Pub Date : 2026-01-01Epub Date: 2025-11-01DOI: 10.1016/j.xkme.2025.101170
Geraldine Venessa Qian Le Boh , Hui-Lin Chin , Yao Chun Zhang , Ru Sin Lim
McCune-Albright syndrome (MAS) is a rare systemic genetic condition classically characterized by childhood-onset polyostotic fibrous dysplasia, café-au-lait skin pigmentation, and precocious puberty. Kidney involvement in MAS is infrequently recognized, particularly in low- and middle-income countries where genomic testing may be limited. We presented the first case report of MAS presenting with Fanconi syndrome and progressive kidney failure, which we postulated represents a phenotypic expansion of the renal phenotype associated with MAS, in addition to hyperthyroidism, osteoid osteoma, bone marrow failure secondary to fibrous dysplasia, and congenital ovarian failure. Initial renal biochemical evaluations were suggestive of proximal tubulopathy; however, secondary investigations were inconclusive. Seventeen years after the patient’s initial presentation, clinically accredited whole exome sequencing conducted under a national genomic research initiative identified a pathogenic GNAS variant (NM_000516:c.[602G>A];p.(Arg201His)), confirming a diagnosis of MAS. This is the first reported case of GNAS-associated Fanconi syndrome and kidney failure. We hypothesized that dysfunction of proximal tubule transporters may be related to elevated circulating cyclic adenosine monophosphate levels and selective expression of G protein-coupled receptors in the proximal tubule, mediated by a gain-of-function in the G-protein α subunit induced by the GNAS pathogenic variant.
{"title":"McCune-Albright Syndrome as a Rare Cause of Fanconi Syndrome and Kidney Failure: A Case Report and Literature Review","authors":"Geraldine Venessa Qian Le Boh , Hui-Lin Chin , Yao Chun Zhang , Ru Sin Lim","doi":"10.1016/j.xkme.2025.101170","DOIUrl":"10.1016/j.xkme.2025.101170","url":null,"abstract":"<div><div>McCune-Albright syndrome (MAS) is a rare systemic genetic condition classically characterized by childhood-onset polyostotic fibrous dysplasia, café-au-lait skin pigmentation, and precocious puberty. Kidney involvement in MAS is infrequently recognized, particularly in low- and middle-income countries where genomic testing may be limited. We presented the first case report of MAS presenting with Fanconi syndrome and progressive kidney failure, which we postulated represents a phenotypic expansion of the renal phenotype associated with MAS, in addition to hyperthyroidism, osteoid osteoma, bone marrow failure secondary to fibrous dysplasia, and congenital ovarian failure. Initial renal biochemical evaluations were suggestive of proximal tubulopathy; however, secondary investigations were inconclusive. Seventeen years after the patient’s initial presentation, clinically accredited whole exome sequencing conducted under a national genomic research initiative identified a pathogenic <em>GNAS</em> variant (NM_000516:c.[602G>A];p.(Arg201His)), confirming a diagnosis of MAS. This is the first reported case of <em>GNAS</em>-associated Fanconi syndrome and kidney failure. We hypothesized that dysfunction of proximal tubule transporters may be related to elevated circulating cyclic adenosine monophosphate levels and selective expression of G protein-coupled receptors in the proximal tubule, mediated by a gain-of-function in the G-protein α subunit induced by the <em>GNAS</em> pathogenic variant.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101170"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787278","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}
Pub Date : 2026-01-01Epub Date: 2025-11-13DOI: 10.1016/j.xkme.2025.101186
Erin E. Tapper , Johanna M. Huusko , Alicia M. Scocchia , Kimberly Gall , Mary-Beth Roberts , Manuel Bernal-Quirós , Satu Valo , Inka Saarinen , Matias Rantanen , Tuuli Pietila , Massimiliano Gentile , Lotta Koskinen , Meenakshi Mahey Kumar , Samuel Myllykangas , Juha Koskenvuo
<div><h3>Rationale & Objective</h3><div>Mounting evidence supports that identifying the specific molecular etiology for individuals with cystic kidney disease (CyKD) is important for prognostication, surveillance, identifying related living donors, and defining familial risk, even in cases in which a clinical diagnosis appears straightforward. In this study, we aimed to investigate the yield of genetic findings and the unique variant characteristics using multigene panel testing (MGPT) in a referral laboratory setting for an unselected population of patients with an indication of CyKD.</div></div><div><h3>Study Design</h3><div>Cross-sectional study.</div></div><div><h3>Setting & Participants</h3><div>A retrospective analysis of 1,235 genetic testing reports from patients with suspected CyKD who pursued MGPT was performed.</div></div><div><h3>Findings</h3><div>A positive result in a gene associated with CyKD was identified in 49.4% (610/1235) of patient reports, identifying 468 unique variants classified as pathogenic or likely pathogenic in 20 unique genes. Variants in <em>PKD1</em>, a gene complicated by homology to 6 different pseudogenes, contributed to 65.6% (400/610) of positive results. Copy number variants (CNVs) were identified in 9.5% (58/610) of positive results, with 30.4% (17/56) of deletions consisting of 4 exons or less. Variants of uncertain significance that were suspicious for being pathogenic (susVUS) were identified in 57.0% (94/165) of patients with inconclusive results.</div></div><div><h3>Limitations</h3><div>Genetic analysis was targeted to the genes included on the panel at the time of testing. As new evidence emerges supporting additional gene-disease associations, there is potential for additional positive results.</div></div><div><h3>Conclusions</h3><div>Thoughtful selection of carefully curated MGPT optimized to detect technically challenging variants can identify the molecular etiology in individuals presenting with CyKD. Further investigation of susVUS through segregation analysis in families may contribute to additional positive results.</div></div><div><h3>Plain-Language Summary</h3><div>Data informing the yield of multigene panel testing (MGPT) for individuals with cystic kidney disease (CyKD) is increasing. In this study, we retrospectively reviewed MGPT results from 1,235 individuals with suspected CyKD. A positive result in one of 20 CyKD-associated genes, including <em>PKD1</em>, was identified in 49.4% (610/1235) of patient reports. Copy number variants (CNVs) accounted for 9.5% (58/610) of positive results, with 30.4% (17/56) of deletions consisting of 4 exons or less. Suspicious variants of uncertain significance were identified in 57.0% (94/165) of patients with inconclusive results. MGPT can identify the molecular etiology of CyKD and, prior to ordering, should be carefully evaluated for relevant gene content, capabilities for technically challenging genes like <em>PKD1,</em> sensitivity to detect
{"title":"Results of Multigene Panel Testing, Including PKD1, in >1,200 Patients With Cystic Kidney Disease: A Retrospective Analysis","authors":"Erin E. Tapper , Johanna M. Huusko , Alicia M. Scocchia , Kimberly Gall , Mary-Beth Roberts , Manuel Bernal-Quirós , Satu Valo , Inka Saarinen , Matias Rantanen , Tuuli Pietila , Massimiliano Gentile , Lotta Koskinen , Meenakshi Mahey Kumar , Samuel Myllykangas , Juha Koskenvuo","doi":"10.1016/j.xkme.2025.101186","DOIUrl":"10.1016/j.xkme.2025.101186","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Mounting evidence supports that identifying the specific molecular etiology for individuals with cystic kidney disease (CyKD) is important for prognostication, surveillance, identifying related living donors, and defining familial risk, even in cases in which a clinical diagnosis appears straightforward. In this study, we aimed to investigate the yield of genetic findings and the unique variant characteristics using multigene panel testing (MGPT) in a referral laboratory setting for an unselected population of patients with an indication of CyKD.</div></div><div><h3>Study Design</h3><div>Cross-sectional study.</div></div><div><h3>Setting & Participants</h3><div>A retrospective analysis of 1,235 genetic testing reports from patients with suspected CyKD who pursued MGPT was performed.</div></div><div><h3>Findings</h3><div>A positive result in a gene associated with CyKD was identified in 49.4% (610/1235) of patient reports, identifying 468 unique variants classified as pathogenic or likely pathogenic in 20 unique genes. Variants in <em>PKD1</em>, a gene complicated by homology to 6 different pseudogenes, contributed to 65.6% (400/610) of positive results. Copy number variants (CNVs) were identified in 9.5% (58/610) of positive results, with 30.4% (17/56) of deletions consisting of 4 exons or less. Variants of uncertain significance that were suspicious for being pathogenic (susVUS) were identified in 57.0% (94/165) of patients with inconclusive results.</div></div><div><h3>Limitations</h3><div>Genetic analysis was targeted to the genes included on the panel at the time of testing. As new evidence emerges supporting additional gene-disease associations, there is potential for additional positive results.</div></div><div><h3>Conclusions</h3><div>Thoughtful selection of carefully curated MGPT optimized to detect technically challenging variants can identify the molecular etiology in individuals presenting with CyKD. Further investigation of susVUS through segregation analysis in families may contribute to additional positive results.</div></div><div><h3>Plain-Language Summary</h3><div>Data informing the yield of multigene panel testing (MGPT) for individuals with cystic kidney disease (CyKD) is increasing. In this study, we retrospectively reviewed MGPT results from 1,235 individuals with suspected CyKD. A positive result in one of 20 CyKD-associated genes, including <em>PKD1</em>, was identified in 49.4% (610/1235) of patient reports. Copy number variants (CNVs) accounted for 9.5% (58/610) of positive results, with 30.4% (17/56) of deletions consisting of 4 exons or less. Suspicious variants of uncertain significance were identified in 57.0% (94/165) of patients with inconclusive results. MGPT can identify the molecular etiology of CyKD and, prior to ordering, should be carefully evaluated for relevant gene content, capabilities for technically challenging genes like <em>PKD1,</em> sensitivity to detect","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101186"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787335","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}
Pub Date : 2026-01-01Epub Date: 2025-09-29DOI: 10.1016/j.xkme.2025.101129
O. Alison Potok , Ronit Katz , Nisha Bansal , Knut A. Langlo , Stein I. Hallan
<div><h3>Rationale & Objective</h3><div>The discrepancy in estimated glomerular filtration rate by cystatin C (eGFRcys) versus creatinine (eGFRcr) has been used as a surrogate for sarcopenia. We studied whether this eGFRcys – eGFRcr difference could improve prediction of kidney failure versus death, which is important in the management of patients with chronic kidney disease (CKD). We hypothesized that it improved the death prediction but not that of kidney failure.</div></div><div><h3>Study Design</h3><div>A five-year cohort study to assess prognostic accuracy.</div></div><div><h3>Setting & Participants</h3><div>The population included 1,146 participants with creatinine (cr) and cystatin C (cys) measurements from the population-based the Nord-Trøndelag Health Study, Norway. Those aged ≤ 65 years or with estimated glomerular filtration rate (eGFR)cr ≥ 45 mL/min/1.73m<sup>2</sup> were excluded.</div></div><div><h3>Exposures</h3><div>The mortality risk equation in patients with CKD (MREK) includes age, sex, eGFRcr, albuminuria, smoking status, history of stroke, diabetes, and heart failure. The kidney failure risk equation includes age, sex, eGFRcr, and albuminuria.</div></div><div><h3>Outcomes</h3><div>Kidney failure or death at 5 years.</div></div><div><h3>Analytical approach</h3><div>The performances of MREK and kidney failure risk equation with and without eGFR_diff (= eGFRcys – eGFRcr) were compared: calibration (likelihood ratio, Akaike information criterion, Brier score), discrimination (C-statistics), reclassification (net reclassification improvement and integrated discrimination improvement).</div></div><div><h3>Results</h3><div>The mean ± SD age was 80 ± 7 years, 42% were men, the mean eGFRcr was 36 ± 8 and eGFR_diff was 1.04 ± 12 mL/min/1.73m<sup>2</sup>; 42 participants (4%) reached kidney failure and 444 (39%) died. C-statistics (95% CI) for MREK improved with eGFR_diff from 70.1% (66.7-73.4) to 73.0% (69.8-76.1) (<em>P</em> = 0.003). The proportion of participants correctly reclassified also improved (net reclassification improvement 14% [10%-17%]), and the separation between the average predicted risk for participants who died versus not (integrated discrimination improvement +0.03 [ 0.02-0.04]).</div></div><div><h3>Limitations</h3><div>Untested generalizability in other populations.</div></div><div><h3>Conclusions</h3><div>Including eGFR_diff into the kidney failure risk and mortality risk equations significantly improved mortality risk prediction, but not kidney failure, in patients with CKD. Serum creatinine level is influenced by many non-GFR determinants, including sarcopenia, and the discrepancy of creatinine versus cystatin C could be helpful in predialytic decision-making.</div></div><div><h3>Plain-Language Summary</h3><div>Patients with chronic kidney disease have a higher mortality risk than those without chronic kidney disease. They are also at risk of kidney failure, which can be treated with dialysis, but this r
{"title":"Using the Difference Between Estimated Glomerular Filtration Rate by Cystatin C and Creatinine to Improve Mortality Risk Prediction in Elderly Patients With CKD in the HUNT Study","authors":"O. Alison Potok , Ronit Katz , Nisha Bansal , Knut A. Langlo , Stein I. Hallan","doi":"10.1016/j.xkme.2025.101129","DOIUrl":"10.1016/j.xkme.2025.101129","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>The discrepancy in estimated glomerular filtration rate by cystatin C (eGFRcys) versus creatinine (eGFRcr) has been used as a surrogate for sarcopenia. We studied whether this eGFRcys – eGFRcr difference could improve prediction of kidney failure versus death, which is important in the management of patients with chronic kidney disease (CKD). We hypothesized that it improved the death prediction but not that of kidney failure.</div></div><div><h3>Study Design</h3><div>A five-year cohort study to assess prognostic accuracy.</div></div><div><h3>Setting & Participants</h3><div>The population included 1,146 participants with creatinine (cr) and cystatin C (cys) measurements from the population-based the Nord-Trøndelag Health Study, Norway. Those aged ≤ 65 years or with estimated glomerular filtration rate (eGFR)cr ≥ 45 mL/min/1.73m<sup>2</sup> were excluded.</div></div><div><h3>Exposures</h3><div>The mortality risk equation in patients with CKD (MREK) includes age, sex, eGFRcr, albuminuria, smoking status, history of stroke, diabetes, and heart failure. The kidney failure risk equation includes age, sex, eGFRcr, and albuminuria.</div></div><div><h3>Outcomes</h3><div>Kidney failure or death at 5 years.</div></div><div><h3>Analytical approach</h3><div>The performances of MREK and kidney failure risk equation with and without eGFR_diff (= eGFRcys – eGFRcr) were compared: calibration (likelihood ratio, Akaike information criterion, Brier score), discrimination (C-statistics), reclassification (net reclassification improvement and integrated discrimination improvement).</div></div><div><h3>Results</h3><div>The mean ± SD age was 80 ± 7 years, 42% were men, the mean eGFRcr was 36 ± 8 and eGFR_diff was 1.04 ± 12 mL/min/1.73m<sup>2</sup>; 42 participants (4%) reached kidney failure and 444 (39%) died. C-statistics (95% CI) for MREK improved with eGFR_diff from 70.1% (66.7-73.4) to 73.0% (69.8-76.1) (<em>P</em> = 0.003). The proportion of participants correctly reclassified also improved (net reclassification improvement 14% [10%-17%]), and the separation between the average predicted risk for participants who died versus not (integrated discrimination improvement +0.03 [ 0.02-0.04]).</div></div><div><h3>Limitations</h3><div>Untested generalizability in other populations.</div></div><div><h3>Conclusions</h3><div>Including eGFR_diff into the kidney failure risk and mortality risk equations significantly improved mortality risk prediction, but not kidney failure, in patients with CKD. Serum creatinine level is influenced by many non-GFR determinants, including sarcopenia, and the discrepancy of creatinine versus cystatin C could be helpful in predialytic decision-making.</div></div><div><h3>Plain-Language Summary</h3><div>Patients with chronic kidney disease have a higher mortality risk than those without chronic kidney disease. They are also at risk of kidney failure, which can be treated with dialysis, but this r","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101129"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145600464","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}
Pub Date : 2026-01-01Epub Date: 2025-11-04DOI: 10.1016/j.xkme.2025.101165
Junaid A. Wali , Yaseen A. Jamal , Mustafa Al-Kawaaz , Graham Rodwell , Megan L. Troxell
Rationale & Objective
Acute kidney injury and hemolysis are rare side effects of rifampin that are sometimes linked with drug re-exposure. We studied this association in a contemporary patient cohort to comprehensively correlate the clinical, laboratory, and biopsy findings.
Study Design
Adult patients who underwent kidney biopsy for acute kidney injury while on rifampin during an 11-year period (2012-2023) were identified. Electronic medical records and biopsy pathology were correlated.
Setting & Participants
Eighteen patients (50% men, ages 43-81) were prescribed rifampin for active pulmonary tuberculosis (7), latent tuberculosis (3), Mycobacterium avium complex infection (4), septic arthritis (3), and Bartonella endocarditis (1). Nine patients had prior rifampin exposure.
Results
Patients most commonly presented with gastrointestinal and ‘flu-like’ symptoms, 1 day to 1 month after rifampin (re-)exposure. Creatinine at biopsy was 2.2-26.1 mg/dL. Importantly, 15 patients had evidence of hemolysis. All biopsies demonstrated acute tubular injury, yet inflammation (acute interstitial nephritis) was variable. Eleven had pigmented casts, 9 with hemoglobin and 2 with myoglobin. Thus, we highlight acute tubular necrosis with hemoglobin casts as a major finding in rifampin kidney injury. Management included supportive care, steroids, and discontinuation of rifampin. Eleven patients required hemodialysis. Fifteen patients had complete renal remission.
Limitations
Retrospective case series without uniformly available clinical and laboratory data.
Conclusions
Hemolytic anemia, hemoglobin cast nephropathy, and acute kidney injury are rare but serious complications of rifampin. Clinicians and patients should be aware of this side effect, and interrupted use of rifampin therapy should be avoided.
Plain-language Summary
Rifampin (also known as rifampicin; brand name Rifadin) is an important antibiotic medication in treating infection, particularly tuberculosis. Rifampin can very rarely cause serious side effects, especially in patients who have taken rifampin previously. We identified 18 patients with kidney injury and kidney biopsy shortly after rifampin (re-)exposure and found that 15 had hemolysis (destruction of red blood cells), most with systemic illness. We found evidence of hemolysis-related casts causing kidney injury in 9 kidney biopsies. Patients and clinicians should be very cautious with rifampin re-exposure, and patients should seek medical attention for malaise, flu-like symptoms, fever, chills, nausea, vomiting, diarrhea, jaundice, decreased urine output, and dark urine.
{"title":"Rifampin-induced Acute Kidney Injury Is Associated With Hemolysis and Drug Re-exposure","authors":"Junaid A. Wali , Yaseen A. Jamal , Mustafa Al-Kawaaz , Graham Rodwell , Megan L. Troxell","doi":"10.1016/j.xkme.2025.101165","DOIUrl":"10.1016/j.xkme.2025.101165","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Acute kidney injury and hemolysis are rare side effects of rifampin that are sometimes linked with drug re-exposure. We studied this association in a contemporary patient cohort to comprehensively correlate the clinical, laboratory, and biopsy findings.</div></div><div><h3>Study Design</h3><div>Adult patients who underwent kidney biopsy for acute kidney injury while on rifampin during an 11-year period (2012-2023) were identified. Electronic medical records and biopsy pathology were correlated.</div></div><div><h3>Setting & Participants</h3><div>Eighteen patients (50% men, ages 43-81) were prescribed rifampin for active pulmonary tuberculosis (7), latent tuberculosis (3), <em>Mycobacterium avium</em> complex infection (4), septic arthritis (3), and <em>Bartonella</em> endocarditis (1). Nine patients had prior rifampin exposure.</div></div><div><h3>Results</h3><div>Patients most commonly presented with gastrointestinal and ‘flu-like’ symptoms, 1 day to 1 month after rifampin (re-)exposure. Creatinine at biopsy was 2.2-26.1 mg/dL. Importantly, 15 patients had evidence of hemolysis. All biopsies demonstrated acute tubular injury, yet inflammation (acute interstitial nephritis) was variable. Eleven had pigmented casts, 9 with hemoglobin and 2 with myoglobin. Thus, we highlight acute tubular necrosis with hemoglobin casts as a major finding in rifampin kidney injury. Management included supportive care, steroids, and discontinuation of rifampin. Eleven patients required hemodialysis. Fifteen patients had complete renal remission.</div></div><div><h3>Limitations</h3><div>Retrospective case series without uniformly available clinical and laboratory data.</div></div><div><h3>Conclusions</h3><div>Hemolytic anemia, hemoglobin cast nephropathy, and acute kidney injury are rare but serious complications of rifampin. Clinicians and patients should be aware of this side effect, and interrupted use of rifampin therapy should be avoided.</div></div><div><h3>Plain-language Summary</h3><div>Rifampin (also known as rifampicin; brand name Rifadin) is an important antibiotic medication in treating infection, particularly tuberculosis. Rifampin can very rarely cause serious side effects, especially in patients who have taken rifampin previously. We identified 18 patients with kidney injury and kidney biopsy shortly after rifampin (re-)exposure and found that 15 had hemolysis (destruction of red blood cells), most with systemic illness. We found evidence of hemolysis-related casts causing kidney injury in 9 kidney biopsies. Patients and clinicians should be very cautious with rifampin re-exposure, and patients should seek medical attention for malaise, flu-like symptoms, fever, chills, nausea, vomiting, diarrhea, jaundice, decreased urine output, and dark urine.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101165"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787287","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}
Pub Date : 2026-01-01Epub Date: 2025-11-10DOI: 10.1016/j.xkme.2025.101185
Christof Aigner , Zoltán Prohászka , Ágnes Szilágyi , Georg A. Böhmig , Klaus Arbeiter , Alice Schmidt , Gere Sunder-Plassmann
Complement mediated thrombotic microangiopathy (C-TMA) is a rare disease resulting in kidney failure and other organ manifestations. Current treatments include the complement C5 blockers eculizumab and ravulizumab as well as plasma therapy. We report on a young adult man with a long-standing history of genetic C-TMA (GC-TMA) because of a likely pathogenic missense variant in CFH. After several years without clinical signs of TMA and normal kidney function (CKD G1A2), without recent specific therapies, he presented with acute kidney injury, microangiopathic hemolysis, and nephrotic range proteinuria. Plasma therapy and ravulizumab failed to stop hemolysis, and he commenced kidney replacement therapy 11 days after admission. Laboratory analyses disclosed suboptimal complement inhibition and low free ravulizumab serum concentrations. Four weeks after admission, we started treatment with crovalimab, a novel humanized anti-C5 antibody. Hemolysis improved immediately and kidney function recovered after 3 months of dialysis treatment and improved continuously during 1 year of therapy with crovalimab. The excellent and rapid response to crovalimab potentially suggests that the engineering of crovalimab, facilitating also subcutaneous administration, may result in a different pharmacokinetic and pharmacodynamic profile of crovalimab as compared with standard C5 inhibitors in patient with nephrotic range proteinuria.
{"title":"Crovalimab Rescue Therapy in a Case With Genetic Complement Mediated Thrombotic Microangiopathy","authors":"Christof Aigner , Zoltán Prohászka , Ágnes Szilágyi , Georg A. Böhmig , Klaus Arbeiter , Alice Schmidt , Gere Sunder-Plassmann","doi":"10.1016/j.xkme.2025.101185","DOIUrl":"10.1016/j.xkme.2025.101185","url":null,"abstract":"<div><div>Complement mediated thrombotic microangiopathy (C-TMA) is a rare disease resulting in kidney failure and other organ manifestations. Current treatments include the complement C5 blockers eculizumab and ravulizumab as well as plasma therapy. We report on a young adult man with a long-standing history of genetic C-TMA (GC-TMA) because of a likely pathogenic missense variant in <em>CFH</em>. After several years without clinical signs of TMA and normal kidney function (CKD G1A2), without recent specific therapies, he presented with acute kidney injury, microangiopathic hemolysis, and nephrotic range proteinuria. Plasma therapy and ravulizumab failed to stop hemolysis, and he commenced kidney replacement therapy 11 days after admission. Laboratory analyses disclosed suboptimal complement inhibition and low free ravulizumab serum concentrations. Four weeks after admission, we started treatment with crovalimab, a novel humanized anti-C5 antibody. Hemolysis improved immediately and kidney function recovered after 3 months of dialysis treatment and improved continuously during 1 year of therapy with crovalimab. The excellent and rapid response to crovalimab potentially suggests that the engineering of crovalimab, facilitating also subcutaneous administration, may result in a different pharmacokinetic and pharmacodynamic profile of crovalimab as compared with standard C5 inhibitors in patient with nephrotic range proteinuria.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101185"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787332","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}
Pub Date : 2026-01-01Epub Date: 2025-11-06DOI: 10.1016/j.xkme.2025.101177
Yuvaram N.V. Reddy MBBS, MPH , Sri Lekha Tummalapalli MD, MBA, MAS , Vishnu S. Potluri MD, MPH , Adam Mussell MA , Joel T. Adler MD, MPH , Amol S. Navathe MD, PhD
{"title":"Transplantation in Mandatory Kidney Payment Models: Understanding the Potential Influence of the ESRD Treatment Choices Model on the Increasing Organ Transplant Access Model","authors":"Yuvaram N.V. Reddy MBBS, MPH , Sri Lekha Tummalapalli MD, MBA, MAS , Vishnu S. Potluri MD, MPH , Adam Mussell MA , Joel T. Adler MD, MPH , Amol S. Navathe MD, PhD","doi":"10.1016/j.xkme.2025.101177","DOIUrl":"10.1016/j.xkme.2025.101177","url":null,"abstract":"","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101177"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787334","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}
Pub Date : 2026-01-01Epub Date: 2025-11-01DOI: 10.1016/j.xkme.2025.101167
Yiting Li , Gayathri Menon , Jane J. Long , Malika Wilson , Byoungjun Kim , Mario P. DeMarco , Babak J. Orandi , Sunjae Bae , Wenbo Wu , Yijing Feng , Terry Gordon , George D. Thurston , Dorry L. Segev , Mara A. McAdams-DeMarco
<div><h3>Rationale & Objective</h3><div>Fine particulate matter (PM<sub>2.5</sub>) is associated with increased mortality and disproportionately affects minoritized patients with kidney failure, particularly Black patients. Among patients with kidney failure, we tested whether neighborhood characteristics (racial and ethnic segregation, socioeconomic deprivation, and built environment) modified the association between PM<sub>2.5</sub> exposure and mortality, overall and by race and ethnicity.</div></div><div><h3>Study Design</h3><div>Cohort study (2003-2019).</div></div><div><h3>Setting & Participants</h3><div>National registry for patients with kidney failure.</div></div><div><h3>Exposures</h3><div>Annualized PM<sub>2.5</sub> concentrations (high, > 9 μg/m<sup>3</sup>), segregation scores (Theil’s H method), deprivation scores (American Community Survey), and built environment factors (medically underserved areas [MUA] and urbanicity) by patients’ residential ZIP code at dialysis initiation.</div></div><div><h3>Outcome</h3><div>All-cause mortality.</div></div><div><h3>Analytical Approach</h3><div>We used multivariable Cox regression with shared state-level frailty to quantify whether neighborhood factors modify the association between PM<sub>2.5</sub> and mortality, overall and stratified by race and ethnicity.</div></div><div><h3>Results</h3><div>High PM<sub>2.5</sub> (vs low) was differentially associated with mortality among patients with kidney failure residing in neighborhoods characterized by high segregation (adjusted hazard ratio [aHR], 1.17; 95% confidence interval [CI], 1.15-1.19; <em>P</em><sub>interaction high vs low</sub> < 0.001), high deprivation (aHR, 1.17; 95% CI, 1.15-1.19; <em>P</em><sub>interaction high vs low</sub> < 0.001), MUA (aHR, 1.15; 95% CI, 1.13-1.16; <em>P</em><sub>interaction</sub> = 0.005), and high-density urban (HDU) areas (aHR, 1.14; 95% CI, 1.12-1.15; <em>P</em><sub>interaction</sub> < 0.001). These differential associations were most prominent among Black patients ([high segregation: aHR, 1.25; 95% CI, 1.21-1.29; <em>P</em><sub>interaction high vs low</sub> = 0.006], [high deprivation: aHR, 1.26; 95% CI, 1.22-1.30; <em>P</em><sub>interaction high vs low</sub> < 0.001], [MUA: aHR, 1.22; 95% CI, 1.19-1.26; <em>P</em><sub>interaction</sub> = 0.02], [HDU areas: aHR, 1.23; 95% CI, 1.20-1.26; <em>P</em><sub>interaction</sub> < 0.001])</div></div><div><h3>Limitations</h3><div>Outdoor PM<sub>2.5</sub> may not reflect individual-level exposures.</div></div><div><h3>Conclusions</h3><div>High levels of PM<sub>2.5</sub> were associated with increased mortality risk among patients with kidney failure residing in neighborhoods characterized by high segregation, high deprivation, MUAs, and HDU areas, particularly among Black patients. Nephrologists should consider closer monitoring of patients, particularly those from minoritized groups who reside in these high-risk neighborhoods, to help mitigate
{"title":"Neighborhood Factors, Air Pollution, and Mortality Among Kidney Failure Patients: Exploring Differences by Race and Ethnicity","authors":"Yiting Li , Gayathri Menon , Jane J. Long , Malika Wilson , Byoungjun Kim , Mario P. DeMarco , Babak J. Orandi , Sunjae Bae , Wenbo Wu , Yijing Feng , Terry Gordon , George D. Thurston , Dorry L. Segev , Mara A. McAdams-DeMarco","doi":"10.1016/j.xkme.2025.101167","DOIUrl":"10.1016/j.xkme.2025.101167","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Fine particulate matter (PM<sub>2.5</sub>) is associated with increased mortality and disproportionately affects minoritized patients with kidney failure, particularly Black patients. Among patients with kidney failure, we tested whether neighborhood characteristics (racial and ethnic segregation, socioeconomic deprivation, and built environment) modified the association between PM<sub>2.5</sub> exposure and mortality, overall and by race and ethnicity.</div></div><div><h3>Study Design</h3><div>Cohort study (2003-2019).</div></div><div><h3>Setting & Participants</h3><div>National registry for patients with kidney failure.</div></div><div><h3>Exposures</h3><div>Annualized PM<sub>2.5</sub> concentrations (high, > 9 μg/m<sup>3</sup>), segregation scores (Theil’s H method), deprivation scores (American Community Survey), and built environment factors (medically underserved areas [MUA] and urbanicity) by patients’ residential ZIP code at dialysis initiation.</div></div><div><h3>Outcome</h3><div>All-cause mortality.</div></div><div><h3>Analytical Approach</h3><div>We used multivariable Cox regression with shared state-level frailty to quantify whether neighborhood factors modify the association between PM<sub>2.5</sub> and mortality, overall and stratified by race and ethnicity.</div></div><div><h3>Results</h3><div>High PM<sub>2.5</sub> (vs low) was differentially associated with mortality among patients with kidney failure residing in neighborhoods characterized by high segregation (adjusted hazard ratio [aHR], 1.17; 95% confidence interval [CI], 1.15-1.19; <em>P</em><sub>interaction high vs low</sub> < 0.001), high deprivation (aHR, 1.17; 95% CI, 1.15-1.19; <em>P</em><sub>interaction high vs low</sub> < 0.001), MUA (aHR, 1.15; 95% CI, 1.13-1.16; <em>P</em><sub>interaction</sub> = 0.005), and high-density urban (HDU) areas (aHR, 1.14; 95% CI, 1.12-1.15; <em>P</em><sub>interaction</sub> < 0.001). These differential associations were most prominent among Black patients ([high segregation: aHR, 1.25; 95% CI, 1.21-1.29; <em>P</em><sub>interaction high vs low</sub> = 0.006], [high deprivation: aHR, 1.26; 95% CI, 1.22-1.30; <em>P</em><sub>interaction high vs low</sub> < 0.001], [MUA: aHR, 1.22; 95% CI, 1.19-1.26; <em>P</em><sub>interaction</sub> = 0.02], [HDU areas: aHR, 1.23; 95% CI, 1.20-1.26; <em>P</em><sub>interaction</sub> < 0.001])</div></div><div><h3>Limitations</h3><div>Outdoor PM<sub>2.5</sub> may not reflect individual-level exposures.</div></div><div><h3>Conclusions</h3><div>High levels of PM<sub>2.5</sub> were associated with increased mortality risk among patients with kidney failure residing in neighborhoods characterized by high segregation, high deprivation, MUAs, and HDU areas, particularly among Black patients. Nephrologists should consider closer monitoring of patients, particularly those from minoritized groups who reside in these high-risk neighborhoods, to help mitigate ","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101167"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787457","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}
Pub Date : 2026-01-01Epub Date: 2025-11-04DOI: 10.1016/j.xkme.2025.101173
Hyunji Kim , Mary Nguyen , Page Salenger , Amanda Tran , Shelly Seidel , Daniel E. Weiner , Klemens B. Meyer , Caroline M. Hsu
Despite often offering a better quality of life than in-center hemodialysis, peritoneal dialysis (PD) at home can be challenging for many. From May 2021 to October 2024, we offered PD assistance at 2 home dialysis clinics in Dialysis Clinic, Inc, a mid-size national dialysis provider. Eligible patients could be incident to or established on PD, with anticipated need for either permanent or temporary assistance. Over 3 years, 6 patients received assisted PD. Three established PD patients needed assistance when their care partners were unavailable. Three other patients required assistance to initiate PD. Assistance duration ranged from 1 day to 5 months. Three patients ultimately transitioned to PD independence, and 3 transferred to in-center hemodialysis. Our greatest challenge was hiring assistants for unpredictable work with odd hours, and we eventually hired 2 postbaccalaureate students preparing for medical careers. Our successes, minimal missed treatments, and a high rate of PD continuation are a testament to their dedication. Assisted PD programs would benefit from economies of scale by being embedded in the health care system. As interest in assisted PD grows, we advocate for sharing of programs’ successes and challenges so that we may together learn how to enable assisted PD in the US.
{"title":"Assisted Peritoneal Dialysis: A Feasibility and Quality Improvement Project","authors":"Hyunji Kim , Mary Nguyen , Page Salenger , Amanda Tran , Shelly Seidel , Daniel E. Weiner , Klemens B. Meyer , Caroline M. Hsu","doi":"10.1016/j.xkme.2025.101173","DOIUrl":"10.1016/j.xkme.2025.101173","url":null,"abstract":"<div><div>Despite often offering a better quality of life than in-center hemodialysis, peritoneal dialysis (PD) at home can be challenging for many. From May 2021 to October 2024, we offered PD assistance at 2 home dialysis clinics in Dialysis Clinic, Inc, a mid-size national dialysis provider. Eligible patients could be incident to or established on PD, with anticipated need for either permanent or temporary assistance. Over 3 years, 6 patients received assisted PD. Three established PD patients needed assistance when their care partners were unavailable. Three other patients required assistance to initiate PD. Assistance duration ranged from 1 day to 5 months. Three patients ultimately transitioned to PD independence, and 3 transferred to in-center hemodialysis. Our greatest challenge was hiring assistants for unpredictable work with odd hours, and we eventually hired 2 postbaccalaureate students preparing for medical careers. Our successes, minimal missed treatments, and a high rate of PD continuation are a testament to their dedication. Assisted PD programs would benefit from economies of scale by being embedded in the health care system. As interest in assisted PD grows, we advocate for sharing of programs’ successes and challenges so that we may together learn how to enable assisted PD in the US.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101173"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787200","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}
Pub Date : 2026-01-01Epub Date: 2025-11-04DOI: 10.1016/j.xkme.2025.101172
Antonio Ulpiano Trillig , Samuel Rotman , Patricia Mehier , Alain Rossier , Gérard Vogel
Acute kidney injury following sucrose-free intravenous immunoglobulins (IVIG) is rare. We report the case of a 67-year-old male who developed a sudden anuric acute kidney injury at day 4 of L-proline stabilized sucrose-free IVIG for a Guillain-Barré Syndrome. The IVIG treatment was halted. The patient did not require renal replacement therapy after an adequate response to diuretics. Amoxicillin was the sole other potential nephrotoxic. The kidney biopsy showed typical features of osmotic nephropathy (ON). Although a certain degree of kidney hypoxia due to dysautonomia and variations of blood pressure might have occurred, histological findings were not compatible with an ischemic acute tubular necrosis. There was no glomerular and vascular involvement. Immunofluorescence of tubular cells cytoplasm was negative, ruling out antibody deposition. The patient had a complete renal recovery after 2 weeks. We hypothesize that proline itself acted as a reabsorbed toxic solute and accumulated in the lysosomes, leading to ON. In this case report we discuss the proline proximal tubular transport, involving pinocytosis in case of high concentration in the filtrate, and potential mechanisms involved in the development of ON.
{"title":"Osmotic Nephropathy Induced by L-Proline Stabilized Sucrose-free Intravenous Immunoglobulins: A Case Report","authors":"Antonio Ulpiano Trillig , Samuel Rotman , Patricia Mehier , Alain Rossier , Gérard Vogel","doi":"10.1016/j.xkme.2025.101172","DOIUrl":"10.1016/j.xkme.2025.101172","url":null,"abstract":"<div><div>Acute kidney injury following sucrose-free intravenous immunoglobulins (IVIG) is rare. We report the case of a 67-year-old male who developed a sudden anuric acute kidney injury at day 4 of L-proline stabilized sucrose-free IVIG for a Guillain-Barré Syndrome. The IVIG treatment was halted. The patient did not require renal replacement therapy after an adequate response to diuretics. Amoxicillin was the sole other potential nephrotoxic. The kidney biopsy showed typical features of osmotic nephropathy (ON). Although a certain degree of kidney hypoxia due to dysautonomia and variations of blood pressure might have occurred, histological findings were not compatible with an ischemic acute tubular necrosis. There was no glomerular and vascular involvement. Immunofluorescence of tubular cells cytoplasm was negative, ruling out antibody deposition. The patient had a complete renal recovery after 2 weeks. We hypothesize that proline itself acted as a reabsorbed toxic solute and accumulated in the lysosomes, leading to ON. In this case report we discuss the proline proximal tubular transport, involving pinocytosis in case of high concentration in the filtrate, and potential mechanisms involved in the development of ON.</div></div>","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101172"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787201","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}
Pub Date : 2026-01-01Epub Date: 2025-10-29DOI: 10.1016/j.xkme.2025.101162
Kunal Malhotra , Tejas Desai , Linda H. Ficociello , Hans-Juergen Arens , Rachel A. Lasky , Michael S. Anger
<div><h3>Rationale & Objective</h3><div>Chronic kidney disease–associated pruritus is commonly related to reduced health-related quality of life, decreased adherence to dialysis, and increased mortality, yet it remains underrecognized and underdiagnosed. We conducted an analysis to characterize the relationship between pruritus and a recognized symptom cluster among hemodialysis patients.</div></div><div><h3>Study Design</h3><div>This retrospective study of adults receiving hemodialysis in a large US dialysis organization analyzed pruritus and the individual symptoms of sleep disturbance, depression, pain, anxiety, and low energy/fatigue. Data from the Kidney Disease Quality of Life 36-Item Short Form Survey (KDQOL-36) and the Patient Health Questionnaire-2 were extracted from electronic medical records.</div></div><div><h3>Results</h3><div>Of the 243,168 adults receiving hemodialysis during the study period who completed a KDQOL-36, 47,477 reported at least moderate bother from pruritus. An additional randomly sampled 33,833 adults not reporting at least moderate pruritus were also included. The KDQOL-36 ratings for each symptom (sleep disturbance, depression, pain, anxiety, and low energy/fatigue) exhibited a significantly (<em>P</em> < 0.001) greater burden with increased pruritus severity. Similar results were observed for KDQOL-36 summary scores. Extreme pruritus was associated with greater than 5-fold and 3-fold increased risk of depressive symptoms and sleep disturbance, respectively. Pruritus was also independently associated with Patient Health Questionnaire-2–defined depressive symptoms. The association of pruritus with co-occurring symptoms was demonstrated across all serum phosphorus concentration subgroups. Patients reporting higher degrees of bother from pruritus were significantly more likely to miss multiple hemodialysis sessions or have shortened treatment sessions.</div></div><div><h3>Limitations</h3><div>The cross-sectional nature of the study limits exploration of temporal relationships between the symptoms.</div></div><div><h3>Conclusions</h3><div>Among hemodialysis patients, pruritus is commonly reported and associated with reduced health-related quality of life. It should be considered alongside the following symptoms commonly observed: sleep disturbance, depression, pain, anxiety, and low energy/fatigue. The presence of one symptom should prompt further investigation, allowing for appropriate diagnosis and management.</div></div><div><h3>Plain-language Summary</h3><div>This study of adults receiving hemodialysis examined the relationship between pruritus and the individual symptoms of sleep disturbance, depression, pain, anxiety, and low energy/fatigue. Data from the Kidney Disease Quality of Life 36-Item Short Form Survey and the Patient Health Questionnaire-2 were extracted from electronic medical records. The analysis found that the presence of at least moderate patient-reported pruritus was independently associa
{"title":"Association of Chronic Kidney Disease–Associated Pruritus With the Sleep Disturbance, Depression, Pain, Anxiety, and Low Energy/Fatigue Symptom Cluster: A Retrospective Cohort Study","authors":"Kunal Malhotra , Tejas Desai , Linda H. Ficociello , Hans-Juergen Arens , Rachel A. Lasky , Michael S. Anger","doi":"10.1016/j.xkme.2025.101162","DOIUrl":"10.1016/j.xkme.2025.101162","url":null,"abstract":"<div><h3>Rationale & Objective</h3><div>Chronic kidney disease–associated pruritus is commonly related to reduced health-related quality of life, decreased adherence to dialysis, and increased mortality, yet it remains underrecognized and underdiagnosed. We conducted an analysis to characterize the relationship between pruritus and a recognized symptom cluster among hemodialysis patients.</div></div><div><h3>Study Design</h3><div>This retrospective study of adults receiving hemodialysis in a large US dialysis organization analyzed pruritus and the individual symptoms of sleep disturbance, depression, pain, anxiety, and low energy/fatigue. Data from the Kidney Disease Quality of Life 36-Item Short Form Survey (KDQOL-36) and the Patient Health Questionnaire-2 were extracted from electronic medical records.</div></div><div><h3>Results</h3><div>Of the 243,168 adults receiving hemodialysis during the study period who completed a KDQOL-36, 47,477 reported at least moderate bother from pruritus. An additional randomly sampled 33,833 adults not reporting at least moderate pruritus were also included. The KDQOL-36 ratings for each symptom (sleep disturbance, depression, pain, anxiety, and low energy/fatigue) exhibited a significantly (<em>P</em> < 0.001) greater burden with increased pruritus severity. Similar results were observed for KDQOL-36 summary scores. Extreme pruritus was associated with greater than 5-fold and 3-fold increased risk of depressive symptoms and sleep disturbance, respectively. Pruritus was also independently associated with Patient Health Questionnaire-2–defined depressive symptoms. The association of pruritus with co-occurring symptoms was demonstrated across all serum phosphorus concentration subgroups. Patients reporting higher degrees of bother from pruritus were significantly more likely to miss multiple hemodialysis sessions or have shortened treatment sessions.</div></div><div><h3>Limitations</h3><div>The cross-sectional nature of the study limits exploration of temporal relationships between the symptoms.</div></div><div><h3>Conclusions</h3><div>Among hemodialysis patients, pruritus is commonly reported and associated with reduced health-related quality of life. It should be considered alongside the following symptoms commonly observed: sleep disturbance, depression, pain, anxiety, and low energy/fatigue. The presence of one symptom should prompt further investigation, allowing for appropriate diagnosis and management.</div></div><div><h3>Plain-language Summary</h3><div>This study of adults receiving hemodialysis examined the relationship between pruritus and the individual symptoms of sleep disturbance, depression, pain, anxiety, and low energy/fatigue. Data from the Kidney Disease Quality of Life 36-Item Short Form Survey and the Patient Health Questionnaire-2 were extracted from electronic medical records. The analysis found that the presence of at least moderate patient-reported pruritus was independently associa","PeriodicalId":17885,"journal":{"name":"Kidney Medicine","volume":"8 1","pages":"Article 101162"},"PeriodicalIF":3.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787346","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}
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