A Sodium Oxalate-Rich Diet Induces Chronic Kidney Disease and Cardiac Dysfunction in Rats

Autor(es)

Crestani, Thayane ^[1] ; Crajoinas, Renato O. ^[1] ; Jensen, Leonardo ^[1] ; Dima, Leno L. ^[1] ; Burdeyron, Perrine ^{[2, 3]} ; Hauet, Thierry ^{[2, 3, 4]} ; Giraud, Sebastien ^{[2, 4]} ; Steichen, Clara ^{[1, 2, 3]}

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Med Sch, Heart Inst, Lab Genet & Mol Cardiol, BR-05403900 Sao Paulo, SP - Brazil

^[2] INSERM U1082 IRTOMIT, F-86000 Poitiers - France

^[3] Univ Poitiers, Fac Med & Pharm, F-86000 Poitiers - France

^[4] CHU Poitiers, Serv Biochim, F-86000 Poitiers - France

• Tipo de documento: Artigo Científico
• Fonte: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES; v. 22, n. 17 SEP 2021.
• Citações Web of Science: 0

Resumo

Chronic kidney disease (CKD) is a worldwide public health issue affecting 14% of the general population. However, research focusing on CKD mechanisms/treatment is limited because of a lack of animal models recapitulating the disease physiopathology, including its complications. We analyzed the effects of a three-week diet rich in sodium oxalate (OXA diet) on rats and showed that, compared to controls, rats developed a stable CKD with a 60% reduction in glomerular filtration rate, elevated blood urea levels and proteinuria. Histological analyses revealed massive cortical disorganization, tubular atrophy and fibrosis. Males and females were sensitive to the OXA diet, but decreasing the diet period to one week led to GFR significance but not stable diminution. Rats treated with the OXA diet also displayed classical CKD complications such as elevated blood pressure and reduced hematocrit. Functional cardiac analyses revealed that the OXA diet triggered significant cardiac dysfunction. Altogether, our results showed the feasibility of using a convenient and non-invasive strategy to induce CKD and its classical systemic complications in rats. This model, which avoids kidney mass loss or acute toxicity, has strong potential for research into CKD mechanisms and novel therapies, which could protect and postpone the use of dialysis or transplantation. (AU)

• Processo FAPESP: 14/14086-7 - Transplante de cardiomiócitos derivados de iPSC pós-infarto do miocárdio em modelo suíno
• Beneficiário: Clara Steichen
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado