Derangements in Phosphate Metabolism in Chronic Kidney Diseases/Endstage Renal Disease: Therapeutic Considerations

Molony, Donald A.; Stephens, Brett W.

doi:10.1053/j.ackd.2011.02.004

Cited by 35 publications

(30 citation statements)

References 118 publications

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“…Currently, strategies that successfully delay progression from CKD to end-stage kidney disease are limited and new strategies are needed. 1,22 We have programmed macrophages ex vivo into M2 to treat experimental CKD. Our group first demonstrated that macrophages derived from spleen and modulated with IL-4 and IL-13 ex vivo to induce an M2 phenotype (M2a) were able to reduce renal injury in mice with AN and mice with streptozotocin-induced diabetic nephropathy.…”

Section: Discussionmentioning

confidence: 99%

Failed renoprotection by alternatively activated bone marrow macrophages is due to a proliferation-dependent phenotype switch in vivo

Cao

Wang

Zheng

et al. 2014

Kidney International

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Alternatively activated macrophages (M2) regulate immune responses and ex vivo polarized splenic M2 are able to ameliorate renal injury including models of renal disease, such as adriamycin nephropathy. Whether M2 derived from other organs have similar protective efficacy is unknown. Here, we report adoptively transferred bone marrow M2 macrophages did not improve renal function or reduce renal injury in adriamycin nephropathy, whereas splenic M2 macrophages were protective. Bone marrow and splenic M2 macrophages showed similar regulatory phenotypes and suppressive functions in vitro. Within the inflamed kidney, suppressive phenotypes in bone marrow but not in splenic M2 macrophages, were dramatically reduced. Loss of the suppressive phenotype in bone marrow M2 was related to strong proliferation of bone marrow M2. Bone marrow M2 proliferation in vivo correlated with M-CSF expression by tubular cells in the inflamed kidney. Inhibition of M-CSF in vitro limited bone marrow M2 proliferation and prevented switch of phenotype. Proliferating cells derived from transfused bone marrow M2 were inflammatory rather than regulatory in their phenotype and function. Thus bone marrow in contrast to splenic M2 macrophages do not protect against renal structural and functional injury in murine adriamycin nephropathy. The failed renoprotection of bone marrow M2 is due to the switch of transfused M2 macrophages from a regulatory to an inflammatory phenotype.

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Section: Discussionmentioning

confidence: 99%

Failed renoprotection by alternatively activated bone marrow macrophages is due to a proliferation-dependent phenotype switch in vivo

Cao

Wang

Zheng

et al. 2014

Kidney International

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“…Elevation in serum calcium levels was noticed before PTX, but phosphate levels were diminished at this time, which was not found in some other studies (Malberti, 2010;Martin & González, 2011;Molony & Stephens, 2011). There has been lack of consensus about augmented phosphate concentration in these patients.…”

Section: Relationship Between Parathyroidectomy Calcium Phosphate Amentioning

confidence: 67%

Hyperparathyroidism in Hemodialyzed Patients – Relation to Melatonin and Reproductive Hormones Before and After Parathyroidectomy

Kancheva¹,

Žofková²,

Hill³

et al. 2012

Hyperparathyroidism

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“…This transient effect on kidney function was observed in both survivors and non-survivors and may at least in part explain why FGF-23 levels did not continuously decline after LVAD implantation and remained markedly elevated until t4, because the synthesis of FGF-23 is increased by elevated serum phosphate levels [8], e.g. as a consequence of impaired kidney function [18]. However, an alternative explanation for the lack of a permanent suppression of FGF-23 levels by LVAD implants is also possible and may involve the altered energy and phosphate metabolism of the failing heart.…”

Section: Discussionmentioning

confidence: 99%

Calciotropic and Phosphaturic Hormones in End-Stage Heart Failure Patients Supported by a Left-Ventricular Assist Device

et al. 2016

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BackgroundCalcium and phosphate are central for myocardial contractility and energy metabolism, and low levels of the calciotropic hormone 1,25-dihydroxyvitamin D (1,25(OH)2D), as well as high levels of the phosphaturic hormone fibroblast growth factor (FGF)-23, are independently associated with poor clinical outcome in heart failure (HF) patients. We therefore aimed to investigate the postoperative time course of the aforementioned hormones in HF patients supported with a left-ventricular assist device (LVAD) implant.MethodsFor the present study, stored biobank plasma samples of 69 patients, collected before LVAD implantation (t0) and 12 days (t1), 30 days (t2), 83 days (t3), and 300 days (t4) post-intervention, were used to measure circulating FGF-23, parathyroid hormone (PTH), 25-hydroxyvitamin D (25OHD), 1,25(OH)2D, and kidney function.ResultsMost patients were male and had baseline INTERMACS levels and cardiac index values ≤ 3 and ≤ 2.7 L/min/m2, respectively. There were significant time effects on estimated glomerular filtration rate (eGFR), FGF-23 and 1,25(OH)2D, but not on PTH or 25OHD. Notably, eGFR values increased and FGF-23 levels decreased only transiently, whereas 1,25(OH)2D increased continuously until t4. The rise in 1,25(OH)2D was largely influenced by those patients who survived the first post-implant year, and was not seen in non-survivors. Variations in 1,25(OH)2D levels could only partly be explained by eGFR values or FGF-23, 25OHD, and PTH levels (multiple R2 = 0.305;P<0.001).ConclusionsThe present study indicates that LVAD implantation has only transient effects on circulating FGF-23 levels, but is associated with a continuous increase in circulating 1,25(OH)2D levels, especially in survivors.

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Derangements in Phosphate Metabolism in Chronic Kidney Diseases/Endstage Renal Disease: Therapeutic Considerations

Cited by 35 publications

References 118 publications

Failed renoprotection by alternatively activated bone marrow macrophages is due to a proliferation-dependent phenotype switch in vivo

Failed renoprotection by alternatively activated bone marrow macrophages is due to a proliferation-dependent phenotype switch in vivo

Hyperparathyroidism in Hemodialyzed Patients – Relation to Melatonin and Reproductive Hormones Before and After Parathyroidectomy

Calciotropic and Phosphaturic Hormones in End-Stage Heart Failure Patients Supported by a Left-Ventricular Assist Device

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