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Res Vet Sci. 2014 Jun;96(3):436-41. doi: 10.1016/j.rvsc.2014.02.011. Epub 2014 Feb 27.

Association between urinary vascular endothelial growth factor excretion and chronic kidney disease in hyperthyroid cats.

Author information

  • 1Department of Veterinary Clinical Sciences, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield AL9 7TA, UK. Electronic address: timwilliams@cantab.net.
  • 2Department of Comparative Biomedical Sciences, Royal Veterinary College, Royal College Street, Camden, London NW1 0TU, UK.
  • 3Department of Veterinary Clinical Sciences, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield AL9 7TA, UK.

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.

KEYWORDS:

NAG; PRA; RAAS; azotaemia; hypoxia; proteinuria

PMID:
24656748
DOI:
10.1016/j.rvsc.2014.02.011
[PubMed - indexed for MEDLINE]
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