scholarly journals Assessment of Zinc-alfa2 Glycoprotein (ZAG) and Lipase Maturation Factor 1 (LMF1) concentration in children with chronic kidney disease

2021 ◽  
pp. 605-613
Author(s):  
Dagmara Roszkowska-Bjanid ◽  
Katarzyna Dyga ◽  
Elżbieta Świętochowska ◽  
Omar Bjanid ◽  
Maria Szczepańska
Keyword(s):  
Chronic Kidney Disease ◽  
Lipid Metabolism ◽  
Kidney Disease ◽  
Transmembrane Protein ◽  
Elevated Serum ◽  
Urine Concentration ◽  
Healthy Children ◽  
Maturation Factor ◽  
Lipase Maturation Factor 1 ◽  
Serum And Urine

ZAG (zinc-α2-glycoprotein) - adipokine, may participate in the mechanism of malnutrition in chronic kidney disease (CKD) as cachexia factor. The transmembrane protein of the endoplasmic reticulum - lipase maturation factor 1 (LMF1) is necessary for the secretion and enzymatic activity of lipases and lowering triglycerides level. The aim of the study was to evaluate these markers - ZAG and LMF1, their potential importance in CKD in children. The study included 59 children and adolescents aged 10.7±5.0 years with CKD. Compared with healthy children, serum and urine ZAG levels were higher in children with CKD. A similar relationship was obtained in the comparison of girls and boys between the above groups. We showed a reduced serum and urine concentration of LMF1 in children with CKD. Additionally, ZAG and LMF1 levels in children below 10 years of age and above 10 were no different. There was also no correlation between these markers and serum creatinine (except negative correlation of urinary ZAG), albumin, cholesterol, triglycerides. LMF1 concentration correlated positively with vitamin D level in dialyzed patients. To conclude, elevated serum ZAG levels in children with CKD document that selective kidney damage results in the rise of ZAG concentration, however the specific role of this marker in malnutrition was not documented. Reduced serum LMF1 concentration in children with CKD, did not correlate with standard parameters used to assess lipid metabolism and severity of CKD. The usefulness of LMF1 as the marker of the lipid metabolism disturbances in children with CKD was not proven.

scholarly journals Osteoprotegerin is a marker of cardiovascular mortality in patients with chronic kidney disease stages 3–5

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gustavo Lenci Marques ◽  
Shirley Hayashi ◽  
Anna Bjällmark ◽  
Matilda Larsson ◽  
Miguel Riella ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Multivariate Analysis ◽  
Kidney Disease ◽  
Cardiovascular Mortality ◽  
Osteoclast Differentiation ◽  
Survival Rates ◽  
Elevated Serum ◽  
High Sensitivity ◽  
Intima Media Thickness

AbstractCardiovascular disease (CVD) is the leading cause of death in patients with chronic kidney disease (CKD). Osteoprotegerin (OPG), known to regulate bone mass by inhibiting osteoclast differentiation and activation, might also play a role in vascular calcification. Increased circulating OPG levels in patients with CKD are associated with aortic calcification and increased mortality. We assessed the predictive role of OPG for all-cause and cardiovascular mortality in patients with CKD stages 3–5 over a 5-year follow-up period. We evaluated the relationship between OPG and all-cause and cardiovascular mortality in 145 CKD patients (stages 3–5) in a prospective observational follow-up study. Inflammation markers, including high-sensitivity C-reactive protein, standard echocardiography, and estimation of intima-media thickness in the common carotid artery, were assessed at baseline, and correlations with OPG levels were determined. The cutoff values for OPG were defined using ROC curves for cardiovascular mortality. Survival was assessed during follow up lasting for up to 5.5 years using Fine and Gray model. A total of 145 (89 men; age 58.9 ± 15.0 years) were followed up. The cutoff value for OPG determined using ROC was 10 pmol/L for general causes mortality and 10.08 pmol/L for CV causes mortality. Patients with higher serum OPG levels presented with higher mortality rates compared to patients with lower levels. Aalen–Johansen cumulative incidence curve analysis demonstrated significantly worse survival rates in individuals with higher baseline OPG levels for all-cause and cardiovascular mortality (p < 0.001). In multivariate analysis, OPG was a marker of general and cardiovascular mortality independent of sex, age, CVD, diabetes, and CRP levels. When CKD stages were included in the multivariate analysis, OPG was an independent marker of all-cause mortality but not cardiovascular mortality. Elevated serum OPG levels were associated with higher all-cause and cardiovascular mortality risk, independent of age, CVD, diabetes, and inflammatory markers, in patients with CKD.

scholarly journals SP436EFFECT OF LEVOCARNITINE ON LIPID METABOLISM AND OXIDATIVE STRESS IN PATIENTS WITH CHRONIC KIDNEY DISEASE

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii522-iii522
Author(s):  
Mariana Koziy ◽  
Liliya Martynyuk
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Lipid Metabolism ◽  
Kidney Disease ◽  
And Oxidative Stress

scholarly journals Quinine-Induced Thrombotic Microangiopathy (Q-TMA): Frequency, Presenting Features, Outcomes

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 1381-1381 ◽  
Author(s):  
Evaren E Page ◽  
Sara K. Vesely ◽  
James N. George
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Conflicts Of Interest ◽  
Elevated Serum ◽  
Kidney Injury ◽  
Long Term Outcome ◽  
Presenting Symptoms ◽  
Immune Mediated ◽  
Organ Systems ◽  
History Of

Abstract Q-TMA is an acute, severe, immune-mediated, drug-induced disorder. Q-TMA is suspected when symptoms suddenly begin within hours following quinine (Q) exposure. Diagnosis of Q-TMA is established by the history of recurrent acute symptoms following recurrent Q exposures and/or by documentation of Q-dependent antibodies reactive with platelets and/or neutrophils. The Oklahoma TTP-HUS Registry enrolls all patients for whom plasma exchange (PEX) is requested for suspected TTP or HUS. Since 1995, when routine measurement of ADAMTS13 activity began, the Registry has diagnosed 78 patients with acquired TTP (ADAMTS13 <10%). During this time we have also diagnosed 17 patients with Q-TMA; 2 additional patients were diagnosed before 1995. Seventeen of these 19 patients were tested for Q-dependent antibodies; all were positive. Nine patients had a history of recurrent acute symptoms with recurrent Q exposure, including the 2 patients not tested for Q-dependent antibodies. Q exposure was a pill in 18 patients, tonic water in one. Remarkably, 18 patients were women; all 19 patients were white. Common presenting symptoms were fever, chills, nausea and vomiting. No patients had focal neurologic abnormalities. All patients had microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and acute kidney injury. Eight patients had elevated serum alanine aminotransferase (231-1345 U/L). Three patients had neutropenia (absolute neutrophil counts, 184-486). Two patients had coagulation abnormalities suggesting disseminated coagulation (DIC). One patient died from complications of the central venous catheter insertion, performed for PEX and dialysis; all other patients recovered normal platelet counts. Three of the 18 surviving patients had end-stage renal disease (2 had kidney transplants). The median estimated glomerular filtration rate (GFR) for the other 15 patients, at 2.7-19.2 years (median, 10.2) after recovery, was 36 ml/min (range, 19-98). Only two patients had normal GFR (≥90 ml/min). Eleven patients had chronic kidney disease, defined by GFR <60 ml/min. Seven of 18 patients have died 4.1-12.7 years (median, 7.8) following recovery at ages 59-87 years. Conclusion. Quinine can cause severe immune-mediated toxicities involving multiple organ systems (Am J Hematol 2016; 91: 461). Q-TMA is an acute disorder causing severe kidney injury and, in some patients, also liver toxicity, neutropenia, and/or DIC. Q-TMA is not rare. During 20 years, we enrolled 17 Q-TMA patients compared to 78 patients with acquired TTP. Chronic kidney disease is a common long-term outcome. Explicit questions are required to discover the association of systemic symptoms with quinine ingestion. Table Table. Disclosures No relevant conflicts of interest to declare.

scholarly journals DIFFERENCES OF SALIVA LEPTIN LEVELS IN CHILDREN WITH CHRONIC KIDNEY DISEASE ON HEMODIALYSIS AND HEALTHY CHILDREN (STUDY IN CHILDREN WITH GINGIVITIS)

2018 ◽  
Vol 11 (4) ◽  
pp. 192
Author(s):  
Berthauli Esther Nurmaida ◽  
Heriandi Sutadi ◽  
Sarworini B Budiardjo ◽  
Eka Laksmi Hidayati
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Immunosorbent Assay ◽  
Enzyme Linked Immunosorbent Assay ◽  
Healthy Children ◽  
Significant Difference ◽  
The Difference

 Objectives: Analyze the difference of salivary leptin in between healthy children with gingivitis and hemodialysis (HD) children with gingivitis.Methods: A total of 20 children, ages 11–16-year-old with gingivitis, were chosen as subjects; 10 were on HD and 10 were healthy children. The level of salivary leptin was measured using the enzyme-linked immunosorbent assay method.Results: The results showed a significant difference of salivary leptin levels between the children on HD (61,300 ± 4151 pg/ml) and the healthy children (57,200 ± 3173 pg/ml).Conclusions: There is a significant difference in the salivary leptin levels in children on HD with gingivitis and healthy children with gingivitis.

scholarly journals SP315INFLUENCE OF LIPID METABOLISM DISORDERS ON ENDOTHELIAL FUNCTION IN CHRONIC KIDNEY DISEASE

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii483-iii483
Author(s):  
Mehman Agayev ◽  
Irada Mammadova ◽  
Shalala Ismayilova
Keyword(s):  
Chronic Kidney Disease ◽  
Lipid Metabolism ◽  
Kidney Disease ◽  
Endothelial Function ◽  
Lipid Metabolism Disorders

scholarly journals Elevated Serum Bone Morphogenetic Protein 4 in Patients with Chronic Kidney Disease and Coronary Artery Disease

2012 ◽  
Vol 6 (2) ◽  
pp. 232-238 ◽  
Author(s):  
Paul F. Stahls ◽  
Daniel J. Lightell ◽  
Stephanie C. Moss ◽  
Corey K. Goldman ◽  
T. Cooper Woods
Keyword(s):  
Coronary Artery Disease ◽  
Chronic Kidney Disease ◽  
Coronary Artery ◽  
Kidney Disease ◽  
Bone Morphogenetic Protein ◽  
Elevated Serum ◽  
Bone Morphogenetic Protein 4 ◽  
Morphogenetic Protein ◽  
Artery Disease

scholarly journals Clusterin deficiency induces lipid accumulation and tissue damage in kidney

2018 ◽  
Vol 237 (2) ◽  
pp. 175-191 ◽  
Author(s):  
Jung-Yoon Heo ◽  
Ji-Eun Kim ◽  
Yongwook Dan ◽  
Yong-Woon Kim ◽  
Jong-Yeon Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Kidney Disease ◽  
Lipid Metabolism ◽  
Kidney Disease ◽  
Lipid Accumulation ◽  
Transforming Growth Factor ◽  
Lipid Levels ◽  
Lipogenic Gene ◽  
Lipogenic Gene Expression ◽  
Deficient Mice

Clusterin is a secretory glycoprotein that is involved in multiple physiopathological processes, including lipid metabolism. Previous studies have shown that clusterin prevents hepatic lipid accumulation via suppression of sterol regulatory element-binding protein (SREBP) 1. In this study, we examined the role of clusterin in renal lipid accumulation in clusterin-knockout mice and NRK52e tubular epithelial cells. Clusterin deficiency increased the expression of SREBP1 and its target genes and decreased malonyl-CoA decarboxylase protein levels in the kidney. Expression of the endocytic receptor, megalin, and scavenger receptor class A was increased in clusterin-deficient mice. Functional analysis of lipid metabolism also revealed that lipid uptake and triglyceride synthesis were increased and fatty acid oxidation was reduced, leading to increased lipid accumulation in clusterin-deficient mice. These phenomena were accompanied by mesangial expansion, fibrosis and increased urinary protein-to-creatinine ratio. High-fat feeding aggravated these clusterin deficiency-induced pathological changes. Clusterin knockdown in NRK52e cells increased lipogenic gene expression and lipid levels, whereas overexpression of clusterin by treatment with adenovirus or recombinant clusterin protein suppressed lipogenic gene expression and lipid levels. Transforming growth factor-beta 1 (TGFB1) expression increased in the kidney of clusterin-deficient mice and suppression of TGFB1 in NRK52e cells suppressed lipid accumulation. These results suggest that clusterin deficiency induces renal lipid accumulation by dysregulating the expression of lipid metabolism-related factors and TGFB1, thereby leading to chronic kidney disease. Hence, clusterin may serve as a therapeutic target for lipid-induced chronic kidney disease.

scholarly journals iTRAQ-based proteomic analysis of plasma reveals abnormalities in lipid metabolism proteins in chronic kidney disease-related atherosclerosis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Magdalena Luczak ◽  
Dorota Formanowicz ◽  
Łukasz Marczak ◽  
Joanna Suszyńska-Zajczyk ◽  
Elżbieta Pawliczak ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Lipid Metabolism ◽  
Kidney Disease ◽  
Proteomic Analysis

Lipid Metabolism in Chronic Kidney Disease: The Role of Statins in Cardiovascular Risk

2007 ◽  
Vol 17 (1) ◽  
pp. 75-78 ◽  
Author(s):  
Christoph Wanner ◽  
Christiane Drechsler ◽  
Vera Krane
Keyword(s):  
Chronic Kidney Disease ◽  
Cardiovascular Risk ◽  
Lipid Metabolism ◽  
Kidney Disease

Elevated Serum Uric Acid Predicts Chronic Kidney Disease

2011 ◽  
Vol 342 (6) ◽  
pp. 461-466 ◽  
Author(s):  
Tamaki Yamada ◽  
Mitsuru Fukatsu ◽  
Tsuneya Wada ◽  
Sadao Suzuki ◽  
Takashi Joh
Keyword(s):  
Chronic Kidney Disease ◽  
Uric Acid ◽  
Kidney Disease ◽  
Serum Uric Acid ◽  
Elevated Serum
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