J Clin Endocrinol Metab
October 2014
Context: The optimal circulating concentration of 25(OH) vitamin D is controversial.
Objective: The aim was to investigate if FGF-23 and 24,25(OH)2D can guide cholecalciferol replacement.
Design: Oral cholecalciferol (10,000 IU weekly) administered to subjects with 25(OH)D levels < 20 ηg/mL and eGFR > 60 mL/min/1.
Background: 25-Hydroxyvitamin D [25(OH)D] is a marker of nutritional status; however, chronic kidney disease (CKD) results in alterations in vitamin D metabolism, including the loss of vitamin D-binding proteins and alterations in CYP27B1 and CYP24 enzymes that metabolize 25(OH)D. This study was designed to determine the predictors of responsiveness to correction of vitamin D deficiency with oral vitamin D2 (ergocalciferol) in adults.
Methods: A retrospective study of 183 veterans with 25(OH)D level <30 ng/mL, who were treated with 50,000 IU per week of vitamin D2, was performed.
Am J Kidney Dis
February 2013
Kidney transplantation, the most effective treatment for the metabolic abnormalities of chronic kidney disease (CKD), only partially corrects CKD-mineral and bone disorders. Posttransplantation bone disease, one of the major complications of kidney transplantation, is characterized by accelerated loss of bone mineral density and increased risk of fractures and osteonecrosis. The pathogenesis of posttransplantation bone disease is multifactorial and includes the persistent manifestations of pretransplantation CKD-mineral and bone disorder, peritransplantation changes in the fibroblast growth factor 23-parathyroid hormone-vitamin D axis, metabolic perturbations such as persistent hypophosphatemia and hypercalcemia, and the effects of immunosuppressive therapies.
View Article and Find Full Text PDFProgressive elevations of fibroblastic growth factor 23 (FGF23) in chronic kidney disease may reduce serum 25-hydroxyvitamin D (25(OH)) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) levels, via stimulation of 24-hydroxylase (Cyp24a1)-mediated catabolism of these vitamin D metabolites. To test this possibility, we measured serum concentrations of 24,25-dihydroxyvitamin D (24,25(OH)(2)D), a product of Cyp24a1 hydroxylation of 25(OH)D, in the Col4a3 knockout mouse, a model of Alport syndrome-derived chronic kidney disease, and in patients with chronic kidney disease of variable severity. There was an inverse correlation between serum FGF23 and both 25(OH)D and 1,25(OH)(2)D in the mouse model, but no significant relationship was observed in the cross-sectional patient cohort.
View Article and Find Full Text PDFThis report describes a novel presentation of chloride resistant metabolic alkalosis in a patient with hypercalcemia related to Multiple Myeloma (MM). A 51-year-old male with newly diagnosed MM presented with widespread skeletal involvement, calcium (Ca(+2)) of 18 mg/dL, phosphorous (PO4) of 6 mg/dL, serum bicarbonate (HCO3) of 37 mEq/L, and serum creatinine (Cr) of 2.6 mg/dL Other causes of metabolic alkalosis such as vomiting, diuretics, alkali ingestion, mineralocorticoid excess and hypokalemia were excluded.
View Article and Find Full Text PDFLupus nephritis (LN) is a common complication of systemic lupus erythematosus (SLE), which is associated with significant morbidity and mortality. Renal involvement in SLE is heterogeneous; therefore, the treatment of LN is determined by the pathological type of LN and ranges from nonspecific measures such as maintenance of adequate blood pressure control and blockade of renin-angiotensin-aldosterone system to the use of immunosuppressive medications. Cyclophosphamide in combination with prednisone has been the standard of care for the treatment of proliferative forms of LN.
View Article and Find Full Text PDFIntroduction: Hypernatremia is a common problem in hospitalized patients and is associated with high morbidity and mortality. This study was designed to evaluate whether physicians follow the recommended guidelines for the rate of correction of hypernatremia of ≤0.5 mEq/L/hr and to evaluate the effect of the rate of correction of severe hypernatremia on the mortality of hospitalized patients.
View Article and Find Full Text PDFSevere lactic acidosis has been reported in patients struggling against restraints, especially in association with the use of stimulant drugs, such as cocaine. Profound acidosis occurring under these conditions can lead to cardiac arrhythmias, autonomic instability and cardiac arrest, a syndrome known as restraint associated asphyxia. Early recognition of this condition and removing the stimulus for lactic acid production (excessive muscle activity) by aggressive sedation and ventilatory assistance, coupled with fluid administration to improve tissue perfusion and lactate metabolism, can be life-saving.
View Article and Find Full Text PDFIntroduction: Although membranoproliferative glomerulonephritis has been reported to occur in association with non-Hodgkin's lymphoma, information concerning the long term effects of treatment of non-Hodgkin's lymphoma on the associated membranoproliferative glomerulonephritis is limited.
Case Presentation: The current report describes a patient who presented with the abrupt onset of hypertension, mixed nephritic/nephrotic syndrome and acute renal failure. Kidney biopsy was consistent with membranoproliferative glomerulonephritis, type 1.