Efficacy and Blood Concentrations of Cetuximab in a Hemodialysis Patient with Tongue Squamous Cell Carcinoma: A Case Report

Treatment with erythropoiesis-stimulating agents in chronic kidney disease patients with cancer

BackgroundPatients with dialysis-dependent end-stage renal disease (ESRD) taking midodrine may be at high risk for poor outcomes following transcatheter aortic valve replacement (TAVR). We evaluated dialysis-dependent ESRD patients taking midodrine. MethodsWe conducted a retrospective analysis of non-clinical trial TAVR patients from February 2012 to December 2020 from 11 facilities in a Western US health system. Patient groups included ESRD patients on midodrine before TAVR (ESRD [+M]), ESRD patients without midodrine (ESRD [−M]), and non-ESRD patients. The endpoints of 30-day and 1-year mortality were represented by Kaplan–Meier survival estimator and compared by log-rank test. ResultsForty-five ESRD (+M), 216 ESRD (−M), and 6898 non-ESRD patients were included. ESRD patients had more comorbid conditions, despite no significant difference in predicted Society of Thoracic Surgeons mortality risk between ESRD (+M) and ESRD (−M) (8.7% vs. 9.2%, p = 0.491). Thirty-day mortality was significantly higher for ESRD (+M) patients vs. ESRD (−M) patients (20.1% vs. 5.6%, p = 0.001) and for ESRD (+M) vs. non-ESRD patients (2.5%, p < 0.001). One-year mortality trended higher for ESRD (+M) vs. ESRD (−M) patients (41.9% vs. 29.8%, p = 0.07), and was significantly higher for ESRD (+M) vs. non-ESRD patients (10.7%, p < 0.001). Compared to ESRD (−M), ESRD (+M) patients had a higher incidence of 30-day stroke (6.7% vs. 1.4%, p = 0.033), 30-day vascular complications (6.7% vs. 0.9%, p = 0.011), and a lower rate of discharge to home (62.2% vs. 84.7%, p < 0.001). In contrast, ESRD (−M) patients had no significant differences from non-ESRD patients for these outcomes. ConclusionsOur experience suggests ESRD patients on midodrine are a higher acuity population with worse survival after TAVR, compared to ESRD patients not on midodrine. These findings may help with risk stratification for ESRD patients undergoing TAVR.

The emerging role of phosphate in vascular calcification

Hypertension in the dialysis patient.

What are the causes of protein-energy malnutrition in chronic renal insufficiency?

Background and Aims Despite evidence suggesting that a lack of fecal oxalate-degrading bacteria colonization is a risk factor for calcium oxalate stone formation, little is known about the oxalate-degrading activity (ODA) in fecal microbiota in end-stage renal disease (ESRD) patients. In addition, to date, there has been a general lack of research on the effect of fecal ODA on oxalate homeostasis in dialysis patients. The present pilot cross-sectional study was performed to compare the oxalate homeostasis profiles depending on ODA in fecal microbiota in ESRD patients. Method The data of a cross-sectional pilot study examining ODA in fecal microbiota, plasma oxalate concentration (POx) and urinary oxalate excretion (UOx) in 32 ESRD patients were represented in this study. Among the patients, there were 21 hemodialysis (HD) patients and 11 peritoneal dialysis (PD) patients. The average age of the patients was 52.5 [39; 65] years. The redoximetric titration with KMnO4 was adopted to evaluate total ODA in fecal microbiota. The results were expressed in % oxalate degradation per 0.01 g of feces. POx concentration and UOx excretion were measured spectrophotometrically using a commercially available kit (MAK-315, Sigma, Spain) and an oxalate oxidase/peroxidase reagent (BioSystems, Spain), respectively. Predialysis plasma samples were collected from HD patients. For further analysis, the patients were allocated to 2 groups according to ODA in feces. Group 1 included the patients with ≥ 1 % oxalate degradation per 0.01 g of feces. Group 2 included the patients with negative ODA (≤ 0 % /0.01 g). For the statistical analysis, we used the nonparametric Kruskal-Wallis test. The median (Me) and interquartile ranges [Q25; Q75] were calculated. The Spearman test was used for the correlation analysis. Univariate logistic regression analysis was used for predicting hyperoxalemia. All statistical analyses were performed using MedCalc. Results ODA in fecal microbiota ranged from -23 to 24 %/0.01 g of feces in ESRD patients and was statistically higher in HD patients compared with PD patients (3.2 [-0.5; 16] vs -4 [-6.5; 6.2], p=0.05). Negative ODA in fecal microbiota (≤ 0 % /0.01 g) was observed in 5/21 (23.8%) HD patients and 7/11 (63.6%) PD patients (χ2=3.9, p=0.04). Consequently, it might be associated with the negative effects of peritoneal dialysis solution. High POx concentration and low UOx excretion were diagnosed in patients with negative ODA in fecal microbiota (Group 2): 30.7 [25.5; 41.5] vs 50 [43.3; 75.5] μmol/L, p=0.01 and 60.9 [51; 65] vs 34.2 [24.4; 39] mg/d, p=0.0002, respectively (Fig. 1). Fecal ODA was directly associated with daily UOx excretion (r=0.85; p&amp;lt;0.0001) (Fig. 2) and had an inverse correlation with POx concentration (r=-0.36; p=0.04) (Fig. 3). In univariate logistic regression analysis, negative fecal ODA was determined as an independent risk factor for high POx concentration (OR: 40; 95% CI: 4.8-331, p&amp;lt;0.0001). Conclusion Our pilot cross-sectional study firstly demonstrated a close association between ODA in fecal microbiota and oxalate homeostasis in ESRD patients: less ODA in fecal microbiota was, higher POx concentration and lower UOx excretion occurred. We suppose that the potential significance of our findings provides preliminary information on the feasibility and necessity of further research in this area.

We do this investigation in order to reveal the relationship between the polymorphism of 1082A/G, anti-inflammatory interleukin-10 gene promoter, and end stage renal disease (ESRD) patients microinflammatory state and arteriosclerosis (AS). We used PCR-RFLP to measure the various kinds of distribution of IL-10 gene-1082A/G genotype and relevant indexes of microinflammatory state and AS of 870 ESRD patients and 1000 healthy persons of control group and to analyze the mechanism of its protection effect keeping ESRD patients away from microinflammation and arteriosclerosis. Compared with the control group, CRP, TNF-alpha, CH50, C3, IL-10 and Alb of ESRD group were in the normal range, but still significantly higher than those of the control group, while IL-10, Alb were significant lower (P < 0.05). The genotype distribution and allele frequency of IL-10A/G gene had no significant differences between the healthy group and the control group (P > 0.05). Levels of CRP, TNF-alpha, CH50 and C3 of ESRD patients with IL-10A/A genotype were significantly higher than those of ESRD patients with G/G and G/A genotype (P < 0.05), while IL-10 and Alb were significantly lower (P < 0.01). The production of IL-10 in serum from patients with IL-10A/A genotype was significantly lower than that of patients with G/G and G/A genotype (P < 0.01). The incidence rate of AS of patients with IL-10-1082A/A genotype was significantly higher than that of patients with G/G and G/A genotype (P < 0.01). The raise of AS incidence rate was correspondent with the decline of serum IL-10 and raise of serum CRP and Fib. The IL-10A/A genotype is a predictable factor of microinflammatory state and high AS incidence rate in ESRD patients. We use IL-10G/G genotype to modulate the high production of serum IL-10, to decline inflammatory reaction and to keep away from microinflammation and AS in ESRD patients. We should work hard on improving the dialysis membrane to reduce the anti-inflammatory factors in uremia for chronic renal failure patients with high arteriosclerosis risk.

Background: End stage renal disease (ESRD) is a well-recognized risk factor for development of sudden cardiac arrest(SCA). There is limited data on outcomes after an in-hospital SCA event in ESRD patients. Methods: Data were obtained from National Inpatient Sample from January 2007 to December 2017. In-hospital SCA was identified using International Classification of Disease, 9th Revision, Clinical Modification, and International Classification of Disease, 10th Revision, Clinical Modification codes of 99.60, 99.63, and 5A12012. ESRD patients were subsequently identified using codes of 585.6 and N18.6. Propensity -matched analysis using logistic regression with SD caliper of 0.2 was used to match patients with and without ESRD. Crude and propensity-matched (PS) cohorts outcomes were calculated. Results: A total of 1,412,985 patients sustained in-hospital SCA during our study period. ESRD patients with in-hospital SCA were younger and had a higher burden of key co-morbidities. Mortality was similar in ESRD and non-ESRD patients in PS matched cohort (70.4% vs. 70.7%, p = 0.45, figure 1) with an overall downward trend over our study years (figure 2). Conclusion: In the context of in-hospital SCA, mortality is similar in ESRD and non-ESRD patients in adjusted analysis. Adequate risk factor modification could further mitigate the risk of in-hospital SCA among ESRD patients

Surgery for diverticulitis is associated with high risk of in-hospital mortality and morbidity in older patients with end-stage renal disease

Some observational studies indicate an association of 25-hydroxy vitamin D (25(OH)D) insufficiency and atherogenic cholesterol concentrations. The aim of this study was to investigate relationship between 25(OH)D concentrations and lipid parameters in end stage renal disease (ESRD) patients, separately for predialysis, hemodialysis and peritoneal dialysis patients. We have adjusted 25(OH)D concentrations for seasonal variability with cosinor analysis, and performed all further analysis using these corrected 25(OH)D concentrations. Concentrations of 25(OH)D and the lipid parameters were determined in 214 ESRD patients and 50 control group participants. The analysis included the measurement of 25(OH)D by HPLC, apolipoprotein (Apo) AI, ApoB and Lp(a) by nephelometry, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) by spectrophotometry and manually calculated ApoB/ApoAI and LDL-C/HDL-C ratio. ESRD patients with adjusted 25(OH)D concentrations of 50 nmol/L had significantly higher TC (P = 0.005) and ApoAI (P = 0.049). Significantly higher HDLC (P = 0.011) and ApoAI (P = 0.020) were found in hemodialysis patients with the 25(OH)D concentrations of 50 nmol/L. The other analyzed lipid parameters differed significantly between predialysis, hemodialysis and peritoneal dialysis patients with 25(OH)D concentrations of < 50 nmol/L. Our study indicate the significant relationship between 25(OH)D repletion and optimal concentrations of lipid parameters in ESRD patients. Further research is necessary to explain whether joint evaluation of vitamin D status and lipid abnormalities could improve cardiovascular outcome in ESRD patients.

Leptin is a 16-kDa protein recently identified as the obese gene product involved in body weight regulation. Administration of recombinant leptin to ob/ob mice, which have a genetic defect in leptin production, reduces food intake and increases energy expenditure. Leptin is synthesized by fat cells, and in normal humans, plasma concentrations are proportional to adiposity. The physiological actions and the degradation pathways of leptin in humans are unknown. We investigated renal elimination of leptin by comparing plasma leptin concentrations in end-stage renal disease (ESRD) patients with normal controls. Our hypothesis was that if renal filtration is a significant route of elimination, the hormone would accumulate in ESRD patients. Mean plasma levels in 141 ESRD patients (26.8 +/- 5.7 and 38.3 +/- 5.6 micrograms/L for males and females, respectively) were significantly higher (P < 0.001) than mean values obtained in normal controls (11.9 +/- 3.1 and 21.2 +/- 3.0 micrograms/L for males and females, respectively). Leptin concentrations in ESRD patients correlated directly with body mass index (BMI; r = 0.77 for men and 0.78 for women). The rate of increase in leptin concentrations with BMI was significantly greater in ESRD patients (5.5 and 6.6 micrograms/L/U BMI for men and women, respectively) than in normal controls (1.4 and 2.6 micrograms/L/U for men and women, respectively). Pre- and postdialysis leptin levels in hemodialysis patients were similar. Western blot of plasma from ESRD patients with high leptin levels showed bands corresponding to the intact protein (16 kDa) with no lesser or greater molecular mass species observed. Leptin concentrations in patients with ESRD did not correlate with measures of residual renal function (serum creatinine, beta 2-microglobulin, PTH, or GH levels). Similarly, we found no correlation between leptin levels and the number of years patients had been on dialysis or with recent weight changes. We conclude that intact leptin is increased in ESRD patients, but does not appear to cause decreased weight. As leptin levels did not correlate with residual renal function, increased production may account for the high levels observed.

The risk of hydrocephalus in end-stage renal disease (ESRD) patients on dialysis has not been studied in depth. Using Taiwan National Health Insurance claims data, we identified 29 684 incident ESRD patients from 2000 to 2010, including 10 030 peritoneal dialysis (PD) patients and 19 654 hemodialysis (HD) patients. The control cohort consisted of 118 736 people randomly selected from those without kidney disease, frequency matched with ESRD patients by age, sex and index year. We also established propensity score-matched cohorts with 10 014 PD and 10 014 HD patients. The incidence rates and hazard ratios (HRs) of hydrocephalus were calculated until the end of 2011. Incidence rates of hydrocephalus were greater in HD and PD patients than in controls (8.44 and 11.0 versus 4.11 per 10 000 person-years, respectively), with an adjusted HR of 1.86 [95% confidence interval (CI) 1.43-2.41] for all ESRD patients compared with controls. A higher proportion of hydrocephalus patients underwent surgical bypass to relieve hydrocephalus in ESRD patients than controls, 40.7% (46/113) versus 24.5% (67/273), with an adjusted odds ratio of 2.11 (95% CI 1.33-3.36). Compared with controls, the adjusted HRs of communicating hydrocephalus for HD and PD patients were 1.77 (95% CI 1.22-2.55) and 2.51 (95% CI 1.61-3.89), respectively. The propensity score-matched analysis showed an HR of 0.72 (95% CI 0.42-1.23) for hydrocephalus in HD patients compared with PD patients. Patients with ESRD are at an increased risk of hydrocephalus. The risk difference between HD and PD patients is not significant.

Introduction: Epicardial adipose tissue (EAT) is the true visceral fat depot of the heart. The relationship between coronary artery disease and EAT was shown in end-stage renal disease (ESRD) patients. One of the established risk factor in this population is dyslipidemia. We aimed to determine the relationship between atherogenic index of plasma (AIP) and EAT in ESRD patients. Methods: This was a cross-sectional study involving 76 ESRD patients receiving PD or HD for ≥6 months and 42 healthy subjects. EAT was measured by using an electrocardiogram-gated 64-multidetector computed tomography (MDCT). Atherogenic index of plasma was calculated as the logarithmically transformed ratio of the serum trigliseride to HDL-cholesterol. Results: The etiology of ESRD patients was diabetic nephropathy (n = 16), chronic glomerulonephritis (n = 10), hypertensive nephropathy (n = 23), polycystic kidney disease (n = 7), nephrolithiasis (n = 5) and unknown (n = 15). There were no differences with respect to the following variables between ESRD patients and healthy subjects: age; sex; BMI; predialysis levels of DBP; serum levels of albumin, HDL-cholesterol and hemoglobin. However, ESRD patients had higher serum levels of trigliseride, hs-CRP and AIP when compared to healthy subjects. There was a statistically significant relationship between EAT, BMI and AIP in ESRD patients (r = 0.42, p < 0.001 and r = 0.25, p = 0.028, respectively). The stepwise linear regression analysis revealed that age, as well as BMI were independent predictors of EAT. Conclusion: We found a relationship between EAT as defined by MDCT and AIP in ESRD patients. Further clinical and experimental studies are needed.

Background: End stage renal disease (ESRD) patients are vulnerable to contract corona virus disease-19 (COVID-19), and they have higher risk of deterioration and mortality rate compared to general population. There are studies on COVID-19 in end stage renal disease (ESRD) patients showing the low rates of deterioration, most of which did not develop into severe pneumonia. Objective: Compare the clinical, laboratory, and radiological findings in COVID-19 patients with and without ESRD and to identify the mortality risk factors in those with ESRD. Methods: We conducted a cross-sectional study involving 87 COVID-19 patients, consisted of 43 ESRD and 44 non-ESRD. Data taken included age, gender, the amount of co-morbid, oxygen saturation when they first arrived, COVID 19 symptoms (mild/moderate/severe-critical), and the data of patients who died. Result: Severe-critical clinical manifestations of COVID-19 were more common in those with ESRD vs those without (p=0.012). However, the mortality was not significantly different. Absolute neutrophil count and neutrophil-lymphocyte ratio (NLR) were significantly higher in those with ESRD. As many as 24% COVID patients died, in which 11% are ESRD patients, and 13% non-ESRD. Multivariate analysis showed that NLR ≥1 had 1.3 times higher death risk compared to NLR&lt;1. Conclusion: Severe-critical clinical manifestations of COVID-19 were more commonly found in ESRD patients. The mortality rate was not significantly different between the ESRD and non-ESRD. In COVID-19 patients with ESRD, NLR ≥1 had 1.3 times higher death risk compared to NLR&lt;1. High NLR is a risk factor for higher mortality in ESRD patients.

Patient Perceptions and Experiences of ESRD Care: Quality and Satisfaction