Proteinuria in autoimmune thyroid disease

Weetman, A P; Tomlinson, K.; Amos, N.; Lazarus, John; Hall, R; McGregor, A. M.

doi:10.1530/acta.0.1090341

Cited by 32 publications

(20 citation statements)

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“…Several studies have shown that hyperthyroid rats have increased proteinuria, which is consistent with the presence of proteinuria in patients with Graves' disease (113). This alteration is unrelated to blood pressure, since antihypertensive therapy was ineffective in reducing proteinuria (93,112).…”

Section: Proteinuriamentioning

confidence: 52%

Vascular and renal function in experimental thyroid disorders

Moreno²,

et al. 2006

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This review focuses on the effects of thyroid hormones in vascular and renal systems. Special emphasis is given to the mechanisms by which thyroid hormones affect the regulation of body fluids, vascular resistance and, ultimately, blood pressure. Vascular function is markedly affected by thyroid hormones that produce changes in vascular reactivity and endothelial function in hyper-and hypothyroidism. The hypothyroid state is accompanied by a marked decrease in sensitivity to vasoconstrictors, especially to sympathetic agonists, alteration that may play a role in the reduced blood pressure of hypothyroid rats, as well as in the preventive effects of hypothyroidism on experimental hypertension. Moreover, in hypothyroid rats, the endothelium-dependent and nitric oxide donors vasodilation is reduced. Conversely, the vessels from hyperthyroid rats showed an increased endothelium-dependent responsiveness that may be secondary to the shear-stress induced by the hyperdynamic circulation, and that may contribute to the reduced vascular resistance characteristic of this disease. Thyroid hormones also have important effects in the kidney, affecting renal growth, renal haemodynamics, and salt and water metabolism. In hyperthyroidism, there is a resetting of the pressure-natriuresis relationship related to hyperactivity of the renin-angiotensin system, which contributes to the arterial hypertension associated with this endocrine disease. Moreover, thyroid hormones affect the development and/or maintenance of various forms of arterial hypertension. This review also describes recent advances in our understanding of thyroid hormone action on nitric oxide and oxidative stress in the regulation of cardiovascular and renal function and in the long-term control of blood pressure.

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Section: Proteinuriamentioning

confidence: 52%

Vascular and renal function in experimental thyroid disorders

Moreno²,

et al. 2006

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“…Recently IL-4 has been defined as an important lymphokine regulating IgE and IgG4 subclass antibody production in man (27). Although it is possible that the isotype restriction we have observed for TSAb may be the result of T cell control, this does not easily account for the fact that all thyroid antibodies are synthesized together in the diseased gland (28,29); it is difficult to envisage how aberrant T cell regulation could affect TSAb IgG isotype selection and not that of Tg or M/TPO antibodies.…”

Section: Discussionmentioning

confidence: 75%

Thyroid-stimulating antibody activity between different immunoglobulin G subclasses.

Weetman¹,

Yateman²,

Ealey³

et al. 1990

J. Clin. Invest.

132

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To investigate the distribution of thyroid-stimulating antibody (TSAb) activity between IgG subclasses, sera from 11 patients with Graves disease (including the National Institute of Biological Standards and Control (NIBSC) Research Standard, long acting thyroid stimulator-B) were fractionated by chromatography on affinity columns of monoclonal IgG subclass antibodies or protein A to deplete all but a single subclass. The resulting fractions were 98% or more pure for a single subclass. In all 11 patients, TSAb activity appeared to be confined to the IgG, fraction as determined by cAMP production on addition of the fractions to the FRTL-5 rat thyroid cell line. In all of eight specimens from seven patients so tested, the whole serum activity was recovered in the IgG, fraction, after adjusting for the recovery of the isotype from the column. TSAb activity in one serum comprised both lambda and kappa light chains but was IgG1 restricted. This IgG subclass restriction was not found when the same fractions were tested for thyroglobulin, microsomal/thyroid peroxidase, or tetanus toxoid antibody activity. Together with previous results showing marked restriction of both light chain usage and isoelectric point of TSAb, these results support the idea that Graves' disease may be the result of an oligo-or possibly monoclonal response at the B cell level. (J. Clin. Invest. 1990. 86:723-727.)

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“…34 The present study shows that hyperthyroid rats have increased proteinuria, consistent with the presence of proteinuria in patients with Graves' disease. 35 This alteration might be secondary to the increased production in hyperthyroid rats of NO, a vasodilator that impairs the glomerular permeability barrier, 36 although the fact that the proteinuria of T 4 -treated rats was unaffected by partial NO blockade argues against this possibility. Moreover, because proteinuria was also unrelated to BP or losartan administration, we suggest that proteinuria in the hyperthyroid state might be produced by a direct action of thyroid hormones, increasing the permeability of the glomerular barrier.…”

Section: Discussionmentioning

confidence: 99%

Increased Pressor Sensitivity to Chronic Nitric Oxide Deficiency in Hyperthyroid Rats

et al. 2003

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Abstract-We studied the effects of a possible interaction between partial nitric oxide deficiency and thyroid hormone excess on the long-term control of blood pressure (BP) and morphological and renal variables and examined the role of the renin-angiotensin system in the increased BP of this interaction. Eight groups (nϭ8 each) of male Wistar rats were used: a control group; 3 groups that were treated with thyroxine (50 g/d), N w -nitro-L-arginine methyl ester (L-NAME; subpressor dose, 1.5 mg · kg, or thyroxine plus L-NAME; and another 4 similarly treated groups that received losartan (20 mg · kg Ϫ1 · d Ϫ1) in their drinking fluid. All treatments were maintained for 3 weeks. The time course of tail systolic BP was recorded once a week. At the end of the experimental period, we measured mean arterial pressure in conscious rats and assessed the morphological, metabolic, plasma, and renal variables. Thyroxine produced a mild BP increase from the second week of treatment and an increase in plasma angiotensin II and plasma nitrates/nitrites by the end of the study. Simultaneous administration of thyroxine and a subpressor dose of L-NAME produced a marked BP increase that reached significance from the first week of treatment. Losartan produced normotension in thyroxine-treated rats and attenuated the BP elevation in thyroxineϩL-NAME-treated rats. Hyperthyroid rats showed relative renal and ventricular hypertrophy, absence of absolute left ventricular hypertrophy, and proteinuria. These alterations were not changed by losartan. We conclude that an impaired nitric oxide system might have a counterregulatory homeostatic role against the prohypertensive effects of thyroid hormone and that the renin-angiotensin system plays an important role in thyroxineϩL-NAME hypertension. Key Words: blood pressure Ⅲ hypertrophy, cardiac Ⅲ losartan Ⅲ nitric oxide Ⅲ hyperthyroidism T he hyperthyroid state is an endocrine disorder associated with important changes in hemodynamic, renal, and cardiac function. 1-3 Hyperthyroidism manifests a hyperdynamic circulation, with increased cardiac output, increased heart rate, and decreased peripheral resistance. 2-4 These characteristic cardiovascular manifestations of hyperthyroidism have been reproduced in rats by thyroid hormone treatment. [1][2][3] Animal studies have reported a dose-and time-related increase in arterial pressure 5,6 and have shown that the hyperthyroid state affects cardiac and renal weight and reduces renal sodium excretion. 2,5,6 It is well known that nitric oxide (NO) plays a major role in the regulation of vascular tone, 7 renal sodium excretion, 8,9 and therefore, of arterial blood pressure (BP). 10 Both acute and chronic administration of NO synthase (NOS) inhibitors increase systemic arterial BP. 11,12 Hyperthyroidism in rats increases the responsiveness of resistance vessels to the endothelium-dependent vasodilator acetylcholine. 13 Fernández et al 14 demonstrated that hyperthyroidism leads to a significant and reversible enhancement in rat liver NOS activity. More rec...

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Proteinuria in autoimmune thyroid disease

Cited by 32 publications

References 0 publications

Vascular and renal function in experimental thyroid disorders

Vascular and renal function in experimental thyroid disorders

Thyroid-stimulating antibody activity between different immunoglobulin G subclasses.

Increased Pressor Sensitivity to Chronic Nitric Oxide Deficiency in Hyperthyroid Rats

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