Background Peritoneal dialysis (PD) has become an increasingly important treatment modality for end-stage renal disease. However, application of PD in patients with liver cirrhosis (LC) and subsequent outcomes have not been thoroughly evaluated. Methods A total of 1,366 patients (≥ 18 years old) who started PD at 4 tertiary referral centers between January 2000 and December 2015 were initially reviewed. Among them, 45 patients with LC were finally analyzed (LC-PD). Using the multivariate Cox hazard ratio (HR) model, outcomes such as technique failure, infection, and mortality in patients with LC-PD were compared with those in non-LC-PD patients (non-LC-PD) or patients with LC who received hemodialysis (LC-HD). All of the patients were selected by 1:1 matching of age, sex, catheter insertion date, and diabetes mellitus. Results During the mean follow-up duration of 43 ± 35.8 months, 12 patients with LC-PD experienced technique failure, and this rate was similar to that of non-LC-PD patients. In evaluating infection episodes, the most common causes for peritonitis and exit-site infection were Escherichia coli (5.8%) and Staphylococcus aureus (19.3%), respectively; these event rates of LC-PD did not differ from those of non-LC-PD. The all-cause mortality rate of the LC-PD group was not different from that of the non-LC-PD and LC-HD groups. Conclusion Dialysis outcomes such as technique failure, infection, and mortality are not affected by the presence of LC. Accordingly, PD therapy is a good option in patients with LC.
Background and Aims Decreased kidney function is a risk factor for the development of contrast-associated acute kidney injury (CA-AKI) in chronic kidney disease (CKD). Although the relationship between CKD and CA-AKI is well established, the mechanistic link between the two, particularly the extent to which this interaction is mediated by inflammation, remains poorly understood. We examined the association between CKD and CA-AKI, as well as potential mediators, including serum albumin and high-sensitivity C-reactive protein (hs-CRP) levels. Method A total of 3,738 patients were enrolled for analysis from 5,299 patients and fulfilled the inclusion criteria among 12,742 patients who underwent coronary angiography (CAG) between 1 January 2007, and 31 December 2016. Multivariable logistic regression and mediation analyses were performed. In addition to the effect as risk factors, direct and indirect effects were also estimated. Results Among 3,738 subjects, 414 developed AKI (11.1%). Pre-procedural albumin and Lnhs-CRP (log-transformed) were independently associated with CA-AKI (odds ratio [OR], 95% confidence interval [CI]): 0.320 (0.272–0.3787), P <0.001 and 1.211 (1.132-1.296), P<0.001, respectively. Direct, and indirect effects were also estimated. Patients with CKD were found to be more likely to exhibit lower serum albumin and higher serum hs-CRP levels. Simple mediation analyses showed that 33.8% and 52.3% of the relationship between CKD and CA-AKI was mediated by the serum albumin and hs-CRP levels, respectively with co-mediation being 13.9%. Conclusion These results represent that, in addition to reduced kidney function, inflammatory parameters are also risk factors and mediators of CA-AKI in patients with CKD.
Background and Aims Serum uric acid (UA) is associated with renal disease. Hyperuricemia can be a risk of hypertension, intrarenal vascular disease and renal injury. We investigate the serum UA has an association with renal disease progression in patients with chronic kidney disease (CKD) with hypertension. Method We recruited 270 CKD patients with hypertension from 4 centers in Korea through the APrODiTe study and followed for 1 year. Serum UA was evaluated as a continuous value and groups divided by quartiles. The renal outcomes were an increase in random urine protein/creatinine ratio (PCR) than baseline value or estimated glomerular filtration rate (eGFR) deterioration which means a decrease in eGFR ≥ 5 (ml/min/1.73m2). Results Baseline serum UA was 6.58 ± 1.73 mg/dl and 6.52 ± 3.59 mg/dl after 1 year. For proteinuria progression, a 1 mg/dl higher serum UA has independent correlation in multivariate regression (odds ratio (OR): 1.272; 95% confidence interval (CI): 1.031-1.568; P = 0.024). The higher quartile of serum UA showed a correlation with the odd ratio than lower quartile (OR: 2.243; 95% CI: 0.862-5.837; P = 0.098, OR:3.417; 95% CI: 1.275-9.152; P= 0.015, OR: 2.754; 95% CI: 1.013-7.488; P < 0.047). In subgroup analysis, the patients with late CKD stage (3-5) showed serum UA has a positive correlation with proteinuria progression (OR: 1.311; 95% CI: 1.022-1.682; P= 0.033) and the top quartile group was correlated with the increased odds ratio compared to lower quartile (OR: 3.811; 95% CI: 1.153-12.59; P = 0.028). For eGFR deterioration, the higher quartile of UA was positively correlated with the odd ratio in only univariate analysis. Conclusion Serum UA level has an independent correlation with proteinuria progression in especially late CKD patient with hypertension. Whereas for eGFR deterioration, serum UA did not show a significant correlation.
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