Effects of subclinical hyperthyroidism on renal handling of water and electrolytes in patients with nodular goiter

Corrales, J. J.; Tabernero, J.; Miralles, José Manuel Pavía; Hernández, María Teresa Gómez

doi:10.1007/bf01649051

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…Although, in overt hyperthyroidism, the enhanced tubular reabsorption of sodium due to increased activity of Na+/H+ exchanger in combination with the decreased load of filtered sodium causes a decrease in the pressure-diuresis-natriuresis response [ 30 ], we did not find a significant difference in electrolytes whether in blood or urine among SCH patients. This is consistent with a previous study that compared patients with SCH and euthyroidism regarding the mean plasma levels of electrolytes and did not reveal any significant differences [ 31 ].…”

Section: Discussionsupporting

confidence: 93%

Renal function changes in patients with subclinical hyperthyroidism: a novel postulated mechanism

Allam,

El-Zawawy,

El-Zawawy

2023

Endocrine

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Background Subclinical hyperthyroidism (SCH) is found to be associated with renal dysfunction. Hyperthyroidism is a well-known cause of secondary systolic hypertension. However, the effect of SCH on the kidney and its vasculature is still unknown. Aim To assess the presence of renal function changes and renal vasodysfunction in SCH patients and their relation to hypertension. Methods The study included 321 patients with SCH and 80 healthy matched controls. Laboratory investigations included thyroid function tests, anti-TSH receptor antibody (TRAb), creatinine, estimated glomerular filtration rate (eGFR), serum osmolarity (S. Osmol), urine osmolarity (U. Osmol), Fractional Excretion of Sodium (FeNa), Fractional Excretion of Potassium (FeK), copeptin (CPP), and aldosterone/renin ratio (ARR). Ultrasound for the thyroid gland, echocardiography, total peripheral resistance (TPR), flow-mediated dilatation (FMD), and Renal Arterial distensibility (RAD) was also done. Results Serum creatinine was significantly lower while eGFR was significantly higher in SCH patients compared to euthyroid subjects (mean 0.59 ± 0.11 mg/dl Vs mean 0.8 ± 0.1 mg/dl, p = 0.001 and mean 128.28 ± 14.69 ml/min/1.73m2 Vs mean 100.49 ± 14.9 ml/min/1.73m2, p = 0.013, respectively). The TPR and FMD showed a significant decrease in SCH group compared to controls (mean 975.85 ± 159.33 mmHg.min/L Vs mean 1120.24 ± 135.15 mmHg.min/L, p = 0.045 and mean 7.03 ± 4.02% Vs mean 13.48 ± 4.57%, p = 0.003, respectively). RAD was significantly higher in hypertensive SCH patients compared to normotensive SCH patients (mean 17.82 ± 2.46 mmHg Vs mean 11.98 ± 3.21 mmHg, p = 0.001). Conclusion SCH patients showed vascular resistance reduction. Alterations in thyroid hormones and blood pressure could be the driving mechanisms for the change in renal functions in patients with SCH.

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Section: Discussionsupporting

confidence: 93%

Renal function changes in patients with subclinical hyperthyroidism: a novel postulated mechanism

Allam,

El-Zawawy,

El-Zawawy

2023

Endocrine

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“…Thyroid hormones and TSH concentrations were measured in the serum of all patients by RIA and by an amplified immunoradiometric assay (for TSH), according to previously described techniques (Corrales et al 1991, Mories et al 1991. For the determination of serum TBII concentrations, the ability of antibodies to block the binding of 125 I-labelled TSH to porcine thyroid membranes was measured by a radioreceptor assay using a commercial kit (TRAK-Assay, Henning, Berlin, Germany).…”

Section: Thyroid Hormones and Autoantibodiesmentioning

confidence: 99%

Methimazole therapy in Graves' disease influences the abnormal expression of CD69 (early activation antigen) on T cells

Corrales

López²,

Ciudad³

et al. 1997

Journal of Endocrinology

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At present, the in vivo response of T, B and natural killer (NK) cells to antithyroid drug therapy remains largely unknown. In the present study, we have prospectively analyzed the in vivo effects of methimazole treatment on a large number of circulating T and NK cell subsets, some of them expressing cell surface activation antigens involved in the very early phase of the immune response, in a group of 17 hyperthyroid, untreated patients with Graves' disease (GD). As one of the first events during T cell activation is the expression of interleukin (IL) receptors, we also studied the binding of IL-2 and IL-6 to T cells. Patients with Graves' disease were sequentially studied at diagnosis/before treatment (day 0) and 7, 14, 30, 90 and 180 days after methimazole therapy. The results were compared with both a group of 19 age- and sex-matched control volunteers and a group of 20 untreated/euthyroid patients with Graves' disease in long-term remission. The combination of flow cytometry and three-color immunofluorescence revealed a clear (P < 0.01) decrease in the percentage of NK cells before and during the whole course of therapy with respect to both controls and patients with Graves' disease who were in long-term remission. Before therapy, a marked increase (P < 0.001) in the ratio of B to NK cells was also observed; thereafter, a slight decrease in this ratio was observed, although normal values were detected only in patients in long-term remission. Expression of the CD69 early activation antigen in the hyperthyroid untreated patients with Graves' disease was clearly increased (P < 0.01) with respect to both controls and patients with Graves' disease who were in long-term remission. This abnormal CD69 expression was found to be significantly reduced (P < 0.001) by methimazole therapy, and this represents a new effect of the drug. Expression of the low-affinity receptor for IL-2 (CD25)--another early T cell activation marker--was not altered in Graves' disease, but the binding of IL-2 and IL-6 to T cells exhibited a progressive and parallel increase during the first 30 days of therapy, decreasing thereafter. Our results show that methimazole therapy downregulates the abnormally high expression of the CD69 early activation antigen on T cells, being less effective on inducing changes in other T cell activation markers and in NK cells.

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“…Thyroid hormones and TSH levels were measured in the serum of all patients by RIA and by an amplified immunoradiometric assay (for TSH), according to previously described techniques (4,20). For the determination of serum TBII levels, a radioreceptor assay that measures the occupancy of TSH receptor was used (TRAK-Assay, Henning, Berlin, Germany).…”

Section: Thyroid Hormones Anti-tsh Receptor Antibodiesmentioning

confidence: 99%

Analysis of IL-2 and IL-6 binding to peripheral blood lymphocytes in Graves disease: Relationship with disease activity

Corrales¹,

Órfão

López

et al. 1997

Cytometry

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Effects of subclinical hyperthyroidism on renal handling of water and electrolytes in patients with nodular goiter

Cited by 7 publications

References 23 publications

Renal function changes in patients with subclinical hyperthyroidism: a novel postulated mechanism

Renal function changes in patients with subclinical hyperthyroidism: a novel postulated mechanism

Methimazole therapy in Graves' disease influences the abnormal expression of CD69 (early activation antigen) on T cells

Analysis of IL-2 and IL-6 binding to peripheral blood lymphocytes in Graves disease: Relationship with disease activity

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