Non-chronic Kidney Disease Patients Research Articles

Effect of ferric citrate hydrate on fibroblast growth factor 23 and platelets in non-dialysis-dependent chronic kidney disease and non-chronic kidney disease patients with iron deficiency anemia.

Iron deficiency anemia (IDA) increases levels of C-terminal fibroblast growth factor 23 (cFGF23) and platelet count (PLT), each of which is associated with cardiovascular events. Therefore, we hypothesized that iron replacement with ferric citrate hydrate (FC) would decrease cFGF23 levels and PLT in patients with IDA. In a randomized, open-label, multicenter, 24-week clinical trial, patients with non-dialysis-dependent chronic kidney disease (CKD) and non-CKD complicated by IDA (8.0 ≤ hemoglobin < 11.0g/dL; and serum ferritin < 50ng/mL [CKD]; < 12ng/mL [non-CKD]) were randomized 1:1 to FC-low (500mg:approximately 120 mg elemental iron/day) or FC-high (1000mg: approximately 240mg elemental iron/day). If sufficient iron replacement had been achieved after week 8, further treatment was discontinued. Seventy-three patients were allocated to FC-low (CKD n = 21, non-CKD n = 15) and FC-high (CKD n = 21, non-CKD n = 16). Regardless of CKD status, FC increased serum ferritin and transferrin saturation, did not change intact FGF23 or serum phosphorus, but decreased cFGF23. In FC-low group, median changes in cFGF23 from baseline to week 8 were -58.00 RU/mL in CKD and -725.00 RU/mL in non-CKD; in FC-high group, the median changes were -66.00RU/mL in CKD and -649.50 RU/mL in non-CKD. By week 8, FC treatment normalized PLT in all patients with high PLT at baseline (>35.2 × 104/µL; FC-low: 1 CKD, 8 non-CKD; FC-high: 3 CKD, 8 non-CKD). Regardless of CKD status, iron replacement with FC decreased elevated cFGF23 levels and normalized elevated PLT in patients with IDA. jRCT2080223943.

Changes in Mortality According to Creatinine/Cystatin C Ratio in Chronic Kidney Disease and Non-chronic Kidney Disease Patients.

BackgroundSerum creatinine and cystatin C are not only good indicators of renal function but have also been confirmed to be related to disease prognosis and mortality in various diseases via creatinine/cystatin C ratio (CCR). However, although they are biomarkers of renal function, there is no study regarding renal impairment as a confounding variable in the relationship between CCR and all-cause mortality.MethodsPatients who had simultaneous measurements of serum creatinine and cystatin C between 2003 and 2020 were enrolled. The patients with chronic kidney disease (CKD) were defined as having an estimated glomerular filtration rate (eGFR) CKD-EPI Cr-Cystatin C < 60 ml/min/1.73 m2. CCR was calculated by dividing the serum creatinine level by the cystatin C level measured on the same day. The main outcome assessed was all-cause mortality according to CCR in CKD or non-CKD groups.ResultsAmong the 8,680 patients in whom creatinine and cystatin C levels were measured simultaneously, 4,301 were included in the CKD group, and 4,379 were included in the non-CKD group, respectively. CCR was 1.4 ± 0.6 in total participants. The non-CKD group showed higher mean CCR, (1.5 ± 0.7 vs. 1.3 ± 0.5) as well as a wider distribution of CCR (p < 0.001) when compared to the CKD group. In non-CKD group, 1st, 4th and 5th quintiles of CCR significantly increased the all-cause mortality risk compared to 2nd quintile of CCR, suggesting U-shaped mortality risk according to CCR in non-CKD. On the other hand, in CKD group, the risk of all-cause mortality linearly increased and 5th quintile of CCR showed 1.82 times risk of mortality compared to 2nd quintile of CCR. In the subgroup analysis of mortality by age and sex, the mortality difference according to CCR were diminished in old age and female sex subgroups.ConclusionWe discovered a U-shaped relationship between mortality and CCR levels in normal renal function, and an increased risk of mortality in CKD with elevated CCR.

Clinical presentation and outcomes of chronic kidney disease patients with COVID-19 admitted to the intensive care unit of a teaching hospital of Northern India during the third wave of the pandemic: A retrospective study.

Chronic kidney disease (CKD) patients have impaired immune status; that's why these patients are prone to develop infection-related complications. The current study compares non-haemodialysis chronic kidney disease and end-stage renal disease (NO-HD-CKD and ESRD, respectively) patient outcomes, the data of which is sparse. Patients diagnosed with COVID-19 infection through reverse transcriptase polymerase chain reaction (RT-PCR) were retrospectively studied using electronic health records. Patients were divided into three categories: non-chronic kidney disease (NO-CKD), NO-HD-CKD, and ESRD, and the outcome was assessed. Out of 745 patients, 92 (12.34%) had NO-HD-CKD and 31 (4.16%) had ESRD. CKD patients who were not on haemodialysis had higher rates of comorbidities and D-dimer and C-reactive protein (CRP) values compared to ESRD patients. The overall unadjusted mortality rate was found to be 17.44%, and it was 10.45% in case of NO-CKD patients, 58.69% for NO-HD-CKD patients, and 48.39% for ESRD patients. It was observed that patients having NO-HD-CKD had greater odds ratio of overall expiry in comparison to those without CKD in univariate analysis (OR: 1.58; 95% CI: 1.31-1.91). It was not significant in fully adjusted models (OR: 1.11; 95% CI: 0.88-1.40). During the third wave of COVID-19, we found higher mortality rates for cases with NO-HD-CKD and, to a lower extent, ESRD. However, patients with ESRD were observed to have good outcomes in comparison to those with NO-HD-CKD. Primary care physicians are the first point of contact for patients. Hence, it is critical for them to manage and to do proper referral of comorbid patients to higher centres.

High-density lipoprotein cholesterol to apolipoprotein A1 ratio and all-cause mortality among incident peritoneal dialysis patients

Background and aimsThe ratio of high-density lipoprotein cholesterol to apolipoprotein A1 (HAR) is associated with all-cause mortality in nonchronic kidney disease patients, but its role in predicting all-cause mortality in patients undergoing peritoneal dialysis (PD) is still unclear. The purpose of this study was to investigate the relationship between HAR and all-cause mortality in patients with PD. Methods and resultsThe medical records of 1199 patients with PD from November 1, 2005, to August 31, 2019, were collected retrospectively. The main outcome was defined as all-cause mortality. The HAR was divided into three groups by X-tile software. The association between HAR and all-cause mortality was evaluated by Cox models. The Kaplan–Meier method was used for the survival curve. The median follow-up period was 35 months (interquartile range: 20–57 months), with a total of 326 deaths recorded. After multiple adjustments, the risk of all-cause mortality in the high HAR group was 1.96-fold higher than that in the low HAR group (hazard ratio: 1.96; 95% CI, 1.22 to 3.15; P = 0.005). The restricted cubic splines showed that the risk of all-cause mortality increased gradually when HAR was >0.37. In the stratified analysis, a high HAR was linked to a high risk of all-cause mortality in males, patients under 55 years old, and patients without diabetes or cardiovascular disease (CVD). ConclusionThis study suggests that HAR is independently related to all-cause mortality in PD patients, especially in males, patients under 55 years old, and patients without diabetes or CVD.

Coronary artery disease in dialysis patients: evidence synthesis, controversies and proposed management strategies.

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality among patients with end-stage renal disease (ESRD). Clustering of traditional atherosclerotic and non-traditional risk factors drive the excess rates of coronary and non-coronary CVD in this population. The incidence, severity and mortality of coronary artery disease (CAD) as well as the number of complications of its therapy is higher in dialysis patients than in non-chronic kidney disease patients. Given the lack of randomized clinical trial evidence in this population, current practice is informed by observational data with a significant potential for bias. Furthermore, guidelines lack any recommendation for these patients or extrapolate them from trials performed in non-dialysis patients. Patients with ESRD are more likely to be asymptomatic, posing a challenge to the correct identification of CAD, which is essential for appropriate risk stratification and management. This may lead to "therapeutic nihilism", which has been associated with worse outcomes. Here, the ERA-EDTA EUDIAL Working Group reviews the diagnostic work-up and therapy of chronic coronary syndromes, unstable angina/non-ST elevation and ST-elevation myocardial infarction in dialysis patients, outlining unclear issues and controversies, discussing recent evidence, and proposing management strategies. Indications of antiplatelet and anticoagulant therapies, percutaneous coronary intervention and coronary artery bypass grafting are discussed. The issue of the interaction between dialysis session and myocardial damage is also addressed.

Impact of Chronic Kidney Disease on Prognosis of Heart Failure with Stable Reduced Ejection Fraction

Background Heart failure with reduced ejection fraction (HFrEF) of Objectives We hypothesized that the presence of CKD can result in a worse prognosis in patients with HFrEF and stable EF of 1 year. Methods At our academic institution, we evaluated 2593 baseline echo studies and their subsequent echo studies to identify HFrEF patients with stable EF of 1 year. Student's T-test and chi-square test were used to assess baseline differences between CKD and non-chronic kidney disease (NCKD) patients. Kaplan Meier survival analysis was conducted and Log-rank p values were calculated to assess the association of the different groups with all-cause mortality, cardiac mortality, and HF hospitalization rates. Multivariate Cox regression was adjusted for age, gender, race, HF etiology, HTN, DLP, DM, CAD, NYHA class, and COPD. Results A total of 205 patients were included in our study. Sixty-six patients (32.1%) had CKD. Table 1 summarizes characteristics of patients. Follow up period was 62.5 ± 30.6 months. CKD patients had higher all-cause mortality (figure 1), cardiac mortality, and HF hospitalization rates than NCKD patients, p-value of 0.0001, 0.001, and 0.001 respectively. In adjusted model, all-cause mortality, cardiac mortality, and HF hospitalization rates remained significantly higher in CKD patients (HR = 2.412, 95% CI = 1.34-4.32, p-value = 0.003), (HR = 2.481, 95% CI = 1.12-5.46, p-value = 0.024), and (HR = 1.766, 95% CI = 1.20-2.59, p-value = 0.004) respectively. Conclusion In patients with HFrEF and stable EF of 1 year, we found that the presence of CKD resulted in significantly higher all-cause mortality, cardiac mortality, and HF hospitalization rates. Further studies are needed to validate our results.

Effect of Chronic Kidney Disease on Mortality Outcomes of Heart Failure with Stable Mid-Range Ejection Fraction

Background Heart failure with mid-range ejection fraction (HFmrEF) of 40-49% is an under-recognized class of CHF. In patients with HFmrEF and stable ejection fraction (EF) of 1 year, the effect of CKD on mortality outcomes is unclear. Objectives We sought to determine if the presence of CKD can result in a higher mortality rate in patients with HFmrEF and stable EF of 1 year. Methods At our academic center, we evaluated 2593 baseline echo studies and their subsequent echo studies to identify HFmrEF patients with stable EF of 1 year. Student's T-test and chi-square test were used to assess baseline differences between CKD and non-chronic kidney disease (NCKD) patients. Kaplan Meier survival analysis was conducted and Log-rank p values were calculated to assess the association of the different groups with all-cause mortality, cardiac mortality, and non-cardiac mortality. Multivariate Cox regression was adjusted for age, gender, race, HTN, DM, CAD, NYHA class, OSA, and Malignancy. Results A total of 132 patients were included in our study. Thirty-three patients (25%) had CKD. The race was the only significantly different characteristic between the two groups, p-value of 0.003. Follow up period was 58.7 ± 29.1 months. CKD patients had higher all-cause and non-cardiac mortality rates (figures 1 and 2) than NCKD patients, p-value of 0.012 and 0.007 respectively. In adjusted model, all-cause and non-cardiac mortality rates remained higher in CKD patients (HR = 2.020, 95% CI = 1.06-3.83, p-value = 0.031) and (HR = 4.461, 95% CI = 1.51-13.11, p-value = 0.007) respectively. Cardiac mortality rate difference was not significant with p-value 0.084. Conclusion We found that patients with CKD and stable mid-range EF of 1 year had significantly higher all-cause mortality and non-cardiac mortality compared to patients with NCKD. Further studies are needed to validate our results.

Correction: Chronic kidney disease (CKD) patients are exposed to more proton pump inhibitor (PPI)s compared to non-CKD patients.

[This corrects the article DOI: 10.1371/journal.pone.0203878.].

Periodontal Status in Chronic Kidney Disease Patients

&lt;div&gt;&lt;p class="AbstractTitle"&gt;&lt;strong&gt;Objectives:&lt;/strong&gt; To compare periodontal status of chronic kidney disease patients with those in non-chronic kidney disease patients and to explore the relationship between periodontitis and chronic kidney disease in a group of Vietnamese.&lt;/p&gt;&lt;/div&gt;&lt;p class="AbstractContent"&gt;&lt;strong&gt;Methods:&lt;/strong&gt; A cross sectional study was conducted on 240 adults including 120 chronic kidney disease patients (group 1) and 120non-chronic kidney disease patients (group 2). The socio-demographic characteristic, dental and smoking habits were investigated by the questionnaire. Periodontal status (PPD, CAL, BOP) were examined. The periodontal status was compared between 2 groups. Multiple logistic regression analysis was performed to examine the relationship between chronic kidney disease and periodontitis after adjusting related factors.&lt;/p&gt;&lt;p class="AbstractContent"&gt;&lt;strong&gt;Results&lt;/strong&gt;: The clinically periodontal parameters in group 1 were all higher compared to those in group 2 (p&amp;lt;0.001). The OR for periodontitis in patients who with age more than 60 years or brushed their teeth less than 2 times per day or had no scaling or in current smokers or with chronic kidney disease were 1.93; 4.27; 7.95; 4.21; 2.94 compared to counterparts, respectively (p&amp;lt;0.05).&lt;/p&gt;&lt;p class="AbstractContent"&gt;&lt;strong&gt;Conclusion:&lt;/strong&gt; The periodontal status of chronic kidney disease patients was found worse than those in non-chronic kidney disease patients. The chronic kidney disease was significantly related to periodontitis.&lt;/p&gt;

Management of Hyperkalemia in Hospitalized Patients

PurposeThe aim of this study was to determine the incidence of treatment of hyperkalemia in hospitalized patients. MethodsThis is a prospective chart review of adults in a tertiary care hospital with hyperkalemia (serum potassium [K+] ≥5.1mEq/L) over a 6-month period. The treatments and their effectiveness, causative factors and associated electrocardiographic (ECG) changes were examined. ResultsThere were 154 hyperkalemic episodes, 32 with K+ ≥6.5mEq/L and 122 with K+<6.5mEq/L. Overall, 97% received treatment for an average K+ of 5.9mEq/L. Sodium polystyrene sulfonate (SPS) was included in 95% of the regimens. incremental doses of sPs monotherapy yielded potassium reductions between 0.7 and 1.1mEq/L, and inadequate responses (K+ <0.5mEq/L) were less frequent with higher doses. There were no differences in the effectiveness of SPS among dialysis-dependent, chronic kidney disease, or nonchronic kidney disease patients. Greater reductions in potassium were observed using a combination of treatments. ECGs were performed in 44% of patients, and 50% showed no ECG changes despite K+ being ≥6.5mEq/L. The most common abnormality, peaked T waves, was associated with a higher frequency of calcium administration but not with the number of K+-lowering therapies. ConclusionsAlmost all the patients were treated for hyperkalemia. Oral SPS monotherapy was the predominant treatment with the best response at the highest dose. Some combination therapies had greater K+ reductions but were used infrequently. An ECG was obtained in about 50% of the cases, but two thirds showed no K+-related changes. Reduced kidney function was associated with 70% of hyperkalemic episodes. Angiotensin-converting enzyme inhibitors and trimethoprim were the most commonly implicated medications.