Peer-reviewed veterinary case report
Urine VEGF linked to kidney disease risk in hyperthyroid cats
By Williams, T L et al.·Published in Research in veterinary science·2014·Department of Veterinary Clinical Sciences, United Kingdom·View original on PubMed →
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Original publication title: Association between urinary vascular endothelial growth factor excretion and chronic kidney disease in hyperthyroid cats.
- Species:
- cat
Plain-English summary
A study looked at hyperthyroid cats and their risk of developing chronic kidney disease (CKD) after treatment. Researchers found that while hyperthyroidism can activate certain systems in the body that might harm the kidneys, the levels of a specific marker in urine (VEGFCR) did not directly link to kidney damage in these cats. This suggests that kidney issues in hyperthyroid cats may not be caused by the expected tubular damage. Overall, the findings indicate that hyperthyroid cats can be monitored for kidney health, but the relationship between hyperthyroidism and kidney disease is more complex than previously thought.
People also search for: hyperthyroid cat kidney disease · cat kidney health monitoring · treatment for hyperthyroid cats
Abstract
Many hyperthyroid cats develop azotaemic chronic kidney disease (aCKD) following treatment, which has led to the hypothesis that hyperthyroidism might be detrimental to renal function. Renin-angiotensin-aldosterone system (RAAS) activation occurs in hyperthyroidism, which could cause peri-tubular hypoxia, tubular damage and the development of aCKD. Urinary vascular endothelial growth factor:creatinine ratio (VEGFCR) is postulated to be a marker of tubular hypoxia. VEGFCR was correlated with plasma renin activity (PRA) and compared between hyperthyroid cats that did and did not develop aCKD following treatment (pre-azotaemic and non-azotaemic groups respectively). PRA was positively correlated with VEGFCR (rs = 0.382; P = 0.028); however, pre-azotaemic hyperthyroid cats had significantly lower VEGFCR than non-azotaemic cats at baseline (median 122.3 fg/g versus 167.0 fg/g; P < 0.001). RAAS activation in hyperthyroidism is associated with increased VEGFCR; however, increased VEGFCR was not correlated with the development of aCKD. Therefore, tubular hypoxia may not be a mechanism for renal damage in hyperthyroid cats.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/24656748/