Kidney360最新文献

{"title":"Sodium-Glucose Cotransporter 2 Inhibitors Prevent Nephrolithiasis in Patients with Diabetes: A TriNetX-Based Real-World Global Comparison.","authors":"Chia-Min Liu, Daniel Hsiang-Te Tsai, Hsiu-Ting Tung, Ze-Hong Lu, Edward Chia-Cheng Lai, Chan-Jung Liu","doi":"10.34067/KID.0000000981","DOIUrl":"https://doi.org/10.34067/KID.0000000981","url":null,"abstract":"<p><strong>Background: </strong>Nephrolithiasis is a prevalent condition associated with diabetes mellitus (DM) and obesity, yet effective pharmacological preventive options remain limited. Sodium-glucose cotransporter 2 inhibitors (SGLT2i), primarily used to manage type 2 DM, have shown potential lithoprotective effects.</p><p><strong>Methods: </strong>This retrospective multinational cohort study utilized electronic health records from the TriNetX database. Adults with DM initiating SGLT2i, dipeptidyl peptidase-4 inhibitors (DPP4i), or glucagon-like peptide-1 receptor agonists (GLP1-RA) were included. Propensity score matching was conducted to balance baseline covariates, yielding 358,096 matched pairs (SGLT2i vs. DPP4i) and 371,374 pairs (SGLT2i vs. GLP1-RA). The primary outcome was incidence of nephrolithiasis.</p><p><strong>Results: </strong>SGLT2i use was associated with a significantly lower risk of nephrolithiasis compared to DPP4i (1.5% vs. 1.9%; HR 0.825, 95% CI: 0.795-0.855; p < 0.001) and GLP1-RA (1.6% vs. 2.0%; HR 0.812, 95% CI: 0.784-0.840; p < 0.001). Subgroup analyses showed consistent protective effects across age, HbA1c, BMI, and renal function strata, although the association was slightly attenuated in older adults, those with suboptimal glycemic control, or impaired renal function.</p><p><strong>Conclusions: </strong>SGLT2 inhibitors may reduce the risk of nephrolithiasis among patients with DM. Possible mechanisms include increased urinary citrate excretion, urinary alkalinization, and anti-inflammatory effects. These findings suggest that SGLT2i may reduce the risk of incident nephrolithiasis in diabetic populations, particularly those with additional metabolic risk factors for nephrolithiasis.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145337363","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 Murine Model of Cardiovascular-Kidney-Metabolic Syndrome Demonstrates Compromised Limb Function in the Ischemic Hind Limb.","authors":"Saran Lotfollahzadeh, Herreet Paul, Joshua Bonifacio, Ricardo Almiron, Isaac Hockestra, Kylla Przekop, Trent Yamamoto, Maria Carmen Piqueras, Wenqing Yin, Kashvi Sethuraman, Asha Jose, Marina Malikova, Jeffrey J Siracuse, Mostafa Belghasem, Howard Cabral, Nazish Sayed, Vipul Chitalia","doi":"10.34067/KID.0000000900","DOIUrl":"https://doi.org/10.34067/KID.0000000900","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular-Kidney-metabolic (CKM) syndrome is a public health problem in the US and results in premature CVD at a relatively preserved GFR. The molecular mediators of CKM are poorly understood, partly due to the lack of a reliable animal model. We set out to generate an animal model with renal and metabolic dysfunctions, using peripheral arterial disease (PAD) as a CKM manifestation.</p><p><strong>Methods: </strong>C57BL/6 male and female mice were randomized into four groups: a normal diet (ND, controls), a 0.2% adenine diet (AD, a CKD model), a high-fat diet (HFD, a metabolic model), and a combination of HFD+AD (a potential CKM model). The mice underwent a hind limb ischemia, followed by an array of structural, endurance and post-exercise hyperemia assays.</p><p><strong>Results: </strong>Compared to control mice, HFD+AD male mice had 23-50% higher weight and GFR than the AD group (P = 0.003). The kidneys of HFD+AD showed tubular atrophy, tubulointerstitial fibrosis, immune infiltration, glomerulomegaly, consistent with glomerular hyperperfusion, hypercholesterolemia, impaired glucose tolerance, and adipophilin in the liver, an early marker of hepatic steatosis, and myocardial fibrosis. The HFD+AD mice showed reductions in the hind limb perfusion ratios, microcapillary density, Type II muscle fibers, and increased muscle fibrosis, immune infiltration, and lowest cross-sectional muscle area. Female CKM mice revealed distinct differences from male mice. Compared to AD and HFD alone, female CKM mice exposed to HFD+AD demonstrated additive phenotypes in endurance assays (distance traveled, exhaustion time, and grip strength) without a similar effect in post-ischemia perfusion, suggesting skeletal muscle and microcapillary dysfunction.</p><p><strong>Conclusions: </strong>A combination of HFD+AD in mice displays features of CKD, metabolic disorders, and cardiovascular disease at a higher GFR, consistent with human CKM. This model can be explored to probe the mechanisms and heterogeneity and sex-specific differences in CKM.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286423","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":"Brachial-Ankle Pulse Wave Velocity is Associated with Kidney Function Decline in Adults Undergoing Cardiovascular Disease Screening.","authors":"Caroline B Ledet, Meliksah Arslan, Kylie Van Dyke, A Rauoof Malik, Iftikhar J Kullo","doi":"10.34067/KID.0000000973","DOIUrl":"https://doi.org/10.34067/KID.0000000973","url":null,"abstract":"<p><strong>Background: </strong>CKD affects 35 million adults in the US and is associated with high morbidity and mortality. We investigated whether brachial-ankle pulse wave velocity (baPWV), a non-invasive measure of arterial stiffness, was associated with kidney function decline in adults undergoing cardiovascular disease (CVD) screening.</p><p><strong>Methods: </strong>In 1,862 patients referred for an exercise ECG test between 2007-2009, baPWV was measured using an Omron Colin oscillometric device. Creatinine-based GFR was estimated (eGFRCr) for participants with available baseline and follow-up creatinine values using the CKD-EPI formula. We performed multivariable linear regression analyses to assess whether baseline baPWV was associated with annualized change in eGFRCr (∆ eGFRCr), after adjustment for age, sex, body mass index (BMI), baseline eGFRCr, and traditional CVD risk factors, including mean arterial pressure (MAP), diabetes and hypertension diagnoses, nephroprotective medication use, smoking status, and total cholesterol. To determine risk of developing CKD and CKD-free survival time by arterial stiffness subgroups, we performed covariable-adjusted Cox proportional hazards modeling and a Kaplan-Meier survival analysis, respectively.</p><p><strong>Results: </strong>After exclusion of participants with missing covariable data and adjustment for covariables, one standard deviation increase in baPWV was associated with a 0.18 mL/min/1.73 m2 BSA greater yearly decrease in eGFRCr (P=0.023) over a median follow-up time of 13.2 years. Participants with higher baseline baPWV had increased risk of CKD (HR (95% CI), P-value; elevated baPWV: 2.4 (1.1, 5.4), P=0.037; borderline-elevated baPWV: 1.8 (1.1, 3.1), P =0.028) and had a shorter CKD-free survival time (median CKD-free survival time (years); normal baPWV: 16.2; borderline-elevated baPWV: 16.0; elevated baPWV: 15.6 (P<0.001)).</p><p><strong>Conclusions: </strong>Elevated baPWV, a noninvasive measure of arterial stiffness that can be obtained in the office setting, was associated with decline in kidney function, risk of CKD development, and CKD-free survival in individuals undergoing CVD screening.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275072","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":"Transdermal GFR Enables Early Detection of Functional Acute Kidney Injury in a Cirrhotic Mouse Model Without Tubular Injury.","authors":"Xuegang Zhao, Xin Sui, Huimin Yi, Jianrong Liu, Yufeng He, Yangbin Li, Lixin Tang, Yunshan Zou, Haijin Lyu","doi":"10.34067/KID.0000001007","DOIUrl":"https://doi.org/10.34067/KID.0000001007","url":null,"abstract":"<p><strong>Background: </strong>AKI is a common complication associated with significant mortality in patients with end-stage liver disease. Current diagnostic criteria primarily rely on serum creatinine levels, which may be influenced by reduced muscle mass commonly observed in cirrhotic patients, thereby delaying the recognition of renal impairment. This study aims to evaluate the efficacy of transdermal glomerular filtration rate (tGFR) measurement for the early diagnosis of renal dysfunction in a AKI murine model of cirrhosis.</p><p><strong>Methods: </strong>A murine model of cirrhosis-associated AKI (cAKI) was established through a 12-week regimen of intragastric administration of 50% carbon tetrachloride (CCl4, 1 mL/kg), followed by a single intraperitoneal injection of lipopolysaccharide (LPS). Renal function was evaluated using transdermal glomerular filtration rate (tGFR) measurement and compared with conventional markers, including serum creatinine and blood urea nitrogen (BUN) levels.</p><p><strong>Results: </strong>Following the induction of the murine model of cAKI, mice received a single intravenous dose of fluorescein-isothiocyanate (FITC)-conjugated sinistrin (75 mg/kg). FITC-sinistrin fluorescence intensity was continuously monitored every 2 seconds for 1.5 to 2 hours using a skin-attached miniaturized sensor. The transdermal glomerular filtration rate (tGFR) was calculated based on a relative fluorescence intensity (RFI) curve using a two-compartment pharmacokinetic model. Serum blood urea nitrogen (BUN) and creatinine (CREA) levels were measured at 2, 4, 8, 12, and 24 hours after LPS administration. Histological analysis revealed that cAKI did not induce significant tubular injury. Notably, tGFR detected a significant reduction in glomerular filtration as early as 2 hours post-LPS ( 0.54± 0.207 vs. 1.06 ± 0.273 μL/min/100 g), whereas BUN levels did not rise significantly until 4 hours (33.94 ± 3.683 vs. 18.7 ± 2.414mmol/L). Serum creatinine and the BUN/CREA ratio showed no significant changes throughout the observation period.</p><p><strong>Conclusions: </strong>Transdermal glomerular filtration rate demonstrates superior sensitivity compared to creatinine- and BUN-based criteria for the early detection of renal impairment in cirrhosis-associated AKI, highlighting its potential clinical utility and warranting further investigation.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355380","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":"Comparative Impact of Early Graft Function on Kidney Transplantation Outcomes According to Donor Types.","authors":"Jeongin Song, Eunjeong Kang, Sehyun Jeong, Hyung Eun Son, Ahram Han, Sangil Min, Jongwon Ha, Jung Pyo Lee, Jong Cheol Jeong, Sehoon Park, Yong Chul Kim, Dong Ki Kim, Yon Su Kim, Hajeong Lee","doi":"10.34067/KID.0000000933","DOIUrl":"https://doi.org/10.34067/KID.0000000933","url":null,"abstract":"<p><strong>Background: </strong>With the rise of high-risk living donor kidney transplantation, the impact of early graft function (EGF) on transplant outcomes remains unclear.</p><p><strong>Methods: </strong>In this retrospective multicenter study, we classified kidney transplantation recipients (KTRs) based on EGF and donor type. EGF within the first post-transplant week was classified as immediate graft function (IGF), slow graft function (SGF), or delayed graft function (DGF), with impaired EGF defined as SGF or DGF. The primary outcomes included biopsy-proven acute rejection (BPAR) within one year, death-censored graft failure (DCGF), and overall mortality.</p><p><strong>Results: </strong>Among 3,261 KTRs, 365 (11.2%) experienced impaired EGF, including 190 (5.8%) with SGF and 175 (5.4%) with DGF. In living donor KTRs, impaired EGF was significantly associated with an increased risk of one-year BPAR (aHR, 2.13; 95% CI, 1.33-3.39) and DCGF (aHR: 2.49, 95% CI: 1.29-4.82) but not mortality. Both SGF and DGF increased the risk of BPAR, while only DGF significantly elevated the risk of DCGF. In deceased donor KTRs, impaired EGF was associated with a higher risk of both DCGF (aHR, 2.18; 95% CI, 1.43-3.31) and mortality (aHR, 2.30; 95% CI, 1.52-3.49) with SGF and DGF demonstrating similar patterns. Notably, prolonged DGF (≥7 days) was linked to progressively worse outcomes.</p><p><strong>Conclusions: </strong>The impact of impaired EGF varies by donor type. In living donor KTRs, impaired EGF increased the risks of BPAR and DCGF, particularly in cases of DGF. In deceased donor KTRs, impaired EGF elevated the risks of DCGF and mortality but not BPAR, highlighting the need for tailored strategies to optimize EGF.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251696","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":"External Validation of the Kidney Donor Profile Index (KDPI) to Predict Long-Term Graft Survival in Kidney Transplant Recipients.","authors":"Bianca Cassão, Renato D Foresto, Maria Amélia Hazin, Ana Paula Morais, Luis Gustavo Modelli de Andrade, José Medina-Pestana, Lúcio Requião-Moura, Helio Tedesco-Silva","doi":"10.34067/KID.0000000946","DOIUrl":"https://doi.org/10.34067/KID.0000000946","url":null,"abstract":"<p><strong>Background: </strong>The Kidney Donor Profile Index (KDPI), developed in the United States, is widely used to predict graft failure after kidney transplantation. However, external validation is crucial to assess its performance in other populations. This study aimed to validate KDPI in Brazilian kidney transplant recipients.</p><p><strong>Methods: </strong>We conducted a single-center, retrospective cohort study involving 1,807 recipients of deceased-donor kidney transplants performed between January 2013 and December 2015, with a 5-year follow-up. The model's discrimination, overall fitness, and calibration were assessed in predicting graft failure.</p><p><strong>Results: </strong>Recipients were 49.2 years old, 60.8% were male, on hemodialysis for 40.1 months. The median KDRI and KDPI were 1.2 and 69%, respectively. The AU-ROC for graft survival was highest in the KDPI >85% category [0.576 (95%CI: 0.521-0.631)], followed by the >35-85% [0.504 (95%CI: 0.460-0.549)] and the 0-35% [0.488 (95%CI: 0.408-0.568)] categories. Discrimination improved in the Cox model incorporating recipient variables and KDPI categories [0.801 (95%CI: 0.775-0.827)]. The KDPI as a continuous variable had a C-index of 0.561 (95%CI: 0.533-0.588), similar to donor age alone [0.560 (95%CI: 0.534-0.587)]. The overall fitness assessed by the Brier score was 0.151, and the calibration plot showed a good performance for KDPI. However, it was similar to what was observed using the donor age as a predictor isolated (0.152).</p><p><strong>Conclusions: </strong>In this transportability external validation study, KDPI performed acceptably as a prediction tool for 5-year graft survival after kidney transplantation. These findings guide organ allocation and support clinical decision-making regarding organ acceptance.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244636","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":"Serum AKR1A1 Levels Predict eGFR Decline Rate in African Americans with Type 2 Diabetes.","authors":"Lijun Ma, Young A Choi, DengFeng Li, Moin A Saleem, Barry I Freedman","doi":"10.34067/KID.0000000966","DOIUrl":"https://doi.org/10.34067/KID.0000000966","url":null,"abstract":"<p><strong>Background: </strong>African Americans have disproportionately high rates of diabetic kidney disease (DKD). Identification of biomarkers predicting early DKD progression is essential to prescribe protective treatments prior to the development of irreversible histologic lesions and markedly reduced kidney function.</p><p><strong>Methods: </strong>We tested whether AKR1A1 was a marker of early DKD progression via knock-out of AKR1A1 in a human kidney proximal tubule cell line, and by measuring serum AKR1A1 concentrations in African Americans with type 2 diabetes (T2D).</p><p><strong>Results: </strong>AKR1A1 knockout cells had reduced cell viability, and the effect was aggravated by administering high dose palmitate. In addition, higher serum AKR1A1 concentrations in African Americans with T2D and preserved kidney function predicted slower decline rate in estimated glomerular filtration rate over time.</p><p><strong>Conclusions: </strong>AKR1A1 appears to play a critical role in countering toxic effects of fatty acid metabolism and may prevent rapid decline of kidney function in African Americans with T2D.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238835","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 Between Urinary Fractional Excretion of Potassium and Proteinuria Remission in Adult Nephrotic Syndrome.","authors":"Ryuto Yoshida, Takashin Nakayama, Ryunosuke Mitsuno, Motoaki Komatsu, Yoichi Oshima, Seiei Iwabuchi, Tomoaki Itoh, Dai Matsumoto, Ei Kusahana, Kenta Hoshi, Kyosei Nakamura, Kentaro Fujii, Yoshikazu Hara, Takahisa Kawaguchi, Koji Futatsugi, Yasuyoshi Yamaji, Hirobumi Tokuyama, Marohito Murakami, Chie Takimoto, Hiroto Matsuda, Takashi Ando, Akinori Hashiguchi, Yuko Kaneko, Tatsuhiko Azegami, Kaori Hayashi","doi":"10.34067/KID.0000000997","DOIUrl":"https://doi.org/10.34067/KID.0000000997","url":null,"abstract":"<p><strong>Background: </strong>Reliable prognostic biomarkers of nephrotic syndrome (NS) are crucial for optimizing patient management. The fractional excretion of potassium (FEK) reflects net tubular potassium handling, but its association with prognosis in NS remains unexplored. We aimed to investigate the association between baseline FEK and proteinuria remission in adult NS.</p><p><strong>Methods: </strong>This multicenter retrospective cohort study was conducted across nine institutions in Japan. We enrolled adult patients diagnosed with NS who underwent a native kidney biopsy and had FEK between January 2012 and June 2022. Patients were categorized based on FEK levels and followed until the first complete remission of proteinuria.</p><p><strong>Results: </strong>A total of 401 patients (median age, 61 years; 43% female) were included. Study participants were stratified into two groups based on the FEK cutoff value of 10%. Patients with high FEK had a significantly lower cumulative incidence of complete remission compared to those with low FEK (P < 0.001, log-rank test). In multivariable Cox regression analysis, high FEK was independently associated with a lower likelihood of complete remission (hazard ratio, 0.53; 95% confidence interval, 0.36-0.78). The trend of this association was observed across most subgroups, including those based on histological diagnosis of minimal change disease (MCD) and non-MCD. Further stratification into four FEK categories revealed a progressive decline in remission rates with increasing FEK, indicating a dose-dependent relationship.</p><p><strong>Conclusions: </strong>Elevated FEK is an independent predictor of a lower likelihood of proteinuria remission in Japanese adults with NS. FEK may serve as a readily accessible and valuable prognostic biomarker in the clinical management of NS.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238862","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":"The Effect of Dialysate Sodium on Endothelial Injury and Microcirculatory Dysfunction.","authors":"Lisa Hur, Yanmin Zhang, Alireza Akbari, Eric K Patterson, Barry G H Janssen, Christopher W McIntyre","doi":"10.34067/KID.0000000949","DOIUrl":"https://doi.org/10.34067/KID.0000000949","url":null,"abstract":"<p><strong>Background: </strong>Hemodialysis (HD) causes injury to the glycocalyx, inducing shedding of syndecan-1. This damage results from hemodynamic stress of HD and injury caused by oncotic shifts in the presence of additional sodium. The aim of this study is to investigate the effects of sodium dialysate concentration on endothelial cell injury and microcirculatory dysfunction during HD. We hypothesize that changes in plasma sodium concentration will result in direct injury to the glycocalyx and reduce microcirculatory perfusion.</p><p><strong>Methods: </strong>Twenty-seven healthy male Wistar Kyoto rats underwent HD: eight were exposed to 140mM sodium dialysate concentration (control), ten were exposed to low sodium dialysate (130mM), and nine were exposed to high sodium dialysate (150mM). Throughout HD, intravital microscopy was used to image the microvasculature perfusion at baseline, during extracorporeal circulation with no dialysate flow (\"Sham\"), at 1 hr into HD, at 2 hrs into HD, and post HD (\"Final\"). Blood samples were collected at the same timepoints corresponding to the intravital microscopy image acquisitions to measure syndecan-1.</p><p><strong>Results: </strong>The findings demonstrate a gradual increase in syndecan-1 concentration in blood plasma and a consistent trend of lower perfusion throughout the duration of the experiment in all experimental groups. Particularly, syndecan-1 concentration in plasma was significantly higher at 2 hrs into HD in the high sodium dialysate group compared to the control and low sodium dialysate group.</p><p><strong>Conclusions: </strong>HD results in direct acute endothelial injury and microcirculatory disturbance. This effect is aggravated by exposure to supraphysiological concentrations of sodium, potentially resulting in sustained injury to the glycocalyx.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225563","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":"Time to Inject Some Contrast into the Nephrotoxicity Debate.","authors":"Nans Florens, Julien Demiselle","doi":"10.34067/KID.0000001019","DOIUrl":"https://doi.org/10.34067/KID.0000001019","url":null,"abstract":"<p><p>Iodinated contrast media have long been feared for causing \"contrast-induced AKI\" (CI-AKI), a concern rooted in early reports with high-osmolar agents. Experimental data suggest potential nephrotoxic mechanisms, yet clinical evidence from older uncontrolled studies was confounded by comorbidities and procedural risks. Contemporary propensity-matched and controlled analyses consistently show that modern low- and iso-osmolar contrast agents (mostly intravenously administered) uncommonly cause true nephrotoxicity, even among high-risk populations such as patients with advanced chronic kidney disease, acute kidney injury, or critical illness. Large randomized trials, including PRESERVE, found no difference in outcomes between sodium bicarbonate and isotonic saline hydration as preventive strategies, nor N-acetylcysteine administration, and highlighted risks like fluid overload. Persistent fear of CI-AKI has fueled \"renalism\": unnecessary avoidance or delay of essential imaging, leading to worse outcomes. Current consensus emphasizes individualized care-avoiding hypovolemia, limiting contrast dose, and withholding nephrotoxins only in severe kidney impairment. A balanced, evidence-based approach should replace outdated caution.</p>","PeriodicalId":17882,"journal":{"name":"Kidney360","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213227","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}