Cardiorenal syndrome (CRS), first defined in 2004 as a consequence of the interactions between the kidneys and other circulatory departments leading to acute heart failure, has since been recognized as a complex clinical entity that is hard to define, diagnose and classify. The framework for the classification of CRS according to pathophysiologic background was laid out in 2008, dividing CRS into five distinct phenotypes. However, determining the timing of individual organ injuries and making a diagnosis of either renal or cardiac failure remains an elusive task. In clinical practice, the diagnosis and phenotyping of CRS is mostly based on using laboratory biomarkers in order to directly or indirectly estimate the degree of end-organ functional decline. Therefore, a well-educated clinician should be aware of the effects that the reduction of renal and cardiac function has on the diagnostic and predictive value and properties of the most commonly used biomarkers (e.g. troponins, N-terminal pro-brain natriuretic peptide, serum creatinine etc). They should also be acquainted, on a basic level, with emerging biomarkers that are specific to either the degree of glomerular integrity (cystatin C) or tubular injury (neutrophil gelatinase-associated lipocalin). This narrative review aims to provide a scoping overview of the different roles that biomarkers play in both the diagnosis of CRS and the prognosis of the disease in patients who have been diagnosed with it, along with highlighting the most important pitfalls in their interpretation in the context of impaired renal and/or cardiac function.
Diabetic kidney disease (DKD) is one of the most common microvascular complications of both type 1 and type 2 diabetes and the most common cause of the end-stage renal disease (ESRD). It has been evidenced that targeted interventions at an early stage of DKD can efficiently prevent or delay the progression of kidney failure and improve patient outcomes. Therefore, regular screening for DKD has become one of the fundamental principles of diabetes care. Long-established biomarkers such as serum-creatinine-based estimates of glomerular filtration rate and albuminuria are currently the cornerstone of diagnosis and risk stratification in routine clinical practice. However, their immanent biological limitations and analytical variations may influence the clinical interpretation of the results. Recently proposed new predictive equations without the variable of race, together with the evidence on better accuracy of combined serum creatinine and cystatin C equations, and both race- and sex-free cystatin C-based equation, have enabled an improvement in the detection of DKD, but also require the harmonization of the recommended laboratory tests, wider availability of cystatin C testing and specific approach in various populations. Considering the complex pathophysiology of DKD, particularly in type 2 diabetes, a panel of biomarkers is needed to classify patients in terms of the rate of disease progression and/or response to specific interventions. With a personalized approach to diagnosis and treatment, in the future, it will be possible to respond to DKD better and enable improved outcomes for numerous patients worldwide.
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