Parathyroid Hormone: A Uremic Toxin

Duque, Eduardo Jorge; Elias, Rosilene Motta; Moysés, Rosa M.A.

doi:10.3390/toxins12030189

Cited by 48 publications

(40 citation statements)

References 94 publications

(116 reference statements)

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“…PTH acts on cardiomyocytes independently of sCa levels promoting left ventricular hypertrophy and fibrosis that lead to diastolic dysfunction and suppressed contractility [ 3 , 11 ]. These effects have been mainly described in patients with chronic kidney disease and long lasting hyperparathyroidism [ 12 ]. In the case reported by Cummings et al, high output heart failure may have resulted or at least contributed in the development of pulmonary edema [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

Acute Respiratory Distress Syndrome Induced by Parathyroid Storm

Zagkotsis¹,

Markou²,

Papanikolaou³

et al. 2021

Cureus

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Hypercalcemic crisis associated with the development of acute respiratory distress syndrome (ARDS) has been rarely documented in the literature. Most cases have been described in patients suffering from malignancies or renal failure with the presence of metastatic calcifications being a prominent feature. Only three cases of ARDS have been reported to date in patients with hypercalcemic crisis due to primary hyperparathyroidism (PHPT). Herein, we report a 72-year-old patient with PHPT that presented with severe hypercalcemic crisis and developed ARDS. He had mild chronic kidney disease and at presentation he had extremely high levels of serum calcium (22.5 mg/dl) and parathormone (3822 pg/ml). After receiving medical treatment for hypercalcemia and the initiation of hemodialysis, he developed ARDS with a fatal outcome, without the presence of pancreatitis, sepsis or heart failure. Although very rare, ARDS should be taken into account as a possible complication of parathyroid crisis, especially in patients with excessive calcium and parathormone levels.

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Section: Discussionmentioning

confidence: 99%

Acute Respiratory Distress Syndrome Induced by Parathyroid Storm

Zagkotsis¹,

Markou²,

Papanikolaou³

et al. 2021

Cureus

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“…Another major characteristic of SHPT is parathyroid hyperplasia. Phosphate accumulation, increased FGF23 levels, decreased vitamin D activity, and hypocalcemia are persistent stimulants of parathyroid hyperplasia and increased PTH secretion [25,26]. Calcitriol, a metabolite of vitamin D, inhibits the cell cycle regulator c-MYC, inhibits transforming growth factor α, and induces p21 to act as cell cycle inhibitor [27].…”

Section: Discussionmentioning

confidence: 99%

Effects of Orai3-Mediated Store-Operated Calcium Entry on Parathyroid Hormone Release in Secondary Hyperparathyroidism

Lin

Wang

Han

et al. 2021

Preprint

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Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease, is characterized by elevated parathyroid hormone (PTH) secretion and Hypocalcemia. Orai3 is a highly selective calcium (Ca2+) channel that plays important roles in tumor development, cardiovascular disease, and autoimmune diseases; however, its role in SHPT is unclear. In the present study, RNA sequencing and western blot assays were used to detect the expression levels of Orai3 in parathyroid tissue from patients with SHPT and from individuals without SHPT. Ca2+ imaging was used to detect the effect of Orai3 channels on Ca2+ signaling in parathyroid gland cells. Enzyme-linked immunosorbent assays were used to detect changes in PTH release. Orai3 knockout rats were used to detect the effect of decreased Orai3 expression on serum PTH levels. We found that the expression of Orai3 in parathyroid tissue obtained from patients with SHPT was significantly higher than that in patients without SHPT. Knockdown of Orai3 in parathyroid cells by transfection with Orai3-specific small inhibitor RNA inhibited store-operated Ca2+ entry (SOCE) in parathyroid cells. Inhibition of SOCE or knockdown of Orai3 significantly inhibited PTH release in parathyroid cells. PTH levels in the blood of Orai3 knockout rat were significantly reduced. Therefore, Orai3 expression and Orai3-mediated Ca2+ signaling may be a mechanism underlying PTH release, and Orai3 may play a role in the development of SHPT.

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“…Parathyroid hormone levels are increased in CKD patients. In a recent review, Duque et al [145] describe the significance of parathyroid hormone as a uremic toxin contributing to the manifestations of the uremic syndrome. In CKD, secondary hyperparathyroidism leads to elevated FGF-23 serum levels, decreased calcitriol production in the kidney, reduced intestinal calcium absorption, and hyperphosphatemia.…”

Section: Vitamin D Fibroblast Growth Factor 23 and Parathyroid Hormonementioning

confidence: 99%

Immune Dysfunction in Uremia 2020

Cohen

2020

Toxins

106

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Cardiovascular disease and infections are major causes for the high incidence of morbidity and mortality of patients with chronic kidney disease. Both complications are directly or indirectly associated with disturbed functions or altered apoptotic rates of polymorphonuclear leukocytes, monocytes, lymphocytes, and dendritic cells. Normal responses of immune cells can be reduced, leading to infectious diseases or pre-activated/primed, giving rise to inflammation and subsequently to cardiovascular disease. This review summarizes the impact of kidney dysfunction on the immune system. Renal failure results in disturbed renal metabolic activities with reduced renin, erythropoietin, and vitamin D production, which adversely affects the immune system. Decreased kidney function also leads to reduced glomerular filtration and the retention of uremic toxins. A large number of uremic toxins with detrimental effects on immune cells have been identified. Besides small water-soluble and protein-bound compounds originating from the intestinal microbiome, several molecules in the middle molecular range, e.g., immunoglobulin light chains, retinol-binding protein, the neuropeptides Met-enkephalin and neuropeptide Y, endothelin-1, and the adipokines leptin and resistin, adversely affect immune cells. Posttranslational modifications such as carbamoylation, advanced glycation products, and oxidative modifications contribute to uremic toxicity. Furthermore, high-density lipoprotein from uremic patients has an altered protein profile and thereby loses its anti-inflammatory properties.

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Parathyroid Hormone: A Uremic Toxin

Cited by 48 publications

References 94 publications

Acute Respiratory Distress Syndrome Induced by Parathyroid Storm

Acute Respiratory Distress Syndrome Induced by Parathyroid Storm

Effects of Orai3-Mediated Store-Operated Calcium Entry on Parathyroid Hormone Release in Secondary Hyperparathyroidism

Immune Dysfunction in Uremia 2020

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