allopurinol and Calcinosis

Gout is a clinical syndrome encompassing a group of metabolic diseases that are all characterized by abnormal uric acid metabolism. In its fullest form, gout is defined by: an increase in the serum urate concentration; characteristic, recurrent, acute arthritic attacks, with monosodium urate monohydrate crystals demonstrable in synovial fluid leukocytes; tophi, usually in and around joints of the extremities, composed of monosodium urate monohydrate deposits; renal disease, often accompanied by hypertension with glomerular, tubular, interstitial, and vascular involvement; and uric acid nephrolithiasis. Any combination of these manifestations may occur, although tophi and urate nephropathy rarely antedate gouty arthritis.

Topics: Acute Disease; Adult; Allopurinol; Anti-Inflammatory Agents; Arthritis; Arthrography; Calcinosis; Chronic Disease; Colchicine; Female; Gout; Humans; Kidney Calculi; Kidney Diseases; Middle Aged; Probenecid; Uric Acid

Studies on kidney transplantation have thus far mainly dealt with surgical techniques, immunology, and transplant tolerance. Disturbed mineral metabolism after renal denervation has not received much attention. Basic physiological research in short-term experiments has shown that experimental renal denervation in rats leads to parathormone (PTH)-independent hyperphosphaturia (HPU). HPU and other metabolic complications also have been described after clinical kidney transplantation. Furthermore, there is an unexpected increase in the risk of bone fracture. However, these studies have examined an organism pre-damaged with regard to the parathyroid and immunosuppression. Experimental investigations in syngeneic rats were performed to see whether HPU also occurs after transplantation and thus after denervation and which target organs are involved.. Thirty-six male Lewis rats subjected to laparotomy (n = 12), unilateral nephrectomy (n = 12), or unilateral transplantation and bilateral nephrectomy (n = 12) were observed for 18 weeks.. Animals that underwent transplantation had a significant loss of phosphate in the urine not associated with decreased calcium, phosphate, or magnesium in bone. Stability test showed no deterioration, despite a slight increase in the bone parameters of alkaline phosphatase, cyclic AMP, and hydroxyproline with unchanged calciotropic hormones. Nephrocalcinosis was not observed. Parallel to HPU, there was a compensatory reduction in fecal phosphate excretion.. The loss of phosphate after clinical kidney transplantation in the predamaged parathyroid hormone control system as well as immunosuppression and a surprising increase in the incidence of bone fractures may be explained by the denervation-related loss of phosphate. The lack of intestinal counter-regulation could be an important pathomechanism.

Topics: Adenosine; Allopurinol; Animals; Bone and Bones; Calcinosis; Disease Models, Animal; Glutathione; Insulin; Kidney Diseases; Kidney Transplantation; Male; Nephrectomy; Organ Preservation; Organ Preservation Solutions; Phosphates; Raffinose; Rats; Rats, Inbred Lew; Tissue and Organ Harvesting; Transplantation, Isogeneic; Urinalysis

Topics: Absorptiometry, Photon; Adolescent; Allopurinol; Amiloride; Calcinosis; Diet, Sodium-Restricted; Diuretics; Drug Therapy, Combination; Glycogen Storage Disease Type I; Gout Suppressants; Humans; Hydrochlorothiazide; Kidney Calculi; Male; Osteoporosis; Recurrence

Topics: Allopurinol; Antineoplastic Agents; Bone Resorption; Calcinosis; Humans; Hypercalcemia; Leukemia, Lymphoid; Male; Middle Aged; Parathyroid Glands; Pulmonary Alveoli; Pulmonary Edema; Spleen