cholecalciferol and Renal-Insufficiency

Treatment using the cell sheet technology has been applied to various organs, including the cornea, heart, esophagus, periodontium, cartilage, middle ear, and lungs. It has been shown that the therapeutic efficacy of cell sheet transplantation involves 2 aspects, supplementation of cells and provision of cytokines to the affected organ. In addition, cell sheet transplantation also promotes repair of damage through the paracrine effects of cytokines derived from the transplanted cells. It is known that in cases of cell transplantation by injection, the transplanted cells are less likely to differentiate into renal tissue to supply cells, but repair is promoted by the actions of the transplanted cell-derived renotropic factors. Renal function requires functional conjugation of various tissues, including blood vessels, glomeruli, renal tubules, and collecting ducts. It is difficult to supply the necessary cells directly to the affected site of the renal tissue composed of complex structures. On the contrary, the 2-dimensional cell sheet can produce proteins such as erythropoietin, and is thus suitable for transplantation into the living body. It would be desirable to develop cell sheet therapy for the suppression of kidney damage in the future, taking advantage of the beneficial characteristics of cell sheets.

Topics: Cell Transplantation; Cells, Cultured; Cholecalciferol; Culture Techniques; Cytokines; Erythropoietin; Humans; Kidney; Kidney Diseases; Regeneration; Renal Insufficiency; Stem Cell Transplantation; Tissue Engineering

Low levels of vitamin D are linked to numerous adverse clinical conditions in hemodialysis (HD) patients, including disturbances of mineral and bone metabolism and increased mortality. Klotho, a molecule involved in such processes as phosphate homeostasis and aging, exists in 2 forms: a transmembrane protein acting as a coreceptor for fibroblast growth factor 23 (FGF-23) and soluble form, which is formed by cleavage of the extracellular domain of this molecule.. The aim of the study was to evaluate the effect of cholecalciferol supplementation on soluble Klotho levels in HD patients.. This was a prospective, open-label trial examining the effects of cholecalciferol supplementation on selected laboratory markers in 22 patients on HD. Vitamin D deficiency was assessed by the measurement of 25-hydroxyvitamin D [25(OH)D] levels. Soluble Klotho, intact FGF-23, intact parathormone (iPTH), and markers of bone formation and resorption were measured at baseline and after 12 weeks of cholecalciferol supplementation.. The levels of 25(OH)D increased, while those of iPTH and cross-linked C-telopeptide of type 1 collagen decreased significantly. Cholecalciferol treatment reduced the median concentration of soluble Klotho (from 438.73 pg/ml; interquartile range, 257.99-865.51 pg/ml; to 370.94 pg/ml; 181.72-710.91 pg/ml; P <0.05). FGF‑23 levels were not affected by the treatment.. Supplementation with cholecalciferol in HD patients decreases soluble Klotho levels without affecting the FGF-23 concentration. Replenishment of vitamin D stores results in a decrease in iPTH levels and reduced bone resorption.

Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Bone Density Conservation Agents; Bone Resorption; Cholecalciferol; Collagen Type I; Dietary Supplements; Female; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Glucuronidase; Humans; Klotho Proteins; Male; Middle Aged; Parathyroid Hormone; Peptides; Prospective Studies; Renal Dialysis; Renal Insufficiency; Young Adult

Vitamin D is synthesized in the skin or supplied. Cholecalciferol is hydroxylated in the liver to 25(OH) vitamin D [25D]. 25D is further hydroxylated in the kidney to 1,25(OH) vitamin D [1,25D]. Catabolism occurs by further hydroxylation. Magnesium is a cofactor of all involved hydroxylases.. To investigate the association between renal function and serum magnesium levels, and the biologically active hormone 1,25D.. Anonymised serum values of 25D, 1,25D, magnesium and creatinine measured in an outpatient cohort over 2 years were analysed.. Renal function and magnesium level did not influence 25D values (r = - 0.144 and 0.030, respectively). Mean serum 1,25D values decreased from 106.5 ± 44.3 pmol/l in individuals with normal renal function to 51.7 ± 18.9 pmol/l in those with severe renal insufficiency (p < 0.01). A weak positive correlation was observed between 1,25D and eGFR (r = 0.317), and between 1,25D and serum magnesium (r = 0.217).. Impaired renal function and low magnesium serum levels are slightly associated with low 1,25D concentrations. Measuring 25D, but not 1,25D, may overestimate the patient's vitamin D status. In patients with renal insufficiency adequate magnesium supply should be ensured.

Topics: Cholecalciferol; Humans; Magnesium; Magnesium Deficiency; Renal Insufficiency; Vitamin D; Vitamin D Deficiency; Vitamins

Knowledge about complications of chronic ultra-high dose vitamin D supplementation is limited. We report a patient with primary progressive multiple sclerosis (MS) who presented with generalized weakness caused by hypercalcemia after uncontrolled intake of more than 50,000 IU of cholecalciferol per day over several months. Various treatment strategies were required to achieve normocalcemia. However, renal function improved only partly and further progression of MS was observed. We conclude that patients need to be informed about the risks of uncontrolled vitamin D intake and neurologists need to be alert of biochemical alterations and symptoms of vitamin D toxicity.

Topics: Cholecalciferol; Drug-Related Side Effects and Adverse Reactions; Humans; Hypercalcemia; Male; Middle Aged; Multiple Sclerosis, Chronic Progressive; Renal Insufficiency; Vitamins

Reduced homoarginine plasma levels are associated with unfavourable cardiovascular outcome in chronic kidney disease (CKD). Cardiovascular events in CKD are fostered by vascular calcification, an active process promoted by hyperphosphatemia and involving osteo-/chondrogenic transformation of vascular smooth muscle cells (VSMCs). The present study explored the effect of homoarginine on phosphate-induced osteo-/chondrogenic signalling and vascular calcification.. Experiments were performed in hyperphosphatemic klotho-hypomorphic mice (kl/kl), in subtotal nephrectomy and vitamin D3-overload mouse calcification models and in primary human aortic smooth muscle cells (HAoSMCs). As a result, plasma homoarginine levels were lower in kl/kl mice than in wild-type mice and in both genotypes significantly increased by lifelong treatment with homoarginine. Surprisingly, homoarginine treatment of kl/kl mice and of mice with renal failure after subtotal nephrectomy augmented vascular calcification and enhanced the transcript levels of plasminogen activator inhibitor 1 (Pai1) and of osteogenic markers Msx2, Cbfa1, and Alpl. Similarly, homoarginine treatment of HAoSMCs increased phosphate-induced calcium deposition, ALP activity, as well as PAI1, MSX2, CBFA1, and ALPL mRNA levels. Homoarginine alone up-regulated osteo-/chondrogenic signalling and indicators of oxidative stress in HAoSMCs. Furthermore, homoarginine reduced citrulline formation from arginine by nitric oxide (NO) synthase (NOS) isoforms. NO formation by NOS was reduced when using homoarginine as a substrate instead of arginine. The osteoinductive effects of homoarginine were mimicked by NOS inhibitor L-NAME and abolished by additional treatment with the NO donors DETA-NONOate and PAPA-NONOate or the antioxidants TEMPOL and TIRON. Furthermore, homoarginine augmented vascular calcification and aortic osteo-/chondrogenic signalling in mice after vitamin D3-overload, effects reversed by the NO donor molsidomine.. Homoarginine augments osteo-/chondrogenic transformation of VSMCs and vascular calcification, effects involving impaired NO formation from homoarginine.

Topics: Animals; Biomarkers; Calcium; Cell Transdifferentiation; Cells, Cultured; Cholecalciferol; Chondrogenesis; Disease Models, Animal; Dose-Response Relationship, Drug; Gene Expression Regulation; Genetic Predisposition to Disease; Glucuronidase; Homoarginine; Humans; Hyperphosphatemia; Klotho Proteins; Mice, Knockout; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Nephrectomy; Nitric Oxide; Nitric Oxide Donors; Nitric Oxide Synthase; Osteogenesis; Phenotype; Renal Insufficiency; Time Factors; Vascular Calcification

Topics: Biopsy; Cholecalciferol; Dietary Supplements; Glucocorticoids; Humans; Male; Nephrocalcinosis; Renal Dialysis; Renal Insufficiency; Tomography, X-Ray Computed; Treatment Outcome; Weight Lifting; Young Adult

Wilson's disease (WD) is not as rare as once believed, and has a wide range of presentations with equally wide range of age of onset. Sometimes the primary presentation might be unusual and may require a thorough investigation to avoid a misdiagnosis. Our case presented with uncontrolled seizures, severe hypokalemia, renal failure, and hypoparathyroidism. After being diagnosed as WD and treated for the same patient made a remarkable recovery.

Topics: Adolescent; Cholecalciferol; Hepatolenticular Degeneration; Humans; Hypocalcemia; Hypokalemia; Hypoparathyroidism; Renal Insufficiency; Seizures; Treatment Outcome; Vitamins; Zinc Acetate

We observed 75 subjects with acute vitamin D3 intoxication (AVD3I). The clinical manifestations of this intoxication are kidneys disorders (65.0%), renal insufficiency (51.0%), gastrointestinal tract disorders (23.0%), arterial hypertension (52.0%). After this intoxication these patients are recommended prolonged rehabilitation.

Topics: Adult; Cholecalciferol; Female; Gastrointestinal Diseases; Humans; Hypertension; Male; Middle Aged; Prognosis; Renal Insufficiency; Retrospective Studies

Parathyroidectomy changes the homeostasis of calcium balance in patients under dialysis for kidney failure. The aim of this work is to value calcium needs in 20 hemodialysed patients who underwent parathyroidectomy, in the department of nephrology of UHC Ibn Rochd of Casablanca from January 1994 to June 1999. These patients, 12 women (60%) and 8 men (40%), aged between 14 and 70 years (mean=46.10+/-13.62 years). Hungry bone syndrome was noted in 8 patients and postoperative hypocalcemia in 15 (75%). Mean minimal serum calcium was 196+/-0.21 mmol/l, with clinical signs in 6 patients. Mean calcium supplement the first postoperative week was 18.1+/-0,54 g/day in the 8 patients with hungry bone syndrome and 14.28+/-0,86 g/day in the 12 remaining patients. Between 6 and 18 months postoperatively, required calcium supplementation was 4.5 to 12 g/day in patients with hungry bone syndrome compared with 3 to 6g/day at the remaining patients. Mean serum calcium remained stable between 2.16 mmol/l to the 3(rd) month and 2.48 mmol/l to the 36(th) month. Postoperative hypocalcemia remains a major concern after parathyroidectomy requiring massive substitution with calcium and active vitamin D metabolite under close supervision to spare these patients from hypercalcemia resulting from parathyroid dysfunction.

Topics: Adolescent; Adult; Aged; Calcium Carbonate; Cholecalciferol; Drug Therapy, Combination; Female; Humans; Hyperparathyroidism; Hypocalcemia; Male; Middle Aged; Parathyroidectomy; Renal Dialysis; Renal Insufficiency; Retrospective Studies; Treatment Outcome

A case of sarcoidosis is described which presented with hypercalcaemia and renal insufficiency. Initially, a calciol intoxication was diagnosed, because a high daily intake was suspected. However, vitamin D3 metabolites in the blood revealed normal concentrations of calcidiol, but extremely high concentrations of calcitriol. These features rejected the first diagnosis and pointed to high endogenous calcitriol production, which may take place in granulomatous diseases. This is caused by an increased 1-alpha-hydroxylation reaction in activated macrophages. Eventually, muscle biopsy revealed non-caseating granulomas, confirming the diagnosis of sarcoidosis.

Topics: Aged; Calcitriol; Cholecalciferol; Diagnosis, Differential; Female; Humans; Hypercalcemia; Muscles; Poisoning; Renal Insufficiency; Sarcoidosis