Iron deficiency anemia and iron losses after renal transplantation.

Iron deficiency contributes to anemia after transplantation. The magnitude of iron loss from blood loss in the peri-transplantation period has not been quantified. We prospectively estimated phlebotomy and surgical losses over the first 12-weeks following transplantation in 39 consecutive renal transplant recipients on hemodialysis (HD), peritoneal dialysis (PD), or chronic kidney disease (CKD).

Differential effects of very high doses of doxercalciferol and paricalcitol on serum phosphorus in hemodialysis patients.

Background: Treatment of secondary hyperparathyroidism (SHPT) includes use of calcitriol (1,25D(3)) to suppress parathyroid hormone (PTH), but dosing of 1,25D(3) is limited by the development of hypercalcemia and a high calcium x phosphorus (Ca x P) product due to gut absorption of calcium and phosphorus as well as enhanced bone resorption. The vitamin D analog 19-Nor-1,25(OH)2-vitamin D2 (paricalcitol) and the prohormone 1alpha-OH-vitamin D2 (doxercalciferol) have been proposed as alternatives which may cause less hypercalcemia and elevated Ca x P, while still suppressing PTH.

Methods: We performed a prospective study to assess the acute bone mobilization effects of very high doses of paricalcitol and doxercalciferol.

Anemia in the kidney-transplant patient.

Anemia, a potentially correctable cardiovascular risk factor, continues to be a major problem in kidney-transplant patients. Erythropoietin levels increase rapidly after successful kidney transplantation, and by 3 months, most patients achieve hemoglobin levels greater than 12 g/dL. Anemia may be caused by problems commonly seen in the general population such as iron deficiency or gastrointestinal blood loss, by immunosuppressive medications, or by more rare abnormalities such as hemolytic uremic syndrome or parvovirus B19-induced aplastic anemia.

Calcineurin is required in urinary tract mesenchyme for the development of the pyeloureteral peristaltic machinery.

Congenital obstructive nephropathy is the principal cause of renal failure in infants and children. The underlying molecular and cellular mechanisms of this disease, however, remain largely undetermined. We generated a mouse model of congenital obstructive nephropathy that resembles ureteropelvic junction obstruction in humans.