scholarly journals The inflammatory profile of chronic kidney disease patients

2021 ◽  
Vol 5 (3) ◽  
pp. 107-111
Author(s):  
Chaker Hanen ◽  
Jarraya Faiçal ◽  
Toumi Salma ◽  
Kammoun Khawla ◽  
Mahfoudh Hichem ◽  
...  

Background: Chronic kidney disease is a worldwide public health issue which is associated with an increased risk of end-stage renal failure and cardiovascular disease. Systemic inflammation exists during chronic renal failure. Recent researches have highlighted the pivotal role of inflammation between renal and cardiovascular disease. The aim of our study is to determine the inflammatory profile of the patient suffering from chronic kidney disease and the influence of hemodialysis on this profile. Methods: We carried out a cross sectional study on 93 patients in the Nephrology Department at Hedi Chaker University Hospital, Sfax, South of Tunisia. Among those patients, 72 patients underwent hemodialysis and 21 patients had chronic kidney disease at stage 3. Clinical data and antecedents were collected. Biological samples were taken after informing the patients and taking their consent. Biological data consisted in lipid profile, albumin rate, hemoglobin rate, uric acid concentration and the usual markers of inflammation noting sedimentation rate, C - reactive protein and orosomucoid. Results: Hemodialysis group of the 72 patients had mean hemodialysis vintage of 54.6 ± 43 months. The inflammatory profile was worse in hemodialysis patients compared to chronic kidney disease patients. Both sedimentation rate, C - reactive protein and orosomucoid were higher in hemodialysis group than in chronic kidney disease group with 71 ± 35.3 mm vs. 42.1 ± 15.5 mm (p < 0.05); 14.6 ± 28.7 mg/l vs. 6.7 ± 8 mg/l (p = 0.02); 1.3 ± 0.7g/l vs. 0.9 ± 0.4 g/l (p = 0.01), respectively. Conclusion: Inflammation increases in dialysis patient. It deserves the nephrologist’s consideration in order to minimize its harmful effects. The monitoring of inflammation markers must be integrated into the nephrologist’s medical practice.

Author(s):  
Paul M Ridker ◽  
Manas Rane

Interleukin-6 (IL-6) is a pivotal cytokine of innate immunity which enacts a broad set of physiologic functions traditionally associated with host defense, immune cell regulation, proliferation, and differentiation. Following recognition of innate immune pathways leading from the NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome to interleukin-1 to IL-6 and on to the hepatically derived clinical biomarker C-reactive protein, an expanding literature has led to understanding of the pro-atherogenic role for IL-6 in cardiovascular disease and thus the potential for interleukin-6 inhibition as a novel method for vascular protection. In this review, we provide an overview of the mechanisms by which IL-6 signaling occurs and how that impacts upon pharmacologic inhibition; describe murine models of IL-6 and atherogenesis; summarize human epidemiologic data outlining the utility of IL-6 as a biomarker of vascular risk; outline genetic data suggesting a causal role for IL-6 in systemic atherothrombosis and aneurysm formation; and then detail the potential role of IL-6 inhibition in stable coronary disease, acute coronary syndromes, heart failure, and the atherothrombotic complications associated with chronic kidney disease and end-stage renal failure. Finally, we review anti-inflammatory and anti-thrombotic findings for ziltivekimab, a novel IL-6 ligand inhibitor being developed specifically for use in atherosclerotic disease and poised to be tested formally in a large scale cardiovascular outcomes trial focused on individuals with chronic kidney disease and elevated levels of C-reactive protein, a population at high residual atherothrombotic risk, high residual inflammatory risk, and considerable unmet clinical need.


2003 ◽  
Vol 42 (1) ◽  
pp. 44-52 ◽  
Author(s):  
Vandana Menon ◽  
Xuelei Wang ◽  
Tom Greene ◽  
Gerald J Beck ◽  
John W Kusek ◽  
...  

2016 ◽  
Vol 97 (6) ◽  
pp. 881-887
Author(s):  
A A Nasybullina ◽  
O V Bulashova ◽  
V M Gazizyanova ◽  
M I Malkova ◽  
E E Mustafin ◽  
...  

Aim. Evaluation of markers of systemic inflammation in patients with chronic heart failure in comorbidity with chronic kidney disease.Methods. The study included 188 patients with heart failure and kidney disease including control group (76 patients) with heart failure with preserved renal function aged 38 to 83 years (mean age 66.8±10.1 years), with the duration of heart failure of about 8 years. Quantitative measurement of C-reactive protein and proteins of blood serum and daily excretion of protein with urine were performed.Results. Glomerular filtration rate in patients without renal pathology was 71.1±11.7 ml/min/1.73 m2, and in the group with heart failure associated with kidney dysfunction it was 51.5±19.1 ml/min/1.73 m2. C-reactive protein, γ-globulin, albumin and total serum protein in patients with chronic kidney disease differed from those in patients with heart failure without kidney damage.Conclusion. C-reactive protein and γ-globulin in the serum significantly increase in patients with heart failure and chronic kidney disease and can be used as markers of cardiac as well as renal events.


2012 ◽  
Vol 187 (4S) ◽  
Author(s):  
Seth A. Cohen ◽  
Kerrin L. Palazzi ◽  
Ryan P. Kopp ◽  
Reza Mehrazin ◽  
Samuel K. Park ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Jeanie Park

Patients with chronic kidney disease are at significantly increased risk for cardiovascular disease and sudden cardiac death. One mechanism underlying increased cardiovascular risk in patients with renal failure includes overactivation of the sympathetic nervous system (SNS). Multiple human and animal studies have shown that central sympathetic outflow is chronically elevated in patients with both end-stage renal disease (ESRD) and chronic kidney disease (CKD). SNS overactivation, in turn, increases the risk of cardiovascular disease and sudden death by increasing arterial blood pressure, arrythmogenicity, left ventricular hypertrophy, and coronary vasoconstriction and contributes to the progression renal disease. This paper will examine the evidence for SNS overactivation in renal failure from both human and experimental studies and discuss mechanisms of SNS overactivity in CKD and therapeutic implications.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Manzoor Parry ◽  
Hamad Jeelani

Abstract Background and Aims The prevalence of chronic kidney disease (CKD) in India varies from 0.16–0.78%. The reported incidence of malnutrition in CKD patients is 37–84%. There is a paucity of data on the quantification of malnutrition and inflammation in undialyzed patients of CKD from north east of India. This study analyzed the prevalence and causes of malnutrition and inflammation in patients with CKD before the initiation of dialysis treatment. Method This study was conducted from May 2017 to May 2019 in the department of nephrology Guahati medical college hospital. Assessment of nutritional and inflammatory status was carried out in patients with CKD before initiation of dialysis. Serum albumin; body mass index (BMI); triceps skin fold thickness (TST); mid-arm muscle circumference (MAMC); and subjective global assessment (SGA) scoring were used for assessment of nutritional parameters. Serum C-reactive protein; serum albumin and serum ferritin level were used to assess the inflammatory status in these patients. Results A total of 528 (male:female= 359:169) patients with CKD participated in this study. Diabetic Nephropathy (35%) was the most common; followed by; hypertension (23%) and chronic glomerulonephritis (20 %). The evidence of malnutrition was noted in 344 (65%). The mean age of patients with malnutrition was 52.8±12.45 years with a male predominance (68%). On the basis of SGA score; malnutrition was noted in 344 patients (mild moderate [36%]; severe; [30%]); remaining (34%) were well nourished. Thus; evidence of Malnutrition was noted in 65% of patients with CKD.). Serum total protein & albumin were higher in the non-malnourished patients in comparison to malnourished (5.83±1.0 vs 5.31±1.12 p&lt;0.05; 3.65±0.7 vs 2.62±0.74) The inflammatory markers (serum ferritin & C reactive protein) were elevated significantly in patients with malnutrition in comparison to those without malnutrition (308.15±60.18 mg/dL vs. 251.64±63.14 mg/dL; p &lt; 0.001; 77% vs. 50%; p &lt; 0.01). Conclusion Malnutrition and inflammation are common in patients with CKD before the commencement of dialysis. This indicates that an emphasis should be placed on the assessment and prevention or correction of malnutrition and inflammatory burden in these patients with CKD.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Changhyun Lee ◽  
Keun Hyung Park ◽  
Young Su Joo ◽  
Ki Heon Nam ◽  
Tae-Ik Chang ◽  
...  

Abstract Background and Aims High-sensitivity C-reactive protein (hs-CRP) level is lower in East Asians than in the Western people and its clinical significance needs to be further explored. We aimed to investigate whether hs-CRP could function as a biomarker in Korean CKD patients. Method We studied the association of hs-CRP with adverse clinical outcomes in 2,018 patients from the KoreaN cohort study for Outcome in patients With Chronic Kidney Disease (KNOW-CKD). The primary outcome was a composite of extended major cardiovascular events (MACE) or all-cause mortality. Extended MACE (eMACE) included non-fatal cardiovascular events, symptomatic arrhythmia, and cardiac death. The secondary endpoints were separate outcome of eMACE, all-cause death, and adverse kidney outcome. We also evaluated predictive ability of hs-CRP for the primary outcome. Results The median hs-CRP level was 0.60 mg/L (IQR 0.2-1.7), and the mean eGFR was 53.6 ml/min/1.73 m2. During the mean follow-up of 3.9 years, there were 125 (6.2%) eMACEs and 80 (4.0%) deaths. The primary composite outcome occurred more frequently in patients with higher hs-CRP level than in those with lower hs-CRP level. In multivariable Cox analysis after adjustment of confounders, there was a graded association of hs-CRP with the primary outcome. The HRs (95% CI) for hs-CRP of 1.0 to 2.99, and ≥ 3.0 mg/L were 1.37 (0.89-2.12) and 2.20 (1.36-3.56), compared with hs-CRP of &lt;1.0 mg/L. In analyses of secondary outcomes, this association was consistent for eMACE and all-cause death; however, hs-CRP was not associated with adverse kidney outcomes. Finally, prediction models failed to show improvement of predictive performance of hs-CRP compared to conventional factors. Conclusion In Korean CKD patients, serum hs-CRP level was low and significantly associated with higher risk of eMACEs and mortality. However, a low serum hs-CRP level was not predictive of adverse kidney outcome, and the predictive performance of hs-CRP was not strong.


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