Mineral metabolism in chronic kidney disease

Kochanek, Malgorzata; Said, Albara; Lerma, Edgar V.

doi:10.1016/j.disamonth.2015.08.003

Cited by 5 publications

(5 citation statements)

References 41 publications

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“…Our study also found that OC, P1NP, and β-CTx were significantly reduced in male and post-menopausal female patients with different UACR, but there was no significant correlation with other bone metabolism indicators, consistent with previous literature that early chronic kidney disease can cause abnormal bone mineral metabolism and appearance of abnormal bone metabolic markers such as OC, P1NP, and β-CTx (14, 15). In addition, the levels of ADPN were significantly reduced and UACR was found to be negatively correlated with ADPN, an insulin–sensitizing hormone and blood lipid regulator, but not significantly correlated with other blood lipid indicators revealing a relationship between UACR and lipid metabolism, or potential associations with early metabolic processes such as insulin resistance and coronary atherosclerosis.…”

Section: Discussionsupporting

confidence: 91%

“…Moreover, 25(OH) Vitamin D3 [25(OH) VD3] and parathyroid hormone (PTH) promote absorption of calcium and phosphorus and increase blood calcium (Ca) and phosphorus (P) concentration thereby promoting bone calcification (8, 9). Previous studies have reported that these bone metabolic indicators may be involved in the crosstalk between bone, islet, and adipose tissues (8, 10–13) and may be associated with early renal damage in DKD (14, 15). However, these findings remain controversial and inconclusive.…”

Section: Introductionmentioning

confidence: 99%

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Correlation Between Serum miR-154-5p and Osteocalcin in Males and Postmenopausal Females of Type 2 Diabetes With Different Urinary Albumin Creatinine Ratios

Ren

Shao

et al. 2019

Front. Endocrinol.

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Purpose: To investigate the serum levels of miR-154-5p, osteocalcin (OC), and other clinical parameters in male and post-menopausal female type 2 diabetes mellitus (T2DM) patients with different urinary albumin creatinine ratio (UACR) levels and to discuss the relationship between miR-154-5p and glycolipid metabolism, bone metabolism, and different urinary albumin excretion rate in T2DM. Methods: Seven hundred thirty-eight T2DM patients were categorized into six groups, including 374 men and 364 post-menopausal women who were sub-divided into three groups based on albumin excretion that involved normal albuminuria, microalbuminuria, and large amount of albuminuria (138, 127, 109, 135, 125, and 104 cases, UACR<30, 30–300, and >300 mg/g, M1, M2, M3, F1, F2, and F3). Measurement of circulating miR-154-5p, OC, and other biochemical indicators were performed by real-time PCR, ELISA, and chemiluminescence assays in T2DM patients and in 141 M0 and 139 F0 control subjects. Results: There are few differences appeared between groups. Comparing with men, women had higher age, waist-to-hip ratio (WHR), adiponectin (ADPN), connective tissue growth factor (CTGF), UACR, procollagen type 1 N-terminal propeptide (P1NP), β-C-terminal telopeptide of type I collagen (β-CTx), OC, and miR-154-5p, but lower FPG, HOMA-IR, and HbA1c. T2DM patients with albuminuria (micro or macro) had lower bone turnover markers (P1NP, β-CTx, and OC) and adiponectin, but higher HbA1c, CTGF, and miR-154-5p. In addition, after regression analysis, UACR was positively correlated with CTGF, HbA1c, and miR-154-5p, and negatively correlated with ADPN and bone turnover markers (P1NP, β-CTx, and OC). However, OC showed a positive correlation with ADPN and other bone turnover markers (P1NP and β-CTx), but negative correlation with CTGF, UACR, and miR-154-5p in all three groups. Conclusion: These findings suggested that increased serum levels of miR-154-5p and decreased OC levels may influence osteogenesis and proteinuria in T2DM and may identify novel targets for diagnosis and treatment of diabetic kidney disease and osteoporosis.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Correlation Between Serum miR-154-5p and Osteocalcin in Males and Postmenopausal Females of Type 2 Diabetes With Different Urinary Albumin Creatinine Ratios

Ren

Shao

et al. 2019

Front. Endocrinol.

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“…The low glomerular filtration rate associated with early CKD development retains excessive phosphorus that causes progressive rise of osteocyte-derived fibroblast growth factor-23 (FGF23) and parathyroid hormone (PTH) production, which adversely affect bone remodeling and resorption eventually ensuring osteoporotic bone complications2. The medications aiming at minimizing phosphorus retention through dietary therapy or alternative vitamin D supplementation improved the abnormal metabolism of minerals and hormones3.…”

mentioning

confidence: 99%

Klotho preservation via histone deacetylase inhibition attenuates chronic kidney disease-associated bone injury in mice

Lin

Chen

et al. 2017

Sci Rep

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Bone loss and increased fracture are the devastating outcomes of chronic kidney disease-mineral and bone disorder (CKD-MBD) resulting from Klotho deficit-related mineral disturbance and hyperparathyroidism. Because Klotho down-regulation after renal injury is presumably affected by aberrant histone deacetylase (HDAC) activities, here we assess whether HDAC inhibition prevents Klotho loss and attenuates the CKD-associated bone complication in a mouse model of CKD-MBD. Mice fed adenine-containing diet developed the expected renal damage, a substantial Klotho loss and the deregulated key factors causally affecting bone remodeling, which were accompanied by a marked reduction of bone mineral density. Intriguingly, administration of a potent HDAC inhibitor trichostatin A (TSA) impressively alleviated the Klotho deficit and the observed alterations of serum, kidney and bone. TSA prevented Klotho loss by increasing the promoter-associated histone acetylation, therefore increasing Klotho transcription. More importantly the mice lacking Klotho by siRNA interference largely abolished the TSA protections against the serum and renal abnormalities, and the deranged bone micro-architectures. Thus, our study identified Klotho loss as a key event linking HDAC deregulation to the renal and bone injuries in CKD-MBD mice and demonstrated the therapeutic potentials of endogenous Klotho restoration by HDAC inhibition in treating CKD and the associated extrarenal complications.

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“…CKD-MBD is characterized by severe renal injury-induced mineral and hormone metabolic disorders accompanied by bone deteriorations (1). In the progression of CKD, low glomerular filtration rate (GFR) is associated with excessive phosphorus (P) levels, which accelerate osteocyte-derived fibroblast growth factor-23 (FGF-23) and parathyroid hormone (PTH) secretion and adversely affects bone remodeling and resorption, eventually resulting in osteoporotic bone complications (2). Previous clinical studies have demonstrated that the severity of CKD is associated with fracture rate (3,4).…”

Section: Introductionmentioning

confidence: 99%

High calcium diet alleviates 5/6 nephrectomy-induced bone deteriorations of lumbar vertebrae in mice

et al. 2018

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Abstract. Dietary calcium (Ca) supplementation has beneficial effects on bone health. However, it is not clear whether a high calcium diet (HCD) following 5/6 nephrectomy (5/6 Nx) is beneficial to bone health. The aim of the present study was to examine the effects of an HCD on bone metabolism using a chronic kidney disease (CKD) mouse model. Male C57BL/6J mice were divided into three groups: Sham group, 5/6 Nx group and 5/6 Nx + HCD group. Mice were sacrificed 12 weeks post-surgery. Calcium (Ca) and creatinine (Cr) were measured using standard colorimetric methods and picric acid methods, respectively. Bone metabolism-associated markers, FGF-23, PTH, ALP-b and TRAP-5b were measured using ELISA kits. Lumbar vertebrae histomorphological analysis was performed using hematoxylin and eosin staining. The expression of osteoprotegerin (OPG) and receptor activator of nuclear factor κB ligand (RANKL) mRNA was detected using reverse transcription-quantitative polymerase chain reaction. Impaired renal function and histopathological damage was indicated in 5/6 Nx mice. However, HCD had no significant effects on these changes in 5/6 Nx mice. Notably, mineral metabolism disorder and histopathological damage to lumbar vertebrae were markedly improved in HCD-treated 5/6 Nx mice. Compared with 5/6 Nx mice, HCD supplementation significantly elevated the ratio of OPG/RANKL and inhibited RANKL mRNA expression in lumbar vertebrae. To conclude, the present findings indicated that increased Ca intake is effective in increasing bone mineral content of the lumbar vertebrae in 5/6 Nx mice. These results may provide a basis for the clinical use of dietary Ca supplementation as a therapeutic approach to treat CKD-induced disturbance of mineral metabolism and bone loss.

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Mineral metabolism in chronic kidney disease

Cited by 5 publications

References 41 publications

Correlation Between Serum miR-154-5p and Osteocalcin in Males and Postmenopausal Females of Type 2 Diabetes With Different Urinary Albumin Creatinine Ratios

Correlation Between Serum miR-154-5p and Osteocalcin in Males and Postmenopausal Females of Type 2 Diabetes With Different Urinary Albumin Creatinine Ratios

Klotho preservation via histone deacetylase inhibition attenuates chronic kidney disease-associated bone injury in mice

High calcium diet alleviates 5/6 nephrectomy-induced bone deteriorations of lumbar vertebrae in mice

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