Ways of calcium reabsorption in the kidney

Moor, Matthias B.; Bonny, Olivier

doi:10.1152/ajprenal.00273.2015

Cited by 97 publications

(95 citation statements)

References 217 publications

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“…In endocrine and other factor-regulated calcium reabsorption, most calcium reabsorption happens in the proximal tubule of the tubular system, with~98% of calcium being reabsorbed. 40 Calbindin D28 was found to have a decreased expression, and its function is to facilitate the reabsorption of calcium ions. 41 Therefore, maleic acid may interfere with calcium reabsorption and decrease serum calcium concentrations indirectly.…”

Section: Endocrine and Other Factor-regulated Calcium Reabsorptionmentioning

confidence: 99%

Proteomic analysis of rat kidney under maleic acid treatment by SWATH‐MS technology

Chien

Xue

Chen

et al. 2020

Rapid Comm Mass Spectrometry

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Rationale Maleic acid is an industrial‐grade chemical that is often used in adhesives, stabilizers, and preservatives. It is unknown whether long‐term consumption of maleic acid modified starch is harmful to humans. However, many studies have indicated that maleic acid causes renal tubular damage in animal models, even as the associated pathways remain unclear. Sequential window acquisition of all theoretical fragment ion spectra (SWATH) is the most innovative of the label‐free quantitative technologies which have better quantification performance. Therefore, SWATH technology was used to investigate the effect of maleic acid on the rat kidney proteome in this study. Methods Sprague‐Dawley(SD) rats were treated with 0 mg/kg (control), 6 mg/kg (low‐dose), 10 mg/kg (medium‐dose), and 60 mg/kg (high‐dose) of maleic acid. After kidney protein extraction, 28% SDS‐PAGE was used, followed by in‐gel digestion and desalting. Next, the samples were analyzed with ultra‐performance liquid chromatography (UPLC) coupled with quadrupole time‐of‐flight mass spectrometry (Q‐TOF MS), and data‐dependent acquisition (DDA) and SWATH technology were also used. The gene ontology and pathway analysis were accomplished. Ultimately, these protein biomarkers were validated by using scheduled high‐resolution multiple reaction monitoring (sMRMHR). Results Comparisons of the control group with the other three groups revealed that 95, 130, and 103 proteins were expressed at significantly different levels in the control group and in the low‐dose, medium‐dose, and high‐dose groups, respectively. According to the gene ontology analysis, the major processes that these proteins were involved in were metabolic processes, biological regulation, cellular processes, and responses to stimuli; the major functions that these proteins were involved in were binding, hydrolase activity, catalytic activity, and oxidoreductase activity; and the major cellular components hat they were involved in were the cytoplasm, extracellular region, membrane, and mitochondria. According to the KEGG pathway analysis, these proteins were involved in 35 pathways, five of which, the carbohydrate metabolism, folate biosynthesis, renal tubular resorption, amino acid metabolism, and Ras signaling pathways, are discussed in this study. Ultimately, 19 proteins involved in 12 important pathways were validated by sMRMHR. Conclusions It was demonstrated that maleic acid caused insufficient energy production, which might lead to a decrease in the activity of the sodium‐potassium ATP pump and hydrogen ion ATP pump, which could in turn have caused renal tubular resorption and hydrogen ion regulation to be blocked, thus leading to the accumulation of hydrogen ions in the renal tubules, which would then result in renal tubular acidification followed finally by Fanconi syndrome.

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Section: Endocrine and Other Factor-regulated Calcium Reabsorptionmentioning

confidence: 99%

Proteomic analysis of rat kidney under maleic acid treatment by SWATH‐MS technology

Chien

Xue

Chen

et al. 2020

Rapid Comm Mass Spectrometry

View full text Add to dashboard Cite

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“…promoting bone resorption (Silva and Bilezikian, 2015) and renal calcium reabsorption (Lau and Bourdeau, 1995, Moor and Bonny, 2016)). In addition, dietary calcium deprivation increases serum PTH levels and so high PTH is associated with increased calcium absorption during periods of low dietary calcium intake.…”

Section: Vitamin D Metabolites Are a Part Of The Hormonal Networkmentioning

confidence: 99%

“…Renal calcium reabsorption occurs through a number of mechanisms that are unique to each segment of the kidney tubule – the full complexity of this process was recently reviewed by Moor and Bonny (Moor and Bonny, 2016). Approximately 90% of renal calcium reabsorption occurs in the proximal tubule and thick ascending limb of the loop of Henle.…”

Section: Vitamin D-mediated Regulation Of Calcium Transport Acrossmentioning

confidence: 99%

The role of vitamin D in the endocrinology controlling calcium homeostasis

Fleet

2017

Molecular and Cellular Endocrinology

204

129

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Vitamin D and its’ metabolites are a crucial part of the endocrine system that controls whole body calcium homeostasis. The goal of this hormonal control is to regulate serum calcium levels so that they are maintained within a very narrow range. To achieve this goal, regulatory events occur in coordination at multiple tissues, e.g. the intestine, kidney, bone, and parathyroid gland. Production of the vitamin D endocrine hormone, 1,25 dihydroxyvitamin D (1,25(OH)2 D) is regulated by habitual dietary calcium intake and physiologic states like growth, aging, and the menopause. The molecular actions of 1,25(OH)2 D on calcium regulating target tissues are mediated predominantly by transcription controlled by the vitamin D receptor. The primary role for 1,25(OH)2 D during growth is to increase intestinal calcium absorption so that sufficient calcium is available for bone mineralization. However, vitamin D also has specific actions on kidney and bone.

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“…In DCT-CNT, calcium enters the cell at the apical side through TRPV5 channels, binds intracellular calbindin-D-28k and exits the cell at the basolateral side by the Na-Ca exchanger (NCX1) and the Ca-ATPase PMCA4 29 any calcium delivered there is subject to precipitation depending most importantly upon the tubular fluid pH. 29 In the PT, the majority of calcium is reabsorbed by passive and hormone-independent paracellular transport. The claudin family of epithelial tight junction proteins are crucial for paracellular calcium permeability.…”

Section: Lo C Aliz Ati On and Fun C Ti On Of C Alci Um And Phos Phamentioning

confidence: 99%

Dent disease: A window into calcium and phosphate transport

Anglani

Gianesello

Beara-Lasić

et al. 2019

J Cellular Molecular Medi

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This review examines calcium and phosphate transport in the kidney through the lens of the rare X‐linked genetic disorder Dent disease. Dent disease type 1 (DD1) is caused by mutations in the CLCN5 gene encoding ClC‐5, a Cl−/H+ antiporter localized to early endosomes of the proximal tubule (PT). Phenotypic features commonly include low molecular weight proteinuria (LMWP), hypercalciuria, focal global sclerosis and chronic kidney disease; calcium nephrolithiasis, nephrocalcinosis and hypophosphatemic rickets are less commonly observed. Although it is not surprising that abnormal endosomal function and recycling in the PT could result in LMWP, it is less clear how ClC‐5 dysfunction disturbs calcium and phosphate metabolism. It is known that the majority of calcium and phosphate transport occurs in PT cells, and PT endocytosis is essential for calcium and phosphorus reabsorption in this nephron segment. Evidence from ClC‐5 KO models suggests that ClC‐5 mediates parathormone endocytosis from tubular fluid. In addition, ClC‐5 dysfunction alters expression of the sodium/proton exchanger NHE3 on the PT apical surface thus altering transcellular sodium movement and hence paracellular calcium reabsorption. A potential role for NHE3 dysfunction in the DD1 phenotype has never been investigated, either in DD models or in patients with DD1, even though patients with DD1 exhibit renal sodium and potassium wasting, especially when exposed to even a low dose of thiazide diuretic. Thus, insights from the rare disease DD1 may inform possible underlying mechanisms for the phenotype of hypercalciuria and idiopathic calcium stones.

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Ways of calcium reabsorption in the kidney

Cited by 97 publications

References 217 publications

Proteomic analysis of rat kidney under maleic acid treatment by SWATH‐MS technology

Proteomic analysis of rat kidney under maleic acid treatment by SWATH‐MS technology

The role of vitamin D in the endocrinology controlling calcium homeostasis

Dent disease: A window into calcium and phosphate transport

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