cholecalciferol and Acute-Kidney-Injury

Topics: Acute Kidney Injury; Animals; Bone Diseases; Calcium; Cholecalciferol; Deficiency Diseases; Dihydroxycholecalciferols; Humans; Hydroxycholecalciferols; Hypoparathyroidism; Kidney; Kidney Transplantation; Nephrectomy; Phosphorus; Rickets; Structure-Activity Relationship; Vitamin D

Acute kidney injury (AKI) is a common complication in patients with potentially life-threatening diseases, and it is also usually associated with unacceptable morbidity and mortality rates. Therefore, new and efficient therapies are urgently required to relieve AKI. It is well known that, reactive oxygen species (ROS), the NF-κB signaling pathways and pyroptosis are involved in AKI induced by ischemia/reperfusion (I/R). The present study seeks to further confirm the internal relationship between vitamin D deficiency and I/R-induced AKI in patients, and to explore the underlying mechanisms of ROS, NF-κB signaling pathways and pyroptosis in the renal ischemia-reperfusion injury, as well as investigating the protective role of cholecalciferol. Patients with vitamin D deficiency show worse renal function reflected by postoperative glomerular filtration rate (GFR) and more release of proinflammatory cytokine IL-1β and IL-18. Renal cell injury and renal dysfunction induced by I/R surgery were attenuated in the ICR mice administered with cholecalciferol. Cholecalciferol reduced ROS production, suppressed activated NF-κB signaling, and inhibited gasdermin D (GSDMD, a pyroptosis execution protein)-mediated pyroptosis. Cholecalciferol therefore has potential, as a clinical drug, to protect renal function in I/R-induced AKI through reducing ROS production, NF-κB activation and GSDMD-mediated pyroptosis.

Topics: Acute Kidney Injury; Animals; Cholecalciferol; Humans; Ischemia; Kidney; Mice; Mice, Inbred ICR; NF-kappa B; Pyroptosis; Reactive Oxygen Species; Reperfusion; Reperfusion Injury; Vitamin D Deficiency

There are many causes of hypercalcemia, with hyperparathyroidism and malignancy accounting for 90% of cases. Sarcoidosis and the intake of vitamin D supplements may also cause hypercalcemia, although the occurrence rate is low if only one is involved. We herein report a sarcoidosis patient who developed hypercalcemia after taking cholecalciferol (vitamin D supplement) for a year.. A 62-year-old Japanese man presented with hypercalcemia and acute kidney injury along with symptoms of fatigue and appetite loss while being followed up for sarcoidosis.. We determined that a combination of cholecalciferol supplementation and sarcoidosis had led to hypercalcemia for several reasons. First, hypercalcemia had not been noted when this patient had first been admitted due to sarcoidosis-related respiratory failure several years earlier, which we presumed that was the highest sarcoidosis disease activity. Second, low serum 25-OH Vit.D3 and high 1,25-(OH)2 Vit.D3 levels were noted despite cholecalciferol supplementation for a year, suggesting that 1-α-hydroxylase overexpression caused by sarcoidosis accelerated the conversion from 25-OH Vit.D3 to 1,25-(OH)2 Vit.D3.. Although initially resistant to preservative management, the hypercalcemia promptly improved after starting corticosteroid treatment.. Hypercalcemia and acute kidney injury were normalized after corticosteroid treatment.. We should be aware of patients' medications, especially in patients with granulomatosis disease. The concomitant measurement of 25-OH Vit.D3 and 1,25-(OH)2 Vit.D3 levels is useful for determining the cause of hypercalcemia.

Topics: Acute Kidney Injury; Calcium; Cholecalciferol; Dietary Supplements; Humans; Hypercalcemia; Male; Middle Aged; Mixed Function Oxygenases; Sarcoidosis; Vitamin D

Increasing evidence demonstrates that reactive oxygen species plays important roles in sepsis-induced acute kidney injury. This study investigated the effects of VitD3 pretreatment on renal oxidative stress in sepsis-induced acute kidney injury. Mice were intraperitoneally injected with lipopolysaccharide (LPS, 2.0mg/kg) to establish an animal model of sepsis-induced acute kidney injury. In VitD3+LPS group, mice were orally pretreated with three doses of VitD3 (25 μg/kg) at 1, 24 and 48 h before LPS injection. As expected, oral pretreatment with three daily recommended doses of VitD3 markedly elevated serum 25(OH)D concentration and efficiently activated renal VDR signaling. Interestingly, LPS-induced renal GSH depletion and lipid peroxidation were markedly alleviated in VitD3-pretreated mice. LPS-induced serum and renal nitric oxide (NO) production was obviously suppressed by VitD3 pretreatment. In addition, LPS-induced renal protein nitration, as determined by 3-nitrotyrosine residue, was obviously attenuated by VitD3 pretreatment. Further analysis showed that LPS-induced up-regulation of renal inducible nitric oxide synthase (inos) was repressed in VitD3-pretreated mice. LPS-induced up-regulation of renal p47phox and gp91phox, two NADPH oxidase subunits, were normalized by VitD3 pretreatment. In addition, LPS-induced down-regulation of renal superoxide dismutase (sod) 1 and sod2, two antioxidant enzyme genes, was reversed in VitD3-pretreated mice. Finally, LPS-induced tubular epithelial cell apoptosis, as determined by TUNEL, was alleviated by VitD3 pretreatment. Taken together, these results suggest that VitD3 pretreatment alleviates LPS-induced renal oxidative stress through regulating oxidant and antioxidant enzyme genes.

Topics: 25-Hydroxyvitamin D 2; Acute Kidney Injury; Animals; Apoptosis; Cholecalciferol; Glutathione; Kidney; Lipid Peroxidation; Lipopolysaccharides; Male; Membrane Glycoproteins; Mice; NADPH Oxidase 2; NADPH Oxidases; Nitric Oxide; Nitric Oxide Synthase Type II; Oxidative Stress; Reactive Oxygen Species; Receptors, Calcitriol; Superoxide Dismutase; Superoxide Dismutase-1; Tyrosine

Vitamin D receptor (VDR) is highly expressed in human and mouse kidneys. Nevertheless, its functions remain obscure. This study investigated the effects of vitamin D3 (VitD3) pretreatment on renal inflammation during lipopolysaccharide (LPS)-induced acute kidney injury. Mice were intraperitoneally injected with LPS. In VitD3 + LPS group, mice were pretreated with VitD3 (25 μg/kg) at 48, 24 and 1 h before LPS injection. As expected, an obvious reduction of renal function and pathological damage was observed in LPS-treated mice. VitD3 pretreatment significantly alleviated LPS-induced reduction of renal function and pathological damage. Moreover, VitD3 pretreatment attenuated LPS-induced renal inflammatory cytokines, chemokines and adhesion molecules. In addition, pretreatment with 1,25(OH)2D3, the active form of VitD3, alleviated LPS-induced up-regulation of inflammatory cytokines and chemokines in human HK-2 cells, a renal tubular epithelial cell line, in a VDR-dependent manner. Further analysis showed that VitD3, which activated renal VDR, specifically repressed LPS-induced nuclear translocation of nuclear factor kappa B (NF-κB) p65 subunit in the renal tubules. LPS, which activated renal NF-κB, reciprocally suppressed renal VDR and its target gene. Moreover, VitD3 reinforced the physical interaction between renal VDR and NF-κB p65 subunit. These results provide a mechanistic explanation for VitD3-mediated anti-inflammatory activity during LPS-induced acute kidney injury.

Topics: Acute Kidney Injury; Animals; Cell Line; Chemokines; Cholecalciferol; Cyclooxygenase 2; Humans; Inflammation; Intercellular Adhesion Molecule-1; Kidney; Lipopolysaccharides; Male; Mice; p38 Mitogen-Activated Protein Kinases; Phosphatidylinositol 3-Kinases; Protein Binding; Proto-Oncogene Proteins c-akt; Receptors, Calcitriol; RNA, Small Interfering; Signal Transduction; Transcription Factor RelA; Transfection; Vascular Cell Adhesion Molecule-1

Vitamin D deficiency is common. It causes osteomalacia, may contribute to osteoporosis and is an independent risk factor for cancer, diabetes, multiple sclerosis, cardiovascular disease and all-cause mortality. We describe patients with a history of sarcoidosis who developed acute kidney injury due to hypercalcaemia following treatment with colecalciferol.

Topics: Acute Kidney Injury; Adult; Cholecalciferol; Humans; Hypercalcemia; Male; Sarcoidosis; Vitamin D Deficiency; Vitamins

Vitamin D toxicity from unactivated vitamin D (calciferol) therapy is currently a rare cause of hypercalcaemia. However, the frequency of this event may increase as high-dose unactivated vitamin D preparations become available. Prolonged vitamin D toxicity can cause reversible hypercalcaemia and partially reversible renal impairment. Parathyroid hormone may not be suppressed with unactivated vitamin D toxicity, especially if renal disease coexists.

Topics: Acute Kidney Injury; Aged; Cholecalciferol; Disease Progression; Female; Humans; Hypercalcemia; Time Factors

To report a case of hypervitaminosis D resulting in hypercalcemia and acute kidney injury in a 70-year-old female who was prescribed a standard dose of vitamin D but given a toxic dose of vitamin D 50,000 IU (1.25 mg) daily resulting from a dispensing error.. A 70-year-old female in her usual state of health was instructed to begin supplementation with vitamin D 1000 IU daily. Three months later she developed confusion, slurred speech, unstable gait, and increased fatigue. She was hospitalized for hypercalcemia and acute kidney injury secondary to hypervitaminosis D. All vitamin D supplementation was discontinued and 5 months after discharge, the patient's serum calcium and vitamin D concentrations, as well as renal function, had returned to baseline values. Upon review of the patient's records, it was discovered that she had been taking vitamin D 50,000 IU daily.. There is an increased interest in vitamin D, resulting in more health care providers recommending--and patients taking--supplemental vitamin D. Hypervitaminosis D is rarely reported and generally only in the setting of gross excess of vitamin D. This report highlights a case of hypervitaminosis D in the setting of a prescribed standard dose of vitamin D that resulted in toxic ingestion of vitamin D 50,000 IU daily due to a dispensing error. As more and more people use vitamin D supplements, it is important to recognize that, while rare, hypervitaminosis D is a possibility and dosage conversion of vitamin D units can result in errors.. Health care providers and patients should be educated on the advantages and risks associated with vitamin D supplementation and be informed of safety measures to avoid hypervitaminosis D. In addition, health care providers should understand dosage conversion regarding vitamin D and electronic prescribing and dispensing software should be designed to detect such errors.

Topics: Acute Kidney Injury; Aged; Cholecalciferol; Confusion; Drug Dosage Calculations; Ergocalciferols; Female; Fractures, Bone; Humans; Hypercalcemia; Medication Errors; Treatment Outcome

Tenofovir-containing antiviral therapy might result in acute renal failure and is able to induce tubular dysfunction with hypocalcemia. On the other hand, hypercalcemia induced by intoxication with colecalciferol has been described to induce renal failure in HIV-positive individuals as well. Here, the authors describe the unusual case of reversible renal failure due to hypercalcemia in a patient with low-dose colecalciferol substitution treated with tenofovir.. A 31-year-old HIV-positive female, CDC stage C3, was admitted to the authors' hospital with progressive renal failure and hypercalcemia. Antiretroviral therapy consisted of tenofovir and emtricitabine in combination with efavirenz. Additionally, she was on low-dose vitamin D(3) substitution (25 microg/d) and calcium supplementation (500 mg/d) due to systemic steroid treatment.. Additionally to regular control of renal function, serologic level of calcium should be supervised in patients concomitantly treated with tenofovir and colecalciferol.

Topics: Acquired Immunodeficiency Syndrome; Acute Kidney Injury; Adenine; Adrenal Cortex Hormones; Adult; AIDS-Related Opportunistic Infections; Alkynes; Anti-HIV Agents; Antitubercular Agents; Benzoxazines; Calcium; Cholecalciferol; Cyclopropanes; Deoxycytidine; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Therapy, Combination; Emtricitabine; Female; Humans; Hypercalcemia; Immune Reconstitution Inflammatory Syndrome; Kidney Function Tests; Mycobacterium avium-intracellulare Infection; Organophosphonates; Osteoporosis; Tenofovir

Topics: Acute Kidney Injury; Adult; Cholecalciferol; Dietary Sucrose; Humans; Male

We studied serum concentrations of calcium, phosphate, intact parathyroid hormone (PTH) and vitamin D3 metabolites in 41 patients with nephropathia epidemica. Thirty-four of the 41 patients had a mild to moderate, mostly nonoliguric acute renal failure (ARF). Hypocalcemia developed in relation to the severity of renal failure, and parathyroid gland response to hypocalcemia was normal. The serum concentration of 1,25-dihydroxyvitamin D3 was lower than normal in patients who developed ARF. Serum phosphate was the most important factor in regulating the serum 1,25(OH)2D3 level, though only mild phosphate retention was seen in the patients. We observed normal or slightly elevated serum phosphate, hypocalcemia accompanied by elevated PTH levels and a decreased serum concentration of 1,25(OH)2D3 in patients with ARF caused by nephropathia epidemica.

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Calcium; Cholecalciferol; Female; Hemorrhagic Fever with Renal Syndrome; Humans; Hypocalcemia; Male; Middle Aged; Nephritis, Interstitial; Orthohantavirus; Parathyroid Hormone; Phosphates

Topics: Acute Kidney Injury; Aged; Bone Marrow Diseases; Cholecalciferol; Female; Humans; Hypercalcemia; Osteoporosis; Sarcoidosis

Topics: Acute Kidney Injury; Cholecalciferol; Humans; Hypercalcemia; Infant; Male

Topics: Acute Kidney Injury; Cholecalciferol; Humans; Hypercalcemia; Infant; Male

Topics: Acute Kidney Injury; Analysis of Variance; Animals; Binding Sites; Chickens; Cholecalciferol; Chromatin; Chromatography; Chromatography, Gel; Cytosol; Evaluation Studies as Topic; Humans; Intestine, Small; Male; Methods; Microchemistry; Periodic Acid; Polyethylene Glycols; Receptors, Drug; Rickets; Silicon Dioxide; Structure-Activity Relationship; Tritium