Kidney Medicine最新文献

{"title":"Association of Proximal Tubule Secretion With Hyperkalemia Risk, Treatment Response, and Outcomes in Heart Failure With Preserved Ejection Fraction","authors":"Nicholas Wettersten, Ronit Katz, Pranav S. Garimella, Alexander L. Bullen, Simon B. Ascher, Jesse C. Seegmiller, Yu Horiuchi, Yoshimitsu Takaoka, Joachim H. Ix","doi":"10.1016/j.xkme.2026.101428","DOIUrl":"10.1016/j.xkme.2026.101428","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Endogenous biomarkers reflecting impaired kidney tubular secretion are associated with risk of hyperkalemia in patients with hypertension and chronic kidney disease. Whether these biomarkers are associated with risk of hyperkalemia, therapeutic response, and adverse cardiovascular and kidney events in heart failure (HF) patients receiving mineralocorticoid receptor antagonists is unknown.</div></div><div><h3>Study Design</h3><div>An observational cohort study.</div></div><div><h3>Setting & Participants</h3><div>Individuals with HF with preserved ejection fraction (HFpEF) enrolled in the TOPCAT study.</div></div><div><h3>Predictors</h3><div>Summary secretion score incorporating urine-to-plasma ratios of 9 secretion markers measured in paired samples at baseline.</div></div><div><h3>Outcomes</h3><div>Change in serum potassium during follow-up, measures of treatment response assessed by change in Kansas City Cardiomyopathy Questionnaire (KCCQ) score and N-terminal pro-B-type natriuretic peptide over 12 months, and adverse cardiovascular and kidney events.</div></div><div><h3>Analytic Approach</h3><div>Linear mixed-effects models, Cox proportional hazards models, and linear regression adjusting for risk factors, estimated glomerular filtration rate, and urine albumin-to-creatinine ratio.</div></div><div><h3>Results</h3><div>Among 372 TOPCAT participants, 179 (48%) were randomized to spironolactone, 45% were women, the mean age was 70 ± 10 years and estimated glomerular filtration rate was 66 ± 18 mL/min/1.73 m<sup>2</sup>. In adjusted models, higher secretion score was not associated with changes in serum potassium, change in KCCQ ≥5 points, change in N-terminal pro-B-type natriuretic peptide, adverse cardiovascular or kidney events. In adjusted models, a higher secretion score was associated with lower KCCQ at 12 months (change −3.5, 95% CI, −6.6 to −0.4) in the spironolactone arm, but not in the placebo arm.</div></div><div><h3>Limitations</h3><div>Low number of events, confounding from Eastern Europe participants who may have not had HFpEF or taken prescribed therapies.</div></div><div><h3>Conclusions</h3><div>Biomarkers of tubular secretion are not associated with risk of hyperkalemia, treatment response, or cardiovascular and kidney events in individuals with HFpEF.</div></div><div><h3>Plain-language Summary</h3><div>People with chronic kidney disease and hypertension with reduced proximal tubule secretion capacity have a greater risk of hyperkalemia. Whether similar associations are seen in individuals with heart failure is unknown. We studied 372 participants with heart failure with preserved ejection fraction enrolled in the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist study. Using blood and urine specimens collected at the time of enrollment, we measured nine biomarkers of proximal tubule secretion capacity and combined them into a composite secretion sco","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101428"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584601","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":"Impact of Using Biomarkers in Eligibility Criteria in Acute Kidney Injury Randomized Controlled Trials: A Systematic Review and Methodological Meta-Analysis","authors":"Fella Chennou, Michael Strader, Roxanne Authier, Patrick T. Murray, William Beaubien-Souligny, Jean-Maxime Côté","doi":"10.1016/j.xkme.2026.101415","DOIUrl":"10.1016/j.xkme.2026.101415","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Many recent randomized controlled trials (RCTs) for acute kidney injury have incorporated biomarkers as part of their eligibility criteria. The sample size calculation of these trials is often based on prior studies that did not include such criteria. This meta-analysis evaluates the impact of a biomarker-based enrichment strategy on the rate of anticipated versus observed primary events and explores the effect of integrating such biomarkers on statistical power.</div></div><div><h3>Study Design</h3><div>We performed a PRISMA-guided systematic review and methodological meta-analysis of RCTs extracted from 6 databases.</div></div><div><h3>Setting & Study Population</h3><div>The RCTs included patients at risk for or diagnosed with acute kidney injury.</div></div><div><h3>Selection Criteria for Studies</h3><div>Clinical trials with a biomarker-based eligibility criterion and either a renal or mortality primary outcome, published between 2010 and 2023.</div></div><div><h3>Data Extraction</h3><div>Data were extracted independently by 2 reviewers.</div></div><div><h3>Analytical Approach</h3><div>The absolute risk difference between anticipated and observed event rates was measured for all patients and stratified for control and intervention groups.</div></div><div><h3>Results</h3><div>Fourteen RCTs involving 3,817 patients were included. Biomarkers of interest were neutrophil gelatinase-associated lipocalin, TIMP-2∗IGFBP7, proteinuria, serum albumin, NT-pro-BNP, homocysteine, and uric acid. The pooled absolute risk difference between anticipated and observed event rates was 0.12 (95% CI; 0.06-0.17). In the control and interventional groups, the absolute risk differences were 0.10 (95% CI, 0.01-0.19) and 0.12 (95% CI, 0.06-0.18), respectively. For kidney damage biomarkers, the risk difference was 0.13 (95% CI, 0.06-0.20). The mean preplanned and achieved statistical powers were 0.84 ± 0.07 and 0.43 ± 0.28, respectively, with no improvement when extrapolating the preplanned sample size.</div></div><div><h3>Limitations</h3><div>Most RCTs were underpowered for their primary outcome. There was a high level of heterogeneity.</div></div><div><h3>Conclusions</h3><div>There is a difference between expected and observed incidence rates that may be partly attributed to biomarker-based enrichment methods. These findings highlight the need for rigorous validation of biomarkers before their incorporation into the eligibility criteria of RCTs.</div></div><div><h3>Plain-Language Summary</h3><div>Clinical trials in acute kidney injury increasingly use specific biomarkers to determine patient eligibility. These tests are meant to identify patients who are most likely to benefit from the intervention. We systematically reviewed 14 randomized trials to assess how this approach affects study results. We found that the number of primary clinical events observed often differed substantially from what researchers expected when p","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101415"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584568","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":"Regarding “Determining Physical Function Measures for Estimating VO2Peak in Patients on Hemodialysis” by Groningen et al.","authors":"Rodrigo Torres-Castro MSc","doi":"10.1016/j.xkme.2026.101446","DOIUrl":"10.1016/j.xkme.2026.101446","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101446"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584571","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":"Alport Syndrome Family Screening and Management: Experience of a Tertiary Center","authors":"Ana M. Gomes, Claudia F. Reis, Joana Dias, Vitória Faria, Jorge Malheiro, Carolina Lemos, Daniela Lopes, Graça Ferreira, Clara Almeida, Idalina Beirão","doi":"10.1016/j.xkme.2026.101419","DOIUrl":"10.1016/j.xkme.2026.101419","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Alport syndrome (AS) is one of the most common causes of inherited chronic kidney disease. Timely diagnosis and treatment of this condition can significantly influence its natural course. The evaluation of at-risk family members allows for the identification of new patients and the initiation of renoprotective measures that help prevent the progression of kidney disease. The aim of this study was to describe the implementation and results of cascade screening among at-risk relatives of a cohort of patients with AS followed at our unit.</div></div><div><h3>Study Design</h3><div>This is a prospective, single-center study conducted at Nephrology Department, Health Local Unit Gaia/Espinho. We provided patients with letters intended for their first-degree relatives, highlighting the benefits of a referral for renal impairment assessment and genetic counseling. A total of 93 at-risk relatives underwent evaluation through biochemical testing (kidney function and urinalysis abnormalities) and were offered molecular screening for the familial <em>COL4</em> variant following genetic counseling. Clinical, genetic, and laboratory data were systematically collected.</div></div><div><h3>Observations</h3><div>Seventy-six (81.7%) at-risk relatives underwent molecular evaluation. A positive molecular test was achieved in 52 (68.4%) relatives, whereas the familial variant was excluded in 24 (31.6%) individuals. 9 (9.6%) individuals declined to proceed with screening and 8 (8.6%) experienced delay in obtaining their results. Among those with a positive molecular screening, 36.5% (n = 19) had urinary protein-creatinine ratio > 0.1 g/g creatinine and 13.5% (n = 7) had glomerular filtration rate (by the CKD-EPI [Chronic Kidney Disease Epidemiology Collaboration] 2021 equation) < 60 mL/min/1.73 m<sup>2</sup>. 30 (57.7%) relatives initiated treatment with a renin-angiotensin-aldosterone system inhibitor. These individuals were older, had higher levels of proteinuria, and had a lower glomerular filtration rate at baseline.</div></div><div><h3>Limitations</h3><div>The relatively small size of this series from a single unit. The cascade screening based on a patient-led approach may not extent to all the at-risk relatives.</div></div><div><h3>Conclusions</h3><div>Cascade screening of relatives of patients with AS is an effective strategy for identifying individuals with ongoing kidney disease or those at risk of future renal impairment. This approach enables the early initiation of nephroprotective measures and ensures timely access to appropriate genetic counseling.</div></div><div><h3>Plain-Language Summary</h3><div>Alport syndrome (AS) is a leading cause of inherited chronic kidney disease. Timely diagnosis and treatment of this condition can significantly influence its natural course. The evaluation of at-risk family members enables the identification of new patients and the early initiation of renoprotective measures to","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101419"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13416653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620580","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":"Place of Death Among Patients Dying of Kidney Failure: Insights From the CDC Wonder Database","authors":"Alyssa Sanchez DO, Nikitha Murthy DO, Thomas Yoo DO, Roy O. Mathew MD, Sayna Norouzi MD, Amir Abdipour MD, Dmitry Abramov MD","doi":"10.1016/j.xkme.2026.101434","DOIUrl":"10.1016/j.xkme.2026.101434","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101434"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13416625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620572","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":"A Novel Entity of Renal Toxicity After Combination Chemotherapy: An Onco-Nephrology Kidney Biopsy Teaching Case","authors":"Gian Marco Berti,&nbsp;Federica Maritati,&nbsp;Francesco Tondolo,&nbsp;Stefano Chilotti,&nbsp;Benedetta Fabbrizio,&nbsp;Gianandrea Pasquinelli,&nbsp;Gaetano La Manna,&nbsp;Gisella Vischini","doi":"10.1016/j.xkme.2026.101439","DOIUrl":"10.1016/j.xkme.2026.101439","url":null,"abstract":"<div><div>Renal injury associated with combination cancer therapies represents a growing diagnostic challenge. Kidney biopsy enables early and appropriate detection of these cases, helping in accurate differential diagnosis and individualized management in these increasingly frequent and complex clinical settings. We report a tricky onco-nephrology teaching case involving a 65-year-old woman with recurrent high-grade Müllerian carcinoma who developed progressive kidney dysfunction, arterial hypertension, and new-onset subnephrotic range proteinuria during treatment with carboplatin, gemcitabine, and bevacizumab. Serologic tests were negative for autoimmune, viral, and hematologic causes. Kidney biopsy showed an advanced membranoproliferative pattern with eosinophilic and periodic acid–Schiff positive intracapillary deposits, diffuse endothelial injury, and unusual tubular myelin figures. Two weeks after kidney biopsy, the patient developed cutaneous purpura that shifted the diagnostic framework toward a systemic vasculopathy. This was supported by the ultrastructural evidence of polyclonal IgM-dominant organized intraluminal deposits and consistent with a drug-induced cryoglobulinemic glomerulonephritis superimposed on gemcitabine-induced chronic thrombotic microangiopathy with unexpected renal lipidosis. To our knowledge, this represents the first reported case of this specific renal injury profile in this clinical setting, underscoring the critical role of kidney biopsy in optimizing personalized care within the emerging field of onco-nephrology.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101439"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13393669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148579175","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":"Associations of Nephron Number, Birth Weight, and Causes of Death in a Community at High Risk of Hypertension and Cardiovascular Disease","authors":"Michael D. Hughson,&nbsp;Rebecca N. Douglas-Denton,&nbsp;Wendy E. Hoy,&nbsp;Cheryl A. Winkler,&nbsp;Jeffrey B. Kopp,&nbsp;John F. Bertram","doi":"10.1016/j.xkme.2026.101432","DOIUrl":"10.1016/j.xkme.2026.101432","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale &amp; Objective&lt;/h3&gt;&lt;div&gt;Low birth weight (LBW) and low nephron number may increase the risk of hypertension and cardiovascular disease (CVD).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study Design&lt;/h3&gt;&lt;div&gt;Total glomerular number was determined by stereological analysis of autopsy kidneys from 336 participants. Health Department-recorded birth weights were obtained for 204 participants who were ≤55 years old.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Outcomes&lt;/h3&gt;&lt;div&gt;Birth weight, nephron number.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Predictors&lt;/h3&gt;&lt;div&gt;Hypertension, CVD, age, biological sex, body mass index, poverty index, and &lt;em&gt;APOL1&lt;/em&gt; genotype.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Analytical Approach&lt;/h3&gt;&lt;div&gt;Relationships were investigated using group comparisons and regression models.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Settings &amp; Participants&lt;/h3&gt;&lt;div&gt;Performance sites: Autopsies, University Medical Center, Jackson, MS; Stereology, Department of Anatomy and Developmental Biology, Monash University, Melbourne; &lt;em&gt;APOL1&lt;/em&gt; genotyping, Basic Research Laboratory, Center for Cancer Research, National Institutes of Health, Frederick, Maryland.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;In total, 170 participants having birth weights were adults, 29% of adults were hypertensive, and 40% died of CVD. Genotyping identified 22 Black participants with 2 &lt;em&gt;APOL1&lt;/em&gt; risk alleles. A median of 718,409 glomeruli per kidney was found for participants with LBW (&lt; 2.5 kg), which was significantly less than the median of 936,937 glomeruli found with birth weights from 3.0 to 4.0 kg (&lt;em&gt;P&lt;/em&gt; &lt; 0.001). Among adults ≤ 55 years old, hypertension correlated with age (&lt;em&gt;P&lt;/em&gt; &lt; 0.001) and the severity of glomerulosclerosis (&lt;em&gt;P&lt;/em&gt; &lt; 0.001), and CVD death correlated with hypertension (&lt;em&gt;P&lt;/em&gt; = 0.01). However, neither LBW nor nephron number was associated with hypertension or CVD death or with an &lt;em&gt;APLO1&lt;/em&gt; high-risk genotype. Among participants aged 65-89 years, increased glomerulosclerosis was associated with a lower median glomerular number (759,623; &lt;em&gt;P&lt;/em&gt; = 0.02) and with hypertension (&lt;em&gt;P&lt;/em&gt; &lt; 0.01).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitations&lt;/h3&gt;&lt;div&gt;Relationships of predictors to outcomes are abridged by death at recruitment.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;LBW and low nephron number were not related to hypertension or CVD in adults ≤ 55 years of age, but a glomerulosclerosis-related reduction in glomerular number may contribute to hypertension and CVD in later life.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain-Language Summary&lt;/h3&gt;&lt;div&gt;The nephron is the basic functional unit of the kidney, and nephron number is directly related to birth weight. It is proposed that hypertension and cardiovascular disease (CVD) risk are the result of reduced nephron numbers in persons born with low birth weight. In this study, we show that the median number of nephrons in persons born at low birth weight is 719,409 (compared with nearly 1,000,000 with normal birth weight). We suggest that a nephron number ≤ 720,000 indi","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101432"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584566","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":"Response to the Letter Regarding “Determining Physical Function Measures for Estimating VO2Peak in Patients on Hemodialysis”","authors":"Kenneth Lim,&nbsp;Nolan W. Groninger,&nbsp;Monique Campos","doi":"10.1016/j.xkme.2026.101447","DOIUrl":"10.1016/j.xkme.2026.101447","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101447"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584700","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":"Thyroid Stimulating Hormone Levels and Risk of Hospital-Acquired Acute Kidney Injury: A Nationwide Cohort Study","authors":"Caoxiang She,&nbsp;Yaduan Lin,&nbsp;Yanan Xie,&nbsp;Shiyu Zhou,&nbsp;Fan Luo,&nbsp;Ruixuan Chen,&nbsp;Luhua Jin,&nbsp;Lantian Li,&nbsp;Linjiang Chen,&nbsp;Xian Shao,&nbsp;Sheng Nie","doi":"10.1016/j.xkme.2026.101414","DOIUrl":"10.1016/j.xkme.2026.101414","url":null,"abstract":"<div><h3>Rationale &amp; Objective</h3><div>The thyroid–renal interaction remains underexplored in acute kidney injury pathophysiology. We aimed to investigate the relationship between thyroid status, defined by thyroid-stimulating hormone (TSH) levels, and incident hospital-acquired acute kidney injury (HA-AKI).</div></div><div><h3>Study Design</h3><div>A retrospective cohort study.</div></div><div><h3>Setting &amp; Participants</h3><div>Patients with TSH quantification within 48 hours after admission from the China Renal Data System (CRDS) database.</div></div><div><h3>Exposure(s)</h3><div>Three TSH levels groups, including hyperthyroid (TSH ≤ 0.5 mIU/L), euthyroid (0.5 &lt; TSH ≤ 5.0 mIU/L), and hypothyroid (TSH &gt; 5.0 mIU/L) TSH levels.</div></div><div><h3>Outcome(s)</h3><div>The primary outcome was HA-AKI.</div></div><div><h3>Analytical Approach</h3><div>Multivariable Cox hazard regression models and restricted cubic spline.</div></div><div><h3>Results</h3><div>A total of 20,317 (5.4%) patients developed HA-AKI, with incidences rates of 8.0%, 5.0%, and 6.4% in patients with hyperthyroid, euthyroid, and hypothyroid TSH levels, respectively. Compared with patients with euthyroid TSH levels, those with hyperthyroid or hypothyroid TSH levels were associated with an increased risk of HA-AKI (hyperthyroid TSH levels: adjusted hazard ratio [aHR], 1.28; 95% confidence interval [CI], 1.21-1.37; <em>P</em> &lt; 0.001; hypothyroid TSH levels: aHR, 1.10; 95% CI, 1.01-1.21; <em>P</em> = 0.03). Additionally, the dose-response curve showed a U-shaped relationship between TSH levels and the risk of new-onset HA-AKI.</div></div><div><h3>Limitations</h3><div>Possible residual confounding.</div></div><div><h3>Conclusions</h3><div>TSH levels in the low (≤0.5 mIU/L) and high (&gt;5.0 mIU/L) ranges were associated with increased risk of HA-AKI. These insights suggest that enhanced vigilance toward AKI may be justifiable in patients with thyroid dysfunction.</div></div><div><h3>Plain-Language Summary</h3><div>The relationship between thyroid dysfunction and chronic kidney disease (CKD) has been extensively studied. However, there is a lack of consensus regarding whether thyroid disorders increase the risk of acute kidney injury (AKI). To address this issue, this national cohort study used thyroid-stimulating hormone (TSH) levels as the primary exposure variable to assess thyroid function, categorizing them into three groups and evaluating the relationship between TSH levels and incident hospital-acquired acute kidney injury (HA-AKI). The results demonstrated that TSH levels in both low and high levels were associated with an increased risk of HA-AKI. Disruptions in the thyroid axis may serve as a predictor of patient outcomes. Therefore, prompt evaluation of thyroid function may be recommended to detect AKI in high-risk populations.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101414"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584693","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":"Estimated Tubular Secretion of Creatinine and Risk of Kidney Failure: The AASK Trial","authors":"Pranav S. Garimella MD, MPH,&nbsp;Kevin M. Cummins PhD,&nbsp;Jennifer Gassman PhD,&nbsp;Francis Gabbai MD,&nbsp;Andrew S. Levey MD,&nbsp;Joachim H. Ix MD, MAS","doi":"10.1016/j.xkme.2026.101433","DOIUrl":"10.1016/j.xkme.2026.101433","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 8","pages":"Article 101433"},"PeriodicalIF":4.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13416659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620622","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}