Sylvia Eleni Rosas

The American Diabetes Association and the European Association for the Study of Diabetes convened a panel to update the consensus statement on the management of type 2 diabetes in nonpregnant adults, published since 2006 and last updated in 2022. The target audience is the multidisciplinary health care team providing diabetes care in the U.S. and Europe. A systematic examination of publications since 2022 informed new recommendations. This update has broadened the focus from the management of hyperglycemia to the holistic management of type 2 diabetes and its risk of associated multiple long-term conditions. Fundamental aspects of diabetes care include promoting healthy lifestyle behaviors (healthy eating, 24-h physical behaviors including sleep, and avoiding tobacco and substance use), alongside the provision of psychological support and weight management interventions. For the management of people living with type 2 diabetes, earlier use, potentially from diagnosis, of sodium–glucose cotransporter 2 (SGLT2) inhibitors and/or glucagon-like peptide 1 (GLP-1)-based therapies to offer organ protection and improve long-term outcomes in type 2 diabetes is advocated. Furthermore, earlier combination use of SGLT2 inhibitors and GLP-1–based therapies should be considered in people with concomitant cardiovascular disease, chronic kidney disease, and heart failure. Finally, the ability to transform outcomes for people living with type 2 diabetes is within our grasp through the consistent, equitable, and systematic implementation of strategies and therapies that are already available.

Background: The imprecision of current metrics to capture the complex genetic admixture and racial identity among Hispanic/Latino individuals in the United States (US) is a concern. We examined the relationship of self-reported race and genetic ancestry with hypertension (HTN) among Hispanics/Latinos. Methods: Cross-sectional study of the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), including 10,586 Hispanic/Latino unrelated adults. Genetic ancestry: West African (AA), Amerindian (AI), and European (EA). Self-reported race: White, Black, Native American, or Multiple/Missing ( More than one race or Unknown/Not reported/Refused ). HTN: systolic (SBP) ≥130 mmHg, diastolic blood pressure (DBP) ≥80 mmHg, and/or use of HTN medications. Age- and sex adjusted models were used. Results: Self-reported race was White (38·6%), Black (3·6%), Native American (4·1%), and Multiple/Missing (53·7%), with Unknown/Not reported/Refused representing 32·7%. Black and White Hispanics/Latinos had the greatest AA (55·7%) and EA (69·3%) ancestries, respectively. Each 10% AA increase was associated with OR 1·15, SBP beta +0.9 mmHg, and DBP beta +0.7 mmHg. Conversely, each 10% AI increase was associated with OR 0·83, SBP beta -0·4 mmHg, and DBP beta -0·6 mmHg. HTN prevalence was highest among those with Black race or in the highest AA quantile (45·6% and 48·0%, respectively), and lowest among those with Native American race or in the highest AI quantile (37·6% and 26·7%, respectively). Conclusion: One-third of Hispanics/Latinos did not self-report race. Black or White self-reporting race did somewhat relate to AA or EA ancestry, respectively. HTN profiles were related to self-reported race and genetic ancestry in this admixed population.

Chronic kidney disease (CKD), prevalent in more than 1 in 7 US adults, is a major noncommunicable disease that increases the risk of cardiovascular disease (CVD), stroke, and mortality. Type 2 diabetes and hypertension are the most common causes of CKD and kidney failure. Early identification and management are critical because CKD is asymptomatic in early stages. However, annual surveillance of high-risk patients is infrequent, and many patients with moderate to severe CKD remain undiagnosed. Barriers to effective CKD care and management include social determinants of health (SDoH), low CKD awareness, communication between patients and health care professionals, health literacy, and the complexity of caring for patients with CKD. SDoH-related factors negatively affect access to health care, increasing the risk of developing CKD and leading to poor health outcomes resulting from delays in diagnosis and treatment. Based on the experience and opinions of the authors, this narrative review of the literature aimed to explore the population-based unmet needs of patients with CKD, address potential solutions to SDoH-related issues, discuss the importance of multidisciplinary care, and offer strategies to overcome clinical inertia to increase screening for CKD and improve patient outcomes. Opportunities for improving the management of patients with CKD in both primary and specialty care include avoiding clinical inertia and optimizing guideline-directed therapy.

BACKGROUND: Sodium–glucose cotransporter 2 (SGLT2) inhibitors slow the progression of chronic kidney disease (CKD), although their potential to prevent the development of CKD in type 2 diabetes needs to be examined. PURPOSE: To evaluate SGLT2 inhibitors for the primary prevention of CKD in people with type 2 diabetes. DATA SOURCES: PubMed and Cochrane Central Register of Controlled Trials (CENTRAL) were searched through October 2025. DATA SYNTHESIS: Randomized controlled trials (RCTs) of SGLT2 inhibitors compared with placebo or other glucose-lowering agents in people with type 2 diabetes without baseline CKD were included. Outcomes were estimated glomerular filtration rate (eGFR) decline and incident albuminuria (i.e., urine albumin-to-creatine ratio [UACR] ≥30 mg/g). Random-effects meta-analyses were performed, and heterogeneity was assessed with I2. Certainty of evidence was evaluated with Grading of Recommendations Assessment, Development and Evaluation (GRADE). RESULTS: Eight RCTs were included: five cardiovascular outcomes trials comparing SGLT2 inhibitors and placebo (24,072 participants) and three trials comparing SGLT2 inhibitors and sulfonylureas (2,889 participants). Compared with placebo, SGLT2 inhibitors reduced the risk of incident albuminuria (three trials; hazard ratio 0.82; 95% CI 0.77–0.88; I2 = 0%, high certainty) and slowed eGFR decline based on the chronic eGFR slope (five trials; mean difference [MD] 0.95 [95% CI 0.84–1.07] mL/min/1.73 m2/year; I2 = 19%, high certainty) and total eGFR slope (four trials; MD 0.76 [0.50–1.03] mL/min/1.73 m2/year; I2 = 88%, moderate certainty). Compared with sulfonylureas, SGLT2 inhibitors slowed eGFR decline based on the chronic eGFR slope (three trials; MD 2.43 [1.72–3.13] mL/min/1.73 m2/year; I2 = 55%, moderate certainty). CONCLUSIONS: In people with type 2 diabetes without CKD, SGLT2 inhibitors slow eGFR decline compared with both placebo and sulfonylureas and prevent incident albuminuria compared with placebo.

Background: Cardiovascular-kidney-metabolic syndrome (CKM) describes the clustering of risk factors and progression of disease at the intersection of metabolic disorders, chronic kidney disease (CKD), and cardiovascular disease (CVD). We aimed to characterize the prevalence of CKM stages and progression of CKM syndrome among diverse U.S. Hispanic/Latino adults. Methods: The Hispanic Community Health Study/Study of Latinos (HCHS/SOL) is a population-based longitudinal cohort of 16,415 Hispanic/Latino adults aged 18-74 years from four U.S. communities. Participants completed examinations at visit 1 (V1, 2008-2011) and visit 2 (V2, 2014-2017). Data collected included body mass index, waist circumference, glucose tolerance, lipids, blood pressure, metabolic syndrome, CKD, 10-year CVD risk (to define subclinical CVD), and clinical CVD. CKM stages were defined using American Heart Association criteria: stage 0 (no CKM risk factors), stage 1 (excess/dysfunctional adiposity), stage 2 (metabolic risk factors or CKD), stage 3 (subclinical CVD or risk equivalents), and stage 4 (clinical CVD). We estimated the age-standardized prevalence of CKM stages at V1 (n=16,123) and CKM stage progression from V1 to V2 (n=11,178). All analyses were weighted and accounted for the HCHS/SOL complex survey design. Results: At V1, the mean age was 41.1 years, and 52.3% were female. The distribution of CKM stages was: stage 0, 10.6% (standard error (SE): 0.4); stage 1, 26.1% (SE: 0.6); stage 2, 50.6% (SE: 0.6); stage 3, 2.4% (SE: 0.2); and stage 4, 10.3% (SE: 0.3). Over an average follow-up of six years, 10.3% (SE: 0.5) regressed to a lower CKM stage, while 21.5% (SE: 0.7) progressed to a higher CKM stage. Conclusions: Among diverse U.S. Hispanic/Latino adults, eight in ten had CKM risk factors or subclinical CVD, and one in five experienced CKM progression over six years. These findings highlight the need for targeted, early-stage interventions to prevent CKM progression and improve CKM health in Hispanic/Latino populations.

OBJECTIVE: To evaluate whether the efficacy and safety of finerenone varied by baseline hemoglobin A1c (HbA1c) level, a proxy of glycemic control, and diabetes duration in people with type 1 diabetes and chronic kidney disease (CKD). RESEARCH DESIGN AND METHODS: Adults with type 1 diabetes, urinary albumin-to-creatinine ratio (UACR) 200 to <5,000 mg/g, and estimated glomerular filtration rate (eGFR) 25 to <90 mL/min/1.73 m2 were randomly assigned (one to one) to finerenone or placebo. UACR change from baseline over 6 months by baseline HbA1c and diabetes duration was analyzed. RESULTS: Baseline HbA1c was available for 240 of 242 participants; mean (SD) HbA1c, diabetes duration, and eGFR were 7.6% (1.1%; 60 [12] mmol/mol), 32.0 (14.2) years, and 58.9 (19.2) mL/min/1.73 m2, respectively. At 6 months, HbA1c (95% CI) remained unchanged (finerenone +0.03% [−0.14%, 0.20%]; placebo 0.00% [−0.12%, 0.11%]; between-group difference +0.04% [−0.17%, 0.24%]; P = 0.74). Over 6 months, median UACR decreased from 574.6 to 373.5 mg/g with finerenone and from 506.4 to 475.6 mg/g with placebo, corresponding to a −25% placebo-corrected change (95% CI –35%, –13%; P = 0.0001). Treatment effects were consistent across HbA1c tertiles (8.1%), with placebo-corrected UACR changes (95% CIs) of −17% (−40%, 13%), −18% (−39%, 10%), and −37% (−55%, −13%), respectively (P interaction = 0.41). Effects were similarly consistent across diabetes duration tertiles (P interaction = 0.70). Overall safety and incidence of hyperkalemia were similar across HbA1c tertiles. CONCLUSIONS: In adults with type 1 diabetes and CKD, finerenone reduced UACR and was well tolerated irrespective of HbA1c level or diabetes duration.

Acute kidney injury (AKI) and chronic kidney disease (CKD) are two interconnected clinical conditions, both defined by degree of functional impairment, but with heterogeneous clinical trajectories. Using new transcriptomic technologies, recent studies have described the cellular diversity in the healthy and injured kidney at the single cell level. Here, we used single nucleus transcriptomics to investigate the molecular diversity and commonalities in kidney biopsies from over 150 participants with AKI and CKD enrolled within the Kidney Precision Medicine Project (KPMP) and did so at the patient participant level. Using an unsupervised approach, we identified two multi-cellular programs associated with clinical and histopathological features of acute injury and chronic damage, respectively. We found that these programs are expressed across patients with AKI and CKD, supporting shared, rather than distinct, underlying molecular mechanisms. These programs capture tissue-level compositional changes towards adaptive and failed-repair states in tubular epithelial cells, as well as intra-cellular molecular changes characteristic of stress in all cell types. We identified subunits of the NFkB and AP-1 complexes, as well as members of the STAT family, as putative upstream regulators of the acute and chronic programs. We were able to map these continuous molecular measures of acute injury and chronic damage to urine and plasma protein profiles obtained at time of biopsy. These non-invasive protein signatures were predictive of renal outcomes in an independent cohort of 44 thousand participants from the UK biobank. In summary, unbiased identification of cellular programs in kidney disease biopsies defined molecular programs of injury cutting across conventional disease categorization and established a non-invasive molecular link to long term patient outcomes. Graphical