Mini review: A reevaluation of nutritional vitamin D in the treatment of chronic kidney disease.

Chronic kidney disease-mineral and bone disorder is a syndrome of mineral and bone metabolism abnormalities caused by chronic kidney disease. Osteoporosis is a systemic metabolic bone disease characterized by low bone mass, disruption of bone microstructure, increased brittleness, and a higher propensity for fractures. Both of these conditions significantly affect bone metabolism and substantially increase the risk of fractures. Nutritional vitamin D is an essential trace element in the human body and an important fat-soluble vitamin. One crucial physiological role of nutritional vitamin D is to achieve mineral-bone metabolism balance by regulating calcium homeostasis. This review summarized the metabolism of vitamin in normal population and its specificity in chronic kidney disease. Over the years, the understanding and application of vitamin D in patients with chronic renal failure is changing. As people pay more attention to hypercalcemia, vascular calcification, osteoporosis, nutritional vitamin D has come into people's attention again. More and more studies are discussing how to prescribe vitamin D supplementation in hemodialysis patients.

Role of nutritional vitamin D in chronic kidney disease-mineral and bone disorder: A narrative review.

Chronic kidney disease-mineral and bone disorder has complex and diverse clinical manifestations, including the simplest abnormalities of calcium, phosphorus and parathyroid hormone detected in blood, abnormalities of bone transformation and mineralization in bone, and calcification of blood vessels or other soft tissues detected on imaging. Patients with CKD-MBD combined low bone mineral density and fragility fractures are referred to as CKD-MBD with low bone mineral density. Vascular calcification refers to ectopic deposition of calcium phosphate in the blood vessel walls and heart valves. The degree of vascular calcification was inversely proportional to bone mineral density. The more severe the degree of vascular calcification, the lower the bone mineral density, and the higher the risk of death, indicating that the bone-vascular axis exists. Activation and alteration of the Wnt signaling pathway are central to the treatment of vascular diseases in uremia. Vitamin D supplementation can prevent secondary hyperparathyroidism, activate osteoblasts, relieve muscle weakness and myalgia, and reduce vascular calcification. Nutritional vitamin D may improve vascular calcification in uremia patients by regulating Wnt signaling pathway.

Refractory hypercalcemia due to an ectopic mediastinal parathyroid gland in a hemodialysis patient: a case report.

BACKGROUND: Hypercalcemia crisis is a complex disorder rarely induced by tertiary hyperparathyroidism, which clinically presents as nonsuppressible parathyroid hyperplasia with persistent increased PTH levels and hypercalcemia. It is one of the major risk factors of morbidity and mortality in end-stage renal disease. Parathyroidectomy should be in consideration in dialysis patients with severe hyperparathyroidism who are refractory to medical therapy. The implications and consequences of it, however, are not fully understood. CASE PRESENTATION: We present a case of a 70 year-old man disturbed by gastrointestinal manifestations due to hypercalcaemic crisis. The patient had longstanding hypercalcaemia and hyperparathyrodism refractory to calcimimetics, calcitonin, hormone and haemodialysis. A ectopic parathyroid gland in anterior mediastinum was found and elucidated by Tc-99 m scan. Futhermore, a video-assisted thoracoscopic parathyroidectomy was performed. Histologically, the tumour consisted of densely arranged chief cells immunohistochemically positive for PTH antigens. Consequently, calcium and parathormone were declining stably without any complications. CONCLUSIONS: On account of refractory hypercalcemia and hyperparathyroidism, radionuclide scanning is useful in the diagnosis of ectopic parathyroid gland. it is of great significance for multidisciplinary therapy combing anesthesia, surgical, endocrinology and nephrology staff.

Autosomal dominant polycystic kidney disease combined with hypertrophic cardiomyopathy: A case report.

INTRODUCTION: This report describes the novel sampling of autosomal dominant polycystic kidney disease (ADPKD) combined with hypertrophic cardiomyopathy (HCM). SYMPTOMS AND CLINICAL FINDINGS: A 48-year-old Chinese man presented with anasarca, hypourocrinia, gross hematuria, and weight gain by 10 kg subsequently developed acute kidney injury after struck by acute respiratory distress syndrome, really a threat to his heart. DIAGNOSES: Abdominal ultrasound revealed multiple small cysts in both kidneys, with the right kidney measuring 11.6 cm in length, and the left kidney measuring 11.5 cm in length, which supported ADPKD. Echocardiography showed left ventricular posterior wall thickness measuring 15.2 mm, interventricular septum measuring 17.2 mm, left atrial size 31.9 mm, ejection fraction measuring 69%, approving the diagnose of HCM. THERAPEUTICS INTERVENTIONS: Because of the failure treatment with tripterygium wilfordii and valsartan, the patient was administered with prednisone 1 mg/kg/day. Continuous renal replacement therapy was required to prevent heart and kidney from failure. OUTCOMES: The patient responded well and his renal function improved. CONCLUSION: This is the first reported case of ADPKD with HCM, with complete remission of acute kidney injury and preservation of cardiac function. Serial checks and measures should be considered for appropriate treatment of ADPKD patient who present with rapid decline of renal function. We present detailed analysis of the patient's disease course and review literature. Written informed consent was obtained from the patient for publication of this case report. It has been permitted by Committee on Ethics of Biomedicine, Second Military Medical University.

Relationship between REL amplification, REL function, and clinical and biologic features in diffuse large B-cell lymphomas.

Although it has been suggested that REL is the critical target gene of 2p12-16 amplification in diffuse large B-cell lymphoma (DLBCL), little experimental evidence supports this notion. In the present study, we sought to evaluate the relationship between REL amplification and REL function in a panel of 46 newly diagnosed DLBCLs and to correlate with DLBCL subgroups as identified by gene expression profiles and clinical features. The results indicate that amplification of the REL locus is not associated with accumulation of the active form of REL, as evaluated by immunofluorescence analysis. Upon subgrouping of the DLBCL cases based on gene expression signatures, REL amplification was detected in all subgroups, while high levels of nuclear-located REL were more frequently detected in activated B-cell-like DLBCL. Correlative analyses of REL copy number and REL nuclear accumulation with clinical parameters did not reveal any significant associations. Together these results indicate that 2p12-16 amplification does not lead to abnormal REL activation, suggesting that REL may not be the functional target of the amplification event. Nonetheless, these data indicate that DLBCLs are heterogeneous with respect to REL and thus nuclear factor-kappaB (NF-kappaB) activity.