American Journal of Kidney Diseases最新文献

{"title":"Sex and the Relationship Between Cardiometabolic Risk Factors and Estimated GFR Decline: A Population-Based Cohort Study.","authors":"Michael K Sullivan, Jennifer S Lees, Brenda M Rosales, Rachel Cutting, Melanie L Wyld, Mark Woodward, Angela C Webster, Patrick B Mark, Nicole De La Mata","doi":"10.1053/j.ajkd.2024.05.007","DOIUrl":"10.1053/j.ajkd.2024.05.007","url":null,"abstract":"<p><strong>Rationale & objective: </strong>Females have a higher prevalence of chronic kidney disease (CKD) than males but are less likely to be treated with kidney replacement therapy (KRT). We studied the interaction between sex and the association of cardiometabolic risk factors for the decline in kidney function over time.</p><p><strong>Study design: </strong>A population-based cohort study.</p><p><strong>Setting & participants: </strong>1,127,731 adults living in Wales, United Kingdom, within the Secure Anonymised Information Linkage Databank.</p><p><strong>Exposure: </strong>Sex and risk factors including age, estimated glomerular filtration rate (eGFR), cardiometabolic conditions, smoking, and socioeconomic deprivation. These risk factors were defined using primary care records.</p><p><strong>Outcome: </strong>The yearly declines in eGFR and the risk of incident kidney failure defined as long-term KRT and/or sustained eGFR<15mL/min/1.73m<sup>2</sup>.</p><p><strong>Analytical approach: </strong>Linear mixed effects models and Cox proportional hazards analysis.</p><p><strong>Results: </strong>The average decline in eGFR at age≤73 years was equal in males and females. After age 73 years, eGFR decline was faster in males than females, particularly for males with heart failure (males-1.22mL/min/1.73m<sup>2</sup> per year [95% CI, -1.25 to-1.20] vs females-0.87mL/min/1.73m<sup>2</sup> per year [95% CI, -0.89 to-0.85]) and current smokers (males-1.58mL/min/1.73m<sup>2</sup> per year [95% CI, -1.60 to-1.55] vs females-1.27mL/min/1.73m<sup>2</sup> per year [95% CI, -1.29 to-1.25]). Socioeconomic deprivation was one of the most impactful risk factors on eGFR decline among females aged>73 years, whereas cardiometabolic risk factors were more important among males. Older females at baseline were less likely to develop incident kidney failure than older males (P for age<0.001).</p><p><strong>Limitations: </strong>Study of people who were almost exclusively White and who had blood laboratory test data. Reliance on creatinine-based eGFR. Albuminuria and body mass index data were incomplete.</p><p><strong>Conclusions: </strong>The eGFR decline was faster in males than in females, especially in the setting of heart failure and smoking. Socioeconomic deprivation was an important risk factor associated with eGFR decline, particularly for females. further work is required to explore less well-recognized risk factors, but these findings may inform clinical management strategies of CKD overall and within sex-specific groups.</p><p><strong>Plain-language summary: </strong>Kidney function is known to decline at a faster rate among males than females. This study incorporated blood laboratory test results from the routine care of 1.1 million adults living in the United Kingdom and found that the decline in kidney function associated with risk factors varied by sex. Before and at the age of 73 years, the decline in kidney function was similar between males and femal","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":"731-741.e1"},"PeriodicalIF":9.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Waiting.","authors":"Justin C Cordova","doi":"10.1053/j.ajkd.2024.03.029","DOIUrl":"10.1053/j.ajkd.2024.03.029","url":null,"abstract":"","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":"A12-A13"},"PeriodicalIF":9.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141490501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal Relationship Between Kidney Function and Cancer Risk: A Mendelian Randomization Study.","authors":"Ellen Dobrijevic, Anita van Zwieten, Andrew J Grant, Clement T Loy, Jonathan C Craig, Armando Teixeira-Pinto, Germaine Wong","doi":"10.1053/j.ajkd.2024.05.016","DOIUrl":"10.1053/j.ajkd.2024.05.016","url":null,"abstract":"<p><strong>Rationale & objective: </strong>Patients treated with kidney replacement therapy experience a 1.5- to 2-fold increased risk of cancer and cancer mortality compared with the general population. Whether this excess risk extends to people with earlier stage chronic kidney disease and whether reduced kidney function is causally related to cancer is unclear.</p><p><strong>Study design: </strong>Two-sample Mendelian randomization (MR).</p><p><strong>Setting & participants: </strong>Genome-wide association study (GWAS) summary statistics for estimated glomerular filtration rate (eGFR) (n=567,460) and urinary albumin-creatine ratio (UACR) (n=127,865) from the CKDGen consortium and cancer outcomes from the UK Biobank (n = 407,329).</p><p><strong>Exposure: </strong>eGFR and UACR.</p><p><strong>Outcome: </strong>Overall cancer incidence, cancer-related mortality and site-specific colorectal, lung, and urinary tract cancer incidence.</p><p><strong>Analytical approach: </strong>Univariable and multivariable MR conducted for all outcomes.</p><p><strong>Results: </strong>The mean eGFR and median UACR were 91.4mL/min/1.73m<sup>2</sup> and 9.32mg/g, respectively, in the CKDGen, and 90.4mL/min/1.73m<sup>2</sup> and 9.29mg/g, respectively, in the UK Biobank. There were 98,093 cases of cancer, 15,850 cases of cancer-related death, 6,664 colorectal, 3584 lung, and 3,271 urinary tract cancer cases, respectively. The genetic instruments for eGFR and UACR comprised 34 and 38 variants, respectively. Genetically predicted kidney function (eGFR and UACR) was not associated with overall cancer risk or cancer death. The association between genetically predicted eGFR and UACR and overall cancer incidence had an odds ratio of 0.88 ([95% CI, 0.40-1.97], P=0.8) and 0.90 ([95% CI, 0.78-1.04], P=0.2) respectively, using the inverse-variance weighted method. An adjusted generalized additive model for eGFR and cancer demonstrated evidence of nonlinearity. However, there was no evidence of a causal association between eGFR and cancer in a stratified MR.</p><p><strong>Limitations: </strong>To avoid overlapping samples a smaller GWAS for UACR was used, which reduced the strength of the instrument and may introduce population stratification.</p><p><strong>Conclusions: </strong>Our study did not show a causal association between kidney function, overall cancer incidence, and cancer-related death.</p><p><strong>Plain-language summary: </strong>Does reduced kidney function cause cancer? Patients with chronic kidney disease have been shown to have an increased risk of cancer and cancer-related death. However, it is not clear whether kidney disease is causally related to cancer or the association is due to other factors such as immune suppression and inflammation or a result of distortion of the analyses from unidentified variables (confounding). We used large, published genetic studies as well a database including 407,329 people in the United Kingdom in a series of Mendelian rand","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":"686-695.e1"},"PeriodicalIF":9.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141858749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cumulative Blood Pressure Load and Incident CKD.","authors":"Hye-Sun Park, Sang Ho Park, Yeseul Seong, Hyo Jeong Kim, Hoon Young Choi, Hyeong Cheon Park, Jong Hyun Jhee","doi":"10.1053/j.ajkd.2024.05.015","DOIUrl":"10.1053/j.ajkd.2024.05.015","url":null,"abstract":"<p><strong>Rationale & objective: </strong>The association of long-term cumulative blood pressure (BP) loads with the risk of incident chronic kidney disease (CKD) remains a matter of debate. This study investigated this association among healthy Korean adults with normal kidney function.</p><p><strong>Study design: </strong>Prospective cohort study.</p><p><strong>Setting & participants: </strong>We analyzed 5,221 participants without CKD in the Korean Genome and Epidemiology Study. Cumulative systolic and diastolic BP (SBP and DBP) loads were calculated as the ratios of the areas under the curve (AUC) for SBP≥120mm Hg or≥80mm Hg for DBP divided by the AUC for all SBP or DBP measurements during the exposure period. These AUCs were categorized into 4 groups: group 0 (reference), cumulative BP load of 0 and groups 1-3, tertiles of cumulative BP loads.</p><p><strong>Outcome: </strong>Primary end point was incident CKD defined as a composite of an estimated glomerular filtration rate (eGFR) below 60mL/min/1.73m<sup>2</sup> or proteinuria greater than 1+on dipstick examination for at least 2 consecutive measurements≥90 days apart.</p><p><strong>Analytical approach: </strong>Multivariable Cox proportional hazards regression to estimate the independent association of cumulative BP loads with incident CKD.</p><p><strong>Results: </strong>Higher cumulative SBP and DBP loads were associated with an increased risk of incident CKD (HR, 1.23 [95% CI, 1.12-1.35] for SBP; and HR, 1.14 [95% CI, 1.04-1.26] for DBP loads for each 1.0-unit greater load). Compared with SBP group 0, groups 2 and 3 were associated with 1.94- and 1.89-fold greater risk of incident CKD. Compared with DBP group 0, groups 2 and 3 were associated with 1.42- and 1.54-fold greater risks. These associations of high cumulative BP loads with an increased risk of incident CKD remained consistent even in the subgroups not taking antihypertensive agents or without prior hypertension diagnosis.</p><p><strong>Limitations: </strong>The assessment of CKD outcomes relied on eGFR and spot urine tests.</p><p><strong>Conclusions: </strong>These findings highlight the association between high cumulative SBP and DBP loads and the occurrence of CKD, even in individuals with normal BP levels.</p><p><strong>Plain-language summary: </strong>Although hypertension is a major risk factor for chronic kidney disease (CKD), most studies have focused on single-point blood pressure (BP) measurements. To explore the association between long-term cumulative BP load and the development of CKD, 5,221 Korean adults with normal kidney function were included in this study. Cumulative systolic BP and diastolic BP load both exhibited a significant association with an increased risk of incident CKD. Notably, the association of cumulative BP loads with elevated risk of incident CKD was evident also in individuals who were not taking antihypertensive agents or who had no previous history of hypertension. These findings underscore ","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":"675-685.e1"},"PeriodicalIF":9.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141858750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing Genetic Testing in Kidney Diseases: Report From a National Kidney Foundation Working Group.","authors":"Nora Franceschini, David L Feldman, Jonathan S Berg, Whitney Besse, Alexander R Chang, Neera K Dahl, Rasheed Gbadegesin, Martin R Pollak, Hila Milo Rasouly, Richard J H Smith, Cheryl A Winkler, Ali G Gharavi","doi":"10.1053/j.ajkd.2024.05.010","DOIUrl":"10.1053/j.ajkd.2024.05.010","url":null,"abstract":"<p><p>About 37 million people in the United States have chronic kidney disease, a disease that encompasses multiple causes. About 10% or more of kidney diseases in adults and as many as 70% of selected chronic kidney diseases in children are expected to be explained by genetic causes. Despite the advances in genetic testing and an increasing understanding of the genetic bases of certain kidney diseases, genetic testing in nephrology lags behind other medical fields. More understanding of the benefits and logistics of genetic testing is needed to advance the implementation of genetic testing in chronic kidney diseases. Accordingly, the National Kidney Foundation convened a Working Group of experts with diverse expertise in genetics, nephrology, and allied fields to develop recommendations for genetic testing for monogenic disorders and to identify genetic risk factors for oligogenic and polygenic causes of kidney diseases. Algorithms for clinical decision making on genetic testing and a road map for advancing genetic testing in kidney diseases were generated. An important aspect of this initiative was the use of a modified Delphi process to reach group consensus on the recommendations. The recommendations and resources described herein provide support to nephrologists and allied health professionals to advance the use of genetic testing for diagnosis and screening of kidney diseases.</p>","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":"751-766"},"PeriodicalIF":9.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Characterization of Kidney Failure of Unknown Etiology in Spain: Findings From the GENSEN Study.","authors":"Miquel Blasco, Borja Quiroga, José M García-Aznar, Cristina Castro-Alonso, Saulo J Fernández-Granados, Enrique Luna, Gema Fernández Fresnedo, Marta Ossorio, María Jesús Izquierdo, Didier Sanchez-Ospina, Laura Castañeda-Infante, Ricardo Mouzo, Mercedes Cao, María L Besada-Cerecedo, Ricardo Pan-Lizcano, Roser Torra, Alberto Ortiz, Patricia de Sequera","doi":"10.1053/j.ajkd.2024.04.021","DOIUrl":"10.1053/j.ajkd.2024.04.021","url":null,"abstract":"<p><strong>Rationale & objective: </strong>Chronic kidney disease of unknown etiology (CKDUE) is one of the main global causes of kidney failure. Genetic studies may identify an etiology in these patients, but few studies have implemented genetic testing of CKDUE in a population-based series of patients, which was the focus of the GENSEN Study.</p><p><strong>Study design: </strong>Case series.</p><p><strong>Settings & participants: </strong>818 patients aged≤45 years at 51 Spanish centers with CKDUE, and either an estimated glomerular filtration rate of<15mL/min/1.73m² or treatment with maintenance dialysis or transplantation.</p><p><strong>Observations: </strong>Genetic testing for 529 genes associated with inherited nephropathies using high-throughput sequencing (HTS). Pathogenic and/or likely pathogenic (P/LP) gene variants concordant with the inheritance pattern were detected in 203 patients (24.8%). Variants in type IV collagen genes were the most frequent (COL4A5, COL4A4, COL4A3; 35% of total gene variants), followed by NPHP1, PAX2, UMOD, MUC1, and INF2 (7.3%, 5.9%, 2.5%, 2.5%, and 2.5%, respectively). Overall, 87 novel variants classified as P/LP were identified. The top 5 most common previously undiagnosed diseases were Alport syndrome spectrum (35% of total positive reports), genetic podocytopathies (19%), nephronophthisis (11%), autosomal dominant tubulointerstitial kidney disease (7%), and congenital anomalies of the kidney and urinary tract (CAKUT, 5%). A family history of kidney disease was reported by 191 participants (23.3%) and by 65 of 203 patients (32.0%) with P/LP variants.</p><p><strong>Limitations: </strong>Missing data, and selection bias resulting from voluntary enrollment.</p><p><strong>Conclusions: </strong>Genomic testing with HTS identified a genetic cause of kidney disease in approximately one quarter of young patients with CKDUE and advanced kidney disease. These findings suggest that genetic studies are a potentially useful tool for the evaluation of people with CKDUE.</p><p><strong>Plain-language summary: </strong>The cause of kidney disease is unknown for 1 in 5 patients requiring kidney replacement therapy, reflecting possible prior missed treatment opportunities. We assessed the diagnostic utility of genetic testing in children and adults aged≤45 years with either an estimated glomerular filtration rate of<15mL/min/1.73m² or treatment with maintenance dialysis or transplantation. Genetic testing identified the cause of kidney disease in approximately 1 in 4 patients without a previously known cause of kidney disease, suggesting that genetic studies are a potentially useful tool for the evaluation of these patients.</p>","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":"719-730.e1"},"PeriodicalIF":9.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141553974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Viral Nephropathies: Core Curriculum 2024.","authors":"Amy A Yau, Sangeetha Murugapandian, Ali W Rizvi, Anna Gaddy","doi":"10.1053/j.ajkd.2024.06.014","DOIUrl":"10.1053/j.ajkd.2024.06.014","url":null,"abstract":"<p><p>Viral-associated nephropathy is when kidney disease results from active viral replication. Because of the high global burden of viral infections, clinicians should be aware of their incidence, kidney manifestations, mechanism of injury, and management. Some viruses, such as hepatitis B, hepatitis C, human immunodeficiency virus (HIV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can lead to nephropathy more commonly than other endemic viruses, such as Epstein-Barr virus, cytomegalovirus, and polyoma virus which are more important causes of nephropathy in the immunosuppressed patient. Other viruses, such as hantavirus and dengue virus, have a high global infectivity rate with rare but severe kidney manifestations. Advances over the past decades have offered us a better understanding of the pathogenesis of viral-associated nephropathies and antiviral therapy options. The patterns of kidney injury include glomerular and tubulointerstitial lesions in the setting of acute and chronic infection. Direct viral infection of kidney parenchymal cells may drive pathologic findings, but kidney pathology may also result from indirect mechanisms due to activation of the innate and adaptive immune system. Some viruses can cause kidney injury due to altered hemodynamics from liver dysfunction or shock. More information about the role of genetics, specifically APOL1 polymorphisms, has come to light in regard to HIV-associated nephropathy and SARS-CoV-2-associated nephropathy. Advances in antiviral therapy help reduce nephrotoxicity and improve morbidity and mortality. In this Core Curriculum, we review common viruses responsible for kidney disease worldwide, discuss mechanisms of pathogenesis, and highlight specific management principles of viral nephropathies. We also discuss other viruses with high endemicity despite low incidence of kidney disease in the immunocompetent and immunosuppressed host.</p>","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":"767-779"},"PeriodicalIF":9.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Reply to \"The Use of Ultrasound in Peritoneal Dialysis Setting\".","authors":"Vandana Dua Niyyar","doi":"10.1053/j.ajkd.2024.04.006","DOIUrl":"10.1053/j.ajkd.2024.04.006","url":null,"abstract":"","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":"798-799"},"PeriodicalIF":9.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141183347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinicopathologic Characteristics of Crystalglobulin-Induced Nephropathy: A Case Series.","authors":"Samih H Nasr, Satoru Kudose, Anthony M Valeri, Ali Kashkouli, Samar M Said, Dominick Santoriello, Glen S Markowitz, Lihong Bu, Lynn D Cornell, Adel Samad, Jahangir Ahmed, Sanjeev Sethi, Nelson Leung, Vivette D D'Agati","doi":"10.1053/j.ajkd.2024.04.019","DOIUrl":"10.1053/j.ajkd.2024.04.019","url":null,"abstract":"<p><strong>Rationale & objective: </strong>Crystalglobulinemia is a rare syndrome characterized by intravascular crystallization of monoclonal immunoglobulins (MIg). Data on kidney involvement are limited to case reports. This series characterizes the clinicopathologic spectrum of crystalglobulin-induced nephropathy (CIN).</p><p><strong>Study design: </strong>Case series.</p><p><strong>Setting & participants: </strong>Nineteen CIN cases identified from the nephropathology archives of Mayo Clinic and Columbia University. CIN was defined by intravascular (extracellular) MIg crystals visible by light microscopy (LM) and electron microscopy (EM).</p><p><strong>Results: </strong>Among the cases, 68% were male, and 65% were Caucasian (median age, 56 years). Most patients presented with severe acute kidney injury (AKI) (median creatinine, 3.5mg/dL), hematuria, and mild proteinuria (median, 1.1g/day). Common extrarenal manifestations were constitutional (67%), cutaneous (56%), and rheumatologic (50%). Fifty percent of cases had hypocomplementemia. The hematologic disorders were monoclonal gammopathy of renal significance (MGRS) (72%), lymphoma (17%), or myeloma (11%), with 65% of these disorders discovered concomitantly with CIN. All patients had MIg identified on serum protein electrophoresis/immunofixation (IgGκ in 65%). The serum free light chain ratio was outside the renal range in 40%, and bone marrow biopsy detected the responsible clone in 67%. On LM, crystals involved glomeruli (100%) and vessels (47%), often with an inflammatory reaction (89%) and fibrin (58%). All cases exhibited crystal substructures (mostly paracrystalline) by EM. Immunofluorescence on paraffin-embedded tissue was more sensitive than frozen tissue (92% vs 47%) for demonstrating the crystal composition (IgGκ in 63%). Follow-up observation (median, 20 months) was available in 16 patients. Eighty-one percent received steroids, 44% plasmapheresis, 38% hemodialysis, and 69% chemotherapy. Ninety-percent of patients who received clone-directed therapy achieved kidney recovery versus 20% of those who did not (P=0.02).</p><p><strong>Limitations: </strong>Retrospective design, small sample size.</p><p><strong>Conclusions: </strong>CIN is a rare cause of nephropathy associated with lymphoplasmacytic disorders (mostly MGRS) and typically presents with severe AKI and extrarenal manifestations. Diagnosis often requires immunofluorescence performed on paraffin-embedded kidney tissue. Prompt initiation of clone-directed therapy, coupled with corticosteroids and plasmapheresis, may lead to recovery of kidney function.</p>","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":"708-718.e1"},"PeriodicalIF":9.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141440018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment Effect Heterogeneity in Acute Kidney Injury Incidence Following Intravenous Antihypertensive Administration for Severe Blood Pressure Elevation During Hospitalization.","authors":"Lama Ghazi, Xinyuan Chen, Michael O Harhay, Liangyuan Hu, Aditya Biswas, Aldo J Peixoto, Fan Li, F Perry Wilson","doi":"10.1053/j.ajkd.2024.09.011","DOIUrl":"https://doi.org/10.1053/j.ajkd.2024.09.011","url":null,"abstract":"<p><strong>Rationale & objective: </strong>Severe hypertension (sHTN) that develops after hospital admission is prevalent in 10% of patients admitted for reasons other than HTN. sHTN is commonly treated with intravenous (IV) antihypertensives and is associated with a greater risk of acute kidney injury (AKI). Our goal was to explore whether there is heterogeneity in IV antihypertensives' effect on AKI incidence among patients who develop sHTN during hospitalization.</p><p><strong>Study design: </strong>Heterogeneity of treatment effect analysis.</p><p><strong>Settings & participants: </strong>Patients who developed sHTN, systolic blood pressure (BP) >180, or diastolic BP >110 mmHg during hospitalization and did not have kidney failure.</p><p><strong>Exposure: </strong>Treatment with IV antihypertensives within 3 hours of BP elevation.</p><p><strong>Outcome: </strong>Time to develop AKI.</p><p><strong>Analytical approach: </strong>An accelerated failure time Bayesian Additive Regression Trees (BART) model to capture the association between the time to develop AKI and predictors. Individual treatment effects estimated for each participant using a counterfactual outcome framework and these estimates were used to identify patient characteristics associated with treatment effect heterogeneity in response to IV antihypertensives.</p><p><strong>Results: </strong>We included 11,951 patients who developed sHTN, 741 were treated with IV antihypertensives, and 11,210 were not, of which 18% and 13% developed AKI, respectively. Most patients would have been harmed from IV antihypertensive treatment except for a small subset of 317 patients who were White, had an SBP on admission ≥156 mmHg, an eGFR ≥70.7 ml/min/1.73m², and a serum bicarbonate <21.7 mmol/L.</p><p><strong>Limitations: </strong>Data-driven, hypothesis-generating approach. Findings were not validated with external data sources.</p><p><strong>Conclusion: </strong>These exploratory findings suggest that most patients who develop sHTN will not benefit from IV antihypertensive treatment. Future studies should assess for heterogeneity when identifying treatment options, if any are needed, for sHTN.</p>","PeriodicalId":7419,"journal":{"name":"American Journal of Kidney Diseases","volume":" ","pages":""},"PeriodicalIF":9.4,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}