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Although progress has been made toward elucidating cellular pathways related to initial cystogenesis in autosomal dominant polycystic kidney disease (ADPKD), the mechanisms that contribute to disease progression and the timing of transitions remain largely unclear. We hypothesized that the predominant kidney biological processes in Pkd1 RC/RC and other ADPKD models are highly dynamic throughout the disease, providing insights into the resulting kidney phenotype and conform well to those observed in human ADPKD. Kidney volume changes by class and age were determined in a large, well-characterized cohort of individuals with ADPKD and long follow-up. Similarly, Pkd1 RC/RC and wild-type (WT) mice were studied longitudinally, and their kidney volume changes and function analyzed. Kidney mRNA profiles (mRNA-sequencing [mRNA-seq]) of Pkd1 RC/RC mice were investigated at early, mid, and late stages, compared with those reported in other ADPKD models and humans with ADPKD. In most individuals with ADPKD, kidney volume continues to increase; however, the rate of growth differs between classes and within severe classes by age. Kidney volume and function changes in Pkd1 RC/RC mice conform well to the kidney volume changes in class 1C patients during adulthood. The kidney transcriptomic profile in Pkd1 RC/RC mice evolves over the course of the disease, underscoring their highly dynamic kidney phenotype, presents several commonalities with other ADPKD models, and is relevant to human ADPKD. Our study suggests that, in ADPKD, different therapeutic strategies might be beneficial at different disease stages and identifies target candidate pathways for biomarker discovery that could be further investigated in humans.

Estimated glomerular filtration rate (GFR, eGFR) from serum creatinine outlines global kidney function, subject to biases in clinical scenarios from muscle wasting and inflammation (prevalent in kidney cancer) and failure to estimate split renal function (SRF, crucial in operative planning). Measured GFR (mGFR) (or true mGFR [mGFRt] without body surface area normalization) from diethylene-triamine-pentaacetate (99mTc-DTPA) tracer clearance is the gold standard for bilateral kidney function, involving extended clearance times and radioactivity. Imaging-derived total kidney volumes are functional proxies but do not probe tissue quality. We employed advanced quantitative diffusion-weighted (DW) magnetic resonance (MR) imaging (MRI) at 3.0 T in addition to kidney volume measurements in a cohort of 27 patients with renal mass (26 and 18 underwent eGFR and mGFR tests, respectively). Cardiac-gated diffusion tensor imaging (DTI) and intravoxel incoherent motion (IVIM) parameters were derived. Individual MR metrics were evaluated for correlation with eGFR and mGFR with Pearson correlations and mixed-model analysis, respectively; LASSO-penalized multivariable regression was employed for mGFR prediction. The metrics were compared between proteinuria groups using 2-sample t tests. Kidney volume correlated with renal function (split volume vs. split mGFR r = 0.54; split volume vs. split mGFRt r = 0.69). MR metrics correlated with individual kidney mGFR and mGFRt (r = 0.76 and 0.81, respectively). Mixed-effects LASSO multiple regression analysis predicted mGFR and mGFRt (R2 = 0.880 and 0.700, respectively). In addition, MR metrics differentiated proteinuria status. Advanced DW MRI metrics may provide surrogates of mGFR and proteinuria. Parameters from bipolar encoding in diastole (emphasizing tubular flow) and flow compensation in systole (emphasizing vascular flow) were often informative.

Urine albumin-to-creatinine ratio (UACR) provides a reliable method for chronic kidney disease screening in patients with type 2 diabetes, yet its use remains underutilized. The CKD-DETECT randomized clinical trial included outpatients &#x2265;18 years with type 2 diabetes without UACR testing in the prior 12 months and no chronic kidney disease. Physicians were randomized to receive either an alert prompting UACR testing or no alert (control). The primary outcome was the proportion of UACR orders within 90 days. The secondary outcome was new chronic kidney disease stage 3-5 diagnoses. Tertiary outcomes were referral to a nephrologist and prescription of chronic kidney disease-related medications, and post-hoc outcomes were UACR &#x2265;10 mg/g and &#x2265;30 mg/g. Overall, 400 patients (mean age 64.7 years; 51.5% female) were included. UACR was ordered in 72 (36.0%) patients in the alert group vs. 23 (11.5%) in the control group (odds ratio [OR] 5.71; 95% confidence interval [CI] 2.58-12.64; P<0.001). New diagnoses of chronic kidney disease occurred in 1 (0.5%) patient in the alert and 2 (1.0%) in the control group (OR 0.50, 95%CI 0.04-5.53; P=0.570). There were no referrals to nephrologists or new prescriptions of chronic kidney disease-related medications. The alert group was associated with increased identification of UACR &#x2265;10 mg/g (21.0% vs. 8.5%; OR 3.41; 95%CI 1.37-8.48; P=0.008) and &#x2265;30 mg/g (9.5% vs. 4.0%; OR 3.71; 95%CI 1.36-10.12; P=0.011). The alert-based CDS program was associated with increased UACR testing and early detection of elevated albuminuria in patients with diabetes. ClinicalTrials.gov identifier, NCT05342545 (prospectively registered on April 18, 2022) FUNDING: : This work was supported by a research grant from Bayer.

Few population-based data exist in the U.S. about adults with IgA nephropathy (IgAN) and risks of kidney, cardiovascular, and mortality outcomes versus those with nonglomerular chronic kidney disease (CKD) or without CKD. We applied natural language processing (NLP) algorithms to electronic health record (EHR) data within a large integrated healthcare delivery system to identify adults with biopsy-proven IgAN between 2010 and 2020. We next identified 2 separate comparison cohorts of adults with nonglomerular CKD and adults without CKD matched on age and sex, and compared the rates of end-stage kidney disease (ESKD), worsening CKD, acute kidney injury (AKI), cardiovascular outcomes, and death through 2021 using multivariable Cox proportional hazards models. We identified 1651 adults with biopsy-confirmed IgAN who had a mean age of 43 years and 48% women, 41% Asian or Pacific Islander, and 3.3% Black. Compared with matched adults with nonglomerular CKD (n = 9863), those with IgAN had higher adjusted rates of ESKD (adjusted hazard ratio [aHR]: 2.79, 95% CI: 2.16-3.62), worsening CKD (aHR: 3.05, 95% CI: 2.68-3.46), and AKI (aHR: 1.45, 95% CI: 1.22-1.73) but no significant adjusted differences in cardiovascular events and death. Compared with matched adults without CKD (n = 16,510), patients with IgAN had substantially higher adjusted rates of adverse kidney outcomes as well as higher adjusted rates of hospitalization for heart failure (aHR: 8.06, 95% CI: 2.90-22.37) and death (aHR: 2.90, 95% CI: 2.08-4.02) but not acute myocardial infarction or stroke/transient ischemic attack. Adults with IgAN are at greater risk of adverse kidney outcomes versus nonglomerular CKD and substantially higher risks of heart failure and death compared with no CKD.

Total kidney volume (TKV) interpreted via the Mayo Imaging Classification (MIC) is the recommended prognostication tool in autosomal dominant polycystic kidney disease (ADPKD), but further risk stratification is often needed. The kidney failure risk equation (KFRE) is validated in chronic kidney disease (CKD) of diverse etiologies, but its use in patients with ADPKD already assessed via the MIC is unclear. This study evaluated the impact of adding KFRE to MIC. Adults with ADPKD with &#x2265;1 computed tomography (CT) or magnetic resonance imaging (MRI) derived TKV available between January 2015 and January 2023 were included in this retrospective observational study. The predictive performance of models including the MIC value, baseline estimated glomerular filtration rate (eGFR), and 5-year KFRE score, and fully adjusted models were examined using the composite outcome of kidney replacement therapy initiation or eGFR decline 40%. The primary analysis was in patients with eGFR < 60 ml/min per 1.73 m2. In the eGFR < 60 ml/min per 1.73 m2 group, compared with the model showing MIC value alone, the adjusted model including age, sex, tolvaptan, KFRE, and MIC value demonstrated the best performance (Akaike information criterion [AIC] = 631, &#x394;C-statistic = 0.47, 0.28, and 0.27 at 1, 3, and 5 years respectively), followed closely by the combination of MIC value and KFRE (AIC = 641, &#x394;C-statistic = 0.47, 0.26, and 0.26), KFRE alone (AIC = 642, &#x394;C-statistic = 0.47, 0.26, and 0.28) at 1, 3, and 5 years respectively. In the cohort with a baseline eGFR < 60 ml/min per 1.73 m2, use of the KFRE in addition to the MIC improved risk prediction, supporting the utilization of these tools together in ADPKD.

Historical case series of monoclonal Ig deposition disease (MIDD) after kidney transplantation (KTx) reported unfavorable outcomes. Recent case series support more acceptable outcomes in selected patients. We performed a pooled analysis of case series and case reports using available individual participant data (IPD). We searched MEDLINE, Web of Science, SCOPUS, Cochrane Library, and gray literature. Recurrence-free survival, graft survival, and overall survival from the time of KTx were analyzed. Sensitivity analyses were performed according to publication type, hematologic response before KTx, exposure to novel agents, and era. Eighty-seven kidney allografts were included from case series and case reports between 1986 and 2023. During the median follow-up of 46 months, recurrence occurred in 47 allografts (54%), at a median of 30 months after KTx. The estimated median recurrence-free survival was significantly longer in patients who achieved a very good partial response (VGPR) hematologic response or better. Graft survival at 5- and 10-years was 67.1% and 45.9% respectively. Recurrence was the main cause of the graft loss in the majority. Among the patients who faced recurrence, the median time from recurrence to graft failure was longer in those who received clone-directed therapies (62 vs. 11 months, P = 0.02). Overall survival rates at 5 and 10 years were 83.8% and 47.4%, respectively. More recent outcomes of patients with MIDD after KTx are favorable. Clone-directed therapies in recurrent disease appear to prolong graft survival.

Chronic kidney disease is a common comorbidity of rheumatoid arthritis. Because there has been scarce and conflicting evidence on the use of biological and targeted synthetic therapy in patients with rheumatoid arthritis and chronic kidney disease, we aimed to examine the effectiveness and persistence of biological and targeted synthetic disease-modifying antirheumatic drugs (DMARDs) for patients with rheumatoid arthritis and chronic kidney disease. This multicentre, prospective cohort study used data from the CorEvitas Rheumatoid Arthritis registry on patients with rheumatoid arthritis who initiated each type of biological and targeted synthetic DMARD (TNF inhibitors, CTLA4 immunoglobulin, IL-6 inhibitors, B-cell depletion therapy, and JAK inhibitors) recruited from 160 rheumatology practices in the USA. Patients were required to have moderate or high disease activity according to the Clinical Disease Activity Index (CDAI; score >10). Chronic kidney disease was defined as an estimated glomerular filtration rate (eGFR) of less than 60 mL/min per 1&#xb7;73 m2 at biological or targeted synthetic DMARD initiation. The primary outcome was the attainment of remission according to CDAI score. Propensity scores were used for overlap weighting to improve the balance of characteristics for patients with and without reduced eGFR. Cox regressions estimated the unadjusted and adjusted hazard ratio (HR) of reduced eGFR for CDAI-based remission. People with lived experience of rheumatoid arthritis were not involved in the study design or conduct. Between Oct 1, 2001, and Dec 31, 2023, 12&#x2009;123 biological and targeted synthetic DMARD treatment initiations in 9601 patients with rheumatoid arthritis, with 51&#x2009;931 person-years of follow-up, were identified. Of 12&#x2009;123 eligible biological and targeted synthetic DMARD treatment initiations, 10&#x2009;857 (89&#xb7;6%) were in patients with preserved eGFR and 1266 (10&#xb7;4%) were in patients with reduced eGFR. Across both groups, median age was 59&#xb7;0 years (IQR 50&#xb7;0-67&#xb7;0), 9720 (80&#xb7;2%) of 12&#x2009;123 treatment initiations were in female patients and 2403 (19&#xb7;8%) were in male patients, and 9908 (81&#xb7;7%) were in non-Hispanic White patients. 3025 (27&#xb7;9%) of 10&#x2009;857 treatment initiations in patients with preserved eGFR resulted in CDAI-based remission versus 246 (19&#xb7;4%) of 1266 treatment initiations in patients with reduced eGFR. Reduced eGFR was associated with a lower likelihood of attaining CDAI-based remission (unadjusted HR 0&#xb7;71 [95% CI 0&#xb7;62-0&#xb7;82], adjusted HR 0&#xb7;76 [0&#xb7;66-0&#xb7;88]) compared with preserved eGFR. Although biological and targeted synthetic DMARDs are generally well tolerated and effective options, patients with rheumatoid arthritis and reduced eGFR have lower likelihood of attaining remission. Tailored treatment strategies for this high-risk population should be established. National Institute of Arthritis and Musculoskeletal and Skin Diseases.

Generalized tonic-clonic seizures are a recognized cause of rhabdomyolysis and may be complicated by acute kidney injury, particularly when muscle injury is severe or prolonged. We describe the case of a 53-year-old man who presented following a witnessed generalized seizure and collapse, with subsequent development of severe rhabdomyolysis and stage three acute kidney injury. Initial assessment focused on neurological and infectious causes of altered consciousness, including neuroimaging and cerebrospinal fluid analysis, which did not demonstrate an acute intracranial or central nervous system infectious process. During admission, renal function progressively deteriorated, accompanied by electrolyte abnormalities. Serial biochemical testing later revealed a marked rise in creatine kinase, peaking at greater than 89,000 international units per liter, confirming severe rhabdomyolysis. Extensive investigations excluded alternative causes of renal impairment, including autoimmune, vasculitic, obstructive, and glomerular pathology. The patient was managed with aggressive intravenous fluid resuscitation, electrolyte correction, and supportive care, resulting in gradual improvement in renal function and down-trending creatine kinase levels without the need for renal replacement therapy. This case highlights the evolving nature of seizure-associated rhabdomyolysis and its potential to cause significant acute kidney injury. It emphasizes the importance of considering rhabdomyolysis in patients presenting after generalized seizures and supports early measurement and monitoring of creatine kinase to guide timely management and reduce the risk of renal complications.

Sex steroids in male patients decrease along with the progression of chronic kidney disease (CKD) and are associated with worse outcomes. This study aimed to increase the knowledge of the pathophysiology of biochemical hypogonadism in male CKD and its reversibility after kidney transplantation (KT). We comprehensively mapped the hypothalamic-pituitary-gonadal (HPG) axis in 120 male patients (age 65 yrs, body mass index [BMI]: 26.8 kg/m2) with CKD stage 1 to 5, and 120 kidney-healthy controls, matched (1:1) for age and BMI. Additionally, we monitored the HPG axis in 50 male kidney transplant recipients (age 60 yrs) from the time of transplantation up to 12 months. Testosterone (T) was measured by liquid chromatography tandem mass-spectrometry. Luteinizing hormone (LH), follicle stimulating hormone (FSH), and inhibin B levels were assessed by immunoassay. T/LH ratio and inhibin B/FSH ratio served as a proxy for the function of Leydig and Sertoli cells, respectively. Hypogonadism is prevalent in CKD and is characterized by depressed T/LH ratio (1.75 [0.71-2.96] vs. 3.99 [2.39-5.20], P < 0.0001) and inhibin B/FSH ratio (14.40 [1.24-33.64] vs. 32.24 [16.27-56.72], P < 0.0001). T levels showed a steady increase shortly after transplantation, whereas LH levels decreased, resulting in a higher T/LH ratio (P < 0.0001). Inhibin B levels decreased after 3 months, resulting in a lower inhibin B/FSH ratio after 3 months (P < 0.0001), with partial recovery after 12 months. Male patients with CKD showed low T/LH and inhibin B/FSH ratios pointing towards testicular failure as underlying pathophysiological mechanism. Male CKD can be considered a state of premature testicular ageing. Leydig cell function rapidly recovered after KT suggesting a functional cause of CKD-induced hypogonadism. In contrast, Sertoli cell function showed a deterioration, especially in the early post-transplant period.

Warfarin is a widely used oral anticoagulant with a narrow therapeutic index and multiple drug-drug interactions that may significantly alter its anticoagulant effect. Torsemide, a loop diuretic commonly prescribed for heart failure and fluid overload, shares metabolic pathways with warfarin, raising the possibility of clinically significant interactions. However, the evidence regarding this interaction remains limited and inconsistent. A 66-year-old male with a history of type 2 diabetes mellitus, hypertension, chronic kidney disease, and prior aortic valve replacement on chronic warfarin therapy presented with extensive soft tissue necrosis of the left leg following minor trauma. During hospitalization, warfarin (3 mg once daily) and Torsemide (20 mg once daily) were initiated concurrently. Subsequently, the patient developed a progressive elevation in international normalized ratio (INR), necessitating repeated fresh frozen plasma transfusions due to increased bleeding risk. Despite supportive management, INR remained elevated. Torsemide was discontinued and replaced with furosemide, after which a gradual stabilization of INR levels was observed. The patient later required left above-knee amputation due to worsening necrosis but recovered following multidisciplinary management. Assessment using the Naranjo Adverse Drug Reaction Probability Scale suggested a possible interaction between warfarin and Torsemide. This case highlights a potential interaction between warfarin and Torsemide resulting in elevated INR and increased bleeding risk. Clinicians should exercise caution and ensure close INR monitoring when initiating Torsemide in patients receiving warfarin therapy.

Coronavirus Disease 2019 (COVID-19) primarily affects the respiratory system but can also cause acute kidney injury (AKI). Infection-related circulatory disturbances driven by systemic inflammation, cytokine release, and reduced effective blood volume play a central role in prerenal AKI. The diagnostic challenge in infection-associated AKI is distinguishing functional hypoperfusion from intrinsic renal injury, particularly when relying solely on serum creatinine. Laboratory investigations showed elevated blood urea nitrogen (BUN) (51&#x202f;mg/dL) and serum creatinine (2.7&#x202f;mg/dL), with reduced estimated glomerular filtration rate (eGFR) of 32.5&#x202f;mL/min. Targeted urinary indices (low urine sodium, high osmolality, and FeNa <1%) were instrumental in identifying a reversible perfusion-related etiology, minimizing the risk of diagnostic misclassification. Renal ultrasonography showed normal kidney size and architecture. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection was confirmed by reverse transcription polymerase chain reaction (RT-PCR). The patient received oxygen therapy, IV Ringer's lactate, furosemide for diuresis, low-molecular-weight heparin for thromboprophylaxis, and ceftriaxone for secondary infection prevention. Potassium imbalance was corrected with intravenous and oral supplementation of potassium chloride. Urine output improved within 48&#x202f;h, and renal function recovered (eGFR 61&#x202f;mL/min/1.73&#x202f;m&#xb2;) without renal replacement therapy. Two consecutive negative RT-PCR tests confirmed viral clearance. The patient was discharged in stable condition with outpatient follow-up.

Autosomal dominant acute porphyrias are rare inherited disorders of haem biosynthesis characterised by accumulation of potentially neurotoxic porphyrin precursors and attacks of severe abdominal pain with autonomic and neuropsychiatric features. Disease severity ranges from asymptomatic individuals to those with recurrent, life-threatening attacks. The International Porphyria Network invited 34 acute porphyria specialists from 17 countries to form an expert panel. The invited group included clinicians from diverse specialities (ie, internal medicine, haematology, endocrinology, gastroenterology, hepatology, neurology, and biochemistry), together with laboratory scientists and patient representatives. The panel met online (in 2023-25) to develop 15 evidence-based recommendations with the use of the Grading of Recommendations, Assessment, Development, and Evaluations framework addressing attack prevention, management of sporadic and recurrent attacks, long-term follow-up, surveillance for primary liver cancer, and family screening. The guidelines support safe, consistent clinical care and improved outcomes, recognising global variation in resources and access to high-cost drugs, and highlighting priorities for future research.

We describe the epidemiology of metabolic dysfunction-associated steatotic liver disease (MASLD) and evidence of advanced liver fibrosis by readily available noninvasive diagnostics and their implications to kidney transplant recipients (KTRs). In this retrospective cohort study of first-time KTRs (2008-2020), we assessed the prevalence and incidence of MASLD (hepatic steatosis on abdominal ultrasound alongside &#x2265; 1 cardiometabolic risk factors) and advanced hepatic fibrosis (Fibrosis-4 (FIB-4) index > 2.67). We fitted multivariable time-dependent Cox regression models to assess associations between MASLD and a composite of graft dysfunction (estimated glomerular filtration rate [eGFR] < 30 mL/min per 1.73 m2), death-censored graft failure (DCGF), death with graft function (DWGF), and each distinct end point. In 650 eligible KTRs (median age 57.2 [interquartile range {IQR}: 45.0-66.0] years, 34% female), prevalence per 100 KTR (95% confidence interval [CI]) at transplantation and 5-years post-transplant, was 21.7 (18.6-25.1) and 42.3 (38.5-46.2), respectively, for MASLD and 42.9 (39.1-46.8) and 69.7 (66.0-73.2), respectively, for advanced fibrosis. Incidence rate per 100 person-years was 5.5 (4.7-6.4) for MASLD and 2.2 (1.6-2.9) for advanced fibrosis in KTRs without MASLD and advanced fibrosis at transplantation, respectively. Adjusted hazard ratios (HR) for the composite, graft dysfunction, DCGF, and DWGF were 1.27 (0.98-1.65), 1.24 (0.86-1.78), 1.14 (0.75-1.73), and 1.56 (1.04-2.33) with versus without MASLD and 1.76 (1.14-2.71), 1.47 (0.71-3.01), 3.28 (1.78-6.06), and 1.68 (0.91-3.13) with FIB-4 > 2.67 versus FIB-4 < 1.3, respectively. KTRs with MASLD and advanced hepatic fibrosis demonstrate lower patient and graft survival, which could be amenable to timely interventions for cardiometabolic risk reduction.

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Recurrent Ig A nephropathy (IgAN; rIgAN) after kidney transplantation is heterogeneous and lacks a guideline or a standard treatment. We evaluated the efficacy and safety of telitacicept as an add-on therapy for rIgAN with persistent proteinuria in kidney recipients. In this prospective, single-center, single-arm cohort study, 25 kidney transplant recipients with biopsy-confirmed rIgAN received add-on telitacicept 240 mg subcutaneously weekly for 12 weeks, then every 2 weeks until week 28. Primary end points were 24-hour urinary protein (24h-UP) and urine albumin-to-creatinine ratio (UACR). Secondary assessments included remission, kidney function, laboratory parameters, and mechanistic biomarkers. Twenty-two participants completed the follow-up. At week 28, 24h-UP and UACR decreased by 51.6% and 62.7% (both P < 0.001), respectively. Complete and partial remission rates were achieved in 47.6% and 57.1% of patients, respectively. Serum albumin increased significantly, whereas serum creatinine (SCr), estimated glomerular filtration rate, and hemoglobin remained stable. Circulating galactose-deficient IgA1 (Gd-IgA1) and asialoglycoprotein receptor (ASGPR) levels declined; Ig levels also decreased, in line with B-cell inhibition and on-target pathways suppression. No treatment-related severe adverse events were reported. The most common adverse events were mild injection site reactions and transient infections. Add-on telitacicept was associated with marked proteinuria reduction and a favorable safety profile in kidney transplant recipients with rIgAN and persistent proteinuria, supporting its potential as a therapeutic option.

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Recent advances in xenotransplantation have gained substantial public and clinical attention as genetically modified porcine organs are now being transplanted into living human recipients. While only case reports have been published to date, the first clinical trials for kidney xenotransplantation are now ongoing. This transition to clinical practice presents multiple implementation challenges for establishing scalable transplant programs while ensuring patient safety. Machine perfusion is expected to play a critical role in addressing these challenges by serving as a central platform for organ preservation, assessment, transport, and therapeutic intervention. Given the limited number of designated pathogen-free (DPF) breeding facilities, regional and international organ transport depends on robust preservation strategies during transit. Additionally, perfusion devices enable essential pre-transplant screening for zoonotic pathogens, a crucial safety measure unique to xenotransplantation. Further, given recent developments that allow for multi-day perfusion of grafts, wild-type grafts could potentially be genetically modified while being perfused ex situ. Beyond these perfusion modalities of isolated whole organs, machine perfusion offers a new therapeutic approach for patients with acute liver failure. Here, cross-circulation between a perfused genetically modified porcine organ and the patient can provide temporary liver replacement therapy. This mini-review summarizes the transformative potential of machine perfusion technology in clinical xenotransplantation with a focus on livers.

The FIDELITY pooled analysis of the FIDELIO-DKD and FIGARO-DKD trials showed a complementary benefit of finerenone and sodium-glucose cotransporter-2 inhibitors (SGLT-2is) in patients with chronic kidney disease (CKD) and type 2 diabetes mellitus (T2D). This study used US electronic health record (EHR) data to create an external control arm (ECA) to augment the FIDELITY comparator group and improve the precision of finerenone's treatment effect estimates. We identified eligible patients from EHR data who met the adapted FIDELITY criteria. These ECA patients were matched (1:1) to the pool of SGLT-2i users within the FIDELITY population using a linear programming method based on baseline demographics and clinical characteristics. We then calculated the treatment effects of finerenone on cardiovascular (CV) and kidney composite end points, hospitalization for heart failure (HHF), and all-cause mortality, incorporating the augmented ECA data. Eligible ECA patients (n = 877) were matched to FIDELITY SGLT-2i users (n = 877), yielding a median (Q1-Q3) absolute standardized mean difference (ASMD) of 0.000 (0.000-0.004). ECA augmentation improved the precision of the trial estimates; data resembled the original FIDELITY estimates but with narrower 95% confidence interval (CI) ranges. For the CV end point and HHF, a significant benefit for finerenone + the SGLT-2i subgroup versus the augmented SGLT-2i controls was observed. Our findings demonstrate that an ECA can effectively augment underrepresented study populations in cardiorenal trials, enhancing the statistical precision of treatment effect estimates when there is sufficient homogeneity between the internal and external control groups.