Global Prevalence of Protein-Energy Wasting in Kidney Disease: A Meta-analysis of Contemporary Observational Studies From the International Society of Renal Nutrition and Metabolism.

OBJECTIVE: To better define the prevalence of protein-energy wasting (PEW) in kidney disease is poorly defined. METHODS: We performed a meta-analysis of PEW prevalence from contemporary studies including more than 50 subjects with kidney disease, published during 2000-2014 and reporting on PEW prevalence by subjective global assessment or malnutrition-inflammation score. Data were reviewed throughout different strata: (1) acute kidney injury (AKI), (2) pediatric chronic kidney disease (CKD), (3) nondialyzed CKD 3-5, (4) maintenance dialysis, and (5) subjects undergoing kidney transplantation (Tx). Sample size, period of publication, reporting quality, methods, dialysis technique, country, geographical region, and gross national income were a priori considered factors influencing between-study variability. RESULTS: Two studies including 189 AKI patients reported a PEW prevalence of 60% and 82%. Five studies including 1776 patients with CKD stages 3-5 reported PEW prevalence ranging from 11% to 54%. Finally, 90 studies from 34 countries including 16,434 patients on maintenance dialysis were identified. The 25th-75th percentiles range in PEW prevalence among dialysis studies was 28-54%. Large variation in PEW prevalence across studies remained even when accounting for moderators. Mixed-effects meta-regression identified geographical region as the only significant moderator explaining 23% of the observed data heterogeneity. Finally, two studies including 1067 Tx patients reported a PEW prevalence of 28% and 52%, and no studies recruiting pediatric CKD patients were identified. CONCLUSION: By providing evidence-based ranges of PEW prevalence, we conclude that PEW is a common phenomenon across the spectrum of AKI and CKD. This, together with the well-documented impact of PEW on patient outcomes, justifies the need for increased medical attention.

Association Between Serum Leptin Level and Mortality in Kidney Transplant Recipients.

OBJECTIVE: Leptin is a hormone made by adipocytes and associated with hypertension, inflammation, and coronary artery disease. Low serum leptin level was associated with higher risk of death in patients with advanced chronic kidney disease. Little is known about the association of serum leptin with outcomes in kidney transplant recipients. DESIGN: Prospective prevalent cohort. SETTING AND SUBJECT: We collected sociodemographic and clinical parameters, medical and transplant history, and laboratory data of 979 prevalent kidney transplant recipients. Associations between serum leptin level and death with a functioning graft, all-cause death, and death-censored graft loss over a 6-year follow-up period were examined in survival models. RESULTS: Serum leptin levels showed moderate negative correlation with eGFR (R = -0.21, P < .001) and positive correlations with BMI (R = 0.48, P < .001) and C-reactive protein (R = 0.20, P < .001). Each 10 ng/mL higher serum leptin level was associated with 7% lower risk of death with functioning graft (hazard ratio [HR] (95% confidence interval [CI]), 0.93 (0.87-0.99)), and this association persisted after adjustment for confounders: HR (95% CI), 0.90 (0.82-0.99). Similar associations were found with all-cause death as outcome. The association between serum leptin level and risk of graft loss was nonlinear, and only low serum leptin level was associated with higher risk of graft loss. CONCLUSIONS: In prevalent kidney transplant recipients, lower serum leptin was an independent predictor of death.

Association between serum resistin level and outcomes in kidney transplant recipients.

Resistin is an adipocytokine that is associated with inflammation, coronary artery disease, and other types of cardiovascular disease among patients with normal kidney function. However, little is known about the association of resistin with outcomes in kidney transplant recipients. We collected socio-demographic and clinical parameters, medical and transplant history, and laboratory data from 988 prevalent kidney transplant recipients enrolled in the Malnutrition-Inflammation in Transplant-Hungary Study (MINIT-HU study). Serum resistin levels were measured at baseline. Associations between serum resistin level and death with a functioning graft over a 6-year follow-up period were examined in unadjusted and adjusted models. The mean±SD age of the study population was 51 ± 13 years, among whom 57% were men and 21% were diabetics. Median serum resistin concentrations were significantly higher in patients who died with a functioning graft as compared to those who did not die during the follow-up period (median [IQR]: 22[15-26] vs. 19[14-22] ng/ml, respectively; P < 0.001). Higher serum resistin level was associated with higher mortality risk in both unadjusted and fully adjusted models: HRs (95% CI): 1.33(1.16-1.54) and 1.21(1.01-1.46), respectively. In prevalent kidney transplant recipients, serum resistin was an independent predictor of death with a functioning graft.

Association of Abdominal Circumference, Body Mass Index, and Inflammation in Kidney Transplant Recipients.

OBJECTIVE: Increased abdominal circumference is a marker of obesity, and it is associated with increased mortality in renal transplant recipients. Recent findings suggest that increased visceral fat deposition is a modifier of inflammation. However, little is known about the association of inflammation with abdominal circumference in kidney transplant recipients. DESIGN: Cross-sectional. SUBJECT: We collected sociodemographic and clinical parameters, medical and transplant history, and laboratory data from 985 prevalent kidney transplant recipients. Abdominal circumference, body mass index (BMI), and inflammatory markers were measured at baseline. Associations of inflammatory markers with abdominal circumference and BMI were examined in unadjusted and adjusted regression models. RESULTS: Mean ± standard deviation age was a 51 ± 13 years, 57% were men, and 21% were diabetics. Patients with abdominal circumference above the median had higher BMI and were older (mean ± standard deviation: 23.9 ± 3.6 vs. 30.1 ± 3.9 kg/m(2), P < .001; and 48 ± 14 vs. 54 ± 11 years, P < .001). Furthermore, patients with higher abdominal circumference had higher inflammatory parameters: median (interquartile range) C-reactive protein (mg/L): 2.3 (3.9) versus 4.1 (6.2), P < .001; and IL-6 (pg/mL): 1.9 (2.2) versus 2.3 (2.4), P < .001. In multivariable-adjusted linear regression models, higher abdominal circumference showed significant linear associations with inflammatory markers (standardized regression coefficients (ß) of abdominal circumference for lnCRP: ßabdominal circumference = 0.29, P < .001; and for lnIL-6: ßabdominal circumference = 0.09, P = .018). Moreover, in multivariable-adjusted linear regression models, higher BMI showed significant linear associations with inflammatory markers (standardized regression coefficients (ß) of BMI for lnCRP: ßBMI = 0.24, P < .001; and for white blood cells: ßBMI = 0.07, P = .041). CONCLUSIONS: Abdominal circumference and BMI are independently associated with inflammatory markers in prevalent kidney transplant recipients.

Photon-counting detector CT reduces the rate of referrals to invasive coronary angiography as compared to CT with whole heart coverage energy-integrating detector.

BACKGROUND: We sought to compare the degree of maximal stenosis and the rate of invasive coronary angiography (ICA) recommendations in patients who underwent coronary CT angiography (CCTA) with photon-counting detector CT (PCD-CT) versus those who underwent CCTA with whole heart coverage energy-integrating detector CT (EID-CT). METHODS: In our retrospective single-center study, we included consecutive patients with suspected CAD who underwent CCTA performed with either PCD-CT or a 280-slice EID-CT. The degree of coronary stenosis was classified as no CAD, minimal (1-24 â€‹%), mild (25-49 â€‹%), moderate (50-69 â€‹%), severe stenosis (70-99 â€‹%), or occlusion. RESULTS: A total of 812 consecutive patients were included in the analysis, 401 patients scanned with EID-CT and 411 patients with PCD-CT (mean age: 58.4 â€‹± â€‹12.4 years, 45.4 â€‹% female). Despite the higher total coronary artery calcium score (CACS) in the PCD-CT group (10 [interquartile range (IQR) â€‹= â€‹0-152.8] vs 1 [IQR â€‹= â€‹0-94], p â€‹< â€‹0.001), obstructive CAD was more frequently reported in the EID-CT vs PCD-CT group (no CAD: 28.7 â€‹% vs 26.0 â€‹%, minimal: 23.2 â€‹% vs 30.9 â€‹%, mild: 19.7 â€‹% vs 23.4 â€‹%, moderate: 14.5 â€‹% vs 9.7 â€‹%, severe: 11.5 â€‹% vs 8.5 â€‹% and occlusion: 2.5 â€‹% vs 1.5 â€‹%, respectively, p â€‹= â€‹0.025). EID-CT was independently associated with downstream ICA (OR â€‹= â€‹2.76 [95%CI â€‹= â€‹1.58-4.97] p â€‹< â€‹0.001) in the overall patient population, in patients with CACS<400 (OR â€‹= â€‹2.18 [95%CI â€‹= â€‹1.13-4.39] p â€‹= â€‹0.024) and in patients with CACS≥400 (OR â€‹= â€‹3.83 [95%CI â€‹= â€‹1.42-11.05] p â€‹= â€‹0.010). CONCLUSION: In patients who underwent CCTA with PCD-CT the number of subsequent ICAs was lower as compared to patients who were scanned with EID-CT. This difference was greater in patients with extensive coronary calcification.

Simultaneous Urea and Phosphate Recovery from Synthetic Urine by Electrochemical Stabilization.

Urine is a widely available renewable source of nitrogen and phosphorous. The nitrogen in urine is present in the form of urea, which is rapidly hydrolyzed to ammonia and carbonic acid by the urease enzymes occurring in nature. In order to efficiently recover urea, the inhibition of urease must be done, usually by increasing the pH value above 11. This method, however, usually is based on external chemical dosing, limiting the sustainability of the process. In this work, the simultaneous recovery of urea and phosphorous from synthetic urine was aimed at by means of electrochemical pH modulation. Electrochemical cells were constructed and used for urea stabilization from synthetic urine by the in situ formation of OH- ions at the cathode. In addition, phosphorous precipitation with divalent cations (Ca2+, Mg2+) in the course of pH elevation was studied. Electrochemical cells equipped with commercial (Fumasep FKE) and developmental (PSEBS SU) cation exchange membranes (CEM) were used in this study to carry out urea stabilization and simultaneous P-recovery at an applied current density of 60 A m-2. The urea was successfully stabilized for a long time (more than 1 month at room temperature and nearly two months at 4 °C) at a pH of 11.5. In addition, >82% P-recovery could be achieved in the form of precipitate, which was identified as amorphous calcium magnesium phosphate (CMP) by using transmission electron microscopy (TEM).

Inflammatory Markers and Outcomes in Kidney Transplant Recipients.

BACKGROUND: Increased levels of TNF-α and IL6 are associated with inflammation and cardiovascular disease among patients with normal kidney function. However, little is known about their association with outcomes in kidney transplant recipients. METHODS: We collected sociodemographic, clinical and laboratory parameters, medical and transplant history from 977 prevalent kidney transplant recipients enrolled in the Malnutrition-Inflammation in Transplant-Hungary study. Serum cytokine levels were measured at baseline. Associations between serum TNF-α and IL6 values and death with a functioning graft over a 6-year follow-up period were examined in unadjusted and adjusted models. RESULTS: The mean ± SD age of the study population was 51 ± 13 years, 57% were men, 21% were diabetics. Median serum TNF-α and IL6 concentrations were significantly higher in patients who died with a functioning graft as compared with those who did not die during the follow-up period (TNF-α: median, 1.92 pg/mL; interquartile range [IQR], 1.43-2.67 pg/mL vs median, 2.25 pg/mL; IQR, 1.63-3.08 pg/mL, P < 0.001; and for IL6: median, 1.91 pg/mL; IQR, 1.21-3.02 pg/mL vs median, 2.81 pg/mL; IQR, 1.65-4.97 pg/mL, P < 0.001). Higher serum TNF-α and IL6 levels were associated with higher mortality risk in both unadjusted and fully adjusted models: TNF-α: hazard ratios (HRs)(1 pg/ml increments), 1.24; 95% confidence interval (CI), 1.13-1.36 and HRs(1 pg/ml increments), 1.19; 95% CI, 1.08-1.32; IL6: HRs(1 pg/ml increments), 1.06; 95% CI, 1.03-1.09 and HRs(1 pg/ml increments), 1.03; 95% CI, 0.99-1.06, respectively. Compared with patients whose serum TNF-α or IL6 levels were in the lowest tertile, those in the middle tertile had similar mortality risk (TNF-α: HR, 1.09; 95% CI, 0.74-1.61; IL6: HR, 1.05; 95% CI, 0.68-1.62), but patients in the highest tertile reported higher risk of mortality: TNF-α: HR, 1.45; 95% CI, 1.01-2.09; IL6: HR, 1.55; 95% CI, 1.04-2.32 in multivariable adjusted models. CONCLUSIONS: In prevalent kidney transplant recipients, serum TNF-α and IL6 were independently associated with death with a functioning graft.

Adipocytokines in renal transplant recipients.

In the last two decades, perceptions about the role of body fat have changed. Adipocytes modulate endocrine and immune homeostasis by synthesizing hundreds of hormones, known as adipocytokines. Many studies have been investigating the influences and effects of these adipocytokines and suggest that they are modulated by the nutritional and immunologic milieu. Kidney transplant recipients (KTRs) are a unique and relevant population in which the function of adipocytokines can be examined, given their altered nutritional and immune status and subsequent dysregulation of adipocytokine metabolism. In this review, we summarize the recent findings about four specific adipocytokines and their respective roles in KTRs. We decided to evaluate the most widely described adipocytokines, including leptin, adiponectin, visfatin and resistin. Increasing evidence suggests that these adipocytokines may lead to cardiovascular events and metabolic changes in the general population and may also increase mortality and graft loss rate in KTRs. In addition, we present findings on the interrelationship between serum adipocytokine levels and nutritional and immunologic status, and mechanisms by which adipocytokines modulate morbidity and outcomes in KTRs.