Statistical analysis identified 10 genes able to discriminate CKD from HD and PD patients (FDR = 5%, P < 0.001) and significantly correlated to CRP levels.
CRPrs2808630 AG compared to the referent AA genotype was associated with CKD in non-Hispanic blacks (n = 1649, 293 of whom had CKD) with an adjusted odds ratio (OR) of 3.09 (95% CI 1.65-5.8; p = 0.001).
We identified ten predictors including sex, diabetes mellitus, lactate dehydrogenase level, C-reactive protein, years since drinking, chronic kidney disease (CKD), stage of CKD, stroke, acute myocardial infarction, and systolic blood pressure.
When compared with the CTR group, subtotal nephrectomy in the CKD group significantly elevated blood pressure; increased the left ventricular mass, end-diastolic left ventricular internal dimension, left ventricular end-diastolic posterior wall thickness and end-diastolic interventricular septum thickness; prolonged the QT interval, corrected QT interval, the interval from the peak to the end of the T wave (Tp-e) and the corrected Tp-e interval; and increased the QT dispersion and the Tp-e/QT ratio; decreased the VFT; and increased the serum concentrations of noradrenaline, C-reactive protein and interleukin-6.
They also had almost 4 times the risk of a CKD-related hospitalisation compared with participants in the lowest CRP tertile (HR=3.91, 95%CI 1.01-15.20, P=0.049) after adjustment for potential confounding factors.
Our research showed that the incidence and severity of infection in CKD5 group were significantly higher than those of CKD1-4 group; the baseline PCT level in CKD patients increased as renal function decreased and strongly correlated with CKD staging (r = 0.749); for CKD1-4 group, PCT, WBC, and N% could predict sepsis with the area under the curve (AUC) of 0.956, 0.854, and 0.917, respectively, but only CRP could predict local infection with AUC of 0.729, and for CKD5 group, only PCT and CRP could predict local infection with AUC of 0.715 and 0.780, respectively, and only PCT and N% could predict sepsis with AUC of 0.823 and 0.683, respectively.
Recent studies have demonstrated that CRP is pathogenic in a number of diseases including hypertensive cardiovascular and kidney complications, diabetic nephropathy, and acute and chronic kidney diseases.
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.
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.