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Chronic hyponatremia may contribute to decreased bone density. We studied 341,003 men and women who underwent DXA testing and observed that individuals with chronic hyponatremia (sodium

Background In the general population, low serum magnesium levels are associated with poor outcomes and death. While limited data suggest that low baseline magnesium levels may be associated with higher mortality in hemodialysis (HD) patients, the impact of changes in magnesium levels over time is unknown. Study Design We examined the association of time-varying serum magnesium levels with all-cause mortality using multivariable time-varying survival models adjusted for clinical characteristics and other time-varying laboratory measures. Setting & Participants 9,359 maintenance HD patients treated in a large dialysis organization between 2007 and 2011. Predictor Time-varying serum magnesium levels across 5 magnesium increments (

Background In the general population, circulating adiponectin is associated with a favorable cardiovascular risk profile (eg, lower triglycerides and body fat) and decreased mortality. Hemodialysis (HD) patients have comparatively higher adiponectin concentrations, but prior studies examining the adiponectin-mortality association in this population have not accounted for body composition or shown a consistent relationship. Study Design Prospective cohort study. Settings & Participants We examined baseline serum adiponectin concentrations in 501 HD patients across 13 dialysis centers from the prospective MADRAD (Malnutrition, Diet, and Racial Disparities in Chronic Kidney Disease) cohort (entry period, October 2011 to February 2013; follow-up through August 2013). Predictor Serum adiponectin concentration in tertiles (tertiles 1, 2, and 3 defined as ≤16.1, 30.1, and ≥30.1-100.0 μg/mL, respectively). Adjustment variables included case-mix and laboratory test results (age, sex, race, ethnicity, vintage, diabetes, serum albumin, total iron-binding capacity, serum creatinine, white blood cell count, phosphate, hemoglobin, and normalized protein catabolic rate), body composition surrogates (subcutaneous, visceral, and total-body fat and lean body mass), and serum lipid levels (cholesterol, high-density lipoprotein cholesterol, and triglycerides). Outcomes All-cause mortality using survival (Cox) models incrementally adjusted for case-mix and laboratory test results. Results Among 501 HD patients, 50 deaths were observed during 631.1 person-years of follow-up. In case-mix- and laboratory-adjusted Cox analyses, the highest adiponectin tertile was associated with increased mortality versus the lowest tertile (HR, 3.35; 95% CI, 1.50-7.47). These associations were robust in analyses that additionally accounted for body composition (HR, 3.18; 95% CI, 1.61-8.24) and lipid levels (HR, 3.64; 95% CI, 1.34-7.58). Limitations Residual confounding cannot be excluded. Conclusions Higher adiponectin level is associated with a 3-fold higher death risk in HD patients independent of body composition and lipid levels. Future studies are needed to elucidate underlying mechanisms and determine therapeutic targets associated with improved outcomes in HD patients.

Background: Protein–energy wasting (PEW) is a common condition in patients with chronic kidney disease (CKD) including dialysis and kidney transplant recipients (TX) and frequently assessed with malnutrition–inflammation score (MIS). We hypothesized that (1) the MIS and PEW parameters are correlated with kidney function and (2) the MIS and PEW parameters are more severe in TX than in non-dialysis (ND) CKD patients with similar eGFR. Methods: In this study, we matched 203 ND-CKD and 203 TX patients from two independently assembled cohorts of patients based on estimated glomerular filtration rate (eGFR) and compared various PEW parameters between the two groups using unadjusted and case-mix adjusted linear regression and conditional logistic regression analysis models. Results: In the combined cohort (n = 406) of patients, the mean ± SD age was 57 ± 12 years; included 55 % men and 35 % diabetics; and demonstrated a mean ± SD baseline eGFR of 29 ± 11 ml/min/1.73 m2. The eGFR correlated positively with serum albumin (ρ = 0.26, p

A significant number of dietary restrictions are imposed traditionally and uniformly on maintenance dialysis patients, whereas there is very little data to support their benefits. Recent studies indicate that dietary restrictions of phosphorus may lead to worse survival and poorer nutritional status. Restricting dietary potassium may deprive dialysis patients of heart-healthy diets and lead to intake of more atherogenic diets. There is little data about the survival benefits of dietary sodium restriction, and limiting fluid intake may inherently lead to lower protein and calorie consumption, when in fact dialysis patients often need higher protein intake to prevent and correct protein-energy wasting. Restricting dietary carbohydrates in diabetic dialysis patients may not be beneficial in those with burnt-out diabetes. Dietary fat including omega-3 fatty acids may be important caloric sources and should not be restricted. Data to justify other dietary restrictions related to calcium, vitamins, and trace elements are scarce and often contradictory. The restriction of eating during hemodialysis treatment is likely another incorrect practice that may worsen hemodialysis induced hypoglycemia and nutritional derangements. We suggest careful relaxation of most dietary restrictions and adoption of a more balanced and individualized approach, thereby easing some of these overzealous restrictions that have not been proven to offer major advantages to patients and their outcomes and which may in fact worsen patients' quality of life and satisfaction. This manuscript critically reviews the current paradigms and practices of recommended dietary regimens in dialysis patients including those related to dietary protein, carbohydrate, fat, phosphorus, potassium, sodium, and calcium, and discusses the feasibility and implications of adherence to ardent dietary restrictions and future research.

© Springer-Verlag Berlin Heidelberg 2014. Muscle wasting is a common complication afflicting maintenance hemodialysis (HD) patients, and it is associated with decreased muscle function, exercise performance, physical function, and quality of life. Meanwhile, numerous epidemiologic studies have consistently shown that greater muscle mass (ascertained by body anthropometry surrogates, body composition tests such as dual x-ray absorptiometry, and/or serum creatinine in patients with little to no residual kidney function) is associated with increased survival in this population. The pathophysiology of muscle wasting in HD patients is complex and may be caused by poor dietary intake, catabolic effects of dialysis therapy, hormonal alterations (e.g., decreased levels or resistance to anabolic hormones, increased levels of catabolic hormones), inflammation, metabolic acidosis, and concurrent comorbidities. Muscle disuse resulting from low physical activity is an important yet under-appreciated risk factor for muscle wasting. Intra-dialytic resistance exercise training has been suggested as a potential strategy to correct and/or prevent this complication in HD patients, but prior studies examining this exercise modality as an anabolic intervention have shown mixed results. In a recently published 12-week randomized controlled trial of a novel intra-dialytic progressive resistance exercise training (PRET) program vs. control therapy conducted in HD and non-HD patients, PRET resulted in increased muscle volume and strength in both groups. At this time, further study is needed to determine if anabolic improvements imparted by resistance exercise translates into improved physical function and quality of life, decreased hospitalization and mortality risk, and greater cost-effectiveness in HD patients.

Protein-energy wasting (PEW), a condition of decreased body protein and fat mass, is highly prevalent in patients with chronic kidney disease (CKD) and a potent predictor of mortality in this population. In adults with CKD, PEW has typically been defined on the basis of (1) deranged biochemical parameters, (2) reduced body mass, (3) reduced muscle mass, and (4) decreased dietary protein intake. Emerging data suggest that PEW may also commonly afflict children with CKD and have a negative impact on growth and development (“uremic failure to thrive”), yet it remains comparatively understudied and less well characterized in these patients. Given the challenges of applying adult-defined PEW criteria to the pediatric population, the authors of a recent study entitled “Protein energy wasting in children with chronic kidney disease” [Abraham et al. (2014) Pediatr Nephrol 29:1231–1238] have sought to develop a scoring system and three alterative definitions for this condition using a combination of biochemical markers, clinical measurements, and subjective reporting in children in the CKiD cohort: (1) minimal PEW definition (≥2 adult-defined PEW criteria); (2) standard PEW definition (≥3 adult-defined PEW criteria); (3) modified PEW definition (≥3 adult-defined PEW criteria, plus short stature or poor growth). These authors observed that meeting the modified PEW definition was associated with a significantly increased risk of hospitalization in unadjusted analyses, i.e., a 2.2-fold higher risk, and trended towards increased risk in multivariable adjusted analyses, i.e., 2.0-fold higher risk. At the present time, future studies validating these findings and developing further refined definitions and/or scoring systems for the detection and management of PEW in children and uremic failure to thrive are urgently needed.

The incidence of early stage renal cell carcinoma (RCC) is increasing and observational studies have shown equivalent oncological outcomes of partial versus radical nephrectomy for stage I tumours. Population studies suggest that compared with radical nephrectomy, partial nephrectomy is associated with decreased mortality and a lower rate of postoperative decline in kidney function. However, rates of chronic kidney disease (CKD) in patients who have undergone nephrectomy might be higher than in the general population. The risks of new-onset or accelerated CKD and worsened survival after nephrectomy might be linked, as kidney insufficiency is a risk factor for cardiovascular disease and mortality. Nephron-sparing approaches have, therefore, been proposed as the standard of care for patients with type 1a tumours and as a viable option for those with type 1b tumours. However, prospective data on the incidence of de novo and accelerated CKD after cancer nephrectomy is lacking, and the only randomized trial to date was closed prematurely. Intrinsic abnormalities in non-neoplastic kidney parenchyma and comorbid conditions (including diabetes mellitus and hypertension) might increase the risks of CKD and RCC. More research is needed to better understand the risk of CKD post-nephrectomy, to develop and validate predictive scores for risk-stratification, and to optimize patient management.

Objective: To compare dialysis transition patterns of chronic kidney disease (CKD) patients with heart failure (HF) and without HF, including inpatient "crash start" initiation of long-term ("maintenance") dialysis, early dialysis initiation as evaluated by estimated glomerular filtration rate (eGFR), and rate of central venous catheter (CVC) use for hemodialysis., Methods: A cross-sectional study was performed within Kaiser Permanente Southern California of patients (age ≥18 years) with observed incidence of CKD who initiated maintenance dialysis between January 1, 2007, and December 31, 2018. Heart failure was further categorized into HF with preserved ejection fraction (>40%) or HF with reduced ejection fraction (≤40%). Associations between HF and risk of inpatient initiation of maintenance dialysis or hemodialysis vascular access were assessed by rate ratio (RR) using Poisson regression with robust variance error., Results: Of 6812 patients with CKD initiating dialysis, 2498 (37%) had HF. Inpatient dialysis initiation occurred in 463 (18.5%) patients with HF vs 416 (9.6%) without HF. Mean (SD) eGFR at dialysis was 11.3 (6.2) mL/min per 1.73 m 2 with HF vs 9.4 (5.2) mL/min per 1.73 m 2 without HF (P<.001). Of 5499 patients who initiated hemodialysis, CVC use occurred in 1302 (58.5%) HF patients vs 1698 (51.9%) non-HF patients. Compared with non-HF patients, patients with HF had multivariate RRs (95% CI) of 1.46 (1.26 to 1.69) and 1.04 (0.99 to 1.10) for inpatient dialysis initiation and CVC use, respectively. Patients with HF with reduced ejection fraction had CVC placement RR of 1.23 (1.14 to 1.33)., Conclusion: Patients with CKD and HF had higher rates of suboptimal dialysis initiation: more frequent inpatient dialysis starts, more frequent CVC placement for hemodialysis access, and higher eGFR at dialysis initiation. Our findings suggest that CKD patients with HF may warrant different management strategies as they progress to dialysis., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Introduction: Niacin is a non-statin lipid-lowering therapy that has been shown to lower triglycerides and improve other risk factors for renal outcomes. Despite these favorable data, the effect of niacin on long-term kidney outcomes remains unclear. The aim of this study was to examine the associations of niacin therapies with incident chronic kidney disease (CKD), end-stage renal disease (ESRD), and death in patients with estimated glomerular filtration rate (eGFR) of at least 60 mL/min/1.73 m2., Methods: In a nationwide historic cohort of 1,139,630 United States (US) veterans with normal baseline eGFR, we examined the association of de novo prescription of niacin with incident CKD (defined as eGFR <60 mL/min/1.73 m2 on two occasions, separated by ≥90 days), ESRD (defined as the initiation of kidney replacement therapy), and death. Associations were examined in Cox proportional hazards models adjusted for demographics, major comorbidities, laboratory measurements, and medications. Prescription time-distribution matching was used to control for survival bias., Results: We identified 133,450 new users of niacin. Overall, patients (n = 1,139,630) had a mean (standard deviation) age of 60 (13) years, with 6% female, 78% white, 16% black, and 6% Hispanic. Niacin users were more likely to be male, white, current, or former smokers, with higher frequencies of comorbidities and statin use. Niacin use (vs. nonuse) was associated with a higher risk of CKD (HR: 1.08, 95% confidence interval:1.07-1.10) but a lower risk of ESRD (0.82, 0.76-0.88) and death (0.90, 0.89-0.91)., Conclusions: In a large national cohort of US veterans with normal kidney function, niacin use was associated with a lower risk of ESRD and death but with a higher risk of incident CKD, which is potentially explained by acute effects on eGFR. Further studies are needed to corroborate the potential benefits of niacin on kidney function and survival., (© 2025 S. Karger AG, Basel.)

Purpose of Review: Protein-energy wasting (PEW) is increasingly more prevalent as chronic kidney disease (CKD) progresses to more advanced stages. There is a global recognition of the importance of preventing and mitigating PEW in the CKD population not on dialysis given the goal of extending dialysis-free time and delaying dialysis initiation and growing evidence of the clinical consequences of PEW which include the risk of death, hospitalization and clinical conditions such as infections. We reviewed the association of PEW and the malnutrition characteristics indicative of PEW on CKD progression., Recent Findings: Studies show the association between low serum albumin levels, low BMI, and diets with inadequate dietary energy and protein intake and CKD progression. Limited studies suggest low muscle mass impacts CKD progression. Optimizing nutrition by dietary management, including a moderately low protein (0.6-0.8 g/kg/day) and plant-based (>50% of protein source, known as PLADO) diet and as needed with supplementation [e.g. during acute kidney injury (AKI) event] administrated orally, enterally, or parenterally are the basis for the prevention and treatment of PEW in CKD and delaying CKD progression. Furthermore, other therapeutic methods such as treating or avoiding comorbidities and AKI, ensuring appropriate exercise and incremental transition to dialysis treatment may help ameliorate and prevent PEW development in CKD patients., Summary: Using tailored precision nutrition approaches and nutritional supplementation with or without other beneficial strategies may help prevent and treat PEW and its consequent occurrence of CKD progression., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Purpose of Review: Initiation of hemodialysis treatment with a thrice-weekly prescription is currently the standard of care irrespective of patients' residual kidney function (RKF), comorbidities, and preferences., Recent Findings: Each year ∼12 000 Veterans with advanced kidney disease progress to end-stage kidney disease (ESKD) requiring dialysis and comprise greater than 10% of the US incident ESKD population. Dialysis is costly and is associated with impaired health-related quality of life (HRQOL) and high mortality risk, especially in the first year of treatment. Evidence suggests an incremental dialysis transition using twice-weekly hemodialysis provides various benefits, including more dialysis-free time, longer RKF preservation, less vascular access damage, and lower patient burden. Pragmatic studies are needed to inform the efficacy and safety of incremental hemodialysis as a personalized dialysis regimen, and could inform its consideration as a conservation strategy during times of supply shortages. Broadly implementing twice-weekly hemodialysis could also potentially allow more Veterans to receive care within VA-based dialysis units. The VA IncHVets Trial is a pragmatic, multicenter, randomized controlled trial comparing the efficacy and safety of twice-weekly incremental vs. thrice-weekly hemodialysis among Veterans transitioning to ESKD., Summary: Further research is needed to determine whether incremental hemodialysis is well tolerated, effective, and facilitates a more favorable transition to dialysis., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

This report represents the conclusions of 15 experts in nephrology and endocrinology, based on their knowledge of key studies and evidence in the field, on the role of continuous glucose monitors (CGMs) in patients with diabetes and chronic kidney disease (CKD), including those receiving dialysis. The experts discussed issues related to CGM accuracy, indications, education, clinical outcomes, quality of life, research gaps, and barriers to dissemination. Three main goals of management for patients with CKD and diabetes were identified: (1) greater use of CGMs for better glycemic monitoring and management, (2) further research evaluating the accuracy, feasibility, outcomes, and potential value of CGMs in patients with end-stage kidney disease (ESKD) on hemodialysis, and (3) equitable access to CGM technology for patients with CKD. The experts also developed 15 conclusions regarding the use of CGMs in this population related to CGMs' unique delivery of both real-time information that can guide monitoring and management of glycemia and continuous and predictive data in this population, which is at higher risk for hypoglycemia and hyperglycemia. The group noted three major clinical gaps: (1) CGMs are not routinely prescribed for patients with diabetes and CKD; (2) CGMs are not approved by the United States Food and Drug Administration (FDA) for patients with diabetes who are on dialysis; and (3) CGMs are not routinely available to all of those who need them because of structural barriers in the health care system. These gaps can be improved with greater stakeholder collaboration, education, and awareness brought to the use of CGM technology in CKD., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: C.M.R. has received honoraria and/or grant support from AstraZeneca, Dexcom, Fresenius, and Vifor. R.Y.G. has nothing to disclose. D.K. has received research support from Abbott Diabetes Care and has been a Consultant to Sanofi, Better Therapeutics, Perfood, and Abbott Diagnostics. A.P.-T. provides consulting and research services to Novo Nordisk, Lilly, Bayer, Dexcom, and Medtronic on behalf of her employer but receives no direct or indirect reimbursement for the services. C.P.K. received consulting feels from Astra Zeneca, Bayer, Boehringer, Ingelheim, Cara Therapeutics, Pharmacosmos, ProKidney, Renibus, and Takeda. R.C.S. has nothing to disclose. A.T.D. has nothing to disclose. R.J.G. has received research support from Novo Nordisk, Dexcom, Boehringer, and Eli Lilly and consulting/advisory/honoraria fees from Abbott, Aztra Zeneca, Bayer, Boehringer, Dexcom, Eli Lilly, Novo Nordisk and Medtronic. R.J.G. is partially supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health (NIH) under Award Numbers P30DK111024 (R.J.G.), K23DK123384 (R.J.G.). and R03DK138255-01. K.K.-Z. has received funding from the NIH to examine CGM in patients with CKD. J.J.N. is partially supported by NIH research grant OT2OD032581 and reports personal fees and other support from Bayer AG, Sanofi, Novo Nordisk, Boehringer Ingelheim, Eli Lilly, Proteomics International, and Dexcom outside the submitted work. I.H.d.B. consults for Alnylam, Boehringer Ingelheim, Lilly, Miter, and Novo Nordisk. I.H.D.B. has also received equipment and supplies for research donated to his institution from Dexcom and Novo Nordisk Research, and funding to his institution from NIDDK and Breakthrough T1D. M.L. has been a consultant or received honoraria from Astra Zeneca, Boehringer Ingelheim, Eli Lilly, Nordic InfuCare, and Novo Nordisk, and has received research grants from Eli Lilly and Novo Nordisk, all outside of the submitted work. S.H.K. reports a relationship with Morphic Medical that includes consulting or advisory. S.H.K. is partially supported by P30DK116074. A.T.A. is a consultant for Liom. C.N.H. is a consultant for Liom. R.E.A. has nothing to disclose. T.T. has nothing to disclose. D.C.K. is a consultant for Afon, embecta, Glucotrack, Lifecare, Novo, Samsung, SynchNeuro, and Thirdwayv.

Iodine is a micronutrient that is required for thyroid hormone synthesis. The iodide cycle in thyroid hormone synthesis consists of a series of transport, oxidation, organification, and binding/coupling steps in thyroid follicular cells. Common sources of iodine include the consumption of an iodine-rich diet or iodine-fortified foods, the administration of amiodarone, iodine-containing supplements, or iodinated contrast media, and other miscellaneous sources. Methods to assess population iodine status include the measurement of urinary iodine concentrations, blood thyroglobulin levels, prevalence of elevated neonatal thyrotropin levels, and thyroid volume. Although excessive iodine intake or exposure is generally well tolerated, an acute iodine load may result in thyroid dysfunction (hypothyroidism or hyperthyroidism) in certain susceptible individuals due to the failure to escape from the Wolff-Chaikoff effect and to the Jod-Basedow phenomenon, respectively. In this review, we discuss the associations between excessive iodine intake or exposure, with particular focus on iodinated contrast media as a common source of excess iodine in health care settings, and risks of incident thyroid dysfunction. We also summarize the risks of iodine excess in vulnerable populations and review current guidelines regarding the screening and monitoring of iodinated contrast-induced thyroid dysfunction. Finally, we discuss the long-term potential nonthyroidal health risks associated with iodine excess and suggest the need for more data to define safe upper limits for iodine intake, particularly in high-risk populations., (Published by Oxford University Press on behalf of the Endocrine Society 2024.)

Introduction: An error grid compares measured versus reference glucose concentrations to assign clinical risk values to observed errors. Widely used error grids for blood glucose monitors (BGMs) have limited value because they do not also reflect clinical accuracy of continuous glucose monitors (CGMs)., Methods: Diabetes Technology Society (DTS) convened 89 international experts in glucose monitoring to (1) smooth the borders of the Surveillance Error Grid (SEG) zones and create a user-friendly tool-the DTS Error Grid; (2) define five risk zones of clinical point accuracy (A-E) to be identical for BGMs and CGMs; (3) determine a relationship between DTS Error Grid percent in Zone A and mean absolute relative difference (MARD) from analyzing 22 BGM and nine CGM accuracy studies; and (4) create trend risk categories (1-5) for CGM trend accuracy., Results: The DTS Error Grid for point accuracy contains five risk zones (A-E) with straight-line borders that can be applied to both BGM and CGM accuracy data. In a data set combining point accuracy data from 18 BGMs, 2.6% of total data pairs equally moved from Zones A to B and vice versa (SEG compared with DTS Error Grid). For every 1% increase in percent data in Zone A, the MARD decreased by approximately 0.33%. We also created a DTS Trend Accuracy Matrix with five trend risk categories (1-5) for CGM-reported trend indicators compared with reference trends calculated from reference glucose., Conclusion: The DTS Error Grid combines contemporary clinician input regarding clinical point accuracy for BGMs and CGMs. The DTS Trend Accuracy Matrix assesses accuracy of CGM trend indicators., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: D.C.K. is a consultant for Afon, Lifecare, Novo, Samsung, embecta, Glucotrack, SynchNeuro, and Thirdwayv. G.F. is CEO of IfDT. G.F./IfDT has/have received research support, speakers’ honoraria or consulting fees in the last three years from Abbott, Ascensia, Berlin Chemie, Boydsense, Dexcom, Glucoset, i-SENS, Lilly, Menarini, Novo Nordisk, Perfood, Pharmasens, Roche, Sinocare, Terumo, Ypsomed. S.P. is an employee of IfDT. B.P.K. declares patent royalties handled by UVA from: DexCom, J&J, Novo Nordisk, and Sanofi; and research support handled by UVA: Dexcom, Novo Nordisk, Tandem Diabetes Care. D.K. has received research support from Abbott Diabetes Care. M.S.D.A. is currently receiving in kind support (CGM devices) from Dexcom Inc for an investigator-initiated clinical study. K.D. receives research funding from Dexcom, Abbott, Sanofi, Viacyte, Insulet, consulting fees from Eli Lilly, Dexcom, Insulet, Oppenheimer, Elsevier, honoraria from Academy for Continued Healthcare Learning, Med Learning Group, Medscape, Impact Education, and royalties from UptoDate. S.M. is in receipt of an investigator-initiated grant from DexCom, has received speaker fees from Sanofi & Lilly, is funded by a Wellcome Trust (223024/Z/21/Z), and is supported by the NIHR Imperial Biomedical Research Centre. A.S. was supported by the NSF Engineering Research Center for Precise Advanced Technologies and Health Systems for Underserved Populations (PATHS-UP) (#1648451). V.N.S. reports receiving personal fees from Sanofi, Embecta, NovoNordisk, Dexcom, Insulet, Tandem Diabetes Care, Ascensia Diabetes Care, Genomelink and LumosFit for consulting, advising or speaking. N.K.T. is a consultant for Roche Diagnostics / Roche Molecular Systems / Radiometer. UC Davis is a Roche Diagnostics Center of Excellence. N.K.T. has received speaking honoraria for Roche Diagnostics, Nova Biomedical, Thermo Fisher, and Radiometer. N.K.T. is also Chair-Elect for the Association for Diagnostic and Laboratory Medicine (ADLM) Critical and Point-of-Care Testing Division, Co-Founder of the Machine Intelligene Learning Optimizer (MILO), Inc, and a member of the International Federation for Clinical Chemistry (IFCC) continuous glucose monitoring workgroup. T.T. is a consultant for Clinical ink. R.E.A. is a consultant for Clinical ink. D.T.A. has received speaker’s honoraria from Abbott, Ascensia Diabetes Care, Insulet, Lilly Diabetes, Mannkind, Novo Nordisk, and Xeris Pharmaceuticals. D.T.A. has received consulting fees from Ascensia Diabetes Care, Lilly Diabetes, and Senseonics. H.K.A. received research grants through University of Colorado from Dexcom, Tandem Diabetes, Medtronic, Mannkind, IM Therapeutics, IAFMS, and received honorarium through University of Colorado for consulting from Dexcom, Tandem Diabetes, and Medtronic. M.E.A.-S. has served on the advisory boards for Abbott, Medtronic, Insulet, VitalAire, Sanofi, Eli Lilly, and Dexcom; has received honoraria for speaking from Abbott, Eli Lilly, Medtronic, Novo Nordisk, Sanofi, VitalAire, and Eli Lilly; and received research support from Medtronic and Sanofi. T.S.B. has received research support from Abbott Rapid Diagnostics, Biolinq, Dexcom, Eli Lilly, Medtronic, Medtrum, Novo Nordisk, Sanofi, Senseonics, and vTv Therapeutics and consulting honoraria from Abbott Diabetes, Abbott Rapid Diagnostics, ACON, CeQur, HagarTech, Intuity Medical, Lifescan, Mannkind, Medtronic, Novo, Perspirion, Sanofi, Sequel Med Tech, and Ypsomed. M.B. currently participates on the Hospital Advisory board with Dexcom and has received research support from Dexcom. L.B. has received research/product support from Dexcom, Ypsomed, and Boehringer Ingelheim; speaker honoraria from Dexcom and Oviva; and participated in advisory boards of Dexcom, Novo Nordisk, Sanofi, Ypsomed, Oviva, and Roche Diabetes Care. Y.M.B. has received honoraria for lectures and scientific advisory from Roche and AstraZeneca in the past 12 months. J.E.B. is on the Speaker’s bureau for Insulet and on the Advisory Board for Cardinal Health and Lifescan. J.E.B. is a consultant for Embecta. J.E.B. receives research support from the Leona M. and Harry B. Helmsley Charitable Trust. E.C. is on the scientific advisory board for Novo Nordisk, Eli-Lilly, Adocia, Arecor, Proventionbio, Portal Insulin, and MannKind. D.C. was a Dexcom employee from August 2018 to May 2024. D.C. is a shareholder of Dexcom, Lilly, Abbott and Tandem. M.C. has received consulting fees from Glooko and research support from Dexcom and Abbott Diabetes Care. G.L.C. is a shareholder of BioTex, Inc., Basepair Biotechnologies Inc., Coordination Centric, Inc., and Shape Memory Medical, Inc. G.L.C. is supported by the NSF Engineering Research Center for Precise Advanced Technologies and Health Systems for Underserved Populations (PATHS-UP) (#1648451). K.K.D. has received honoraria, travel, or fees for advisory boards from AstraZeneca, Novo Nordisk, Boehringer Ingelheim, Eli Lilly, Abbott Diabetes, Menarini, and Sanofi in the last 12 months. J.E. receives federal funding from FDA, NIMHD, and NCATS and is a consultant for Sanofi. C.F. receives royalties from Dexcom and Novo Nordisk managed through her institution. G.A.F. is an advisor for 180 Life Sciences, 89bio, Adocia, Abbott, AdipoPharma, Aerami, Amolyt, Carthera, Catalyst, Cohen Global, CMC Magnetics, Diasome, Eleos, Entera Bio, Enterin, Glyscend, Hagar, Hogan Lovells, IM Therapeutics, Innoneo, Intarcia, Levicure, Lilly Asia Ventures, Lumos, Mars Symbioscience, Melior, metaLead Therapeutics, Microbiotix, MMD, Modular Medical, New Amsterdam, Northwestern, NuSirt, NuVox, Oramed, Pano, Pasithea, PhylloPharma, Pleiogenix, Recordati, Regor, Remodeless, Renaissance, RenovoRx, Rivus, RxMP, Sera Biopharma, Seraxis, Serpin, SFC Fluidics, Skinject, SROne, Stalicla, Surf Bio, TIXiMED, Veroscience, Verthermia, WaveBreak, Zealand Pharma, and Zucara. M.A.L.G. is a consultant for Abbott, Medtronic, Novonordisk, and Roche. R.J.G. received research support from Novo Nordisk, Dexcom and Eli Lilly and consulting fees/advisory fees from Abbott Diabetes Care, Aztra Zeneca, Bayer, Boehringer, Dexcom, Eli Lilly, Novo Nordisk, and Medtronic, outside of this work. R.J.G. is partially supported by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health under Award Numbers P30DK111024, K23DK123384, R03DK138255, and U2CD137135. A.M.G.-M. reports speaker fees from Novo Nordisk, Sanofi, Elli Lilly, Boehringer Ingelheim, Abbott, and Medtronic. L.H. is a consultant for a number of companies that are developing innovative solutions for the treatment of people with diabetes. N.H. reports Advisory Board member fees from Abbott Diabetes Care and Insulet as well as honoraria for lectures from Berlin-Chemie AG, Becton Dickenson, Sanofi Germany, Roche Diabetes Care, and Dexcom Germany. T.H. serves on the advisory board for Acella and Horizons Therapeutics (no financial compensation). S.H. has served on the advisory board for Tandem, Dexcom, and Medtronic, and received honoraria for nonpromotional educational and/or consultancy work from Abbott, Insulet, Dexcom, Roche, and Sanofi. P.G.J. is a shareholder of Pacific Diabetes Technologies Inc. and serves on the advisory board for Eli Lilly. P.G.J. received grant support from SFC Fluidics and research support from Eli Lilly and Dexcom. J.J. has received fees from lectures and or advisory boards from Abbott, Astra Zeneca, Boeringer Ingelheim, Eli Lilly, Medtronic, Nordic Infucare, Novo Nordisk, and Sanofi. S.R.J is a consultant for USV, Marico, Glenmark, Franco Indian, Twin Health, Biocon, and Zydus Lifesciences. S.R.J. received speaking honoraria from Abbott, Novo Nordisk, MSD, Sanofi, Boehringer Ingelheim, AstraZeneca, Lupin, Bayer Zydus, USV, DRL, Meyer Organics, Servier, Natco. R.A.L. is a consultant for Abbott Diabetes Care, Biolinq, Capillary Biomedical, Deep Valley Labs, Gluroo, PhysioLogic Devices, Portal Insulin, Sanofi, and Tidepool. R.A.L. has served on advisory boards for. ProventionBio and Lilly. R.A.L. receives research support through his institution from Insulet, Medtronic, Tandem, and Sinocare. L.A.L. has received research funding from, has provided CME on behalf of, and/or has acted as an advisor to Abbott, AstraZeneca, Boehringer Ingelheim, Eli Lilly, Lexicon, Merck, Novo Nordisk, Pfizer, and Sanofi. M.L. has been a consultant or received honoraria from Astra Zeneca, Boehringer Ingelheim, Eli Lilly, Nordic InfuCare, and Novo Nordisk, and has received research grants from Eli Lilly and Novo Nordisk, all outside of the submitted work. J.K.M. is a member of advisory boards of Abbott Diabetes Care, Becton-Dickinson, Biomea Fusion, Eli Lilly, Embecta, Medtronic, NovoNordisk A/S, Roche Diabetes Care, Sanofi-Aventis, and Viatris and received speaker honoraria from A. Menarini Diagnostics, Abbott Diabetes Care, AstraZeneca, Boehringer Ingelheim, Dexcom, Eli Lilly, Medtrust, MSD, NovoNordisk A/S, Roche Diabetes Care, Sanofi, Viatris, and Ypsomed. J.K.M. is a shareholder of decide Clinical Software GmbH and elyte Diagnostics. A.M. reports speaker fees from Novo Nordisk. M.M. has an existing research & development relationship with Scientific Bioprocessing, Inc and has been a consultant for Abbott. S.-J.M. is a consultant for Abbott, Curestream, Daewoong, EOFlow, G2e, Huons, iSense, Medtronic, Novo Nordisk, and Sanofi. D.N.O. has served on advisory boards for Abbott Laboratories, Medtronic, Merck Sharp & Dohme, Novo Nordisk, Roche, and Sanofi; received research support from Medtronic, Novo Nordisk, Roche, Eli Lilly and Company, and Sanofi; and received travel support from Novo Nordisk and Merck Sharp & Dohme. F.J.P. has received research support (to Emory University) from Dexcom, Insulet, Novo Nordisk, Tandem, and Ideal Medical Technologies, and has received consulting fees from Dexcom. A.L.P. is on the advisory board of Medscape, Vertex, and Lilly; receives research support from Insulin and Abbott; and has stock options in Omada Health. R.P.-B. receives grant support from Novo Nordisk, Lexicon Pharmaceuticals, and Medtronic and received consulting fees from Bayer, Lexicon Pharmaceuticals, Novo Nordisk, and Roche. C.M.R. has received honoraria and/or grant support from AstraZeneca, Dexcom, Fresenius, and Vifor. D.B.S. is supported by the Intramural Research Program of the National Institutes of Health. S.S. was a Novo Nordisk employee from 2022-2023. S.S. has served as advisor for Novo Nordisk and has received speaker fees from Novo Nordisk and Nordic Infucare within the past three years. G.D.S’s employer, nonprofit International Diabetes Center, HealthPartners Institute, has received educational grant funds from Abbott Diabetes Care, Medscape, and Sanofi-Aventis Groupe. G.D.S receives no personal income/honorarium from these activities. K.S. received grant supports from Arkray, Terumo, and Dexcom. E.K.S. is partly supported by the VA Merit Award (1I01CX001825) from the US Department of Veterans Affairs Clinical Sciences Research and has received unrestricted research support from Dexcom and Tandem Diabetes (to Baltimore VA Medical Center and to University of Maryland) for the conduction of clinical trials. N.L.S. received funding from Novo Nordisk for an investigator-initiated research grant unrelated to the current project. G.E.U. is partly supported by research grants from National Institutes of Health (NIH/NATS UL 3UL1TR002378-05S2) from the Clinical and Translational Science Award program, and from National Institutes of Health and National Center for Research Resources (NIH/NIDDK 2P30DK111024-06). G.E.U. has received research support (to Emory University) from Abbott, Bayer, and Dexcom; and has participated in advisory boards for Dexcom and GlyCare. E.W. has received consulting fees from Abbott Diabetes Care, Ascensia, Bayer, Boehringer, Ingelheim, Embecta, GlaxoSmithKline, Lilly, Medtronic, Renalytix, and Sanofi. E.W. has received honoraria from Abbott Diabetes Care, Bayer, Boehringer Ingelheim, GlaxoSmithKline, Lilly, Medtronic, Renalytix, and Sanofi. E.W. is on the Speakers’ Bureau from Abbott Diabetes Care, Bayer, Boehringer, Ingelheim, GlaxoSmithKline, Lilly, Renalytix, and Sanofi. M.Z. is a consultant for DexCom, Inc. M.A.K. is Chief Medical Officer of QuesGen, Inc. C.T., C.L., B.V.H., J.S.K., W.A.L., S.Y.R., J.J.S., K.W., C.W., K.R., C.N.H., A.T.A., A.A., R.R.B., E.M.B., J.G.C., K.Y.C., A.D., N.E., S.K.K., U.M., N.M., C.M., J.H.N., A.P., P.R., S.M.S., B.S., M.V., H.W.V., J.W., A.H.B.W., and S.Y. have nothing to disclose.

Objective: In the general population, continuous glucose monitoring (CGM) provides convenient and less-invasive glucose measurements than conventional self-monitored blood glucose and results in reduced hypoglycemia and hyperglycemia and increased time in target glucose range. However, accuracy of CGM versus blood glucose is not well established in hemodialysis patients., Research Design and Methods: Among 31 maintenance hemodialysis patients with diabetes hospitalized from October 2020 to May 2021, we conducted protocolized glucose measurements using Dexcom G6 CGM versus blood glucose, with the latter measured before each meal and at night, plus every 30-min during hemodialysis. We examined CGM-blood glucose correlations and agreement between CGM versus blood glucose using Bland-Altman plots, percentage of agreement, mean and median absolute relative differences (ARDs), and consensus error grids., Results: Pearson and Spearman correlations for averaged CGM versus blood glucose levels were 0.84 and 0.79, respectively; Bland-Altman showed the mean difference between CGM and blood glucose was ∼+15 mg/dL. Agreement rates using %20/20 criteria were 48.7%, 47.2%, and 50.2% during the overall, hemodialysis, and nonhemodialysis periods, respectively. Mean ARD (MARD) was ∼20% across all time periods; median ARD was 19.4% during the overall period and was slightly lower during nonhemodialysis (18.2%) versus hemodialysis periods (22.0%). Consensus error grids showed nearly all CGM values were in clinically acceptable zones A (no harm) and B (unlikely to cause significant harm)., Conclusions: In hemodialysis patients with diabetes, although MARD values were higher than traditional optimal analytic performance thresholds, error grids showed nearly all CGM values were in clinically acceptable zones. Further studies are needed to determine whether CGM improves outcomes in hemodialysis patients., (© 2024 by the American Diabetes Association.)

Diabetes is the leading cause and a common comorbidity of advanced chronic kidney disease. Glycaemic management in this population is challenging and characterised by frequent excursions of hypoglycaemia and hyperglycaemia. Current glucose monitoring tools, such as HbA 1c , fructosamine and glycated albumin, have biases in this population and provide information only on mean glucose exposure. Revolutionary developments in glucose sensing and insulin delivery technology have occurred in the last decade. Newer factory-calibrated continuous glucose monitors provide real-time glucose data, with predictive alarms, allowing improved assessment of glucose excursions and preventive measures, particularly during and between dialysis sessions. Furthermore, integration of continuous glucose monitors and their predictive alerts with automated insulin delivery systems enables insulin administration to be decreased or stopped proactively, leading to improved glycaemic management and diminishing glycaemic fluctuations. While awaiting regulatory approval, emerging studies, expert real-world experience and clinical guidelines support the use of diabetes technology devices in people with diabetes and advanced chronic kidney disease., (© 2024. The Author(s).)