney disease described here illustrates the main mechanisms and factors of organ dysfunction and its outcomes as a con sequence of colorectal cancer treatment. The necessity of multidisciplinary cooperation in determining the management and treatm ent tactics of such patients is shown, that is essential for the long-term prognosis.
{"title":"Onconephrology: acute kidney disease after preventive ileostomy in a patient with colorectal cancer","authors":"K. S. Suprunovich, I. Paltyshev, A. Zakharenko, V. Dobronravov","doi":"10.36485/1561-6274-2023-27-1-102-107","DOIUrl":"https://doi.org/10.36485/1561-6274-2023-27-1-102-107","url":null,"abstract":" The risk of acute kidney injury (AKI) in cancer patients is much higher than in the general population. Common causes of AKI in this group of patients are toxicity of chemotherapy com ponents and water-electrolyte imbalances. The risks of AKI increase significantly if the patient has a history of chronic kidney disease of any etiology. Risk assessment and correction, prevention and treatment of acute and chronic renal dysfunction are the standard tasks of onconephrology The clinical case of acute kidney disease described here illustrates the main mechanisms and factors of organ dysfunction and its outcomes as a con sequence of colorectal cancer treatment. The necessity of multidisciplinary cooperation in determining the management and treatm ent tactics of such patients is shown, that is essential for the long-term prognosis.","PeriodicalId":19089,"journal":{"name":"Nephrology (Saint-Petersburg)","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90468077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-07DOI: 10.36485/1561-6274-2023-27-1-48-60
T. A. Yagupova, O. Kurochkina, O. A. Minchenkova, Yu. I. Sevalneva, P. A. Bubnova, A. V. Sokolov, K. Vishnevskii, D. Sadovskaya
Перенести в английский вариант BACKGROUND. Hyperphosphatemia in CKD is spread widely, represents as independent factor of mortality at all stages of CKD, after transplantation, reduces the effectiveness of nephroprotection, leads to vascular calcification, stimulates hyperparathyroidism. Achieving the phosphatemia target is a difficult task and is based on a combination of a hypophosphate diet, effective dialysis, the antihyperparathyroidic measures and the phosphate-binders (PBs). THE AIM. The aim is to evaluate the effectiveness of sevelamertherapy in real clinical practice as part of a hypophosphatemic strategy with clarification of the conditions and measures under which it is optimal. PATIENTS AND METHODS. In an eight-month study in a region where there are no restrictions on access to calcium-free PBs, 127 patients were included in the study after the "washing period ": the of sevelamer doses were titrated until phosphatemia reaches below 1.58 mmol/l in parallel with individual measures of four-component hypophosphatemic strategy. RESULTS. From the starting dose of 3-6 tablets/day, 38 patients experienced either dose increase (+ 1016 ± 760 mg) or in 28 patients– decrease (- 1427 ± 1059 mg). By the third month of therapy, the proportion of patients with phosphatemia < 1.58 mmol/l reached 70 %, < 1.78 mmol/l – 90 %. The decrease magnitude depended on the initial phosphatemia, the level of PTH (maximum in the range of 150-600 pg/ml), occurs more slowly in men. During therapy, there was a decrease in the need for antihyperparathyroid therapy in the absence of dynamics in the parathyroid hormone level. In multiple regression analysis models, the independent factors associated with phosphatemia during treatment were sevelamer dose, dialysis dose, baseline phosphate and parathyroid hormone levels; the magnitude of phosphatemia reduction was independently associated with sevelamer dose, dialysis dose, baseline parathyroid hormone level, and assessment of treatment compliance. CONCLUSION. Sevelamer in a moderate well–tolerated doses as part of an individualized hyperphosphatemia correction strategy is able to achieve target phosphatemia (< 1.58 mmol/L) in 70 % of cases, and relatively safe level (< 1.78 mmol/L) – in 90 %.
{"title":"Selamerex: regional real-world practice and perspective of therapy optimisation","authors":"T. A. Yagupova, O. Kurochkina, O. A. Minchenkova, Yu. I. Sevalneva, P. A. Bubnova, A. V. Sokolov, K. Vishnevskii, D. Sadovskaya","doi":"10.36485/1561-6274-2023-27-1-48-60","DOIUrl":"https://doi.org/10.36485/1561-6274-2023-27-1-48-60","url":null,"abstract":" Перенести в английский вариант BACKGROUND. Hyperphosphatemia in CKD is spread widely, represents as independent factor of mortality at all stages of CKD, after transplantation, reduces the effectiveness of nephroprotection, leads to vascular calcification, stimulates hyperparathyroidism. Achieving the phosphatemia target is a difficult task and is based on a combination of a hypophosphate diet, effective dialysis, the antihyperparathyroidic measures and the phosphate-binders (PBs). THE AIM. The aim is to evaluate the effectiveness of sevelamertherapy in real clinical practice as part of a hypophosphatemic strategy with clarification of the conditions and measures under which it is optimal. PATIENTS AND METHODS. In an eight-month study in a region where there are no restrictions on access to calcium-free PBs, 127 patients were included in the study after the \"washing period \": the of sevelamer doses were titrated until phosphatemia reaches below 1.58 mmol/l in parallel with individual measures of four-component hypophosphatemic strategy. RESULTS. From the starting dose of 3-6 tablets/day, 38 patients experienced either dose increase (+ 1016 ± 760 mg) or in 28 patients– decrease (- 1427 ± 1059 mg). By the third month of therapy, the proportion of patients with phosphatemia < 1.58 mmol/l reached 70 %, < 1.78 mmol/l – 90 %. The decrease magnitude depended on the initial phosphatemia, the level of PTH (maximum in the range of 150-600 pg/ml), occurs more slowly in men. During therapy, there was a decrease in the need for antihyperparathyroid therapy in the absence of dynamics in the parathyroid hormone level. In multiple regression analysis models, the independent factors associated with phosphatemia during treatment were sevelamer dose, dialysis dose, baseline phosphate and parathyroid hormone levels; the magnitude of phosphatemia reduction was independently associated with sevelamer dose, dialysis dose, baseline parathyroid hormone level, and assessment of treatment compliance. CONCLUSION. Sevelamer in a moderate well–tolerated doses as part of an individualized hyperphosphatemia correction strategy is able to achieve target phosphatemia (< 1.58 mmol/L) in 70 % of cases, and relatively safe level (< 1.78 mmol/L) – in 90 %.","PeriodicalId":19089,"journal":{"name":"Nephrology (Saint-Petersburg)","volume":"23 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89770735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-07DOI: 10.36485/1561-6274-2023-27-1-61-68
E. Barinov, Kh. V. Grigoryan, Y. Malinin
BACKGROUND. To date, the mechanisms of small stone elimination by lithokinetic therapy (LCT) have not been elucidated. THE AIM of this investigation was to estimate the activity of receptors controlling the contraction and relaxation of smooth muscle cells (SMC) against the background of α1A-adrenoreceptor blockade during LCT in patients with small stones localization in the middle third of ureter. PATIENTS AND METHODS. The study was prospective and included 40 patients in whom standard LCT was done for localization of small concrements (≤6 mm) in the middle third of ureter. The functional activity of receptors modulating ureteric peristalsis was analyzed in vitro using platelet suspension. The agonists used were ATP, ADP, adenosine, epinephrine, angiotensin-2 (Sigma-Aldrich Chemie GmbH, Germany) at EC50 concentrations causing aggregation at 50 % in healthy subjects. Platelet aggregation was assessed by turbidimetric method on ChronoLog analyzer (USA). RESULTS. No differences in the rate of small concrements elimination from the middle third of ureter was found in presence and absence of α1A-adrenoreceptor blocker in LCT. Before LCT, α2-adrenoreceptor hyperresponsiveness, normoreponsiveness of purine P2X1- and P2Y-receptors, adenosine A2-receptor and angiotensin AT1-receptor were found. After 9 days of LCT with verified elimination of concrements, an increase in P2X1-receptor and AT1-receptor activity (p < 0.001) was found regardless of the administration of α1A-adrenoceptor blocker. P2Y-receptor hyperresponsiveness was seen in the presence and normoreponsiveness in the absence of α1A-adrenoreceptor blocker in LCT. CONCLUSION. At the lithokinetic therapy irrespective of α1A-adrenoreceptor blocker prescription, compensatory mechanisms, aimed at enhancement of contractile activity and preservation of smooth muscle cell relaxation take part in the traffics of small concrements from the middle third of ureter.
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