Retinol‐Binding Protein in Serum and Urine of Hyperthyroid Cats before and after Treatment with Radioiodine

Hoek, Ingrid van; Meyer, Evelyne; Duchateau, Luc; Peremans, K.; Smets, Pascale; Daminet, Sylvie

doi:10.1111/j.1939-1676.2009.0364.x

Cited by 27 publications

(25 citation statements)

References 36 publications

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“…32 Both these proteins are also found in cat sera, and have been shown to interact in a complex with thyroxine in vitro. 33,34 Serum RBP concentrations are similar in hyperthyroid and healthy cats. 34 Therefore, limited availability of RBP for retinol binding in the presence of high serum T4 could explain higher free retinol concentrations in hyperthyroid cats, which resolved with a return to normal serum T4 concentrations.…”

Section: Discussionmentioning

confidence: 97%

Antioxidant Status in Hyperthyroid Cats before and after Radioiodine Treatment

Branter

Drescher

Padilla

et al. 2012

Veterinary Internal Medicne

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Background: Reversible antioxidant depletion is found in hyperthyroid humans, and antioxidant depletion increases the risk of methimazole toxicosis in rats.Objectives: To determine whether abnormalities in concentrations of blood antioxidants or urinary isoprostanes were present in hyperthyroid cats, and were reversible after radioiodine treatment. To determine whether or not antioxidant abnormalities were associated with idiosyncratic methimazole toxicosis.Animals: Hyperthyroid cats presented for radioiodine treatment (n = 44) and healthy mature adult control cats (n = 37).Methods: Prospective, controlled, observational study. Red blood cell glutathione (GSH), plasma ascorbate (AA), plasma free retinol (vitamin A), a-tocopherol (vitamin E), and urinary free 8-isoprostanes in hyperthyroid cats were compared to healthy cats and to hyperthyroid cats 2 months after treatment.Results: Blood antioxidants were not significantly different in hyperthyroid cats (mean GSH 1.6 ± 0.3 mM; AA 12.8 ± 4.9 lM, and vitamin E, 25 ± 14 lg/mL) compared to controls (GSH 1.4 ± 0.4 mM; AA 15.0 ± 6.6 lM, and vitamin E, 25 ± 17 lg/mL). Urinary isoprostanes were increased in hyperthyroid cats (292 ± 211 pg/mg creatinine) compared to controls (169 ± 82 pg/mg; P = .006), particularly in hyperthyroid cats with a USG < 1.035. Plasma free vitamin A was higher in hyperthyroid cats (0.54 ± 0.28 lg/mL versus 0.38 ± 0.21 in controls; P = .007). Both abnormalities normalized after radioiodine treatment. No association was found between oxidative status and prior idiosyncratic methimazole toxicosis.Conclusion and Clinical Importance: Increased urinary isoprostane could reflect reversible renal oxidative stress induced by hyperthyroidism, and this requires additional evaluation.

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Section: Discussionmentioning

confidence: 97%

Antioxidant Status in Hyperthyroid Cats before and after Radioiodine Treatment

Branter

Drescher

Padilla

et al. 2012

Veterinary Internal Medicne

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“…When tubular cells are damaged, they release tubular enzymes into the ultrafiltrate, increasing urinary enzyme activities. Urinary markers of tubular damage (33), such as retinol-binding protein or N-acetyl-␤-glucosaminidase, are elevated in hyperthyroid humans (12,29) and cats (42). In this paper, we analyzed the urinary excretion of GluAP, AlaAP, CysAp, and AspAp as possible biomarkers of tubular dysfunction in thyroid disorders and after an increased saline intake.…”

Section: E285mentioning

confidence: 99%

Salt sensitivity in experimental thyroid disorders in rats

Pérez-Abud

Rodríguez-Gómez

Villarejo

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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This study assessed salt sensitivity, analyzing the effects of an increased saline intake on hemodynamic, morphological, and oxidative stress and renal variables in experimental thyroid disorders. Six groups of male Wistar rats were used: control, hypothyroid, hyperthyroid, and the same groups treated with salt (8% via food intake). Body weight, blood pressure (BP), and heart rate (HR) were recorded weekly for 6 wk. Finally, BP and HR were recorded directly, and morphological, metabolic, plasma, and renal variables were measured. High-salt intake increased BP in thyroxine-treated rats but not in control or hypothyroid rats. High-salt intake increased cardiac mass in all groups, with a greater increase in hyperthyroid rats. Urinary isoprostanes and H 2O2 were higher in hyperthyroid rats and were augmented by high-salt intake in all groups, especially in hyperthyroid rats. High-salt intake reduced plasma thyroid hormone levels in hyperthyroid rats. Proteinuria was increased in hyperthyroid rats and aggravated by high-salt intake. Urinary levels of aminopeptidases (glutamyl-, alanyl-, aspartyl-, and cystinylaminopeptidase) were increased in hyperthyroid rats. All aminopeptidases were increased by salt intake in hyperthyroid rats but not in hypothyroid rats. In summary, hyperthyroid rats have enhanced salt sensitivity, and high-salt intake produces increased BP, cardiac hypertrophy, oxidative stress, and signs of renal injury. In contrast, hypothyroid rats are resistant to salt-induced BP elevation and renal injury signs. Urinary aminopeptidases are suitable biomarkers of renal injury. salt intake; hyperthyroidism; hypothyroidism; aminopeptidases; blood pressure RENAL FUNCTION AND SALT AND water metabolism can be considerably impaired by thyroid disorders (3, 46). Some authors reported that hypothyroid rats have a lesser ability to concentrate urine and show increased natriuresis after salt or water loading (10,18,25,39) and have a reduced capacity to conserve sodium, which produces a negative sodium balance and death when subjected to dietary sodium restriction (13). However, our group did not observe increased sodium excretion in hypothyroid methimazole-treated rats under some of the above conditions (44) or in pressure-diuresis-natriuresis studies (43). On the other hand, thyroxine (T 4 )-treated rats showed changes in renal hemodynamics and sodium resorption (46), increased blood volume (34), polydipsia/polyuria (15), reduced ability to excrete sodium after hypertonic saline loading (44), and a blunted pressure-diuresis-natriuresis response (43).These data indicate that thyroid disorders are accompanied by major changes in renal sodium handling.Hypothyroidism reduces blood pressure (BP) and prevents experimental hypertension (46), whereas T 4 administration to rats increases BP (6) and accelerates the course of hypertension (46). Although numerous systems can influence BP over the short term, long-term BP regulation depends on the renal excretion of sodium (22). An increased BP in response to dietary sodium (sal...

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“…On the contrary, recent evidence suggests that hyperthyroidism contributes to development and further progression of chronic kidney disease with detrimental implications for kidney function in cats with untreated or poorly regulated hyperthyroidism (van Hoek et al, 2009b). Medical, and perhaps nutritional, management is the only viable choice in such animals.…”

Section: Treatment Of a Newly Diagnosed Hyperthyroid Cat With Pre-eximentioning

confidence: 99%

Feline hyperthyroidism: diagnosis and treatment

Kasabalis

Soubasis

Petanides

2017

J Hellenic Vet Med Soc

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Hyperthyroidism is a common endocrinopathy in cats older than 8 years, with no sex or breed predisposition. Benign adenomas and adenomatous hyperplasia of the thyroid gland is observed in the majority of cases. Symptoms reflect the effect of thyroid hormone excess in various systems, with weight loss, polyphagia, polyuria-polydipsia, cardiovascular and gastrointestinal abnormalities being common clinical manifestations. On clinical examination, there is frequently prominent thyroid enlargement. Common laboratory abnormal findings include increased activity of alkaline phosphatase and alanino-aminotransferase, hyperphosphataemia, azotaemia and decreased concentration of ionized calcium and creatinine. Definite diagnosis of the disease is based on the demonstration of increased blood concentration of thyroid hormones.Measurement of thyroxine concentration, alone or in conjunction with concentration of free thyroxine, is usually sufficient to reach a diagnosis. When diagnosis is uncertain, thyroid stimulating hormone, scintigraphy and dynamic function tests can be used. The possibility of concurrent diseases (e.g., renal failure, diabetes mellitus) must be investigated, as their presence has implications on diagnosis and treatment. Medical therapy, thyroidectomy, radionine therapy and low iodine diet are also valid options for treatment. Each has advantages and disadvantages that a clinician must take into consideration before instigating treatment. Prognosis for hyperthyroidism is favourable if no severe disease exists concurrently.

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Retinol‐Binding Protein in Serum and Urine of Hyperthyroid Cats before and after Treatment with Radioiodine

Cited by 27 publications

References 36 publications

Antioxidant Status in Hyperthyroid Cats before and after Radioiodine Treatment

Antioxidant Status in Hyperthyroid Cats before and after Radioiodine Treatment

Salt sensitivity in experimental thyroid disorders in rats

Feline hyperthyroidism: diagnosis and treatment

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