scholarly journals MO210SERUM LEVELS OF PLASMINOGEN ACTIVATOR UROKINASE RECEPTOR AND CARDIOTROPHIN-LIKE CYTOKINE FACTOR 1IN PATIENTS WITH NEPHROTIC SYNDROME

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Natalia Chebotareva ◽  
Anatoliy Vinogradov ◽  
Wenjing Cao ◽  
Alla Gindis ◽  
Igor Alentov ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Iga Nephropathy ◽  
Plasminogen Activator ◽  
Immunosuppressive Treatment ◽  
Laboratory Data ◽  
Serum Levels ◽  
Urokinase Receptor ◽  
Tubulointerstitial Fibrosis ◽  
Chronic Glomerulonephritis ◽  
Serum Samples

Abstract Background and Aims The pathogenesis of primary focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) remains unknown to date. Some circulating permeability factors are discussed. This work assessed molecule candidates for permeability in serum samples of patients with nephrotic syndrome (NS). Method Forty-one patients with chronic glomerulonephritis (CGN) were included in our study. Seventeen patients had FSGS, 7 patients had MCD, 5 patients had membranoproliferative glomerulonephritis (MPGN), 6 patients had IgA nephropathy, and 6 patients had membranous nephropathy (MN). The laboratory data were compared with the clinical and histological features of nephritis. Serum levels of uPAR and CLCF-1 were measured by ELISA. Results The serum levels of plasminogen activator urokinase receptor (uPAR) were higher in FSGS patients before treatment than in patients with other morphological forms (MCD, IgA nephropathy, MN and MPGN). The levels of uPAR in serum did not correlate with daily proteinuria, serum creatinine/eGFR, arterial hypertension, the number of sclerosed glomeruli or tubulointerstitial fibrosis. No correlations were found between the levels of cardiotrophin-like cytokine factor 1 (CLCF-1) in serum and creatinine levels/glomerular filtration rate, the percentage of sclerosed glomeruli or the severity of tubulointerstitial fibrosis. There were no significant differences between the histological variants of nephritis. However, we found correlations between CLCF-1 levels and proteinuria (Rs = 0. 397, p = 0.015) and triglycerides levels (Rs = 0. 475, p = 0.003). Conclusion The data indicate an increase in the serum uPAR levels of FSGS before treatment. CLCF-1 levels in serum do not depend on histological forms of CGN, kidney function or immunosuppressive treatment, but they correlate with proteinuria and serum lipids in patients with NS.

Serum levels of plasminogen activator urokinase receptor and cardiotrophin-like cytokine factor 1 in patients with nephrotic syndrome

2021 ◽  
Author(s):  
Natalia Chebotareva ◽  
Anatoliy Vinogradov ◽  
Venzsin Cao ◽  
Alla Gindis ◽  
Angelina Berns ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Plasminogen Activator ◽  
Serum Levels ◽  
Urokinase Receptor

scholarly journals Elevated serum levels of checkpoint molecules in patients with adult Still’s disease

2020 ◽  
Author(s):  
Yuya Fujita ◽  
Tomoyuki Asano ◽  
Haruki Matsumoto ◽  
Naoki Matsuoka ◽  
Jumpei Temmoku ◽  
...  
Keyword(s):  
Disease Activity ◽  
Immunosuppressive Treatment ◽  
Elevated Serum ◽  
Serum Levels ◽  
Chronic Arthritis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Still’S Disease ◽  
Serum Samples ◽  
Still's Disease ◽  
Adult Still's Disease

Abstract Background: The interaction between galectin-9 (Gal-9) and its ligand, T cell immunoglobulin and mucin-containing-molecule-3 (TIM-3), one of the coinhibitory receptors, transduce the inhibitory signaling to regulate immune responses. The dysregulated expression of checkpoint molecules has been reported under various inflammatory or autoimmune conditions. The aim of this study is to investigate the levels of these checkpoint molecules and their associations between proinflammatory markers in patients with adult Still’s disease (ASD). Methods: Serum samples were collected from 47 patients with active ASD, 116 patients with rheumatoid arthritis (RA), and 37 healthy controls (HCs). Serum levels of Gal-9, soluble TIM-3 (sTIM-3), and IL-18 were determined using enzyme-linked immunosorbent assay (ELISA). Results were compared with clinical features of ASD. Results: Serum Gal-9 levels in patients with ASD (median: 21.57 ng/ml, interquartile range IQR [11.41–39.72]) were significantly higher compared to those in patients with RA (7.58 ng/ml, IQR [5.57–10.20] p < 0.001) as well as those in HCs (4.51 ng/ml, [IQR; 3.58–5.45], p < 0.001). Similarly, serum sTIM-3 levels in patients with ASD were significantly higher than those in patients with RA and HCs. Serum levels of Gal-9 or sTIM-3 showed positive correlations with IL-18 levels (Gal-9; r = 0.90, p< 0.001, sTIM-3; r = 0.78, p< 0.001) in patients with ASD. Serum levels of Gal-9 or sTIM-3 correlated with serum ferritin (Gal-9; r = 0.77, p< 0.001, sTIM-3; r = 0.71, p< 0.001) and ASD disease activity score (Pouchot’s score, Gal-9; r = 0.66, p< 0.001, sTIM-3; r = 0.59, p< 0.001). Whereas there was no significant correlation between serum Gal-9 or sTIM-3 and CRP. ASD patients with chronic arthritis phenotype had a significantly higher Gal-9/ferritin and sTIM-3/ferritin ratio than those without this phenotype. After immunosuppressive treatment, Gal-9 and sTIM-3 levels showed a significant decline in parallel to the disease activity scores. Conclusions: Serum levels of the coinhibitory checkpoint molecules were elevated and correlated with disease activity in patients with ASD. These coinhibitory checkpoint molecule may be implicated in the autoinflammatory process seen in ASD.

Thrombotic Thrombocytopenic Purpura (TTP) and Systemic Lupus Erythematosus (SLE): Distinct but Potentially Overlapping Syndromes.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 858-858
Author(s):  
Laura Hunt ◽  
Xiaoning Li ◽  
Judith James ◽  
Deirdra R. Terrell ◽  
Bernhard Lammle ◽  
...  
Keyword(s):  
Clinical Diagnosis ◽  
Lupus Erythematosus ◽  
Immunosuppressive Treatment ◽  
Laboratory Data ◽  
First Episode ◽  
P Value ◽  
Serum Samples ◽  
Sledai Score ◽  
Previous Diagnosis ◽  
Adamts13 Deficiency

Abstract A systematic literature review suggests that SLE and TTP co-exist: we identified 51 articles reporting 87 patients who were diagnosed with both TTP and SLE. SLE was diagnosed prior to TTP in 53 (61%), subsequent to TTP in 11 (13%) and simultaneously with TTP in 23 (26%) patients. However a critical distinction is that TTP is a rapidly fatal disease without plasma exchange (PE) treatment while SLE is typically a more chronic disease with intermittent acute flares and PE is not an essential treatment. Therefore when TTP is suspected in a patient with an established diagnosis of SLE, the relative benefits and risks of PE are difficult to assess, since the diagnosis of TTP may be unclear and PE is a procedure with risk for major complications and death. The Oklahoma TTP-HUS Registry has collected serum samples on 185 of 206 (90%) of prospectively enrolled patients with a clinical diagnosis of TTP or HUS from 11/13/1995 to 12/31/2003; all patients have been followed to the present time. We compared presenting features and clinical outcomes of the first episode of TTP-HUS between the 14 (7%) patients in whom SLE had been previously diagnosed to the 22 patients in whom the diagnosis of TTP was supported by severely deficient (<5%) ADAMTS13. None of the 14 patients with a previous diagnosis of SLE had severe ADAMTS13 deficiency (range 7–100%, median 50%). SLE disease activity as measured by the SLEDAI score ranged from 3–32, median 10, indicating that SLE manifestations were severe in most patients. Only 2 patients had inactive lupus as indicated by a SLEDAI score <4. SLE was not considered at the time of diagnosis of the first episode of TTP in the 22 patients with severe ADAMTS13 deficiency. Only 1/22 patients has been subsequently diagnosed with SLE; at the time of an apparent relapse of TTP he had serositis and positive serologic tests; his ADAMTS13 activity at that time was 30%. This patient’s course documents the potential overlap of these two disorders. SLE-TTP(n=14) TTP (n=22) p-value Median values are presented for continuous data. Laboratory data are most abnormal values at diagnosis of TTP-HUS ±7 days Age (years) 39 39 0.820 Race (% Black) 36% 45% 0.563 Gender (% female) 100% 82% 0.140 Obesity (BMI ≥ 30 kg/m²) 14% 55% 0.016 Severe neurologic abnormalities 71% 45% 0.126 Platelet count 21 9 0.010 Hematocrit 22 21 0.660 LDH 707 1431 0.043 Acute renal failure 64% 5% <0.001 Response to PE 36% 86% 0.003 Death 64% 23% 0.018 Relapse in 30 day survivors 0% 44% 0.031 Although the demographic (age, race, gender) and some presenting clinical features of patients with SLE and a clinical diagnosis of TTP-HUS were not different from patients with TTP and severe ADAMTS13 deficiency, other presenting features and the outcomes were different. Response to PE was poor, all cause mortality was high, and relapses of TTP have not occurred in patients with a previous diagnosis of SLE. These differences suggest that these 2 groups of patients in our Registry are distinct. Therefore in patients with an established diagnosis of SLE in whom the additional diagnosis of TTP-HUS is considered, more intensive immunosuppressive treatment for SLE is appropriate initial management in addition to considering the relative benefits and risks of PE.

scholarly journals Elevated serum levels of checkpoint molecules in patients with adult Still’s disease

2020 ◽  
Author(s):  
Yuya Fujita ◽  
Tomoyuki Asano ◽  
Haruki Matsumoto ◽  
Naoki Matsuoka ◽  
Jumpei Temmoku ◽  
...  
Keyword(s):  
Disease Activity ◽  
Immunosuppressive Treatment ◽  
Elevated Serum ◽  
Serum Levels ◽  
Chronic Arthritis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Still’S Disease ◽  
Serum Samples ◽  
Still's Disease ◽  
Adult Still's Disease

Abstract Background: The interaction between galectin-9 (Gal-9) and its ligand, T cell immunoglobulin and mucin-containing-molecule-3 (TIM-3), one of the coinhibitory receptors, transduce the inhibitory signaling to regulate immune responses. The dysregulated expression of checkpoint molecules has been reported under various inflammatory or autoimmune conditions. The aim of this study is to investigate the levels of these checkpoint molecules and their associations between proinflammatory markers in patients with adult Still’s disease (ASD). Methods: Serum samples were collected from 47 patients with active ASD, 116 patients with rheumatoid arthritis (RA), and 29 healthy controls (HCs). Serum levels of Gal-9, soluble TIM-3 (sTIM-3), and IL-18 were determined using enzyme-linked immunosorbent assay (ELISA). Results were compared with clinical features of ASD. Results: Serum Gal-9 levels in patients with ASD (median: 21.57 ng/ml, interquartile range IQR [11.41–39.72]) were significantly higher compared to those in patients with RA (7.58 ng/ml, IQR [5.57–10.20] p < 0.001) as well as those in HCs (4.74 ng/ml, [IQR; 4.27–5.63], p < 0.001). Similarly, serum sTIM-3 levels in patients with ASD were significantly higher than those in patients with RA and HCs. Serum levels of Gal-9 or sTIM-3 showed positive correlations with IL-18 levels (Gal-9; r = 0.90, p< 0.001, sTIM-3; r = 0.78, p< 0.001) in patients with ASD. Serum levels of Gal-9 or sTIM-3 correlated with serum ferritin (Gal-9; r = 0.77, p< 0.001, sTIM-3; r = 0.71, p< 0.001) and ASD disease activity score (Pouchot’s score, Gal-9; r = 0.66, p< 0.001, sTIM-3; r = 0.67, p< 0.001). Whereas there was no significant correlation between serum Gal-9 or sTIM-3 and CRP. ASD patients with chronic arthritis phenotype had a significantly higher Gal-9/ferritin and sTIM-3/ferritin ratio than those without this phenotype. After immunosuppressive treatment, Gal-9 and sTIM-3 levels showed a significant decline in parallel to the disease activity scores. Conclusions: Serum levels of the coinhibitory checkpoint molecules were elevated and correlated with disease activity in patients with ASD. These coinhibitory checkpoint molecule may be implicated in the autoinflammatory process seen in ASD.

scholarly journals ASSOCIATION OF HLA AND PROINFLAMMATORY CYTOKINES OF BLOOD IN PATIENTS WITH GLOMERULONEPHRITIS

2017 ◽  
pp. 35-41 ◽  
Author(s):  
M. Kolesnyk ◽  
V. Driyanska ◽  
M. Velychko ◽  
G. Drannik ◽  
O. Petrina
Keyword(s):  
Renal Failure ◽  
Nephrotic Syndrome ◽  
Proinflammatory Cytokines ◽  
Prognostic Markers ◽  
Hla Antigens ◽  
Serum Levels ◽  
High Serum ◽  
Chronic Glomerulonephritis ◽  
Healthy Donors ◽  
Negative Marker

Introduction. Cytokines and HLA are of important part of immunogenesis of many diseases, therefore the analysis of these indices and this associations in dependence of glomerulonephritis (GN) can define their value as the additional prognostic markers. Aim of the work is to determine the peculiarities of associations the high serum levels ofproinflammatory cytokines (TNF a, MCP-1, IL-18) and some HLA in phenotype to substantiate of chronic glomerulonephritis with nephrotic syndrome (CGN, NS) immunogenesis and to ascertain the additional prognostic markers. Materials and methods. There was studied the HLA-antigens distribution in the 264 CGN, NS adult patients and 350 healthy donors by typing the lymphocytes with the aid of standard microlymphocytotoxic test (Terasaki’s test). Using IFA, the level of the proinflammatory cytokines was studied in the blood serum - MCP-1 in 39, IL-18 – 40 and TNF-a - 96patients. Results. HLA-A23, -24, -B8, -38, -41, -44, DR1, -4, -w52 in adults patients have associations (RR>2) CGN, NS; the attributive risk (a>0,1) to develop GN detected in patients have A24, B8, DR 1, 4, w52. The relative risk (RR) to develop chronic renal failure (CRF) is in detection of HLA-10, -29, -30, -41, -51, DR4; attributive risk (AR) - A10. The CGN, NS patients showed statistically higher level of the serum proinflammatory cytokines – TNF-6, IL-17, MCP-1 with more high indices of the TNF-a in patients with HLA-A23, -A28, -B44 (RR of CGN, NS), -A10 (AR of CRF), IL-18 - A24 (AR of CGN, NS) ma A10 (AR of CRF). The highest levels of MCP-1 detected in adults case have risk antigens - relative B41, attributive - A28, B8, and predictor of CRF B41, wich may be negative marker for prognosis. Conclusion. It was to determine associations the serum levels of some cytokines and HLA in patients with CGN, NS. We think it appropriate to study HLA and proinflammatory cytokines TNF-a, IL-18 and MCP-1 in blood as additional negative prognostic predictors for the differentiating approach to treatment.

scholarly journals Terápiás megfontolások IgA-nephropathiában a legutolsó vizsgálatok (STOP-IgAN, TESTING, NEFIGAN) eredményei alapján

2017 ◽  
Vol 158 (49) ◽  
pp. 1946-1952 ◽  
Author(s):  
Judit Nagy ◽  
Balázs Sági ◽  
Judit Máté ◽  
Tibor Vas ◽  
Tibor Kovács
Keyword(s):  
Renal Function ◽  
Iga Nephropathy ◽  
Immunosuppressive Treatment ◽  
Renin Angiotensin System ◽  
Steroid Treatment ◽  
Chronic Glomerulonephritis ◽  
Systemic Steroid ◽  
Supportive Treatment ◽  
Level Of Evidence ◽  
Distal Small Intestine

Abstract: IgA nephropathy is an immune-mediated chronic glomerulonephritis with a great variability in clinical presentation and outcome. The disease can progress to end-stage renal failure in 25% of patients. For this reason we should identify patients with potential to progress. Most important risk factors for progression are persistent proteinuria, hypertension, decreased renal function and some histological lesions. The actually suggested treatment is summarized in KDIGO Clinical Practice Guideline from 2012. They suggest to give firstly non-specific supportive treatment (especially renin-angiotensin system blocking agents). Recommendation about steroid/immunosuppression treatment is based on low level of evidence. Recently three studies were organised concerning benefits and risk of steroid/immunosuppressive treatment added together with specific supportive treatment. In the STOP-IgAN study, systemic steroid/immunosuppressive treatment significantly decreased proteinuria but did not stop progression. In the TESTING study, systemic steroid treatment significantly decreased proteinuria and progression. However, the study was recently discontinued due to several severe side effects of steroid treatment. Involvement of intestinal mucosal immunity in the pathogenesis of IgA nephropathy suggested the NEFIGAN study with budesonide treatment. Budesonide releases corticosteroid in distal small intestine and colon. Proteinuria was significantly decreased and renal function remained stabile. High number of withdrawals owing to adverse effects is a major concern implying a substantial systemic effect of budesonide. We need further information on the characteristics of patients who most likely benefit from steroid/immunosuppressive treatment given after or together with specific supportive treatment. Orv Hetil. 2017; 158(49): 1946–1952.

scholarly journals BK Virus Load Associated with Serum Levels of sCD30 in Renal Transplant Recipients

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Haidar A. Shamran ◽  
Salma N. Malik ◽  
Jinan M. Al-Saffer ◽  
Rana S. Jawad
Keyword(s):  
Renal Transplant ◽  
Immunosuppressive Treatment ◽  
Elevated Serum ◽  
Serum Levels ◽  
Bk Virus ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Serum Samples ◽  
Virus Load ◽  
Significant Difference

Background. Rejection is the main drawback facing the renal transplant operations. Complicated and overlapping factors, mainly related to the immune system, are responsible for this rejection. Elevated serum levels of sCD30 were frequently recorded as an indicator for renal allograft rejection, while BV virus is considered as one of the most serious consequences for immunosuppressive treatment of renal transplant recipients (RTRs).Aims. This study aimed to determine the association of BK virus load with serum levels of sCD30 in RTRs suffering from nephropathy.Patients and Methods. A total of 50 RTRs with nephropathy and 30 age-matched apparently healthy individuals were recruited for this study. Serum samples were obtained from each participant. Real-time PCR was used to quantify BK virus load in RTRs serum, while ELISA technique was employed to estimate serum levels of sCD30.Results. Twenty-two percent of RTRs had detectable BKV with mean viral load of 1.094E+ 06 ± 2.291E+ 06. RTRs showed higher mean serum level of sCD30 (20.669±18.713 U/mL) than that of controls (5.517±5.304 U/mL) with significant difference. BK virus load had significant positive correlation with the serum levels of sCD30 in RTRs group.Conclusion. These results suggest that serum levels of sCD30 could be used as an indicator of BK viremia, and accordingly the immunosuppressive regime should be adjusted.

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