Effect of Thyroxine Replacement on Creatinine, Insulin-Like Growth Factor 1, Acid-Labile Subunit, and Vascular Endothelial Growth Factor

Schmid, Christoph; Brändle, Michael; Zwimpfer, Cornelia; Zapf, J.; Wiesli, Peter

doi:10.1373/clinchem.2003.021022

Cited by 49 publications

(35 citation statements)

References 31 publications

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“…This association between renal function and hypothyroidism has been observed and in other studies using the Modification of Diet in Renal Disease (MDRD) creatinine-based equation and/or the newly introduced Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation (46,47). Data from studies using more precise GFR measuring methods (inulin or 51 Cr-EDTA) concluded that hypothyroidism is associated reduced GFR (10). All these studies confirmed that restoration of thyroid hormone levels can CysC equations in patients with thyroid disorders should be interpreted with caution (13).…”

Section: Thyroid Disorders and Glomerular Filtration Ratesupporting

confidence: 52%

“…Additionally, a chloride load in distal tubuli of hypothyroid rats, caused by a disturbed activity of chloride channels CIC-2, activated the tubulo-glomerular feedback leading to decreased GFR (49). Moreover, hypothyroidism causes a reduction of the expression of several glomerular vasodilators including insulin-like growth factor 1 (IGF-1) and vascular endothelial growth factor (VEGF), contributing to the reduction of GFR (51). In contrast, hyperthyroidism has the opposite effect on Scr and GFR.…”

Section: Impact Of Thyroid Hormones On Kidney Growth and Developmentmentioning

confidence: 99%

“…Hypothyroidism is associated with a decrease in transporter function and the opposite occurs (7) decreased (7) Peripheral vascular resistance decreased (7) increased (7) RAS activity increased (17) decreased (17) RBF increased (49) decreased (48,49) Glomerular vasoconstriction decreased (53) increased (50,51) Glomerular surface area increased (48) decreased (26) Tubulo-glomerular feedback increased (54) increased (49) Filtration pressure increased (53) decreased (48) GFR increased (11,12) decreased (8-10) Proteinuria increased (7) increased (7) Activity of tubular ion transport increased (65,66) decreased (56,59) Tubular mass increased (64) decreased (49) Urine concentrating ability decreased (68, 69) decreased (48) CO = cardiac output; GFR = glomerular filtration rate; RAS = renin-angiotensin system; RBF = renal blood flow.…”

Section: Thyroid Disorders and Tubular Functionmentioning

confidence: 99%

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The Thyroid and the Kidney: A Complex Interplay in Health and Disease

et al. 2014

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Thyroid hormones may directly affect the kidney and altered kidney function may also contribute to thyroid disorders. The renal manifestations of thyroid disorders are based on hemodynamic alterations or/and to direct effects of thyroid hormones. The renin-angiotensin system plays a crucial role in the cross-talk between the thyroid and the kidney. Hypothyroidism may be accompanied by an increase of serum creatinine and reduction of glomerular filtration rate (GFR), whereas hyperthyroidism may increase GFR. Treatment of thyroid disorders may lead to normalization of GFR. Primary and subclinical hypothyroidism and low triiodothyronine (T3) syndrome are common features in patients with chronic kidney disease (CKD). In addition low levels of thyroid hormones may predict a higher risk of cardiovascular and overall mortality in patients with end-stage renal disease. The causal nature of this correlation remains uncertain. In this review, special emphasis is given to the thyroid pathophysiology, its impact on kidney function and CKD and the interpretation of laboratorial findings of thyroid dysfunction in CKD.

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Section: Thyroid Disorders and Glomerular Filtration Ratesupporting

confidence: 52%

Section: Impact Of Thyroid Hormones On Kidney Growth and Developmentmentioning

confidence: 99%

Section: Thyroid Disorders and Tubular Functionmentioning

confidence: 99%

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The Thyroid and the Kidney: A Complex Interplay in Health and Disease

et al. 2014

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“…Second, although IGF-I expression is regulated by growth hormone, circulating IGF-I concentration is dependent on the presence of IGF-binding proteins (IGF-BPs). Sleep deprivation has diverse effects on metabolic function and hormone levels (15,22,48), which in turn may alter production of IGF-I, IGF-BPS, or decouple IGF-I production from growth hormone (38,45,51). Restoration of growth hormone alone may not have been sufficient to restore IGF-I levels.…”

Section: Discussionmentioning

confidence: 99%

Growth hormone rescues hippocampal synaptic function after sleep deprivation

Kim

Grover

Bertolotti

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Kim E, Grover LM, Bertolotti D, Green TL. Growth hormone rescues hippocampal synaptic function after sleep deprivation. Am J Physiol Regul Integr Comp Physiol 298: R1588 -R1596, 2010 doi:10.1152/ajpregu.00580.2009.-Sleep is required for, and sleep loss impairs, normal hippocampal synaptic N-methyl-D-aspartate (NMDA) glutamate receptor function and expression, hippocampal NMDA receptor-dependent synaptic plasticity, and hippocampaldependent memory function. Although sleep is essential, the signals linking sleep to hippocampal function are not known. One potential signal is growth hormone. Growth hormone is released during sleep, and its release is suppressed during sleep deprivation. If growth hormone links sleep to hippocampal function, then restoration of growth hormone during sleep deprivation should prevent adverse consequences of sleep loss. To test this hypothesis, we examined rat hippocampus for spontaneous excitatory synaptic currents in CA1 pyramidal neurons, long-term potentiation in area CA1, and NMDA receptor subunit proteins in synaptic membranes. Three days of sleep deprivation caused a significant reduction in NMDA receptor-mediated synaptic currents compared with control treatments. When rats were injected with growth hormone once per day during sleep deprivation, the loss of NMDA receptor-mediated synaptic currents was prevented. Growth hormone injections also prevented the impairment of long-term potentiation that normally follows sleep deprivation. In addition, sleep deprivation led to a selective loss of NMDA receptor 2B (NR2B) from hippocampal synaptic membranes, but normal NR2B expression was restored by growth hormone injection. Our results identify growth hormone as a critical mediator linking sleep to normal synaptic function of the hippocampus.hippocampal area CA1; long-term potentiation; NMDA receptor; sleep deprivation SLEEP IS A CRITICAL REGULATOR of biological functions, including brain function, yet the signals linking sleep to brain function are not known. Previous investigations showed that growth hormone, which is normally secreted during sleep and reduced during sleep deprivation (5, 15, 21, 52), regulates synaptic function in the hippocampus (33, 57). Growth hormone could therefore be a link between sleep and brain function, but this possibility has not yet been tested. Growth hormone is released from somatotroph cells in the anterior pituitary and is essential for somatic growth and metabolism (18). Recent studies have shown that growth hormone can cross the blood-brain barrier (9,19,42) and that the growth hormone receptor is expressed in several brain regions including the hippocampus (24, 30). Growth hormone effects on brain and cognitive function (41) may involve growth hormone regulation of synaptic plasticity in the hippocampus and hippocampal-dependent learning and memory (25,27,43). In the hippocampus, N-methyl-D-aspartate (NMDA) receptors play critical roles in memory formation and induction of long-term potentiation (LTP), a widely used synaptic model of learning an...

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“…However, in our opinion, while VEGF concentration is investigated, the thyrometabolic state of the patient should be considered. Moreover, the increase of P-PP VEGF concentration in response to L-T 4 administration may, at least in part, improve endothelial function and renal blood flow, thereby contributing to the decrease of serum creatinine concentration, observed in hypothyroid patients treated with L-T 4 [50].…”

Section: Discussionmentioning

confidence: 99%

Influence of L-Thyroxine Administration on Poor-platelet Plasma VEGF Concentrations in Patients with Induced Short-term Hypothyroidism, Monitored for Thyroid Carcinoma

et al. 2007

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Abstract. Angiogenesis is a process of new blood vessel development from pre-existing vasculature. It is a crucial process in normal physiology, as well as in several pathological conditions. The vascular endothelial growth factor (VEGF) represents a family of specific endothelial cell mitogens, involved in normal angiogenesis and in tumour development. The aim of the present study was to estimate the influence of L-thyroxine (L-T 4 ) administration on poorplatelet plasma (P-PP) VEGF concentrations in patients with induced short-term hypothyroidism, monitored for differentiated thyroid carcinoma. In the present study, P-PP concentrations of VEGF, thyroglobulin, thyrotropin and free thyroid hormones were investigated in a population of 24 hypothyroid patients, who were withdrawn from L-T 4 treatment for 5 weeks and studied before and after 2 months of L-T 4 therapy. Only healthy female patients with no evidence of metastasis in whole body scintigraphy were included in the study. They were then compared with 20 healthy control subjects, matched for age, sex and body mass index (BMI). The patients had significantly lower plasma VEGF concentrations before treatment with L-T 4 than after administration of that hormone. There was no significant difference in plasma VEGF levels, either between the patients treated with L-T 4 , and the controls, or between the patients untreated with L-T 4 , and the controls. Even short-time changes in thyrometabolic profile exert an important influence on P-PP VEGF concentrations, even if there is no thyroid tissue.

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Effect of Thyroxine Replacement on Creatinine, Insulin-Like Growth Factor 1, Acid-Labile Subunit, and Vascular Endothelial Growth Factor

Cited by 49 publications

References 31 publications

The Thyroid and the Kidney: A Complex Interplay in Health and Disease

The Thyroid and the Kidney: A Complex Interplay in Health and Disease

Growth hormone rescues hippocampal synaptic function after sleep deprivation

Influence of L-Thyroxine Administration on Poor-platelet Plasma VEGF Concentrations in Patients with Induced Short-term Hypothyroidism, Monitored for Thyroid Carcinoma

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