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Multidisciplinary care can improve the outcomes of chronic kidney disease (CKD), however the contribution of self-care behavior and knowledge about CKD is unclear. This study enrolled 454 participants with CKD stages 1–5 not on dialysis. Structured questionnaires were used to evaluate self-care behavior and kidney disease knowledge. Rapid decline in renal function was defined as the decline in estimated filtration rate > 3 ml/min per 1.73 m 2 /year within 1-year prior to enrollment. The mean age of all study participants was 65.8 ± 12.1 years and 55.9% were male. The elderly had better self-care behavior while younger participants had better disease knowledge. Both high self-care and high disease knowledge scores were significantly associated with and had a synergistic effect on decreasing the risk of rapid decline in renal function. CKD patients with better self-care behavior and better kidney disease knowledge had lower risk of rapid decline in renal function.

Aims/Introduction Few studies have assessed whether dynamic kidney function prior to sodium–glucose cotransporter‐2 inhibitor (SGLT2i) initiation influenced subsequent renal outcomes. Thus, the study aimed to investigate whether combining estimated glomerular filtration rate (eGFR) slope and urinary albumin/creatinine ratio (UACR) change prior to using SGLT2i contributes to subsequent kidney outcomes. Materials and Methods This retrospective cohort study utilized data from the Kaohsiung Medical University Hospital Research Database (KMUHRD) in Taiwan. We identified 975 SGLT2i new users with type 2 diabetes from 2016 to 2020, who had an eGFR >60 mL/min/1.73 m2 and UACR <30 mg/g 1 year prior to using SGLT2i. Patients were categorized into four groups based on an eGFR decline rate of 2.5 mL/min/1.73 m2/year and a UACR increase of 30%. The primary study outcomes included a >30% eGFR decline with a drop in eGFR categories and a >43% UACR increase with progression in UACR categories. Results After SGLT2i treatment, compared with the non‐progressive renal function group, the glomerular injury group significantly lowered the risk of eGFR decline (adjusted hazard ratio [95% CI] 0.384 [0.199, 0.740]) and UACR progression (adjusted hazard ratio [95% CI] 0.514 [0.313, 0.846]). In addition, for those with a major eGFR decline before starting SGLT2i, significant improvements in the eGFR slope (P < 0.05) were observed after the treatment, irrespective of UACR increase. Conclusions Early initiation of SGLT2i among type 2 diabetes patients with low‐risk renal disease progression and glomerular injury renal status may prevent them from progressing into chronic kidney disease.

The factors associated with the timely creation of distal vascular access for hemodialysis initiation are unclear. We aimed to explore the association between the slope of estimated glomerular filtration rate (eGFR) and the successful usage of vascular access upon hemodialysis initiation. This single center retrospective cohort study enrolled chronic kidney disease patients who undertook a multidisciplinary care program from 2003 to 2016. Using eGFR slope as predictor, we evaluated the vascular access created timely upon hemodialysis initiation. Among the 987 patients, vascular access was created at a median eGFR of 5.8 min/ml/1.73 m 2 , with a median duration of 3.1 months before hemodialysis. The proportions of vascular access created timely, created not timely (vascular access immature), and not created were 68.5%, 8.8%, and 22.7%, respectively. There was a significant negative association of eGFR upon vascular access creation with eGFR slope (r = − 0.182, P < 0.001). The fastest eGFR slope patients (the first quartile or < − 10 min/ml/1.73 m 2 /year) had the lowest percentage of vascular access created timely. In the multivariable logistic regression analysis, only higher eGFR upon vascular access creation (P = 0.001) and eGFR slope (P = 0.009) were significantly associated with vascular access created timely. The adjusted odds ratios of each quartile of eGFR slopes for vascular access created timely were 0.46 (95% confidence interval 0.27–0.86), 1.30 (0.62, 2.72), 1.00 (reference), and 0.95 (0.48–1.87), respectively. eGFR slope is associated with the timely creation of vascular access for the initiation of hemodialysis in a reverse-J-shaped pattern and may help determine the time of vascular access creation.

Protein-bound uremic toxins (Indoxyl sulfate [IS] and p-cresyl sulfate [PCS]) are both associated with cardiovascular (CV) and all-cause mortality in subjects with chronic kidney disease (CKD). Possible mechanisms have not been elucidated. In hemodialysis patients, we investigated the relationship between the free form of IS and PCS and 181 CV-related proteins. First, IS or PCS concentrations were checked, and high levels were associated with an increased risk of acute coronary syndrome (ACS) in 333 stable HD patients. CV proteins were further quantified by a proximity extension assay. We examined associations between the free form protein-bound uremic toxins and the quantified proteins with correction for multiple testing in the discovery process. In the second step, the independent association was evaluated by multivariable-adjusted models. We rank the CV proteins related to protein-bound uremic toxins by bootstrapped confidence intervals and ascending p -value. Six proteins (signaling lymphocytic activation molecule family member 5, complement component C1q receptor, C–C motif chemokine 15 [CCL15], bleomycin hydrolase, perlecan, and cluster of differentiation 166 antigen) were negatively associated with IS. Fibroblast growth factor 23 [FGF23] was the only CV protein positively associated with IS. Three proteins (complement component C1q receptor, CCL15, and interleukin-1 receptor-like 2) were negatively associated with PCS. Similar findings were obtained after adjusting for classical CV risk factors. However, only higher levels of FGF23 was related to increased risk of ACS. In conclusion, IS and PCS were associated with several CV-related proteins involved in endothelial barrier function, complement system, cell adhesion, phosphate homeostasis, and inflammation. Multiplex proteomics seems to be a promising way to discover novel pathophysiology of the uremic toxin.

Low transferrin saturation (TSAT), calculated by serum iron divided by total iron-binding capacity (TIBC), indicates iron deficiency. Because malnutrition and inflammation are associated with low TIBC in chronic kidney disease (CKD), TSAT might not reflect iron status or risk for anemia. We examined whether low serum iron was a risk factor for anemia in CKD patients with normal TSAT. Thus we compare the risk for anemia in 2500 CKD stage 1–4 patients divided by TSAT (cutoff: 20%) and serum iron (cutoff: 70 μg/dL in men, 60 μg/dL in women). Our results confirmed low TIBC (< 200 μg/dL) was associated with hypoalbuminemia and high C-reactive protein. In fully-adjusted logistic regression, both “normal TSAT low iron” and “low TSAT low iron” groups were associated with baseline anemia (hemoglobin < 11 g/dL) (odds ratios (OR) 1.56; 95% confidence interval (CI) 1.13–2.16 and OR 2.36; 95% CI 1.76–3.18, respectively) compared with the reference group (normal TSAT normal iron). Sensitivity tests with different cutoffs for TSAT and iron also showed similar results. In patients without anemia, both groups were associated with anemia after 1 year (OR 1.69; 95% CI 1.00–2.83 and OR 1.94; 95% CI 1.11–3.40, respectively). In conclusion, CKD stage 1–4 patients with normal TSAT but low serum iron are still at risk for anemia.

Pyuria is common in chronic kidney disease (CKD), which could be due to either urinary tract infection (UTI) or renal parenchymal inflammation. Only little is known regarding the association of pyuria or UTI with renal outcomes. We investigated 3226 patients with stage 3–5 CKD. Pyuria was defined as ≥ 50 WBC per high-power field (hpf) and was correlated to old age, female, diabetes, hypoalbuminemia, lower eGFR, and higher inflammation status. In Cox regression, patients with more than one episode of pyuria in the first year (11.8%) had increased risks for end-stage renal disease (ESRD) [hazard ratio (95% CI): 1.90 (1.58–2.28); p  <  0.001 ], rapid renal function progression [odds ratio (95% CI): 1.49 (1.13–1.95); p  =  0.001 ], and all-cause mortality [hazard ratio: 1.63 (1.29–2.05); p  <  0.001 ], compared to those without pyuria. In a subgroup analysis, the risk of pyuria for ESRD was modified by CKD stages. We investigated the effects of UTI (urinary symptoms and treated by antibiotics) and pyuria without UTI (urine WBC < 50 to ≥ 10/hpf without any episodes of ≥ 50 WBC/hpf or UTI), while both groups were associated with clinical outcomes. In conclusion, CKD stage 3–5 patients with frequent pyuria or UTI episodes have increased risks of renal outcomes.

Chronic kidney disease (CKD) and hepatitis C virus (HCV) infection are closely linked and both increase patient mortality. The association of HCV and risk of developing end-stage renal disease (ESRD) has not been analyzed with competing risk model. We enrolled a prospective cohort of 4,185 patients (mean age, 62 years; 41% female) registered in the CKD integrated care program at two affiliated hospitals of Kaohsiung Medical University in Taiwan between November 11, 2002 and May 31, 2009. With competing risk model, we analyzed the association of HCV infection, defined by seropositive of anti-HCV antibody, and hepatitis B virus (HBV) infection, defined by seropositive of HBV surface antigen, with the risk of entering ESRD. The prevalence of HCV infection was 7.6% and it increased with the CKD stages (trend test, P<0.001), while the prevalence of HBV infection was 7.4% and no specific trend among CKD stages (tend test, P = 0.1). During the 9,101 person-year follow-up period, there were 446 death and 1,205 patients entering ESRD. After adjusting death as the competing risk, the estimated 5-year cumulative incidence rate of ESRD among patients with and without HCV infection were 52.6% and 38.4%, respectively (modified log-rank, P<0.001). Multivariable analysis showed that HCV infection, but not HBV infection, had higher risk of developing ESRD compared with cases without infection (HCV, HR: 1.32, 95% CI: 1.07-1.62; HBV, HR: 1.10, 95% CI: 0.89-1.35). Subgroup analyses showed consistent results. With death-adjusted competing risk analysis, HCV infection is associated with an increased risk of developing ESRD in CKD cohort.

Aims/Introduction Fatty acid desaturase (FADS) genetic polymorphisms are strongly correlated with the risk of dyslipidemia and cardiovascular disease. In this study, we examined the impact of FADS1 and FADS2 genetic variants on plasma lipid status, and assessed interactions between FADS genetic polymorphisms and plasma n‐3/n‐6 fatty acids regarding lipid status within a population of 816 Taiwanese patients with type 2 diabetes. Materials and Methods Selected tag single‐nucleotide polymorphisms (FADS1 rs174546 [T/C]; FADS2 rs174602 [A/G] and rs2072114 [A/G]) were genotyped (n = 816). Results The distribution of genotypes were compared with reports publicly available in the Genome Aggregation Database for East Asian populations (https://gnomad.broadinstitute.org). In the subgroup of patients not taking lipid‐lowering medications (n = 192), we observed that the G allele of FADS2 rs174602 was statistically significantly correlated with lower low‐density lipoprotein cholesterol (LDL‐C) concentrations (P = 0.001), whereas the G allele of rs2072114 was marginally associated with LDL‐C concentrations (P = 0.091). Using a general linear model adjusted for confounding factors, statistically significant interactions (P = 0.016) between single‐nucleotide polymorphisms in rs2072114 and a low alpha‐linolenic acid (18:3n‐3)/linoleic acid (18:2n‐6) ratio; the G allele correlated with lower LDL‐C levels among individuals with a low alpha‐linolenic acid/linoleic acid ratio. Interaction between rs174602 single‐nucleotide polymorphisms and low alpha‐linolenic acid/linoleic acid values on LDL‐C was only marginally significant (P = 0.063). Conclusions Our results show the role of n‐3/n‐6 dietary polyunsaturated fatty acids in modifying the effects of genetic susceptibility on lipoprotein concentrations in patients with type 2 diabetes. Our findings highlight the potential of interventions with dietary polyunsaturated fatty acids regarding developing individualized prevention strategies for type 2 diabetes presenting with co‐occurring dyslipidemia and cardiovascular diseases.

Diabetic retinopathy (DR) is associated with increased cardiovascular risk, but evidence of its relationship with heart failure (HF) in people with diabetes and chronic kidney disease (CKD) is limited. Therefore, we examined the association between DR severity and concurrent HF status, as well as the risk of subsequent HF hospitalization in this population. A total of 1,503 patients with both diabetes and CKD underwent fundus photography. DR severity was classified into three groups: Group 1 (no apparent DR, mild non-proliferative DR [NPDR], moderate NPDR), group 2 (severe NPDR, very severe NPDR), and group 3 (proliferative DR [PDR], and high-risk PDR). Associations between HF status and DR severity were analyzed using ordinal regression. Cox proportional hazard models examined the association between DR severity and subsequent HF hospitalization. HF was positively associated with worse DR grade (adjusted odds ratio 2.09, 95% confidence interval [CI] 1.37–3.18). In patients without HF at baseline, a higher incidence of acute HF hospitalization over 5 years was identified in group 2 (hazard ratio 1.37, 95% CI 0.83–2.26) and group 3 (hazard ratio 1.86, 95% CI 1.22–2.83) compared to patients with less severe DR. In summary, DR severity is independently associated with both concurrent HF and risks for HF hospitalization over 5 years among those with diabetes and CKD and could aid cardiovascular risk stratification.