Kidney Medicine最新文献

{"title":"A2/A2B Deceased Donor Kidney Transplantation Using A2 Titers Improves Access to Kidney Transplantation: A Single-Center Study","authors":"Erik L. Lum ,&nbsp;Afshin Pirzadeh ,&nbsp;Nakul Datta ,&nbsp;Gerald S. Lipshutz ,&nbsp;Andrea M. McGonigle ,&nbsp;Anum Hamiduzzaman ,&nbsp;Natalie Bjelajac ,&nbsp;Bethany Hale-Durbin ,&nbsp;Suphamai Bunnapradist","doi":"10.1016/j.xkme.2024.100843","DOIUrl":"10.1016/j.xkme.2024.100843","url":null,"abstract":"<div><h3>Rationale &amp; Objective</h3><p>The option for A2/A2B deceased donor kidney transplantation was integrated into the kidney allocation system in 2014 to improve access for B blood group waitlist candidates. Despite excellent reported outcomes, center uptake has remained low across the United States. Here, we examined the effect of implementing an A2/A2B protocol using a cutoff titer of<!--> <!-->≤1:8 for IgG and<!--> <!-->≤1:16 for IgM on blood group B kidney transplant recipients at a single center.</p></div><div><h3>Study Design</h3><p>Retrospective observational study.</p></div><div><h3>Setting &amp; Participants</h3><p>Blood group B recipients of deceased donor kidney transplants at a single center from January 1, 2019, to December 2022.</p></div><div><h3>Exposure</h3><p>Recipients of deceased donor kidney transplants were analyzed based on donor blood type with comparisons of A2/A2B versus blood group compatible.</p></div><div><h3>Outcomes</h3><p>One-year patient survival, death-censored allograft function, primary nonfunction, delayed graft function, allograft function as measured using serum creatinine levels and estimated glomerular filtration rate at 1 year, biopsy-proven rejection, and need for plasmapheresis.</p></div><div><h3>Analytical Approach</h3><p>Comparison between the A2/A2B and compatible groups were performed using the Fisher test or the χ² test for categorical variables and the nonparametric Wilcoxon rank-sum test for continuous variables.</p></div><div><h3>Results</h3><p>A total of 104 blood type B patients received a deceased donor kidney transplant at our center during the study period, 49 (47.1%) of whom received an A2/A2B transplant. Waiting time was lower in A2/A2B recipients compared with blood group compatible recipients (57.9 months vs 74.7 months, <em>P</em> <!-->=<!--> <!-->0.01). A2/A2B recipients were more likely to receive a donor after cardiac death (24.5% vs 1.8%, <em>P</em> <!-->&lt;<!--> <!-->0.05) and experience delayed graft function (65.3% vs 41.8%). There were no observed differences in the average serum creatinine level or estimated glomerular filtration rate at 1 month, 3 months, and 1 year post kidney transplantation, acute rejection, or primary nonfunction.</p></div><div><h3>Limitations</h3><p>Single-center study. Small cohort size limiting outcome analysis.</p></div><div><h3>Conclusions</h3><p>Implementation of an A2/A2B protocol increased transplant volumes of blood group B waitlisted patients by 83.6% and decreased the waiting time for transplantation by 22.5% with similar transplant outcomes.</p></div><div><h3>Plain-Language Summary</h3><p>Recipient blood type is one of the main determinants of waiting time to receive a deceased donor kidney transplant. Patients with blood type B have some of the longest waiting times for a kidney in the United States. Minorities comprise a large percentage of blood group B waitlist patients, contributing to observed racial differences in kid","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000542/pdfft?md5=92f55a86a71fc81898e1dda383ac65f6&pid=1-s2.0-S2590059524000542-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141133589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urine Epidermal Growth Factor and Kidney Function Decline in Middle-Aged Adults","authors":"Merve Postalcioglu ,&nbsp;Rebecca Scherzer ,&nbsp;Joachim H. Ix ,&nbsp;David R. Jacobs Jr ,&nbsp;Cora E. Lewis ,&nbsp;Sucheta Vaigankar ,&nbsp;Michelle M. Estrella ,&nbsp;Orlando M. Gutierrez ,&nbsp;Michael G. Shlipak","doi":"10.1016/j.xkme.2024.100846","DOIUrl":"10.1016/j.xkme.2024.100846","url":null,"abstract":"<div><h3>Rationale &amp; Objective</h3><p>The diagnosis and prognostication of chronic kidney disease (CKD) largely rely on glomerular measures that may not reflect tubular damage. We investigated the associations of urine kidney tubule biomarkers with estimated glomerular filtration rate (eGFR) change among middle-aged adults, when chronic diseases typically emerge.</p></div><div><h3>Study Design</h3><p>An observational cohort study.</p></div><div><h3>Setting &amp; Participants</h3><p>A total of 1,145 participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study without CKD, hypertension, or cardiovascular disease at the year 20 visit.</p></div><div><h3>Exposures</h3><p>Seven different biomarkers of tubular health: urine epidermal growth factor (EGF), alpha-1-microglobulin (α1m), interleukin-18, kidney injury molecule-1, monocyte chemoattractant protein-1, uromodulin, and chitinase-3-like protein 1.</p></div><div><h3>Outcomes</h3><p>Ten-year eGFR change and incident reduced eGFR (new onset of eGFR<!--> <!-->&lt;<!--> <!-->60<!--> <!-->mL/min/1.73<!--> <!-->m²).</p></div><div><h3>Analytical Approach</h3><p>We examined associations of tubular health biomarkers with 10-year eGFR change and incident reduced eGFR with linear mixed models and interval-censored proportional hazards regression models, respectively. Both minimally and fully adjusted models were controlled for urine creatinine levels.</p></div><div><h3>Results</h3><p>The mean age of participants was 44.8<!--> <!-->±<!--> <!-->3.7 years, with 39% African American and 56% female. The average 10-year change in eGFR was -18.6<!--> <!-->mL/min/1.73<!--> <!-->m² (95% CI, -19.4 to -17.8). In contrast to the other tubular biomarkers, which showed conflicting results, EGF demonstrated strong, consistent associations with both kidney outcomes. Each 1-standard deviation (SD) higher EGF was associated with a 2.37<!--> <!-->mL/min/1.73<!--> <!-->m² (95% CI, 0.64-4.10) smaller 10-year decrease in eGFR and a 42% (95% CI, 4%-64%) lower risk of incident reduced eGFR in the fully adjusted model.</p></div><div><h3>Limitations</h3><p>Observational design, measurements of eGFR were done only at 5-year intervals during follow-up.</p></div><div><h3>Conclusions</h3><p>In middle-aged, community-dwelling adults without hypertension, cardiovascular disease or CKD, higher urine EGF concentrations are associated with slower eGFR decline, whereas other kidney tubule biomarkers lacked a consistent association with kidney function decline.</p></div><div><h3>Plain Language Summary</h3><p>Current measures of chronic kidney disease (CKD) rely on markers of glomerular health and function. This approach inadequately captures the role of kidney tubule health, a known histopathological predictor of CKD development. We investigated associations of 7 biomarkers of kidney tubule health with 10-year estimated glomerular filtration rate (eGFR) change and incident reduced eGFR. ","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000578/pdfft?md5=63afe19094ca813342c047a024fd52cf&pid=1-s2.0-S2590059524000578-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141140528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Kidney Disease Stage and Cardiovascular and Mortality Events Among Older Adults: The SPRINT Trial","authors":"Valentina Turbay-Caballero ,&nbsp;Ana C. Ricardo ,&nbsp;Jinsong Chen ,&nbsp;Celestin Missikpode ,&nbsp;James P. Lash ,&nbsp;Gustavo Aroca-Martinez ,&nbsp;Carlos G. Musso","doi":"10.1016/j.xkme.2024.100845","DOIUrl":"10.1016/j.xkme.2024.100845","url":null,"abstract":"<div><h3>Rationale &amp; Objective</h3><p>The risk implications of the Kidney Disease: Improving Global Outcomes (KDIGO) chronic kidney disease classification in older adults are controversial. We evaluated the risk of adverse outcomes in this population across categories of estimated glomerular filtration rate (eGFR) and urinary albumin-creatinine ratio (UACR).</p></div><div><h3>Study Design</h3><p>Prospective cohort.</p></div><div><h3>Settings &amp; Participants</h3><p>In total, 2,509 participants aged<!--> <!-->≥75 years in the Systolic Blood Pressure Intervention Trial (SPRINT).</p></div><div><h3>Exposure</h3><p>KDIGO eGFR and UACR categories. We combined KDIGO categories G1 and G2, G3b and G4, as well as A2 and A3.</p></div><div><h3>Outcomes</h3><p>Primary SPRINT outcome (composite of myocardial infarction, other acute coronary syndromes, stroke, heart failure, or death from cardiovascular causes), and all-cause death.</p></div><div><h3>Analytical Approach</h3><p>Multivariable Cox proportional hazard models.</p></div><div><h3>Results</h3><p>Mean age was 79.8 years, and 37.4% were female. The mean eGFR was 64.0<!--> <!-->mL/min/1.73<!--> <!-->m², and the median UACR was 13.1<!--> <!-->mg/g. In multivariable Cox proportional hazard analysis, compared with participants with eGFR<!--> <!-->≥<!--> <!-->60<!--> <!-->mL/min/1.73<!--> <!-->m² and UACR<!--> <!-->&lt;<!--> <!-->30<!--> <!-->mg/g, there was no statistically significant difference in the risk of the primary outcome among participants with eGFR 45-59 or 15-44<!--> <!-->mL/min/1.73<!--> <!-->m² and UACR<!--> <!-->&lt;<!--> <!-->30<!--> <!-->mg/g. However, those with eGFR 45-59 or 15-44<!--> <!-->mL/min/1.73<!--> <!-->m² and UACR<!--> <!-->≥<!--> <!-->30<!--> <!-->mg/g had higher risk of the primary outcome (HR [95% CI], 1.97 [1.27-3.04] and 3.32 [2.23-4.93], respectively). The risk for all-cause death was higher for each category of abnormal eGFR and UACR, with the highest risk observed among those with eGFR 15-44<!--> <!-->mL/min/1.73<!--> <!-->m² and UACR<!--> <!-->≥<!--> <!-->30<!--> <!-->mg/g (3.34 [2.05-5.44]).</p></div><div><h3>Limitations</h3><p>Individuals with diabetes and urine protein<!--> <!-->&gt;1<!--> <!-->g/day were excluded from SPRINT.</p></div><div><h3>Conclusion</h3><p>Among older adults SPRINT participants, low eGFR without albuminuria was associated with higher mortality but not with increased risk of cardiovascular events. Additional studies are needed to evaluate an adapted chronic kidney disease stage-based risk stratification for older adults.</p></div><div><h3>Plain-Language Summary</h3><p>Using data from participants in the SPRINT trial, we evaluated the association of chronic kidney disease stage with adverse clinical outcomes among adults older than 75 years without diabetes. We found that low level of kidney function determined by a low estimated glomerular filtration rate with moderately or severely inc","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000566/pdfft?md5=574ad26fcf880b684cde618eaef02325&pid=1-s2.0-S2590059524000566-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141135125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atomoxetine for Intradialytic Hypotension in a Patient on Hemodialysis: A Case Report","authors":"Yi-Hsin Chen ,&nbsp;Chih-Tsung Chen","doi":"10.1016/j.xkme.2024.100840","DOIUrl":"10.1016/j.xkme.2024.100840","url":null,"abstract":"<div><p>Intradialytic hypotension significantly affects patient safety and clinical outcomes during hemodialysis. Despite various pharmacological and nonpharmacological interventions, effective management remains elusive. In this report, we detail a case of intradialytic hypotension in a male patient in his 40s, undergoing hemodialysis with a history of polycystic kidney disease. Eight years ago, the patient underwent bilateral nephrectomy because of a severe cystic infection, after which his systolic blood pressure (BP) persistently remained at 50-70<!--> <!-->mm Hg during dialysis sessions. The initial treatment strategy for hypotension included fludrocortisone, midodrine, and prednisolone, leading to a slight temporary increase in BP, which subsequently declined. As the patient’s condition deteriorated, the administration of norepinephrine or dopamine became necessary to sustain BP during dialysis. Given the patient’s resistance to these treatments, a daily dose of 25<!--> <!-->mg of atomoxetine was introduced. Following this treatment, there was a gradual improvement in the patient’s vertigo, weakness, and BP. This case illustrates that low-dose atomoxetine can alleviate symptoms and elevate BP in patients experiencing severe intradialytic hypotension during hemodialysis.</p></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000517/pdfft?md5=d74e8429e43b1b9ca37c2cb2a24f7ad3&pid=1-s2.0-S2590059524000517-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141046266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antibrush Border Antibody Disease: A Case Series","authors":"Michelle Pengshung ,&nbsp;Vivek Charu ,&nbsp;Megan L. Troxell ,&nbsp;Shreeram Akilesh ,&nbsp;Kelly D. Smith ,&nbsp;J. Ashley Jefferson","doi":"10.1016/j.xkme.2024.100841","DOIUrl":"10.1016/j.xkme.2024.100841","url":null,"abstract":"<div><p>Antibrush border antibody (ABBA) disease is a rare cause of kidney disease characterized by progressive renal tubular injury associated with immune complex deposition along the basement membranes of the proximal tubule and circulating autoantibodies to brush border antigens. Several antigens have been identified as targets of autoantibodies in this disease, including low-density lipoprotein receptor related protein 2 (LRP2), cubilin, and amnionless proteins. We present 9 patients from 2 academic medical centers and describe the clinicopathologic characteristics and outcome data. All patients presented with acute kidney injury and proteinuria. Pathology confirmed immune complex deposition along proximal tubular basement membranes in all patients, but the majority (6/8) also showed segmental glomerular subepithelial immune complexes. Two of 3 patients treated with rituximab demonstrated stabilization of kidney function; 1 of these patients had mantle cell lymphoma. One patient with lung cancer showed stabilization of disease after treatment of the malignancy. The remaining patients progressed to end-stage kidney disease with either conservative therapy (3 patients) or immunosuppression with glucocorticoids (2 patients). This series highlights the poor prognosis of ABBA disease, but a potential benefit of anti-B cell therapy or treatment of an underlying malignancy in some cases.</p></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000529/pdfft?md5=2ef0e5fa2d5c6c5c74deccdb243d9b86&pid=1-s2.0-S2590059524000529-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141048768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"APOL1 High-Risk Genotypes and Kidney Disease Risk in Middle-Aged Black Adults: More Questions Than Answers","authors":"Orlando M. Gutiérrez","doi":"10.1016/j.xkme.2024.100842","DOIUrl":"10.1016/j.xkme.2024.100842","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000530/pdfft?md5=54380f6f9db2beabd25c9ccf34caf2c9&pid=1-s2.0-S2590059524000530-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141032853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SGLT2 Inhibitor Use for Treatment of Hypocitraturia in a Distal Renal Tubular Acidosis","authors":"Stefan Scherr ,&nbsp;Sara H. Ksiazek ,&nbsp;Christoph Schwarz ,&nbsp;Marcus D. Säemann","doi":"10.1016/j.xkme.2024.100839","DOIUrl":"10.1016/j.xkme.2024.100839","url":null,"abstract":"<div><p>5-Amino salicylic acid (5-ASA) is a known culprit for the development of tubulointerstitial nephritis. Together with impaired kidney function, tubulointerstitial nephritis can lead to specific tubular malfunctions including distal renal tubular acidosis. Distal renal tubular acidosis is an acid-base disorder in which acid secretion in the distal part of the renal tubular system is decreased. Patients with distal renal tubular acidosis are predisposed to recurrently form calcium phosphate kidney stones. This results from the inability to acidify the urine properly as well as from a decreased citrate concentration in the urine, which is another pathognomonic feature of distal renal tubular acidosis. We present the case of a man in his late 40s with Crohn’s disease who developed tubulointerstitial nephritis associated with 5-ASA leading to the development of distal renal tubular acidosis and recurrent calcium phosphate nephrolithiasis. After steroid therapy and partial recovery of kidney function, we observed an increase of citraturia in response to treatment with dapagliflozin, potentially indicating beneficial effects of sodium/glucose cotransporter 2 inhibition on the recurrence of calcium phosphate stone disease in interstitial nephritis-induced distal tubular acidosis.</p></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000505/pdfft?md5=abd716ee101896c7809ecd2730e6c62b&pid=1-s2.0-S2590059524000505-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141040076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dialysis Patient With a Unique Rash","authors":"Alissa Cyriac ,&nbsp;Steven L. Allen ,&nbsp;Sophia Cyriac ,&nbsp;Kenar D. Jhaveri","doi":"10.1016/j.xkme.2024.100838","DOIUrl":"10.1016/j.xkme.2024.100838","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000499/pdfft?md5=a4f928f733ccdfc17ec0b598d4d1cf22&pid=1-s2.0-S2590059524000499-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141056326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute Kidney Injury in Inflammatory Bowel Disease Patients: A Nationwide Comparative Analysis","authors":"Manish K. Saha ,&nbsp;Susan L. Hogan ,&nbsp;Ronald J. Falk ,&nbsp;Edward L. Barnes ,&nbsp;Yichun Hu ,&nbsp;Abhijit V. Kshirsagar ,&nbsp;Carolyn T. Thorpe","doi":"10.1016/j.xkme.2024.100836","DOIUrl":"10.1016/j.xkme.2024.100836","url":null,"abstract":"<div><h3>Rationale &amp; Objective</h3><p>About 25%-40% of patients with inflammatory bowel disease (IBD) may have extraintestinal manifestations, mainly involving the liver, skin, and joints. Kidney involvement in patients with IBD has been reported, but there are no estimates of its prevalence in population-based studies in the United States. We compared the frequency of acute kidney injury (AKI) among hospitalizations with IBD with that among hospitalizations with collagen vascular diseases and hospitalizations with neither condition.</p></div><div><h3>Study Design</h3><p>Retrospective, population-based cohort study.</p></div><div><h3>Setting &amp; Participants</h3><p>Healthcare Cost and Utilization Project-Nationwide Inpatient Sample database.</p></div><div><h3>Outcomes</h3><p>AKI and AKI requiring dialysis.</p></div><div><h3>Analytical Approach</h3><p>Regression models were used to compare the occurrence of AKI among groups. Inverse probability of treatment weighting was applied to balance groups on covariates.</p></div><div><h3>Results</h3><p>The final sample comprised 5,735,804 hospitalizations, including 57,121 with IBD, 159,930 with collagen vascular diseases, and 5,518,753 with neither IBD nor collagen vascular diseases. AKI was observed in 13%, 15%, and 12.2% of hospitalizations with IBD, collagen vascular diseases, and the general population, respectively. When adjusting for demographic, hospital, and clinical characteristics using inverse probability of treatment weighting, hospitalizations with IBD had higher odds of being diagnosed with AKI than both those with collagen vascular diseases (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.27-1.38) and the general population (OR, 1.27; 95% CI, 1.23-1.31) and also had higher odds of being diagnosed with AKI requiring dialysis than those with collagen vascular diseases (OR, 1.59; 95% CI, 1.31-1.94) or than the general population (OR, 1.45; 95% CI, 1.25-1.68).</p></div><div><h3>Limitations</h3><p>Cross-sectional analysis, underreporting of International Classification of Diseases codes, and analyses relevant to in-hospital stays only.</p></div><div><h3>Conclusions</h3><p>The prevalence and risk of AKI among hospitalizations with IBD is greater than that of hospitalizations with collagen vascular diseases and the general population. Coexisting kidney disease should be considered among patients with a known diagnosis of IBD.</p></div><div><h3>Plain Language Summary</h3><p>As a nephrologist, we have evaluated many patients with inflammatory bowel disease with various forms of kidney disease, both inflammatory and noninflammatory. Based on a multitude of factors, we have always wondered if there are shared immune mechanisms between the gut and kidney that could explain the underlying inflammation in both organs. In addition, based on recent studies of other autoimmune/inflammatory diseases, there is growing interest in the role of the gut microbiome (microorganisms that reside in our g","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000475/pdfft?md5=592a6b011520efa07b2ef4839389995a&pid=1-s2.0-S2590059524000475-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141054146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Volume and Body Composition in Hemodialysis Patients: A Bioimpedance Study Assessing Differences by Sex","authors":"Sebastian Mussnig MD ,&nbsp;Janosch Niknam MD ,&nbsp;Christoph Matthias ,&nbsp;Susanne Widmer ,&nbsp;Dilara Gülmez ,&nbsp;Simon Krenn MD ,&nbsp;Matthias Lorenz MD ,&nbsp;Charles Chazot PhD ,&nbsp;Peter Wabel PhD ,&nbsp;Daniel Schneditz PhD ,&nbsp;Manfred Hecking PhD","doi":"10.1016/j.xkme.2024.100837","DOIUrl":"10.1016/j.xkme.2024.100837","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590059524000487/pdfft?md5=b2721d16bbe6c2fa06c1b8fd3bcc1bdc&pid=1-s2.0-S2590059524000487-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141029929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}