Transthyretin amyloid cardiomyopathy (ATTR-CM) is a type of progressive cardiomyopathy that is characterized by the accumulation of misfolded transthyretin protein within the myocardium. Cardiorenal dysfunction is common among patients with ATTR-CM, and its presence is associated with worse outcomes. As such, monitoring kidney dysfunction has important implications for disease prognostication. There remains an unmet need to better characterize renal biomarkers to enhance risk stratification and assessment of treatment response in affected patients. The goal of this review is to detail how cardiorenal dysfunction influences the clinical natural history of ATTR-CM and how it may be modified by treatment. An increasing body of evidence has evaluated the usefulness of various renal biomarkers in ATTR-CM. Beyond traditional measures such as estimated glomerular filtration rate(eGFR), measures of albuminuria, cystatin C, and uromodulin may better reflect glomerular and tubular vulnerability, while congestion related measures such as outpatient diuretic intensification may better capture disease trajectory. Emerging data also suggest that disease modifying therapies and supportive treatments may influence renal function over time. Cardiorenal biomarkers in ATTR-CM may provide insight into the evolving disease biology and the interplay between cardiac dysfunction and kidney injury. As disease modifying therapies become more widely used, incorporating dynamic renal measures (including eGFR trajectories and albuminuria) may refine prognostic precision and support longitudinal assessment of treatment effect.
Jefferson et al. (Thu,) studied this question.