Kidney Medicine最新文献

{"title":"Kidney Function and Incident Stroke and Dementia Using an Updated Estimated Glomerular Filtration Rate Equation Without Race: The Multi-Ethnic Study of Atherosclerosis","authors":"Samuel R. Moen , Jeffrey R. Misialek , Timothy M. Hughes , Craig W. Johnson , Mark J. Sarnak , Sarah N. Forrester , W.T. Longstreth Jr. , Mercedes R. Carnethon , James S. Pankow , Sanaz Sedaghat","doi":"10.1016/j.xkme.2024.100961","DOIUrl":"10.1016/j.xkme.2024.100961","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Equations for estimated glomerular filtration rate (eGFR) have previously included a coefficient for African American race. We evaluated and compared risk of incident stroke and dementia between old and new equations of eGFR for African American and non-African American participants.</div></div><div><h3>Study Design</h3><div>Prospective observational study.</div></div><div><h3>Setting & Participants</h3><div>Baseline values were collected from 6,814 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) cohort between 2000 and 2002. Participants were followed up until 2018. The analytic sample consisted of 6,646 participants (mean [SD] age 62 [10] years; 53% female; 39% White, 27% African American, 12% Chinese American, and 22% Hispanic/Latino).</div></div><div><h3>Exposure</h3><div>eGFR equation from 2021 based on serum creatinine and cystatin C levels without race.</div></div><div><h3>Outcome</h3><div>Incident stroke and dementia.</div></div><div><h3>Analytical Approach</h3><div>Cox proportional regression adjusting for demographic, lifestyle, and clinical variables was performed to estimate associations between different eGFR measures and risk of incident stroke and dementia.</div></div><div><h3>Results</h3><div>During a median follow-up period of 17 years, 349 (5.3%) participants experienced an incident stroke event, and 574 (8.6%) participants experienced incident dementia. In the fully adjusted model, overall participants with eGFR<!--> <!--><60 compared with those<!--> <!-->>90<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup> were at significantly increased risk of dementia (HR, 95% CI: 1.73, 1.21-2.45). A lower eGFR was not significantly associated with incident stroke (1.30, 0.75-2.24). African American participants tended to be reclassified to a lower group of eGFR in the new equations, whereas non-African American participants were reclassified to a higher group of eGFR. When comparing older versus newer equations of eGFR in African American and non-African American participants in association with incident stroke and dementia, differences were minimal.</div></div><div><h3>Limitations</h3><div>Incident dementia was ascertained through International Classification of Diseases (Ninth and Tenth Revisions) codes.</div></div><div><h3>Conclusions</h3><div>Our findings illustrate participants with 2021 eGFR<!--> <!--><<!--> <!-->60 compared with those with eGFR<!--> <!-->><!--> <!-->90<!--> <!-->mL/min/1.73<!--> <!-->m<sup>2</sup> have higher risk of dementia in both African American and non-African American participants, but not of stroke.</div></div><div><h3>Plain Language Summary</h3><div>Existing research has established that declined kidney function is associated with stroke and dementia. Kidney function is commonly estimated using inputs of blood proteins alongside demographic inputs of age, sex at birth, and race. Inclusion of race to estimate kidney function has gained","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100961"},"PeriodicalIF":3.2,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143268329","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":"Sepsis-Associated Acute Kidney Disease Incidence, Trajectory, and Outcomes","authors":"Hsiu-Yin Chiang , Chih-Chia Liang , Ya-Luan Hsiao , Uyen-Minh Le , Yi-Ching Chang , Pei-Shan Chen , David Ray Chang , I-Wen Ting , Hung-Chieh Yeh , Chin-Chi Kuo","doi":"10.1016/j.xkme.2024.100959","DOIUrl":"10.1016/j.xkme.2024.100959","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Systematic evaluation of the prognosis from sepsis-associated acute kidney disease (SA-AKD) using real-world data is limited. This study aimed to use data algorithms on the electronic health records to trace the SA-AKD trajectory from acute kidney injury (AKI) to chronic kidney disease (CKD).</div></div><div><h3>Study Design</h3><div>A retrospective cohort study.</div></div><div><h3>Setting & Participants</h3><div>Adult inpatients with first sepsis episode surviving 90 days after AKD in a quaternary referral medical center.</div></div><div><h3>Exposure</h3><div>We defined SA-AKD as having sustained ≥1.5-fold increased serum creatinine levels or initiating kidney replacement therapy after the SA-AKI, and we classified SA-AKD into recovery, relapse, and persistent SA-AKD subgroups.</div></div><div><h3>Outcomes</h3><div>All-cause mortality, kidney replacement therapy (KRT), <em>de novo</em> nondialysis dependent CKD (CKD-ND), and late-recovery AKD during 1-year follow-up.</div></div><div><h3>Analytical Approach</h3><div>A multivariable Cox proportional hazards models.</div></div><div><h3>Results</h3><div>Of 24,038 eligible inpatients with sepsis, 42.2% had SA-AKI, and 17.6% progressed to SA-AKD (43.6% recovery, 8.3% relapse, 32.2% persistent, and 15.9% unclassified). Compared with the recovery subgroup, the 1-year mortality risk for the relapse, persistent, and unclassified SA-AKD subgroups were 1.57 (adjusted hazard ratios [aHRs]; 95% CI, 1.22-2.01), 1.36 (1.13-1.63), and 0.65 (0.48-0.89), respectively. Risks of KRT initiation were 3.27 (2.14-4.98), 6.01 (4.41-8.19), and 0.98 (0.55-1.74), respectively, and corresponding aHRs for <em>de novo</em> CKD-ND were 3.84 (2.82-5.22), 3.35 (2.61-4.29), and 0.48 (0.30-0.77), respectively. Patients with relapse SA-AKD had a higher likelihood of late recovery (aHR, 3.62; 95% CI, 2.52-5.21) than the persistent SA-AKD.</div></div><div><h3>Limitations</h3><div>Selection bias and information bias could be present because of limiting population to sepsis survivors and because of no standardized follow-up protocol for kidney function.</div></div><div><h3>Conclusions</h3><div>SA-AKD without recovery is associated with increased and long-term risks of KRT initiation, mortality, and increased risk of <em>de novo</em> CKD-ND for patients initially free of CKD. Further studies are warranted for managing AKI to AKD to CKD in real-world settings.</div></div><div><h3>Plain Language Summary</h3><div>Systematic evaluation of the prognosis for sepsis-associated acute kidney injury (AKI) and sepsis-associated acute kidney disease (AKD) using real-world data remain limited. We applied standard definitions of sepsis and AKI/AKD and comprehensively profiled the AKI-AKD-chronic kidney disease (CKD) trajectory among sepsis survivors in a large, longitudinal hospital-based cohort. Our study showed that sepsis-associated AKD without recovery is associated with elevated and long-term risks","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100959"},"PeriodicalIF":3.2,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143131167","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":"High-Frequency Vessel Wall Vibrations Associate With Stenosis Formation and Arteriovenous Fistula Failure","authors":"Luca Soliveri MS , Sofia Poloni MS , Paolo Brambilla MD , Anna Caroli PhD , Andrea Remuzzi EngD , Michela Bozzetto PhD , Kristian Valen-Sendstad PhD","doi":"10.1016/j.xkme.2024.100957","DOIUrl":"10.1016/j.xkme.2024.100957","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100957"},"PeriodicalIF":3.2,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143349145","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 Serum Amphiregulin Levels With Kidney Failure and Mortality: The Chronic Renal Insufficiency Cohort (CRIC)","authors":"Insa M. Schmidt MD, MPH , Eirini Kefalogianni PhD , Runqi Zhao MS , Ashish Verma MD , Venkata Sabbisetti PhD , Mahboob Rahman MD , Nishigandha Pradhan MD , Anand Srivastava MD, MPH , Jiang He MD, PhD , Jing Chen MD, MSc , Sushrut S. Waikar MD, MPH , Andreas Herrlich MD, PhD","doi":"10.1016/j.xkme.2024.100958","DOIUrl":"10.1016/j.xkme.2024.100958","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100958"},"PeriodicalIF":3.2,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143471246","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":"INVS Mutation-Related NPHP2 Nephronophthisis With Glomerulocystic Disease: A Case Report","authors":"Yuichiro Sawada ,&nbsp;Akinari Sekine ,&nbsp;Yuki Oba ,&nbsp;Masayuki Yamanouchi ,&nbsp;Tatsuya Suwabe ,&nbsp;Kei Kono ,&nbsp;Keiichi Kinowaki ,&nbsp;Kenichi Ohashi ,&nbsp;Yutaka Yamaguchi ,&nbsp;Takuya Fujimaru ,&nbsp;Takayasu Mori ,&nbsp;Eisei Sohara ,&nbsp;Shinichi Uchida ,&nbsp;Takehiko Wada ,&nbsp;Naoki Sawa ,&nbsp;Yoshifumi Ubara","doi":"10.1016/j.xkme.2024.100956","DOIUrl":"10.1016/j.xkme.2024.100956","url":null,"abstract":"<div><div>We examined a 68-year-old woman with decreased renal function (serum creatinine level of 1.77<!--> <!-->mg/dL) and polycystic kidney disease. Magnetic resonance imaging revealed multiple bilateral renal cysts with uniform low intensity on T1-weighted images and uniform high intensity on T2-weighted ones but no mixed intensity cysts. Kidney biopsy findings included collapsed glomerular structures within dilated cyst-like structures. Glomerulocystic disease was diagnosed. Genetic analysis revealed 2 different INVS (nephronophthisis 2 [NPHP2]) compound heterozygous missense mutations. The NPHP2 is usually found in infants, and to our knowledge, this is the first report of an older patient with NPHP2.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 4","pages":"Article 100956"},"PeriodicalIF":3.2,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143637646","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":"Metabolomics to Identify Unclassified Uremic Toxins: A Comprehensive Literature Review","authors":"Raymond Vanholder ,&nbsp;Griet Glorieux ,&nbsp;Angel Argiles ,&nbsp;Stéphane Burtey ,&nbsp;Gerald Cohen ,&nbsp;Flore Duranton ,&nbsp;Laetitia Koppe ,&nbsp;Ziad A. Massy ,&nbsp;Alberto Ortiz ,&nbsp;Rosalinde Masereeuw ,&nbsp;Dimitrios Stamatialis ,&nbsp;Joachim Jankowski ,&nbsp;European Uremic Toxins Work Group (EUTox)","doi":"10.1016/j.xkme.2024.100955","DOIUrl":"10.1016/j.xkme.2024.100955","url":null,"abstract":"<div><div>A comprehensive review of known uremic retention molecules goes back to more than 10 years ago and did not consider metabolomic analyses. The present analysis searches for as of yet unclassified solutes retained in chronic kidney disease (CKD) by analyzing metabolites associated with relevant outcomes of CKD. This untargeted metabolomics-based approach is compared with a conventional targeted literature search. For the selected molecules, the literature was screened for arguments regarding toxic (harmful), beneficial, or neutral effects in experimental or clinical studies. Findings were independently crosschecked. In total, 103 molecules were selected. No literature on any effect was found for 55 substances, 3 molecules had no significant effect, and 13 others showed beneficial effects. For the remaining 32 compounds, we found at least one report of a toxic effect. Whereas 62.5% of the compounds with at least one study on a toxic effect was retrieved via the bottom-up approach, 69.2% of the substances originating from metabolomics-based approaches showed a beneficial effect. Our results suggest that untargeted metabolomics offer a more balanced view of uremic retention than the targeted approaches, with higher chances of revealing the beneficial potential of some of the metabolites.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100955"},"PeriodicalIF":3.2,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143131168","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":"High-Density Lipoprotein Lipidomics, Endothelial Dysfunction, and Fistula Maturation in Patients With Advanced Chronic Kidney Disease","authors":"Benjamin Lidgard MD ,&nbsp;Andrew N. Hoofnagle MD, PhD ,&nbsp;Leila R. Zelnick PhD ,&nbsp;Ian H. de Boer MD ,&nbsp;Amanda M. Fretts PhD ,&nbsp;Bryan R. Kestenbaum MD ,&nbsp;Rozenn N. Lemaitre PhD ,&nbsp;Cassianne Robinson-Cohen PhD ,&nbsp;Nisha Bansal MD","doi":"10.1016/j.xkme.2024.100954","DOIUrl":"10.1016/j.xkme.2024.100954","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100954"},"PeriodicalIF":3.2,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143131344","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":"Hyponatremia Correction and Osmotic Demyelination Syndrome Risk: A Systematic Review and Meta-Analysis","authors":"Supawadee Suppadungsuk ,&nbsp;Pajaree Krisanapan ,&nbsp;Sara Kazeminia ,&nbsp;Nasrin Nikravangolsefid ,&nbsp;Waryaam Singh ,&nbsp;Larry J. Prokop ,&nbsp;Kianoush B. Kashani ,&nbsp;Juan Pablo Domecq Garces","doi":"10.1016/j.xkme.2024.100953","DOIUrl":"10.1016/j.xkme.2024.100953","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale &amp; Objective&lt;/h3&gt;&lt;div&gt;Osmotic demyelination syndrome (ODS) is a rare but severe condition often attributed to the rate of sodium collection. We evaluated the association between the overly rapid sodium correction in adult hospitalized patients with ODS.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study Design&lt;/h3&gt;&lt;div&gt;Systematic review and meta-analysis.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Setting &amp; Study Populations&lt;/h3&gt;&lt;div&gt;Adults hospitalized hyponatremia patients.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Selection Criteria for Studies&lt;/h3&gt;&lt;div&gt;The studies comparing the incidence of ODS with and without rapid sodium correction inception to January 2024.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Data Extraction&lt;/h3&gt;&lt;div&gt;Two reviewers independently extracted data and assessed the risk of bias and the certainty of evidence.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Analytic Approach&lt;/h3&gt;&lt;div&gt;The incidence of ODS following a rapid and nonrapid sodium correction was pooled using the random effects model. Subgroup and meta-regression analyses were performed for the robustness and the source of heterogeneity.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Eleven cohort studies were included with 26,710 hospitalized hyponatremia patients. The definition of hyponatremia varied from&lt;!--&gt; &lt;!--&gt;&lt;116 to&lt;!--&gt; &lt;!--&gt;&lt;130&lt;!--&gt; &lt;!--&gt;mmol/L, and overly rapid sodium correction was defined as&lt;!--&gt; &lt;!--&gt;&gt;8 to 12&lt;!--&gt; &lt;!--&gt;mmol/L within 24 hours. The overall incidence of ODS was 0.23%. The incidence of ODS in rapid and nonrapid sodium correction was 0.73% and 0.10%, respectively. Meta-analysis demonstrated that a rapid rate of sodium correction was associated with a higher incidence of ODS (odds ratio 3.16, 95% CI, 1.54-6.49, I&lt;sup&gt;2&lt;/sup&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;27%), whereas some patients with hyponatremia developed ODS without rapid sodium level correction. The sensitivity analysis based on the quality of the studies was consistent with the main result.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitation&lt;/h3&gt;&lt;div&gt;Various definition criteria for ODS diagnosis across studies, lack of potential electrolyte and treatment data that may affect the incidence of ODS.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;The rapid rate of sodium correction had a statistical correlation with a higher incidence of ODS. Among ODS without rapid correction, further studies are recommended to evaluate and comprehend the relationship for better and proper management of hospitalized patients with hyponatremia.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain Language Summary&lt;/h3&gt;&lt;div&gt;Hyponatremia is a common electrolyte disorder that is essential to treat symptoms to prevent further neurologic complications, even from hyponatremia itself or following treatment. This meta-analysis evaluated the association between sodium correction rate and osmotic demyelination syndrome (ODS). The finding demonstrated that rapid correlation&lt;!--&gt; &lt;!--&gt;&gt;8&lt;!--&gt; &lt;!--&gt;mmol/L/24&lt;!--&gt; &lt;!--&gt;h had a statistical correlation with a higher risk of ODS. Rapid sodium correction occurred in 21.5% of patients with hyponatremia. The overall incidence ","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100953"},"PeriodicalIF":3.2,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143131298","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":"Utility of Activated Partial Thromboplastin Time Screening in Prospective Living Kidney Donors: A Single Center Cohort Study","authors":"Lucy S. Wang BA ,&nbsp;Emily Ertmann BS ,&nbsp;Eli Feldman BA ,&nbsp;Meredith Kossoff BS ,&nbsp;Brian Lu BS ,&nbsp;John C. Lin BS, AB ,&nbsp;Allyson Pishko MD, MSCE ,&nbsp;Robert Redfield MD ,&nbsp;Amanda Leonberg-Yoo MD ,&nbsp;Adam Cuker MD, MS","doi":"10.1016/j.xkme.2024.100951","DOIUrl":"10.1016/j.xkme.2024.100951","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100951"},"PeriodicalIF":3.2,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143131345","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":"Is Amanita phalloides Nephrotoxicity due to Mitochondrial Toxicity?","authors":"Jules Weinhard ,&nbsp;Justine Serre ,&nbsp;Perrine Frère ,&nbsp;Clovis Adam ,&nbsp;Marie Camille Lafargue ,&nbsp;David Buob ,&nbsp;Cédric Rafat","doi":"10.1016/j.xkme.2024.100952","DOIUrl":"10.1016/j.xkme.2024.100952","url":null,"abstract":"<div><div><em>Amanita phalloides</em>-related kidney toxicity is poorly documented and remains to be elucidated. Herein, we describe the case of a 43-year old patient who presented with severe liver failure following the ingestion of <em>Amanita phalloides</em>. Although liver injury subsided following the administration of N-acetyl cystein and silibinin, the patient subsequently developed KDIGO stage 3 acute kidney injury. Histopathological examination of the kidney displayed moderate tubular injury characterized by dilated tubular lumens and flattening of the tubular epithelium on optic microscopy. Electron microscopy showed mitochondrial changes including swelling and decreased number of cristae. Immunofluorescence for the key mitochondrial protein TOM20 found significantly decreased expression compared with ischemic acute tubular injury. Despite these changes, histoenzymology showed preserved succinate cytochrome c oxidase (COX) expression, suggesting that mitochondrial complex IV function was maintained. Our findings suggest that <em>Amanita phalloides</em> elicits acute tubular injury via mitochondrial damage, possibly through a pathway that spares COX function.</div></div><div><h3>Plain-Language Summary</h3><div>Kidney damage caused by Amanita phalloides (death cap mushroom) is not well understood. We report the case of a 43-year-old patient who experienced severe liver failure after eating this mushroom. While treatment with N-acetyl cysteine and silibinin improved the liver damage, the patient later developed severe kidney injury. Tests on the kidney showed damage to its tubules inside, with changes in their structure under a microscope. Closer examination revealed that the energy-producing parts of the cells, called mitochondria, were swollen and had fewer folds (cristae), which are essential for energy production. However, one key mitochondrial function, involving an enzyme called complex IV, appeared to be unaffected.This case suggests that the death cap mushroom may harm kidneys by damaging mitochondria in a way that leaves certain functions intact.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 3","pages":"Article 100952"},"PeriodicalIF":3.2,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143131175","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}