interleukin-8 has been researched along with Albuminuria* in 16 studies
1 review(s) available for interleukin-8 and Albuminuria
1 trial(s) available for interleukin-8 and Albuminuria
15 other study(ies) available for interleukin-8 and Albuminuria
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Albumin Urinary Excretion Is Associated with Increased Levels of Urinary Chemokines, Cytokines, and Growth Factors Levels in Humans.
The aim of the present study was to study the associations between urine albumin excretion, and a large number of urinary chemokines, cytokines, and growth factors in a normal population. We selected 90 urine samples from individuals without CVD, diabetes, stroke or kidney disease belonging to the Prospective Investigation of the Vasculature in Uppsala Seniors Study (41 males and 49 females, all aged 75 years). Urinary cytokine levels were analyzed with two multiplex assays (proximity extension assays) and the cytokine levels were correlated with urine albumin. After adjustment for sex, body mass index (BMI), estimated glomerular filtration rate (eGFR), smoking and multiplicity testing, 11 biomarkers remained significantly associated with urine albumin: thrombospondin 2, interleukin 6, interleukin 8, hepatocyte growth factor, matrix metalloproteinase-12 (MMP-12), C-X-C motif chemokine 9, tumor necrosis factor receptor superfamily member 11B, osteoprotegerin, growth-regulated alpha protein, C-X-C motif chemokine 6, oncostatin-M (OSM) and fatty acid-binding protein, intestinal, despite large differences in molecular weights. In this study, we found associations between urinary albumin and both small and large urine proteins. Additional studies are warranted to identify cytokine patterns and potential progression markers in various renal diseases. Topics: Aged; Albuminuria; Chemokines; Cytokines; Female; Glomerular Filtration Rate; Hepatocyte Growth Factor; Humans; Interleukin-6; Interleukin-8; Male; Oncostatin M; Thrombospondins | 2021 |
Evidence for interactions between inflammatory markers and renin-angiotensin system molecules in the occurrence of albuminuria in children with sickle cell anemia.
Sickle cell anemia (SCA) is an important cause of chronic kidney disease, but its pathophysiology is not completely understood. The aim of this study was to compare inflammatory biomarkers in urine samples of SCA children with and without albuminuria, and to explore correlations with renin-angiotensin system (RAS) molecules. A cross-sectional study of 213 children selected from the Minas Gerais state cohort were assigned to two groups: Group 1-89 children with SCA who had albuminuria; Group 2-124 children with SCA and normal albuminuria matched by age and sex with group 1. A subset of 89 children was prospectively followed for a median time of 1.1 year. Inflammatory biomarkers (chemokines and cytokines) in urine were measured using cytometric beads array, and RAS molecules were measured by ELISA. Children with albuminuria had significantly higher urinary levels of IP-10/CXCL10, MCP-1/CCL2, MIG/CXCL9, IL-8/CXCL8, IL-12p70, TNF, IL-10, and IL-6 than patients with normal albuminuria. In the correlation analysis, albumin/creatinine ratio was significantly and positively correlated with IP-10/CXCL10, MCP-1/CCL2, MIG/CXCL9, IL-8/CXCL8, TNF, IL-10, and IL-6. Significant correlations were found between inflammatory and RAS molecules. In the prospective analysis, cumulative risk of persistent albuminuria was higher for children with urinary levels of IP-10/CXCL10 or IL-6 above the 50th percentile. Our data showed that inflammatory markers and RAS molecules might contribute to the occurrence of albuminuria in children with SCA, suggesting that both pathways interact in sickle cell nephropathy. Topics: Adolescent; Albuminuria; Anemia, Sickle Cell; Biomarkers; Chemokine CCL2; Chemokine CXCL10; Chemokine CXCL9; Chemokines; Child; Child, Preschool; Cross-Sectional Studies; Cytokines; Female; Follow-Up Studies; Humans; Infant; Inflammation; Interleukin-10; Interleukin-12; Interleukin-6; Interleukin-8; Kidney Diseases; Male; Prospective Studies; Renin-Angiotensin System; Tumor Necrosis Factor-alpha; Young Adult | 2020 |
Pro-inflammatory cytokines are associated with podocyte damage and proximal tubular dysfunction in the early stage of diabetic kidney disease in type 2 diabetes mellitus patients.
To evaluate if there is a link between inflammation (expressed by inflammatory cytokines) and the early stage of diabetic kidney disease (DKD), as shown by markers of podocyte damage and proximal tubular (PT) dysfunction.. In this study were enrolled 117 type 2 DM patients (36-normoalbuminuria, 42-microalbuminuria, 39- macroalbuminuria), and 11 healthy subjects. Serum and urinary IL-1 alpha, IL-8, IL-18, urinary albumin:creatinine ratio (UACR), eGFR, biomarkers of podocyte damage (podocalyxin, synaptopodin, nephrin) and of PT dysfunction (KIM-1, NAG) were assessed.. Pro-inflammatory interleukins are associated with podocyte injury and PT dysfunction in early DKD. These could exert a key role in the pathogenesis of early DKD, before the development of albuminuria. Topics: Aged; Albuminuria; Cytokines; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Humans; Inflammation; Interleukin-18; Interleukin-1alpha; Interleukin-8; Kidney Tubules, Proximal; Middle Aged; Podocytes | 2020 |
Epicardial, pericardial and total cardiac fat and cardiovascular disease in type 2 diabetic patients with elevated urinary albumin excretion rate.
Background We evaluated the association of cardiac adipose tissue including epicardial adipose tissue and pericardial adipose tissue with incident cardiovascular disease and mortality, coronary artery calcium, carotid intima media thickness and inflammatory markers. Design A prospective study of 200 patients with type 2 diabetes and elevated urinary albumin excretion rate (UAER). Methods Cardiac adipose tissue was measured from baseline echocardiography. The composite endpoint comprised incident cardiovascular disease and all-cause mortality. Coronary artery calcium, carotid intima media thickness and inflammatory markers were measured at baseline. Cardiac adipose tissue was investigated as continuous and binary variable. Analyses were performed unadjusted (model 1), and adjusted for age, sex (model 2), body mass index, low-density lipoprotein cholesterol, smoking, glycated haemoglobin, and systolic blood pressure (model 3). Results Patients were followed-up after 6.1 years for non-fatal cardiovascular disease ( n = 29) or mortality ( n = 23). Cardiac adipose tissue ( p = 0.049) and epicardial adipose tissue ( p = 0.029) were associated with cardiovascular disease and mortality in model 1. When split by the median, patients with high cardiac adipose tissue had a higher risk of cardiovascular disease and mortality than patients with low cardiac adipose tissue in unadjusted (hazard ratio 1.9, confidence interval: 1.1; 3.4, p = 0.027) and adjusted (hazard ratio 2.0, confidence interval: 1.1; 3.7, p = 0.017) models. Cardiac adipose tissue ( p = 0.033) was associated with baseline coronary artery calcium (model 1) and interleukin-8 (models 1-3, all p < 0.039). Conclusions In type 2 diabetes patients without coronary artery disease, high cardiac adipose tissue levels were associated with increased risk of incident cardiovascular disease or all-cause mortality even after accounting for traditional cardiovascular disease risk factors. High cardiac adipose tissue amounts were associated with subclinical atherosclerosis (coronary artery calcium) and with the pro-atherogenic inflammatory marker interleukin-8. Topics: Adipose Tissue; Adiposity; Aged; Albuminuria; Biomarkers; Cardiovascular Diseases; Carotid Intima-Media Thickness; Coronary Angiography; Denmark; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Echocardiography; Female; Humans; Incidence; Inflammation Mediators; Interleukin-8; Kaplan-Meier Estimate; Linear Models; Male; Middle Aged; Nonlinear Dynamics; Pericardium; Prognosis; Proportional Hazards Models; Prospective Studies; Risk Assessment; Risk Factors; Time Factors | 2017 |
Helicobacter pylori infection associated with type 2 diabetic nephropathy in patients with dyspeptic symptoms.
The aim of this conventional case-control study was to investigate the prevalence and relationship between Helicobacter pylori infection in type 2 diabetes mellitus (DM) and diabetic nephropathy (DN).. A total of 241 type 2 DM patients and 69 non-diabetic subjects with dyspeptic symptoms were enrolled in the study. Gastroduodenal lesions were observed by gastrointestinal endoscopy and the presence of H. pylori was identified by rapid urease test and serum IgG antibodies to H. pylori. According to the urinary albumin excretion rate (UAE), patients were classified into diabetes mellitus group (DM group, with UAE <30 mg/24h); diabetic nephropathy group 1 (DN group 1, with UAE 30 mg/24 h to <300 mg/24 h); and diabetic nephropathy group 2 (DN group 2 ≥ 300 mg/24 h). The 69 non-diabetic subjects were used as control group. The serum levels of inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-8 were determined using ELISA.. The prevalence of H. pylori infection in DN group 1 and DN group 2 was 45/72 (62.5%) and 34/53 (64.15%), respectively, which was significantly higher than in control [28/65 (43.1%)] and DM groups [42.9% (27/63)]. No significant differences of H. pylori prevalence were detected between DN groups as well as DM and control groups. Interestingly, in both DN groups, higher levels of IL-8, TNF-α and urinary albumin excretion rate were found in H. pylori positive subjects.. Diabetic nephropathy patients are more susceptible to H. pylori infection. Our data support an association between H. pylori infection and diabetic nephropathy. Topics: Adult; Albuminuria; Case-Control Studies; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Female; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-8; Male; Middle Aged; Prevalence; Tumor Necrosis Factor-alpha | 2015 |
Urinary albumin and interleukin-8 levels are not good indicators of ongoing vesicoureteral reflux in children who have no active urinary tract infection.
Vesicoureteral reflux (VUR) is a risk factor for kidney scarring, hypertension and declining renal function. Standard diagnostic methods are invasive and can cause exposure to radiation and urinary tract infections (UTIs). We aimed to investigate urine albumin and interleukin-8 levels as markers of ongoing VUR and renal damage in children without UTIs.. Random urine samples were collected from 51 children, including 16 children with VUR (group A), 17 children with resolved VUR (group B) and 18 normal children (group C). The diagnosis of VUR or resolved VUR was confirmed by voiding cystourethrogram (VCUG) or direct radionuclide cystography (DRNC). All children had normal kidney function and had no evidence of UTI in the preceding three months. Random urine specimens were assayed for albumin (Alb), creatinine (Cr) and interleukin-8 (IL-8) and mean values were compared by one way ANOVA.. In groups A and B, the mean age at first UTI was 31.7 ± 2.4 and 27 ± 2.0 months respectively. In group A, the mean duration between VUR diagnosis and study entrance was 30 ± 9.1 months. In group B, the mean duration between VUR diagnosis and recovery was 19.9 ± 1.3 months. Overall, 76.4% of affected children had bilateral VUR and 41.2% had severe VUR. There were no significant differences in urinary Alb, IL-8, Alb/Cr and IL-8/Cr between the three groups.. The current study does not support the hypothesis that microalbuminuria or urinary IL-8 are good indicators of ongoing VUR and renal injury in children. Topics: Albuminuria; Analysis of Variance; Biomarkers; Case-Control Studies; Child; Child, Preschool; Cross-Sectional Studies; Female; Humans; Interleukin-8; Male; Urinary Tract Infections; Vesico-Ureteral Reflux | 2013 |
Purple corn anthocyanins retard diabetes-associated glomerulosclerosis in mesangial cells and db/db mice.
Diabetic glomerulosclerosis is the hardening of the renal glomeruli that can lead to kidney failure. In the early stage of glomerulosclerosis occur renal mesangial expansion and renal filtration dysfunction. Purple corn has been classified as a functional food and is rich in anthocyanins exerting potential disease-preventive activities. The in vitro study using human renal mesangial cells examined that anthocyanin-rich purple corn butanol fraction (PCB) can attenuate high glucose (HG)-promoted mesangial cell proliferation and matrix accumulation.. Cells were cultured for 3 days in media containing 33 mM glucose in the presence of 1-20 μg/mL PCB. In the in vivo animal study, db/db mice were treated with 10 mg/kg anthocyanin-rich polyphenolic extracts of purple corn (PCE) for 8 weeks.. HG enhanced mesangial production of the fibrosis biomarkers of collagen IV and connective tissue growth factor (CTGF), which was markedly attenuated by adding PCB. Such mesangial fibrosis entailed interleukin-8 activation via eliciting Tyk2-STAT signaling pathway. PCB dampened HG-promoted mesangial hyperplasia that appeared to be attributed to increased expression of platelet-derived growth factor. The 8-week administration of PCE lowered plasma glucose level of db/db mice and ameliorated severe albuminuria. Moreover, PCE lessened collagen fiber accumulation in kidney glomeruli and CTGF expression via retarding TGF-β signaling. Protein expressions of nephrin and podocin, key proteins for filtration barrier function of the glomerular capillary wall, were repressed by treating mice with PCE.. Purple corn may be a potent therapeutic agent for the treatment for diabetes-associated glomerulosclerosis accompanying proteinuria and kidney filtration dysfunction. Topics: Albuminuria; Animals; Anthocyanins; Biomarkers; Blood Glucose; Cell Proliferation; Collagen Type IV; Connective Tissue Growth Factor; Diabetic Nephropathies; Fibrosis; Humans; Interleukin-8; Intracellular Signaling Peptides and Proteins; Male; Membrane Proteins; Mesangial Cells; Mice; Plant Extracts; Platelet-Derived Growth Factor; Proteinuria; Signal Transduction; STAT Transcription Factors; Transforming Growth Factor beta; TYK2 Kinase; Zea mays | 2012 |
Regression of microalbuminuria in type 1 diabetes is associated with lower levels of urinary tubular injury biomarkers, kidney injury molecule-1, and N-acetyl-β-D-glucosaminidase.
Elevated urinary albumin excretion in patients with type 1 diabetes reverts to normoalbuminuria in a majority of patients but advances toward proteinuria in some. In order to gain valuable insights into the early pathophysiology of diabetic nephropathy we evaluated the association of kidney tubular injury biomarkers with changes in albuminuria in patients with type 1 diabetes mellitus. Urine levels of kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), and some inflammatory markers were determined in 38 healthy individuals and 659 patients with type 1 diabetes mellitus having varying degrees of albuminuria. Urinary interleukin-6, CXCL10/IP-10, NAG, and KIM-1 levels were very low in healthy individuals, increased in type 1 patients with normoalbuminuria, and were highest in diabetic patients that had microalbuminuria. Low baseline concentrations of urinary KIM-1 and NAG both individually and collectively were significantly associated with the regression of microalbuminuria over the subsequent 2 years; an effect independent of clinical characteristics. Progression and regression of microalbuminuria were unrelated to urinary levels of interleukins 6 and 8, CXCL10/IP-10, and monocyte chemoattractant protein-1. Thus our results show that lower urinary KIM-1 and NAG levels were associated with the regression of microalbuminuria in type 1 diabetes mellitus. Hence, tubular dysfunction is a critical component of the early course of diabetic nephropathy. Topics: Acetylglucosaminidase; Adult; Albuminuria; Biomarkers; Case-Control Studies; Chemokine CCL2; Chemokine CXCL10; Cross-Sectional Studies; Diabetes Mellitus, Type 1; Diabetic Nephropathies; Disease Progression; Female; Follow-Up Studies; Hepatitis A Virus Cellular Receptor 1; Humans; Inflammation Mediators; Interleukin-6; Interleukin-8; Male; Membrane Glycoproteins; Middle Aged; Receptors, Virus; Remission, Spontaneous | 2011 |
Association between Duffy antigen receptor for chemokines expression and levels of inflammation markers in sickle cell anemia patients.
Since inflammation plays a prominent role in the pathogenesis of sickle cell anemia (SCA) and Duffy antigen receptor for chemokines (DARC) modulates the function of inflammatory processes, we analyzed the relationship between the erythrocyte DARC phenotype and clinical expression of SCA. DARC locus was genotyped in 212 SS adult patients followed by the sickle cell center of Guadeloupe (French West Indies). After patients' stratification according to RBC DARC expression, the prevalence of renal disease, leg ulcers, priapism and osteonecrosis was compared between patient groups as well as hematological variables and plasma levels of chemokines. Duffy-positive patients exhibited higher counts of white blood cells (9.95+/-2.36 vs 8.88+/-2.32 10(9)/L, p=0.0066), polynuclear neutrophils (5.1+/-1.73 vs 4.51+/-1.71 10(9)/L, p=0.0227), higher plasma levels of IL-8 (4.46+/-1.22 vs 1.47+/-0.5 pg/mL, p=0.0202) and RANTES (27.8+/-4.3 vs 18.1+/-2.3 ng/mL, p=0.04) than Duffy-negative patients. No association was detected between RBC expression of DARC and the studied complications. Topics: Adult; Albuminuria; Anemia, Sickle Cell; Blood Cell Count; Chemokine CCL5; Creatinine; Duffy Blood-Group System; Female; Gene Frequency; Guadeloupe; Heterozygote; Homozygote; Humans; Inflammation; Interleukin-8; Leg Ulcer; Leukocyte Count; Male; Middle Aged; Neutrophils; Osteonecrosis; Polymorphism, Single Nucleotide; Priapism; Receptors, Cell Surface; Tumor Necrosis Factor-alpha; Young Adult | 2010 |
Serum concentrations of markers of TNFalpha and Fas-mediated pathways and renal function in nonproteinuric patients with type 1 diabetes.
The aim of our study was to examine serum markers of the TNF and Fas pathways for association with cystatin-C based estimated glomerular filtration rate (cC-GFR) in subjects with type 1 diabetes (T1DM) and no proteinuria.. The study group (the 2nd Joslin Kidney Study) comprised patients with T1DM and normoalbuminuria (NA) (n = 363) or microalbuminuria (MA) (n = 304). Impaired renal function (cC-GFR <90 ml/min) was present in only 10% of patients with NA and 36% of those with MA. We measured markers of the tumor necrosis factor alpha (TNFalpha) pathway [TNFalpha, soluble TNF receptor 1 (sTNFR1), and 2 (sTNFR2)], its downstream effectors [soluble intercellular and soluble vascular adhesion molecules (sICAM-1 and sVCAM-1), interleukin 8 (IL8/CXCL8), monocytes chemoattractant protein-1 (MCP1), and IFNgamma inducible protein-10 (IP10/CXCL10)], the Fas pathway [soluble Fas (sFas) and Fas ligand (sFasL)], CRP, and IL6.. Of these, TNFalpha, sTNFRs, sFas, sICAM-1, and sIP10 were associated with cC-GFR. However, only the TNF receptors and sFas were associated with cC-GFR in multivariate analysis. Variation in the concentration of the TNF receptors had a much stronger impact on GFR than clinical covariates such as age and albumin excretion.. Elevated concentrations of serum markers of the TNFalpha and Fas-pathways are strongly associated with decreased renal function in nonproteinuric type 1 diabetic patients. These effects are independent of those of urinary albumin excretion. Follow-up studies are needed to characterize the role of these markers in early progressive renal function decline. Topics: Adult; Albuminuria; Apoptosis; Biomarkers; C-Reactive Protein; Chemokine CCL2; Chemokine CXCL10; Cross-Sectional Studies; Cystatin C; Diabetes Mellitus, Type 1; Diabetic Nephropathies; Fas Ligand Protein; fas Receptor; Female; Glomerular Filtration Rate; Humans; Intercellular Adhesion Molecule-1; Interleukin-6; Interleukin-8; Kidney; Male; Middle Aged; Receptors, Tumor Necrosis Factor, Type I; Receptors, Tumor Necrosis Factor, Type II; Signal Transduction; Tumor Necrosis Factor-alpha; Vascular Cell Adhesion Molecule-1 | 2009 |
Proinflammatory and proapoptotic effects of methylglyoxal on neutrophils from patients with type 2 diabetes mellitus.
To determine the effect of methylglyoxal (MG) on cytokine production by, and apoptosis of, neutrophils from type 2 diabetes mellitus (T2DM) patients.. The levels of plasma MG, cytokines released by isolated neutrophils and the apoptotic status of neutrophils were determined.. The higher level of plasma MG in T2DM patients was correlated positively with glycated hemoglobin levels, fasting plasma glucose levels and urine albumin/creatinine ratios. The basal levels of cytokines released from neutrophils were markedly higher in patients. MG treatment of the neutrophils isolated from diabetic patients either did not alter, or decreased, the production of cytokines. In contrast, MG induced the release of cytokines from neutrophils of non-diabetics. Moreover, the neutrophils from T2DM patients showed a greater proclivity for apoptosis, which was further increased by in vitro MG treatment.. MG stimulated neutrophils to release more cytokines, which might play a role in the development of infection in T2DM. Topics: Aged; Albuminuria; Anti-Inflammatory Agents; Apoptosis; Blood Glucose; Caspase 3; Creatine; Cytokines; Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Enzyme-Linked Immunosorbent Assay; Female; Flow Cytometry; Glycated Hemoglobin; Humans; Interleukin-6; Interleukin-8; Male; Middle Aged; Neutrophils; Nitric Oxide; Pyruvaldehyde; Tumor Necrosis Factor-alpha | 2007 |
Anti-interleukin 8 antibody abolishes effects of lipoid nephrosis cytokine.
Supernatant factor from peripheral blood mononuclear cell (PBMC) cultures of idiopathic minimal lesion nephrotic syndrome (IMLNS) patients in relapse induces in vivo albuminuria and increases 35sulfate uptake by glomerular basement membrane (GBM) in rats. The purpose of this study was to evaluate the effect of anti-interleukin 8 (IL8) neutralizing antibody on the effects induced by the supernatant factor. Supernatant factor collected from six cultures of PBMC from IMLNS patients in relapse were combined and aliquotted into two samples. Anti-IL8 neutralizing antibody (750 ng) was added to one. Supernatant factor or supernatant factor and anti-IL8 antibody were infused for 5 days into the left renal artery of Wistar rats using an osmotic pump. On the last day of infusion, rats were injected with 35sulfate (1.0 mCi/200 g) intraperitoneally and killed after 8 h. Glomeruli were isolated and GBM obtained. There was a significant increase in 35sulfate uptake of the infused kidney (169 +/- 52 cpm/mg dry glomerular weight, mean +/- SEM) compared with the uptake seen in the contralateral kidney (116 +/- 41, P < 0.05) when the supernatant factor was infused alone. No significant differences in 35sulfate incorporation were seen between infused kidney (173 +/- 5) and contralateral kidney (190 +/- 49) when supernatant factor and anti-IL8 antibody were administered. A significant increase in albuminuria was seen on the last day of infusion (0.43 +/- 0.11 albumin/ creatinine ratio, mean +/- SEM) compared with the ratio prior to infusion of the supernatant factor alone (0.18 +/- 0.03, P <0.05). No significant differences in urinary albumin/creatinine ratios prior to and on the 5th day of infusion were seen when the supernatant factor was administered with anti-IL8 antibody. Supernatant factor effects were abolished by the addition of anti-IL8 neutralizing antibody, suggesting that the described effects are mediated by IL8. Topics: Adolescent; Adult; Albuminuria; Animals; Antibodies; Child; Child, Preschool; Female; Humans; Infant; Interleukin-8; Kidney Glomerulus; Leukocytes, Mononuclear; Male; Nephrosis, Lipoid; Rats; Sulfates | 1998 |
Effect of interleukin-8 on glomerular sulfated compounds and albuminuria.
To evaluate the effect of interleukin-8 (IL8) on glomerular basement membrane (GBM) sulfated compounds and albuminuria, we infused IL8 in 1% bovine serum albumin (BSA) for 5 days into the left renal artery of Holtzman male rats at the rate of 10 microliters/h using an osmotic pump. Control rats received 1% BSA. A significant increase in urinary albumin/creatinine ratio was seen on the last day of IL8 infusion (0.38 +/- 0.11, mean +/- SEM) when compared with albumin/creatinine ratio prior to infusion (0.19 +/- 0.04, P = 0.04). No significant differences in urinary albumin excretion prior to and after infusion of 1% BSA were observed. On the last day of infusion, rats were injected with 35sulfate (1.0 mCi/200 g body weight) intraperitoneally and killed after 8 h. Glomeruli were isolated and GBM obtained. After 5 days of IL8 administration, there was a significant increase in 35sulfate uptake by GBM of the infused kidney (76 +/- 10 cpm/dry glomerular weight, mean +/- SEM) compared with the uptake seen in the contralateral kidney (53 +/- 9, P = 0.05). The in vivo infusion of IL8 increased the 35sulfate uptake by GBM and augmented the urinary albumin/creatinine ratio, suggesting that IL8 may induce albuminuria by altering the metabolism of the GBM sulfated compounds. This hypothesis needs to be confirmed by studies on glomerular charge selectivity and GBM anionic sites during the course of the infusion. Moreover, the persistence of the effect needs to be evaluated by prolonging the infusion for more than 5 days. Topics: Albuminuria; Animals; Cell Membrane Permeability; Creatinine; Glomerular Mesangium; Glycosaminoglycans; Heparitin Sulfate; Infusions, Intravenous; Interleukin-8; Kidney Glomerulus; Male; Rats; Renal Artery; Sulfates; Sulfur Radioisotopes | 1997 |
Urine interleukin-6 and interleukin-8 in children with acute pyelonephritis, in relation to DMSA scintigraphy in the acute phase and at 1-year follow-up.
The relationship between urine interleukin-6 (IL-6) and interleukin-8 (IL-8)/creatinine quotients and 99mTc-dimercaptosuccinic acid (DMSA) scintigraphy, performed within 10 days of acute first-time pyelonephritis and after 1 year, was studied in 41 children. The urine IL-6 and IL-8/creatinine quotients were also related to the urine N-acetyl-beta-D-glucosaminidase (NAG) and albumin/creatinine quotients. Presence of DMSA uptake defects, reflecting local inflammation, in children in the acute phase of pyelonephritis, were associated with elevated urine IL-6/creatinine quotients (median 27 pg/mumol); in children without DMSA changes there was no increase in quotients (median non-detectable) (P < 0.05). Persistent DMSA changes at the 1-year follow-up, probably reflecting renal scarring, were only seen in children with increased urine IL-6/creatinine quotients in the acute phase (P < 0.01). No correlation was found between urine IL-8 and DMSA uptake defects. Vesicoureteral reflux (VUR) at 6-8 weeks did not correlate with the urine cytokine levels in the acute phase. The urine excretion of NAG and albumin, reflecting renal dysfunction, was associated with values of both urine IL-6 and IL-8/creatinine quotients, but not with DMSA defects or VUR. Thus, the initial urine IL-6/creatinine quotients might be used as an indicator of risk for persistent renal damage in acute pyelonephritis. Topics: Acetylglucosaminidase; Acute Disease; Albuminuria; Child; Child, Preschool; Creatinine; Follow-Up Studies; Humans; Infant; Infant, Newborn; Interleukin-6; Interleukin-8; Kidney; Organotechnetium Compounds; Pyelonephritis; Radionuclide Imaging; Succimer; Technetium Tc 99m Dimercaptosuccinic Acid; Vesico-Ureteral Reflux | 1994 |
Prevention of proteinuria by the administration of anti-interleukin 8 antibody in experimental acute immune complex-induced glomerulonephritis.
Glomerular infiltration by neutrophils is a hallmark of acute glomerulonephritis. The pathophysiological role of interleukin 8 (IL-8), a potent neutrophil chemotactic cytokine (chemokine), was explored in an animal model of acute immune complex-mediated glomerulonephritis by administering a neutralizing antibody against IL-8. Repeated injection of bovine serum albumin (BSA) into rabbits caused the deposition of immune complexes consisting of BSA and rabbit IgG in glomeruli. Histological analyses revealed a small but significant number of neutrophils in glomeruli and the fusion of epithelial cell foot processes. Concomitantly, urinary levels of protein and albumin increased markedly (3.20 +/- 0.97 and 1.39 +/- 0.53 mg/h, respectively) compared with those of untreated animals (0.77 +/- 0.21 and 0.01 +/- 0.01 mg/h, respectively). Anti-IL-8 antibody treatment decreased the number of neutrophils in glomeruli by 40% and dramatically prevented the fusion of epithelial cell foot process. Furthermore, treatment with anti-IL-8 antibody completely normalized the urinary levels of protein and albumin (0.89 +/- 0.15 and 0.02 +/- 0.01 mg/h, respectively). These results indicated that IL-8 participated in the impairment of renal functions in experimental acute immune complex-mediated glomerulonephritis through activating as well as recruiting neutrophils. Topics: Acute Disease; Albuminuria; Animals; Antibodies, Monoclonal; Antigen-Antibody Complex; Glomerulonephritis; Interleukin-8; Kidney Glomerulus; Male; Mice; Proteinuria; Rabbits | 1994 |