Calcium salts are increasingly used as phosphorus binders in patients with chronic renal failure. Calcium carbonate is the principal salt presently utilized, however, other calcium salts may be more effective and safer phosphorus binders. Theoretical calculations, in vitro experiments, and in vivo studies in normal subjects have shown calcium acetate to be a more effective phosphorus binder than other calcium salts. This salt has not previously been studied in patients with chronic renal failure. We used a one-meal gastrointestinal balance technique to measure phosphorus absorption, calcium absorption and phosphorus binding in six patients with chronic renal failure. Calcium acetate was compared with calcium carbonate and placebo. Equivalent doses (50 mEq Ca++) of calcium acetate bound more than twice as much phosphorus (106 +/- 23 mg) as calcium carbonate (43 +/- 39 mg) P less than 0.05. When phosphorus binding was factored for calcium absorption, calcium acetate bound 0.44 mEq HPO4 =/mEq absorbed Ca++ compared with 0.16 mEq HPO4 = bound/mEq Ca++ absorbed with calcium carbonate. More efficient phosphorus binding permits serum phosphorus concentration to be controlled with lower doses of calcium salts. The higher phosphorus binding/calcium absorption ratio coupled with a lower dose indicates that less calcium will be absorbed when calcium acetate is used for phosphorus control. Markedly positive calcium balance, hypercalcemia and ectopic calcification should be less likely to occur with this drug than other calcium salts.
The clinical diagnosis of SGF/DGF can be made 6 h post-operatively based on urine output and serum creatinine. Basiliximab can be started post-operatively in these patients and decreased levels of TAC can be used to achieve acceptably low rates of rejection in these patients. However, SGF/DGF patients, regardless of their need for dialysis, have worse function at 1 yr and lower 2-yr actuarial graft survival compared with non-SGF/DGF patients. Most of the poor survival can be attributed to the SGF group. Further strategies to either prevent SGF/DGF or to optimize treatment in these patients are needed.
Objective: To investigate immunoexpression of p53 in parathyroid tumors and hyperplasias and correlate it with the histopathological diagnosis and severity of hyperparathyroidism. Design: A total of 102 parathyroid tissues from archival paraffin-embedded specimens or obtained at surgery between 1988 and 1997 from 65 consecutive individuals with hyperparathyroidism were studied. Methods: p53 immunoexpression, gland mass, preoperative serum calcium and intact parathyroid hormone (PTH) were analyzed; 14 normal parathyroid glands were used as controls. Results: The histopathological findings were: adenomas (n=28), primary hyperplasias (n=12), secondary nodular and diffuse hyperplasias (patients with uremia, n=57), carcinomas (n=4) and carcinomatous metastatic tissue (n=1). Nuclear p53 was detected in 36% of the adenomas, 42% of the primary hyperplastic glands, 72% of the diffuse hyperplasias, 44% of nodular hyperplasias and 40% of the carcinomatous tissues, and was absent from normal glands. p53 expression was significantly more frequent in diffuse hyperplasias than in adenomas (P=0·037). Serum ionized calcium tended to be higher in p53-positive glands in all histopathological groups; however, the difference was only significant in nodular hyperplasias (P=0·018). The same trend was observed for serum intact PTH levels of adenomas and nodular hyperplastic glands. Gland mass was not significantly different according to p53 staining. Conclusions: p53 immunoexpression was not useful in differentiating between the histopathological parathyroid subgroups. p53 immunodetection was particularly frequent in secondary hyperplastic glands of uremic patients. Our study suggests that p53, whether wild-type or mutant, is regulated in parathyroid tumors and hyperplasias. Changes in wild-type p53 may be part of a cellular response to a hyperproliferative condition.
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