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ObjectivesREVEAL-CKD aims to estimate the prevalence of, and factors associated with, undiagnosed stage 3 chronic kidney disease (CKD).DesignMultinational, observational study.SettingData from six country-specific electronic medical records and/or insurance claims databases from five countries (France, Germany, Italy, Japan and the USA [two databases]).ParticipantsEligible participants (≥18 years old) had ≥2 consecutive estimated glomerular filtration rate (eGFR) measurements (calculated from serum creatinine values, sex and age) taken from 2015 onwards that were indicative of stage 3 CKD (≥30 and <60 mL/min/1.73 m2). Undiagnosed cases lacked an International Classification of Diseases 9/10 diagnosis code for CKD (any stage) any time before, and up to 6 months after, the second qualifying eGFR measurement (study index).Main outcome measuresThe primary outcome was point prevalence of undiagnosed stage 3 CKD. Time to diagnosis was assessed using the Kaplan-Meier approach. Factors associated with lacking a CKD diagnosis and risk of diagnostic delay were assessed using logistic regression adjusted for baseline covariates.ResultsThe prevalence of undiagnosed stage 3 CKD was 95.5% (19 120/20 012 patients) in France, 84.3% (22 557/26 767) in Germany, 77.0% (50 547/65 676) in Italy, 92.1% (83 693/90 902) in Japan, 61.6% (13 845/22 470) in the US Explorys Linked Claims and Electronic Medical Records Data database and 64.3% (161 254/250 879) in the US TriNetX database. The prevalence of undiagnosed CKD increased with age. Factors associated with undiagnosed CKD were female sex (vs male, range of odds ratios across countries: 1.29–1.77), stage 3a CKD (vs 3b, 1.81–3.66), no medical history (vs a history) of diabetes (1.26–2.77) or hypertension (1.35–1.78).ConclusionsThere are substantial opportunities to improve stage 3 CKD diagnosis, particularly in female patients and older patients. The low diagnosis rates in patients with comorbidities that put them at risk of disease progression and complications require attention.Trial registrationNCT04847531.

Novel biomarkers may improve our ability to predict which patients with chronic kidney disease (CKD) are at higher risk for progressive loss of renal function. Here, we assessed the performance of urine neutrophil gelatinase–associated lipocalin (NGAL) for outcome prediction in a diverse cohort of 3386 patients with CKD in the Chronic Renal Insufficiency Cohort study. In this cohort, the baseline mean estimated glomerular filtration rate (eGFR) was 42.4ml/min per 1.73m2, the median 24-h urine protein was 0.2g/day, and the median urine NGAL concentration was 17.2ng/ml. Over an average follow-up of 3.2 years, there were 689 cases in which the eGFR was decreased by half or incident end-stage renal disease developed. Even after accounting for eGFR, proteinuria, and other known CKD progression risk factors, urine NGAL remained a significant independent risk factor (Cox model hazard ratio 1.70 highest to lowest quartile). The association between baseline urine NGAL levels and risk of CKD progression was strongest in the first 2 years of biomarker measurement. Within this time frame, adding urine NGAL to a model that included eGFR, proteinuria, and other CKD progression risk factors led to net reclassification improvement of 24.7%, but the C-statistic remained nearly identical. Thus, while urine NGAL was an independent risk factor of progression among patients with established CKD of diverse etiology, it did not substantially improve prediction of outcome events.

Correspondence to Professor Dinesh Khullar, Nephrology and Renal Transplant Medicine, Max Super Speciality Hospital Saket, New Delhi, India, India; drdineshkhullar@gmail.com An 85-year-old woman, a case of diabetes mellitus, hypothyroidism, dementia and stage 4 chronic kidney disease, was admitted with an Escherichia coli urinary tract infection with a rise in serum creatinine from 1.8 to 4.6 mg/dL. Renal excretion of memantine is significantly reduced in alkaline urine and in patients with severe renal impairment.1 The area under the curve (AUC) for memantine increases significantly in patients with glomerular filtration rate (GFR) <50 mL/min/1.73 m2 with a recommended maximum dose of 5 mg two times per day (half the routine dose).2 3 This may predispose patients with chronic kidney disease to develop adverse effects related to memantine accumulation. Prolonged unconsciousness associated with memantine exposure has been previously described in two patients, one of whom had a low GFR.4 Episodic loss of consciousness, myoclonus and seizures has also been described with memantine.5 Psychosis and seizures due to memantine may be explained by reduction of gamma aminobutyric acid (GABA) mediated inhibitory signals in the cerebral cortex.5 Ketamine, another NMDA antagonist, is used as an anaesthetic agent.

Written by an interdisciplinary team of experts, this book contains historical information as well as current update on renal replacement therapy. New technology and techniques are presented in a concise, easy-to-read style that keeps the reader interested. The contributors include physicians who practise uremia therapy since its conception to more recent graduates, along with surgeons, pioneers and physicians who are patients themselves, thus giving readers the broadest perspective.

Reviews all the latest basic and clinical research findings With contributions from leading international experts in the field, this book is dedicated to all facets of uremic toxins research, including low molecular weight solutes, protein-bound solutes, and middle molecules. Moreover, it covers everything from basic mass spectrometry research to the latest clinical findings and practices. Uremic Toxins is divided into three sections: * Section One, Uremic Toxins, explores the definition, classification, listing, and mass spectrometric analysis of uremic toxins * Section Two, Selected Uremic Toxins, describes key uremic toxins, explaining chemical structures, metabolism, analytical methods, plasma levels, toxicity, clinical implications, and removal methods. Among the uremic toxins covered are indoxyl sulfate, asymmetric dimethylarginine, PTH, ß2-microglobulin, and AGEs * Section Three, Therapeutic Removal of Uremic Toxins, describes how uremic toxins can be removed by hemodialysis, peritoneal dialysis, and oral sorbent All chapters are based on the authors' thorough review of the literature as well as their own personal laboratory and clinical experience. References at the end of each chapter provide a gateway to the literature in the field. Reviewing all the latest basic and clinical research findings, Uremic Toxins will help bench scientists in nephrology advance their own investigations. It will also help clinicians take advantage of the latest tested and proven treatments for the management of chronic kidney disease.

Objective： Coronary artery calcification （CAC） is thought to be a controlled metabolic process that is very similar to the formation of new bone. In patients with chronic renal failure （CRF）, CAC is very common, and CAC severity correlates with the deterioration of renal lilnction. We summarized the current understanding and emerging findings of the relationship between CAC and CRF. Data Sources： All studies were identified by systematically searching PubMed, Embase, and CNKI databases for the terms ＂coronary calcification＂, ＂＇chronic renal failure＂, ＇~vascular smooth muscle cell＂, and their synonyms until September 2017. Study Selection： We examined the titles and abstracts of all studies that met our search strategy thoroughly. The full text of relevant studies was evaluated. Reference lists of retrieved articles were also scrutinized for the additional relevant studies. Results： CRF can accelerate CAC progression. CRF increases the expression of pro-inflamrnatory factors, electrolyte imbalance （e.g., of calcium, phosphorus）, parathyroid hon~none, and uremic toxins and their ability to promote calcification. These factors, through the relevant signaling pathways, trigger vascular smooth muscle cells to transtbrm into osteoblast-like cells while inhibiting the reduction of vascular calcification factors, thus inducing further CAC. Conclusions： Coronary heart disease in patients with CRF is due to multiple factors. Understanding the mechanism of CAC can help interventionists to protect the myocardium and reduce the prevalence of coronary heart disease and mortality.

Among patients with type 2 diabetes and stage 4 chronic kidney disease, bardoxolone methyl, as compared with placebo, did not reduce the risk of end-stage renal disease or cardiovascular death. Cardiovascular events in the bardoxolone group prompted trial termination. Type 2 diabetes mellitus is the most important cause of progressive chronic kidney disease in the developed and developing worlds. Various therapeutic approaches to slow progression, including restriction of dietary protein, glycemic control, and control of hypertension, have yielded mixed results. 1 – 3 Several randomized clinical trials have shown that inhibitors of the renin–angiotensin–aldosterone system significantly reduce the risk of progression, 4 – 6 although the residual risk remains high. 7 None of the new agents tested during the past decade have proved effective in late-stage clinical trials. 8 – 12 Oxidative stress and impaired antioxidant capacity intensify with the progression of chronic kidney disease. 13 In . . .

In Dialysis Without Fear, psychiatrist and dialysis patient Dr. Daniel Offer joins with his wife, Marjorie Kaiz Offer, and daughter, Susan Offer Szafir, to reveal how life can be lived, and lived well, on dialysis. Drawing on his long medical career and more than seven years of personal experience with dialysis, Dr. Offer dispels many misconceptions surrounding this treatment, explaining how you can adapt to the new diet, travel, work and continue to partake in life's joys and celebrations. But the fears and hardships can be quite real, and Dr. Offer brings his years as a psychiatrist to bear as he provides practical advice on how patients can overcome them. Walking through each step of dialysis, he explains different types of treatment, examines the pros and cons of a transplant, and discusses side effects. Since dialysis affects the entire family, Dr. Offer and his co-authors also provide realistic insights into how relatives can cope and thrive together, sharing the humour, courage, and triumphs of real families who have successfully faced the challenges of dialysis. The result is an inspiring, practical guide that will help patients and their families learn to overcome the difficulties of dialysis, live without fear, and enjoy every day.

Background: The biological properties of oxidized and non-oxidized PTH are substantially different. Oxidized PTH (oxPTH) loses its PTH receptor-stimulating properties, whereas non-oxidized PTH (n-oxPTH) is a full agonist of the receptor. This was described in more than 20 well published studies in the 1970 s and 80 s . However, PTH oxidation has been ignored during the development of PTH assays for clinical use so far. Even the nowadays used third generation assay systems do not consider oxidation of PTH We recently developed an assay to differentiate between oxPTH and n-oxPTH. In the current study we established normal values for this assay system. Furthermore, we compare the ratio of oxPTH to n-oxPTH in different population with chronic renal failure: 620 children with renal failure stage 2-4 of the 4C study, 342 adult patients on dialysis, and 602 kidney transplant recipients. In addition, we performed modeling of the interaction of either oxPTH or n-oxPTH with the PTH receptor using biophysical structure approaches. Results: The children had the highest mean as well as maximum n-oxPTH concentrations as compared to adult patients (both patients on dialysis as well as kidney transplant recipients). The relationship between oxPTH and n-oxPTH of individual patients varied substantially in all three populations with renal impairment. The analysis of n-oxPTH in 89 healthy control subjects revealed that n-oxPTH concentrations in patient with renal failure were higher as compared to healthy adult controls (2.25-fold in children with renal failure, 1.53-fold in adult patients on dialysis, and 1.56-fold in kidney transplant recipients, respectively). Computer assisted biophysical structure modeling demonstrated, however, minor sterical- and/or electrostatic changes in oxPTH and n-oxPTH. This indicated that PTH oxidation may induce refolding of PTH and hence alters PTH-PTH receptor interaction via oxidation induced three-dimensional structure alteration of PTH. Conclusion: A huge proportion of circulating PTH measured by current state-of-the-art assay systems is oxidized and thus not biologically active. The relationship between oxPTH and n-oxPTH of individual patients varied substantially. Non-oxidized PTH concentrations are 1.5 - 2.25 fold higher in patients with renal failure as compared to health controls. Measurements of n-oxPTH may reflect the hormone status more precise. The iPTH measures describes most likely oxidative stress in patients with renal failure rather than the PTH hormone status. This, however, needs to be demonstrated in further clinical studies.