Serum CRP decreased in both groups (from 15.1±5.2 to 14.0±5.6 mg/L, p=0.01 in the KTx group and from 16.5±3.9 to 15.4±4.3 mg/L in the CKD group p=0.05).
However, in individuals with the highest levels (3rd tertile) of C-reactive protein (CRP) or fibrinogen, we observed robust associations of PR with eGFR and CKD, suggesting that systemic inflammation may modify the PR-eGFR and PR-CKD relationships.
Despite no change in serum C-reactive protein, the endotoxin-lowering effect of sevelamer may help to attenuate the inflammatory status of patients with chronic kidney disease.
Randomized controlled trials assessing the effects of vitamin D supplementation or treatment on glycemic control, lipid profiles, and C-reactive protein (CRP) among patients with CKD were included.
To determine the association between inflammatory markers (interleukin (IL)-12, IL-18, highly sensitive C-reactive protein (hsCRP)) and non-invasive markers of arterial stiffness (24-h pulse pressure (PP)) with DD in stages 3-4 CKD patients.
A blood culture should be considered for patients with ABSSSI with diabetes mellitus or chronic kidney disease or those exhibiting abnormal CRP, glucose, or albumin levels because of the positive correlation between bacteremia and mortality.
The evaluation of the benefits of drugs may lead to individualized therapy for CKD patients: Cholesterol-lowering treatment for CKD patients with high levels of both LDLc and CRP is suggested.
Abdominal and Chest X-rays were unremarkable, blood tests showed worsening Acute Kidney Injury (AKI) on Chronic Kidney Disease (CKD); and raised C-Reactive Protein (CRP) with no obvious symptoms or focus of infection.
In contrast, coexisting chronic obstructive pulmonary disease and higher C-reactive protein levels were independent risk factors for 1-year mortality in the HF without CKD group.
Our results highlighted that probiotic supplements exerted a statistically significant effect on urea levels in non-dialysis CKD population, while no evidence suggested that probiotics possessed meaningful impacts on the reduction of uric acid, C-reactive protein, creatinine and estimated glomerular filtration rate preservation of CKD population.
The objective of this hypothesis-generating post hoc subgroup analysis was to explore the effects of icosapent ethyl at 2 or 4 g/day (prescription pure ethyl ester of the omega-3 fatty acid eicosapentaenoic acid [EPA]) on atherogenic lipid, apolipoprotein, inflammatory parameters (high-sensitivity C-reactive protein [hsCRP], lipoprotein-associated phospholipase A<sub>2</sub> [Lp-PLA<sub>2</sub>]), and oxidative parameters (oxidized-LDL [ox-LDL]) in statin-treated patients from ANCHOR with stage 3 CKD.
In the CKD group, older age, smoking, larger waist circumference, reduced eGFR (OR: 0.97, 95% CI: 0.95-0.99, P < 0.001), proteinuria (OR: 2.01, 95% CI: 1.09-3.74, P < 0.001) and raised serum C-reactive protein (1.01, 1.00-1.03, P < 0.001) were significantly associated with AF.
Stress hyperglycaemia was diagnosed in 34.6% of the cases; the majority of these cases were patients with high-serum urea, CRP, and chronic kidney disease.
Association of elevated blood serum high-sensitivity C-reactive protein levels and body composition with chronic kidney disease: A population-based study in Taiwan.
It was the aim of this study to analyze the number and localization of MCs and DCs, macrophages, T- and B-cells as well as the expression of markers of inflammation such as CRP and NFκB in calcified and non-calcified atherosclerotic plaques of patients with CKD and control patients.
Hepatocyte nuclear factors as possible C-reactive protein transcriptional inducer in the liver and white adipose tissue of rats with experimental chronic renal failure.
The PWV ratio was associated with age and C-reactive protein (beta: 0.08 z-score, 95%CI 0.02-0.14; p=0.01) or active disease (beta: 0.43 z-score, 95%CI 0.003-0.857; p=0.048) in patients with UC and with age and glomerular filtration rate (beta: -0.56 z-score, 95%CI -1.05 to -0.07; p=0.02) in patients with CKD.
Among the patients with infection, there was no difference between those who died and those who survived in terms of baseline CRP level, but a significant difference emerged in CRP level at 48 and 96 h. Factors which were found to significantly reduce survival time were the presence of chronic kidney disease, chronic obstructive pulmonary disease, hypoxia and tachycardia at admission, APACHE-II score over 20.5, initial albumin level below 2.44 g/dL, and serum CRP clearance rates of less than 11% at 48 h and 20% at 96 h.
Using patients with non-CKD and low CRP as a reference group, the adjusted hazard ratios (HR, 95% confidence interval) for CVD were 1.88 (0.25-9.44) for patients with CKD/low CRP and 9.71 (3.27-31.97) for those with CKD/high CRP.