Key result
Rodent models of chronic kidney disease provide unique insights into the whole-organism pathophysiology of cardiovascular complications, though they have limitations in fully recapitulating human disease.
High-quality animal models remain a key tool in improving the understanding of the pathophysiology of CKD-associated cardiovascular disease.
Rodent CKD models advance CV pathophysiology research; leaves open improved systems for human translation.
Chronic kidney disease (CKD) is a heterogeneous range of disorders affecting up to 11% of the world's population. The majority of patients with CKD die of cardiovascular disease (CVD) before progressing to end-stage renal disease. CKD patients have an increased risk of atherosclerotic disease as well as a unique cardiovascular phenotype. There remains no clear aetiology for these issues and a better understanding of the pathophysiology of CKD-associated CVD is urgently needed. Although nonanimal studies can provide insights into the nature of disease, the whole-organism nature of CKD-associated CVD means that high-quality animal models, at least for the immediate future, are likely to remain a key tool in improving our understanding in this area. We will discuss the methods used to induce renal impairment in rodents and the methods available to assess cardiovascular phenotype and in each case describe the applicability to humans.
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Sadeghi‐Alavijeh et al. (2017) conducted a review in Chronic kidney disease-associated cardiovascular disease. Animal models was evaluated. Rodent models of chronic kidney disease provide unique insights into the whole-organism pathophysiology of cardiovascular complications, though they have limitations in fully recapitulating human disease.
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