scholarly journals Glomerular filtration rate, readiness to apoptosis and late apoptosis of peripheral blood lymphocytes in different variants of bronchial asthma

Author(s):  
V Mineev ◽  
T Vasilyeva ◽  
I Nesterovich
2020 ◽  
Vol 24 (4) ◽  
pp. 55-60
Author(s):  
V. N. Mineev ◽  
A. A. Kuzmina ◽  
T. M. Lalaeva

INTRODUCTION. We have previously postulated the similarity of molecular pathogenetic mechanisms in bronchial asthma (BA) and chronic kidney disease (CKD). Understanding these mechanisms in such a comorbidity pathology is of interest to the clinicians. In recent years, the attention of BA pathogenesis researchers has attracted low-investigated adipokine – apelin. On the other hand, apelin is considered as a renoprotective adipokine that can prevent the progression of CKD. THE AIM of the study is to identify the relationship between apelin/APJ signaling system and glomerular filtration rate in different BA variants. PATIENTS AND METHODS. The 12 of practically healthy persons and 36 bronchial asthma patients were examined. Levels of apelin-12, apelin-36, and APJ receptor of apelines on peripheral blood lymphocytes were determined, as well as levels of TNF-α, IL-6 IL-4 by immunoenzyme method according to standard protocol. Glomerular filtration rate (eGFR) by CKD-EPI was calculated. RESULTS. With the help of factor analysis, it was revealed that the glomerular filtration rate in bronchial asthma is associated with the level of apelin-36. A high level of glomerular filtration rate corresponds to a high level of apelin-36. In bronchial asthma, the negative association of pro-inflammatory adipokines TNF-α and IL-6 with the glomerular filtration rate was revealed. On the other hand, the IL-4 was found to be directly related to the glomerular filtration rate according to the factorial analysis. CONCLUSION. The obtained data suggest a possible renoprotective effect of apelin-36 in bronchial asthma.


2021 ◽  
Vol 25 (4) ◽  
pp. 64-70
Author(s):  
V. N. Mineev ◽  
T. S. Vasilieva ◽  
A. V. Smirnov ◽  
O. V. Galkina ◽  
V. I. Trofi mov

INTRODUCTION. Previously, we postulated the common pathogenetic mechanisms in bronchial asthma (BA) and chronic kidney disease (CKD). The kidney injury molecule-1 (KIM-1) is considered as an early biomarker of the proximal renal tubules damage. In the available literature, there is only one clinical study of KIM-1 in children BA.THE AIM of the study is to  assess KIM-1 levels in different variants of BA.PATIENTS AND METHODS. The 24 BA patients were examined. Glomerular filtration rate (eGFR) by CKD-EPI was calculated. The concentration of the kidney injury molecule -1 (KIM-1) in urine was determined by enzyme immunoassay. Urinary albumin was determined by the immunoturbidimetric method. VEGF-A in serum was determined by enzyme immunoassay (sandwich variant).RESULTS. In the urine of BA patients, KIM-1 was detected, and its level in patients with a non-allergic variant is significantly higher than in patients with an allergic variant of the disease. Factor analysis was carried out, the following was revealed: the KIM-1 component with a high positive factor load is associated with a key characteristic of BA such as the severity of the disease course, as well as with a high negative factor load – with a component of the glomerular filtration rate; the KIM-1 component with a high positive factor load is associated with the presence of drug intolerance in BA patients; the microalbuminuria component is negatively associated with the severity of BA disease course, as well as with the components KIM-1, VEGF-A, which seems to be associated with the use of systemic glucocorticoids in severe BA disease course; the KIM-1 component is positively associated with the VEGF-A component, which may indicate possible KIM-1 involvement in hypoxic kidney injury in BA. CONCLUSION. The obtained data suggest that in BA, first of all, in a non-allergic variant of the disease and in a severe course of BA, kidney injure is formed, detected using kidney injure molecule-1 KIM-1.


2016 ◽  
Vol 26 (2) ◽  
pp. 196-200
Author(s):  
V. N. Mineev ◽  
T. S. Vasil'eva ◽  
T. M. Lalaeva

2019 ◽  
Vol 3 (3) ◽  
pp. 113-123 ◽  
Author(s):  
Yeon Joo Lee ◽  
Ilya G Glezerman ◽  
Roni Tamari ◽  
Craig S Sauter ◽  
Susan E Prockop ◽  
...  

Background: The epidemiology of BK polyoma virus nephropathy in hematopoietic cell transplant recipients is poorly characterized. Kidney dysfunction after hematopoietic cell transplant is often attributed to treatment toxicities and kidney biopsies are rarely performed. Methods: We reviewed pathology-confirmed BK polyoma virus nephropathy cases in adult and pediatric patients who had undergone a hematopoietic cell transplant between 1 January 2015 and 31 December 2017 at our institution. Plasma and urine BK polyoma virus was assessed by a quantitative polymerase chain reaction assay and were obtained at the clinician discretion. Glomerular filtration rate was estimated by the Chronic Kidney Disease Epidemiology Collaboration equation. BK polyoma virus nephropathy was scored by the Banff Working Group Proposal. Results: Eight (7 adult and 1 pediatric) cases of BK polyoma virus nephropathy were identified among 685 hematopoietic cell transplant recipients, 14 of whom had undergone a kidney biopsy. Five patients (62.5%) had received a CD34+-selected peripheral blood hematopoietic cell transplant; two had received a cord blood allograft and one an unmodified peripheral blood hematopoietic cell transplant. Two patients developed acute graft-versus-host disease grade II. Early post–hematopoietic cell transplant BK polyoma viruria was documented with onset at a median of 54 days (range, 6–91) post–hematopoietic cell transplant and median urine BK polyoma viral load was 9.6 log10 copies/mL (range, 8.6–10.0). BK polyoma virus nephropathy was diagnosed at a median of 267 days after hematopoietic cell transplant (range, 133–637). At BK polyoma virus nephropathy diagnosis, all patients had decreased renal function with glomerular filtration rate (median 29 mL/min/1.73 m2; range, 9–98 ) and creatinine (median 2.4 mg/dL; range, 0.8–7.5) ; median plasma BK polyoma viral load was 6.3 log10 copies/mL (range, 5.5–7.1) and median CD4+ lymphocyte count was 82 cell/mcL (range, 21–172). Conclusions: We report eight biopsy-proven BK polyoma virus nephropathies in hematopoietic cell transplant recipients from a single center. BK polyoma virus nephropathy should be considered in hematopoietic cell transplant recipients with worsening kidney function and high BK polyoma viremia.


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