Background/Objectives: Albuminuria is an early marker of kidney damage and an independent predictor of adverse outcomes, making its reduction a key therapeutic goal. Finerenone, a selective nonsteroidal mineralocorticoid receptor antagonist, has demonstrated renal and cardiovascular benefits in patients with diabetic kidney disease (DKD), although the magnitude of the antiproteinuric response may vary in clinical practice. This post hoc analysis aimed to characterize the six-month antiproteinuric response to finerenone and to descriptively explore baseline clinical and treatment characteristics across response categories in the FINDKDLATAM cohort. Methods: A subgroup analysis was performed on a real-world, multicenter, retrospective, observational study that included patients from the FINDKDLATAM study who had urinary albumin-to-creatinine ratio (UACR) measurements taken at baseline and six months. Patients were classified as absolute responders (≥50% reduction in UACR), partial responders (30–49% reduction), and non-responders (<30% reduction or no reduction in UACR) at six months of follow-up. Sociodemographic, clinical, biochemical, therapeutic, and safety variables were analyzed. Results: Of the 347 patients included in the original cohort, 334 had complete UACR data at six months and were included in the analysis. Of these, 80.2% (n = 268) were absolute responders, 11.7% (n = 39) partial responders, and 8.1% (n = 27) non-responders. Median UACR decreased from 350.7 to 67.0 mg/g among absolute responders and from 240.5 to 143.0 mg/g among partial responders (both p < 0.0001), whereas no significant change was observed among non-responders. No baseline clinical characteristic consistently distinguished responders from non-responders. Serum potassium increased during follow-up, particularly among non-responders. Conclusions: In this retrospective Latin American cohort, most patients experienced a reduction in UACR after six months of finerenone treatment. However, the uncontrolled observational design, concomitant therapies, UACR variability, and regression to the mean preclude attributing these changes exclusively to finerenone. These exploratory findings do not support selecting patients according to a particular responder phenotype but rather support prescribing finerenone according to currently approved clinical criteria. Prospective studies with adjusted analyses are needed to identify independent predictors of response.
Cardiorenal-metabolic syndrome (CRMS) is a pathophysiological interaction of metabolic, cardiovascular, and renal dysfunctions, sharing mechanisms such as chronic inflammation, insulin resistance, neurohormonal activation and vascular dysfunction. This progressive condition can begin in subclinical stages and evolve into established cardiovascular and renal disease. The CRMS staging classification stratifies patients from a stage with no risk factors (stage 0) to clinical cardiovascular disease with or without kidney failure (stages 4a and 4b). This framework guides interventions based on absolute risk and disease progression. The recently developed PREVENT model improves prediction of total cardiovascular risk (myocardial infarction, heart failure, stroke, and mortality) by incorporating variables from the cardio-renal-metabolic axis. Using this tool, therapeutic strategies can be personalized and patients who benefit most from intensive or combination therapies can be identified. Compared to traditional comorbidity-based approaches, CRMS demands an interdisciplinary, anticipatory, and patient-centered strategy. The implementation of integrated models improves clinical outcomes and promotes health equity. CRMS should be considered a strategic priority in precision medicine, public health, and global health policy.
La enfermedad hepática esteatósica asociada a disfunción metabólica (MASLD) ha dejado de entenderse como una alteración confinada al hígado para consolidarse como una entidad sistémica con repercusiones cardiovasculares, metabólicas y renales, con una prevalencia cada vez más elevada a nivel mundial. Así mismo, la enfermedad renal crónica (ERC) continúa aumentando en todo el mundo, impulsada en gran medida por la obesidad, la resistencia a la insulina, la diabetes tipo 2 y otras expresiones del síndrome cardiovascular-reno-metabólico. En este contexto, la coexistencia entre MASLD y ERC no parece obedecer únicamente a factores de riesgo compartidos, sino a mecanismos biológicos convergentes que favorecen la lesión glomerular y tubular, la inflamación persistente, el estrés oxidativo, la lipotoxicidad, la activación neurohormonal y la fibrosis progresiva. Esta revisión analiza la relación entre MASLD y ERC desde una perspectiva clínica, con énfasis en los ejes fisiopatológicos compartidos y las implicaciones diagnósticas y terapéuticas. Reconocer esta interacción no solo mejora la estratificación del riesgo, sino que también abre la puerta a estrategias de intervención más tempranas y multidimensionales.
Introducción: La polimiositis es una miopatía idiopática autoinmune que se caracteriza por trastornos de colágeno y afecta principalmente a los músculos proximales y a los pulmones. Su inicio es subagudo y evoluciona a lo largo de semanas. Es más prevalente en mujeres que en hombres. Las manifestaciones renales son poco comunes, pero cuando están presentes, las principales incluyen la necrosis tubular aguda relacionada con hemoglobinuria y la mioglobinuria asociada a rabdomiólisis aguda. Además, pueden presentarse síntomas como disfagia y disnea. Reporte de caso: Se reporta el caso de una paciente femenina de 40 años con antecedentes de dermatitis herpetiforme e hiperprolactinemia, quien consultó por un cuadro clínico de un mes de evolución, caracterizado por fiebre, anasarca, debilidad muscular, proteinuria significativa y derrame pericárdico. La electromiografía evidenció hallazgos compatibles con miopatía inflamatoria y la biopsia muscular confirmó el diagnóstico de polimiositis. La biopsia renal mostró un aumento de la matriz mesangial con depósitos de IgM en inmunofluorescencia, compatible con glomerulopatía mesangial. La paciente fue tratada con pulsos de corticoides y presentó una evolución clínica favorable. Discusión: La afectación renal en pacientes con polimiositis (PM) es infrecuente y suele limitarse al daño tubular secundario a rabdomiólisis o a glomerulopatías, como la glomeruloesclerosis focal y segmentaria o la nefritis túbulo-intersticial. La aparición de un síndrome nefrótico en este contexto requiere una evaluación etiológica detallada. En el caso presentado, la biopsia renal evidenció una nefropatía mesangial por IgM, una entidad rara y aún controvertida, que ha sido discutida como una variante de enfermedad por cambios mínimos o GEFS. La literatura reporta escasos casos de glomerulopatías asociadas a PM, predominando hallazgos de glomerulonefritis membranosa o por inmunocomplejos. La fisiopatología podría implicar mecanismos inmunitarios comunes, entre ellos la activación de células T CD8+ y la liberación de citocinas capaces de inducir daño glomerular. Conclusión: La remisión completa del síndrome nefrótico tras tratamiento inmunosupresor dirigido a la PM sugiere un posible origen inmunomediado compartido.
BACKGROUND Patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) face high renal and cardiovascular risks. Finerenone, a selective non-steroidal mineralocorticoid receptor antagonist, has demonstrated efficacy in reducing these risks in clinical trials. However, its real-world safety and effectiveness remain underexplored in local settings. AIM To evaluate the real-world safety and effectiveness of finerenone in patients with T2DM and CKD across seven Latin American countries. METHODS We conducted an observational, multicenter, retrospective cohort study based on real-world data in 347 patients with T2DM and CKD [urinary albumin-creatinine ratio (UACR) > 30 mg/g]. Patients received finerenone (10 mg or 20 mg daily), and clinical and laboratory parameters were evaluated at baseline and after six months of treatment. RESULTS At baseline, median values (interquartile range) were: Glycated hemoglobin A1c 7.6% (6.8%-8.1%); estimated glomerular filtration rate 39.0 mL/minute/1.73 m2 (30.0-50.0); UACR 345 mg/g (189-760); systolic blood pressure 143 mmHg (130-160); diastolic blood pressure 79 mmHg (70-82); and serum potassium 4.4 mmol/L (4.1-4.7). After six months, significant reductions were observed: Glycated hemoglobin A1c to 7.0% (6.5%-7.9%); UACR to 81 mg/g (28-167); systolic blood pressure to 130 mmHg (120-140); and diastolic blood pressure to 73 mmHg (70-80). Serum potassium increased to 4.7 mmol/L (4.3-5.0), while estimated glomerular filtration rate remained stable at 41.6 mL/minute/1.73 m2 (27.0-52.0). CONCLUSION In our cohort of patients with CKD associated with T2DM, finerenone proved to be an effective short-term therapy for reducing albuminuria, demonstrating very good tolerance and a low risk of hyperkalemia.
