Kidney Medicine最新文献

{"title":"Microscopic Tubulovenous Communications in Nonneoplastic Kidneys: A Single-Center Case Series and Review of the Literature","authors":"Cullen M. Lilley, Jonathan E. Zuckerman","doi":"10.1016/j.xkme.2025.101071","DOIUrl":"10.1016/j.xkme.2025.101071","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Pathological connection between the kidney tubules and veins is known as a microscopic tubulovenous communication we refer to as a tubulovenous fistula (TVF). This finding has been reported in a few small case reports, but no systematic examination of cases across various clinical settings detailing their histologic spectrum and associated clinical/pathologic findings has been performed.</div></div><div><h3>Study Design</h3><div>Case series and literature review.</div></div><div><h3>Setting & Participants</h3><div>Nonneoplastic kidney pathology reports from an academic medical center (February 1, 1990, to February 1, 2024) were queried for mention of TVF. In total, 30,537 nonneoplastic kidney reports were queried, and 22 cases of TVF were identified.</div></div><div><h3>Results</h3><div>In total, 72.7% of TVF cases were from native kidney biopsies. Median patient age was 66 (range, 25-84) with a male predominance (68.2%). Clinically, 82.4% had microscopic hematuria, and 17.6% had gross hematuria. TVFs were usually singular and involved arcuate size veins. Microscopically, 95.5% of cases had acute tubular injury, and 73.3% had at least focal pathologic intratubular casts/calcium crystals. In total, 56.3% of native cases had interstitial nephritis. Of the transplant cases (n<!--> <!-->=<!--> <!-->6), 66.7% exhibited rejection.</div></div><div><h3>Limitations</h3><div>Laboratory data, clinical follow-up, and original slides were not available in all cases examined. Although rare in our repository, TVFs are likely an under-reported finding. In addition, the focality of TVFs could play a role in their limited rate of detection.</div></div><div><h3>Conclusions</h3><div>This is the largest case series exploring the clinical and histologic features associated with TVFs in the kidney. Our findings support the assertion that TVFs are associated with hematuria without glomerulonephritis and occur in the setting of significant tubular injury, intratubular casts/crystals, and obstructive phenomena likely because of disruption of tubular basement membranes adjacent to veins.</div></div><div><h3>Plain Language Summary</h3><div>Our study explores a rare feature found in medical kidney biopsies called tubulovenous communications, in which small blood vessels connect with kidney tubules. These communications can sometimes be overlooked or not recognized because of their rarity. We reviewed a series of biopsies to identify and describe these communications and their associated findings in the kidney. By looking at these biopsies, we learned that these communications are more common when there is background kidney inflammation. Our findings highlight the importance of recognizing tubulovenous communications, which could potentially explain blood in the urine in patients with kidney inflammation but no damage to the glomerulus. Our findings also suggest that inflammation may be a mechanistic explanation for the formatio","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 9","pages":"Article 101071"},"PeriodicalIF":3.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Dialysis Medical Director Rotation for Nephrology Fellows: A Single Center’s 10-Year Experience","authors":"Harshil A. Fichadiya , Jing Miao , James R. Gregoire","doi":"10.1016/j.xkme.2025.101070","DOIUrl":"10.1016/j.xkme.2025.101070","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Many nephrology fellows will eventually become dialysis unit medical directors, yet few receive formal training on the responsibilities of this position. This study reports on our 10-year experience conducting a dedicated medical director rotation for nephrology fellows.</div></div><div><h3>Study Design</h3><div>An observational longitudinal study of a month-long medical director rotation designed to prepare nephrology fellows for leadership roles in dialysis facilities.</div></div><div><h3>Setting & Participants</h3><div>From 2014 to 2023, 36 nephrology fellows at the Mayo Clinic in Rochester, MN completed the rotation.</div></div><div><h3>Quality Improvement Activities</h3><div>Fellows were surveyed before and immediately after the rotation. Postgraduation surveys assessed the rotation’s effect on the fellows’ clinical practice.</div></div><div><h3>Outcomes</h3><div>The study evaluated how well the rotation improved fellows’ understanding of the medical director role, its influence on their clinical practice, and the importance of incorporating this training into fellowship programs.</div></div><div><h3>Analytic Approach</h3><div>Quantitative and qualitative survey responses from fellows before and after the rotation and postgraduation were analyzed.</div></div><div><h3>Results</h3><div>Before the rotation, only 5% of fellows had a strong understanding of the medical director’s role, increasing to 100% after completion. None felt well prepared for the role before rotation, whereas 81% reported feeling well prepared afterward. Among graduated fellows, nearly half served as a dialysis facility medical director, 70% found the rotation valuable to their practice, and 30% found it somewhat valuable. Additionally, 85% considered it very important to include a medical director rotation in fellowship training.</div></div><div><h3>Limitations</h3><div>Single-center study.</div></div><div><h3>Conclusions</h3><div>A structured medical director rotation within a general nephrology fellowship effectively prepares fellows for leadership roles in dialysis facilities and could serve as a model for other institutions.</div></div><div><h3>Plain Language Summary</h3><div>The increasing prevalence of patients with kidney failure has expanded the role of dialysis facility medical directors, yet many nephrology fellows receive little formal training for this leadership position. To address this gap, our fellowship program introduced a dedicated medical director rotation in 2014. We surveyed current and graduated fellows to assess the rotation’s effect. Results showed that participation significantly improved fellows’ understanding and preparedness for the role. Graduates found the rotation highly beneficial, though they identified areas for improvement, such as financial management training. Our study highlights the importance of a structured medical director education in nephrology fellowships, demonstrating that such","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 9","pages":"Article 101070"},"PeriodicalIF":3.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sarcoidosis Induced by Metal Particles From a Left Elbow Prosthesis","authors":"Daihi Sato ,&nbsp;Naoki Sawa ,&nbsp;Shusaku Matuoka ,&nbsp;Daisuke Ikuma ,&nbsp;Yuki Oba ,&nbsp;Hiroki Mizuno ,&nbsp;Akinari Sekine ,&nbsp;Masayuki Yamanouchi ,&nbsp;Eiko Hasegawa ,&nbsp;Tatsuya Suwabe ,&nbsp;Takehiko Wada ,&nbsp;Kei Kono ,&nbsp;Keiichi Kinowaki ,&nbsp;Kenichi Ohashi ,&nbsp;Tamiko Takemura ,&nbsp;Kei Takahashi ,&nbsp;Yoshifumi Ubara","doi":"10.1016/j.xkme.2025.101066","DOIUrl":"10.1016/j.xkme.2025.101066","url":null,"abstract":"<div><div>A 74-year-old woman with rheumatoid arthritis had developed severe pain in her left elbow 7 years previously and undergone joint replacement. Recently, the joint replacement surgery had to be repeated, and 3 months later, she was hospitalized because of rapid deterioration of kidney function, blurred vision, and eye pain. Levels of serum albumin-adjusted calcium (10.6<!--> <!-->mg/dL), serum 1,25-dihydroxyvitamin D₃ (115<!--> <!-->pg/mL), and lysozyme (27.5<!--> <!-->μg/mL) were elevated, and kidney function was impaired (serum creatinine, 2.48<!--> <!-->mg/dL). Biopsies of periarticular tissue and a left axillary lymph node revealed CD68-positive, non-caseating granulomatous tissue with multinucleated giant cells containing metal particles. In addition, kidney biopsy showed granulomatous tubulointerstitial nephritis with positive CD68 and 1α-hydroxylase staining. Sarcoidosis was diagnosed. We assumed that macrophages had phagocytosed metal particles generated by wear of the joint prosthesis, leading to formation of granulomas, which spread to the left axillary lymph nodes and then to the lung field and kidneys, where they caused acute granulomatous tubulointerstitial nephritis. Eventually, the granuloma cells acquired 1α-hydroxylase activity, resulting in 1,25-dihydroxyvitamin D₃ production and hypercalcemia, which caused acute kidney injury.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 9","pages":"Article 101066"},"PeriodicalIF":3.4,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renal Prognostic Identification in Patients With Autosomal Dominant Polycystic Kidney Disease by Whole Genome Sequencing: A Prospective, Observational Study","authors":"Hirayasu Kai ,&nbsp;Joichi Usui ,&nbsp;Eri Okada ,&nbsp;Ryota Ishii ,&nbsp;Taka-Aki Sato ,&nbsp;Takuro Tamura ,&nbsp;Hiroyuki Nishiyama ,&nbsp;Kunihiro Yamagata","doi":"10.1016/j.xkme.2025.101059","DOIUrl":"10.1016/j.xkme.2025.101059","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale &amp; Objective&lt;/h3&gt;&lt;div&gt;The association between autosomal dominant polycystic kidney disease (ADPKD) genetic variants and renal prognosis remains unclear. We conducted whole genome sequencing to identify the factors contributing to disease severity.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study Design&lt;/h3&gt;&lt;div&gt;Prospective, observational study.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Setting &amp; Population&lt;/h3&gt;&lt;div&gt;Using data collected from a 2-year prospective cohort of 200 patients with ADPKD, gene mutations were identified using whole genome sequencing.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Exposure&lt;/h3&gt;&lt;div&gt;None.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Outcomes&lt;/h3&gt;&lt;div&gt;The primary endpoint was the rate of increase in total kidney volume. The secondary endpoints were composite renal endpoints (induction of dialysis, kidney transplantation, or a decrease in the estimated glomerular filtration rate of&lt;!--&gt; &lt;!--&gt;≥25%).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Analytical Approach&lt;/h3&gt;&lt;div&gt;Logistic regression analyses were performed to determine the factors associated with the outcomes.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Among 169 patients for whom genetic diagnosis was performed, genetic mutations were identified in 144 cases, with 109 (75.7%) &lt;em&gt;PKD1&lt;/em&gt;, 34 (23.6%) &lt;em&gt;PKD2&lt;/em&gt;, and 1 (0.7%) &lt;em&gt;GANAB&lt;/em&gt; variants identified. The median annual increase in total kidney volume was 5.9%. Among the patients who were followed, 60 patients (33.5%) achieved the composite renal endpoint. The independent risk factors for reaching the renal composite endpoint were estimated glomerular filtration rate at enrollment (OR, 0.93; 95% CI, 0.91-0.96) and &lt;em&gt;PKD1&lt;/em&gt; truncation (OR, 3.05; 95% CI, 1.11-8.40). Hypertension and overweight exacerbated disease severity, particularly in patients with &lt;em&gt;PKD1&lt;/em&gt; truncation. The annual rate of kidney function deterioration was higher in the order of &lt;em&gt;PKD1&lt;/em&gt; truncating, &lt;em&gt;PKD1&lt;/em&gt; non-truncating, &lt;em&gt;PKD2&lt;/em&gt; truncating, and &lt;em&gt;PKD2&lt;/em&gt; non-truncating variants. The rate of Mayo imaging classification 1C-1E was highest in the same order.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitations&lt;/h3&gt;&lt;div&gt;Owing to the various &lt;em&gt;PKD&lt;/em&gt; variants, the sample size for each variant was insufficient for comprehensive evaluation of kidney function.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;&lt;em&gt;PKD1&lt;/em&gt; truncation is a sensitive severity marker in patients with ADPKD, and &lt;em&gt;PKD2&lt;/em&gt; non-truncation is the least severe. Genetic diagnosis is useful for predicting renal prognosis.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain-Language Summary&lt;/h3&gt;&lt;div&gt;This prospective study included 200 patients with autosomal dominant polycystic kidney disease (ADPKD), with the objectives of the following: (1) ascertaining the feasibility of conducting comprehensive ADPKD genetic diagnosis using whole genome sequencing with next-generation sequencing, and (2) identifying factors associated with renal prognosis and disease severity. This study showed that differences in genotype influence the rate of kidney function deterioration and disease se","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 9","pages":"Article 101059"},"PeriodicalIF":3.4,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of Genetically Predicted CKD With Urinary Tract Cancer and Lung Cancer: A Mendelian Randomization Analysis","authors":"Li Luo ,&nbsp;Ron T. Gansevoort ,&nbsp;Lyanne M. Kieneker ,&nbsp;Rudolf A. de Boer ,&nbsp;Zekai Chen ,&nbsp;Joseph Pierre Aboumsallem ,&nbsp;Harold Snieder ,&nbsp;Chris H.L. Thio","doi":"10.1016/j.xkme.2025.101065","DOIUrl":"10.1016/j.xkme.2025.101065","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale &amp; Objective&lt;/h3&gt;&lt;div&gt;Chronic kidney disease (CKD) is reported to be associated with cancer, especially for urinary tract and lung cancer. However, whether this suggests causality has not been resolved. This study aimed to investigate the causal relation of CKD to overall, urinary tract, and lung cancer.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study Design&lt;/h3&gt;&lt;div&gt;Mendelian randomization (MR) analysis.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Setting &amp; Participants&lt;/h3&gt;&lt;div&gt;Single-nucleotide polymorphism (SNP)-CKD data were obtained from genome-wide association studies of a meta-analysis of CKDGen and UK Biobank. SNP-cancer data from genome-wide association studies of several community-based and cancer-specific consortia were extracted and then meta-analyzed.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Exposures&lt;/h3&gt;&lt;div&gt;Impaired kidney function (creatinine-based estimated glomerular filtration rate [eGFRcr]&lt;!--&gt; &lt;!--&gt;&lt;60&lt;!--&gt; &lt;!--&gt;mL/min/1.73&lt;!--&gt; &lt;!--&gt;m&lt;sup&gt;2&lt;/sup&gt;), increased albuminuria (urinary albumin-creatinine ratio [UACR]&lt;!--&gt; &lt;!--&gt;&gt;30&lt;!--&gt; &lt;!--&gt;mg/g), and on a continuous scale, eGFRcr, cystatin C-based eGFR (eGFRcys), and UACR.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Outcomes&lt;/h3&gt;&lt;div&gt;Incidences of overall cancer, urinary tract cancer, and lung cancer.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Analytical Approach&lt;/h3&gt;&lt;div&gt;Pooled MR estimates of single-SNP Wald ratios were obtained using an inverse variance-weighted method.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;In inverse variance-weighted MR analyses, a higher genetic liability to impaired kidney function was not significantly associated with higher overall cancer risk (OR, 1.00; 95% CI, 1.00-1.01; &lt;em&gt;P&lt;/em&gt;&lt;sub&gt;OR&lt;/sub&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;0.06). No associations of other kidney phenotypes including increased albuminuria, eGFRcr, eGFRcys, and UACR with overall cancer risk were found at the Bonferroni-corrected significance level (all &lt;em&gt;P&lt;/em&gt;&lt;sub&gt;OR&lt;/sub&gt; &lt;!--&gt;&gt;&lt;!--&gt; &lt;!--&gt;0.0025). Similarly, risk estimates of generally null were detected in the associations of all these CKD phenotypes with specifically urinary tract and lung cancer (all &lt;em&gt;P&lt;/em&gt;&lt;sub&gt;OR&lt;/sub&gt; &lt;!--&gt;&gt;&lt;!--&gt; &lt;!--&gt;0.0025). The results of our sensitivity analyses, including pleiotropy-robust MR, reverse MR, and multivariable MR analyses, corroborated the results of our main analyses.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitations&lt;/h3&gt;&lt;div&gt;Uncertain extrapolation to other ethnicities.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Genetically predicted CKD is not associated with the risk of incident overall, urinary tract, and lung cancer. Our findings thus provide no genetic evidence for a causal relationship between CKD and cancer.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain-Language Summary&lt;/h3&gt;&lt;div&gt;Despite growing evidence for an association between chronic kidney disease (CKD) and cancer, causality remains unresolved because of the confounding bias inherent to observational studies. To test causality, we applied Mendelian randomization, which uses genetic variants to minimize confounding. We genetically predicted 5 CKD traits ","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 9","pages":"Article 101065"},"PeriodicalIF":3.4,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Humoral Immune Responses in Dialysis Patients After mRNA Omicron JN.1 Vaccination","authors":"Metodi V. Stankov PhD ,&nbsp;Markus Hoffmann PhD ,&nbsp;Christine Happle MD ,&nbsp;Karsten Lürken MD ,&nbsp;Amy Kempf ,&nbsp;Inga Nehlmeier ,&nbsp;Andrea Stölting ,&nbsp;Stefan Pöhlmann PhD ,&nbsp;Alexandra Dopfer-Jablonka MD ,&nbsp;Georg M.N. Behrens MD","doi":"10.1016/j.xkme.2025.101067","DOIUrl":"10.1016/j.xkme.2025.101067","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 9","pages":"Article 101067"},"PeriodicalIF":3.4,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144895402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary Ewing Sarcoma Within an Autosomal Dominant Polycystic Kidney: A Case Report","authors":"Shengliang He ,&nbsp;Jonathan Davick ,&nbsp;Prerna Rastogi ,&nbsp;Sarat Kuppachi","doi":"10.1016/j.xkme.2025.101064","DOIUrl":"10.1016/j.xkme.2025.101064","url":null,"abstract":"<div><div>Ewing sarcoma, that originates from neuroectoderm, is typically encountered in the bone and soft tissue of children and young adults and rarely presents as a primary renal tumor. Autosomal dominant polycystic kidney disease, which is the most common type of inherited kidney disease, has been debated to be associated with an increased risk of kidney cancer. This report describes the first documented case of primary Ewing sarcoma arising within an autosomal dominant polycystic kidney. A 44-year-old male with end-stage kidney disease secondary to autosomal dominant polycystic kidney disease presented with left flank pain. Imaging revealed a 14<!--> <!-->cm heterogeneous mass in the lower pole of the polycystic left kidney. The patient underwent laparoscopic left nephrectomy, and pathology examination confirmed the diagnosis of primary Ewing sarcoma. He received 12 cycles of adjuvant chemotherapy, including vincristine, dactinomycin, and cyclophosphamide. Despite treatment, disease relapse occurred 13 months after the initial diagnosis, and the patient died 3 months later. Primary Ewing sarcoma of the kidney is a rare malignancy with nonspecific clinical and imaging features. It is associated with a poor prognosis due to delayed diagnosis, high metastatic potential, and frequent recurrence.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 9","pages":"Article 101064"},"PeriodicalIF":3.4,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations Between Lymphopenia and the Development/Recovery of Acute Kidney Injury Among Patients Hospitalized With Respiratory Virus Infections","authors":"Guohui Fan ,&nbsp;Xin Liu ,&nbsp;Feiya Xu ,&nbsp;Xiaomeng Zhang ,&nbsp;Chaozeng Si ,&nbsp;Tingyu Yin ,&nbsp;Yanshuang Lyu ,&nbsp;Jing Ma ,&nbsp;Bing Liu ,&nbsp;Weizhong Yang ,&nbsp;Cunbo Jia ,&nbsp;Dingyi Wang","doi":"10.1016/j.xkme.2025.101063","DOIUrl":"10.1016/j.xkme.2025.101063","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale &amp; Objective&lt;/h3&gt;&lt;div&gt;Lymphopenia may have a potential mechanism on the development of acute kidney injury (AKI) after respiratory virus infection but has never been revealed. We aimed to investigate the relationship between lymphopenia and AKI in patients hospitalized with respiratory virus infections.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study &amp; Design&lt;/h3&gt;&lt;div&gt;A single-center and retrospective cohort study.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Setting &amp; Participants&lt;/h3&gt;&lt;div&gt;Data were retrospectively collected from electronic medical records of patients hospitalized with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), influenza, or other respiratory virus infections from 2016- 2023.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Exposure&lt;/h3&gt;&lt;div&gt;Prolonged lymphopenia (&lt;1.1 ×&lt;!--&gt; &lt;!--&gt;10&lt;sup&gt;9&lt;/sup&gt;/L) was defined as continuous lymphopenia lasting for&lt;!--&gt; &lt;!--&gt;≥1&lt;!--&gt; &lt;!--&gt;day before AKI diagnosis. Serial measurements of serum creatinine levels and lymphocyte counts before AKI were collected.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Outcomes&lt;/h3&gt;&lt;div&gt;AKI developed after infection was identified according to the KDIGO guideline.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Analytical Approach&lt;/h3&gt;&lt;div&gt;Multivariable logistic regression models and Cox proportional regression models were conducted to evaluate associations between lymphopenia or blood count ratios and AKI.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;A total of 3,104 patients were analyzed, including 1,945 infected with SARS-CoV-2, 597 with influenza, and 472 with other respiratory virus infections. The AKI incidences were 18.0%, 23.3%, and 16.3%, respectively. Serum creatinine level was significantly negatively correlated with lymphocyte count in SARS-CoV-2 and influenza infections. Multivariable regression showed lymphopenia, especially prolonged lymphopenia, was significantly associated with AKI in all virus groups, especially in influenza. The risk magnitudes of monocyte-to-lymphocyte ratio, neutrophil-to-lymphocyte ratio, and platelet-to-lymphocyte ratio on admission for AKI varied by different viral infections. Lymphopenia or not was not associated with AKI stages or AKI recovery.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitations&lt;/h3&gt;&lt;div&gt;The results were limited by the retrospective, single-center setting and the probability of underestimation of the prevalence of both lymphopenia and AKI.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;Lymphopenia, especially prolonged lymphopenia, and neutrophil-to-lymphocyte ratio on admission were risk factors for AKI after respiratory virus infection, with the highest risk observed in patients with influenza.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain-Language Summary&lt;/h3&gt;&lt;div&gt;Lymphopenia may play a role in acute kidney injury (AKI) after respiratory virus infections, but this link has not been well studied. Our research explored the relationship between lymphopenia and AKI in hospitalized patients with COVID-19, influenza, and other respiratory viruses. By reviewing medical records from 2016-2023, we found that prolonged lymphopenia was sign","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 9","pages":"Article 101063"},"PeriodicalIF":3.4,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"APOL1 Mediated Kidney Disease: A Review and Look Toward the Future","authors":"Vinay Srinivasan ,&nbsp;Paolo Nikolai So ,&nbsp;Edward P.K. Kwakyi ,&nbsp;Edgar V. Lerma ,&nbsp;Nasim Wiegley","doi":"10.1016/j.xkme.2025.101062","DOIUrl":"10.1016/j.xkme.2025.101062","url":null,"abstract":"<div><div>Individuals of recent African ancestry are disproportionately affected by kidney disease. The discovery of the Apolipoprotein L1 (<em>APOL1)</em> gene and, subsequently, the G1 and G2 risk alleles has helped to understand some of these disparities. The <em>APOL1</em> gene does not appear to be necessary for normal kidney function, and the high-risk alleles appear to be gain of function mutations offering protection against <em>Trypanosoma</em> species. In the United States, ∼6 million African Americans have a high-risk genotype. However, not all patients with high-risk genotypes will develop kidney disease, leading to the idea of a second hit hypothesis by certain genetic, environmental, and inflammatory triggers. Recent clinical trials have focused on the different postulated mechanisms of cellular toxicity, and one promising candidate, inaxaplin, has advanced to a phase 3 study. This mini-review discusses the development of <em>APOL1</em> risk alleles, clinical implications of a high-risk genotype, and a suggested framework for nephrologists to pursue genetic testing in countries where it is easily accessible.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 9","pages":"Article 101062"},"PeriodicalIF":3.4,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Plasma KIM-1, TNFR-1, and TNFR-2 With Cardiovascular Outcomes and All-Cause Mortality in Individuals With Chronic Kidney Disease: An Ancillary Analysis of SPRINT","authors":"Nicholas Wettersten ,&nbsp;Ronit Katz ,&nbsp;Simon B. Ascher ,&nbsp;Rebecca Scherzer ,&nbsp;Alexander L. Bullen ,&nbsp;Teresa K. Chen ,&nbsp;Kasey Campos ,&nbsp;Pranav S. Garimella ,&nbsp;Michelle M. Estrella ,&nbsp;Michael G. Shlipak ,&nbsp;Joachim H. Ix","doi":"10.1016/j.xkme.2025.101024","DOIUrl":"10.1016/j.xkme.2025.101024","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Rationale &amp; Objective&lt;/h3&gt;&lt;div&gt;Among individuals with chronic kidney disease (CKD), higher blood levels of kidney injury molecule-1 (KIM-1) and soluble tumor necrosis factor receptors (TNFR-1 and TNFR-2) have been associated with greater risk of CKD progression. Their associations with risk of cardiovascular disease (CVD) and all-cause mortality in individuals with CKD remain uncertain.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Study Design&lt;/h3&gt;&lt;div&gt;An observational cohort study.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Setting &amp; Participants&lt;/h3&gt;&lt;div&gt;Systolic Blood Pressure Intervention Trial participants with hypertension and CKD (eGFR&lt;!--&gt; &lt;!--&gt;&lt;60&lt;!--&gt; &lt;!--&gt;mL/min/1.73&lt;!--&gt; &lt;!--&gt;m&lt;sup&gt;2&lt;/sup&gt;) but without diabetes.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Predictors&lt;/h3&gt;&lt;div&gt;Plasma KIM-1, TNFR-1, and TNFR-2.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Outcomes&lt;/h3&gt;&lt;div&gt;A composite CVD outcome (acute coronary syndrome/myocardial infarction, stroke, heart failure, and CVD death) and all-cause mortality.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Analytic Approach&lt;/h3&gt;&lt;div&gt;Cox proportional hazards models, adjusting for CVD risk factors, eGFR, and urine albumin-to-creatinine ratio.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Total of 2,350 participants with a mean age of 73&lt;!--&gt; &lt;!--&gt;±&lt;!--&gt; &lt;!--&gt;9 years, eGFR of 46&lt;!--&gt; &lt;!--&gt;±&lt;!--&gt; &lt;!--&gt;10&lt;!--&gt; &lt;!--&gt;mL/min/1.73m&lt;sup&gt;2&lt;/sup&gt; and 25% prevalence of CVD. Over more than 3 years follow-up, 293 CVD events (12%) and 160 deaths (7%) occurred. Higher KIM-1, TNFR-1, and TNFR-2 were associated with higher risk of the composite CVD outcome after adjusting for CVD risk factors, but associations were no longer significant after adjusting for eGFR and urine albumin-to-creatinine ratio (KIM-1: HR&lt;!--&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;1.13, 95% CI, 0.99-1.30; TNFR-1: HR&lt;!--&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;1.03, 95% CI, 0.72-1.46; TNFR-2: HR&lt;!--&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;0.98, 95% CI, 0.76-1.26). In contrast, in fully adjusted models, higher plasma KIM-1 and TNFR-1, but not TNFR-2, were associated with higher risk of all-cause mortality (KIM-1: HR&lt;!--&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;1.23, 95% CI, 1.01-1.49; TNFR-1: HR&lt;!--&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;2.09, 95% CI, 1.14-3.83; TNFR-2: HR&lt;!--&gt; &lt;!--&gt;=&lt;!--&gt; &lt;!--&gt;1.19, 95% CI, 0.85-1.66).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Limitations&lt;/h3&gt;&lt;div&gt;No individuals with diabetes or stroke.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;In individuals with hypertension and nondiabetic CKD, associations of higher plasma KIM-1, TNFR-1, and TNFR-2 concentrations with CVD events were not independent of eGFR and albuminuria, whereas higher levels of plasma KIM-1 and TNFR-1 were independently associated with greater risk of all-cause mortality.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Plain-Language Summary&lt;/h3&gt;&lt;div&gt;Blood levels of kidney injury molecule-1 (KIM-1) and soluble tumor necrosis factor receptors (TNFR-1 and TNFR-2) have been associated with progression of kidney disease. We evaluated if these biomarkers were associated with risk of cardiovascular events and all-cause mortality in individuals without diabetes with hypertension and chronic kidney disease from the Systolic B","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"7 7","pages":"Article 101024"},"PeriodicalIF":3.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144571339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}