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Renal Osteodystrophy and the Status of Aluminum and Other Trace Metals in CAPD Patients: A Panel * Review
Author(s) -
Campese Vito,
Easterling Ronald E.,
Finkelstein Fred,
Mattern William,
Ogden David A.,
Steiner Robert W.,
Oreopoulos Dimitrios G.
Publication year - 1984
Publication title -
peritoneal dialysis international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.79
H-Index - 83
eISSN - 1718-4304
pISSN - 0896-8608
DOI - 10.1177/089686088400400305
Subject(s) - peritoneal dialysis , calcium , renal osteodystrophy , endocrinology , medicine , parathyroid hormone , tonicity , secondary hyperparathyroidism , osteomalacia , hyperparathyroidism , hemodialysis , osteodystrophy , phosphate , chemistry , vitamin d and neurology , kidney disease , biochemistry
Most reports indicate that in patients on CAPD, hyperparathyroid bone disease progresses, while osteomalacia improves. With 1.5g% Dianeal, and when dialysate Ca is 7mg%, peritoneal mass transfer of calcium is positive, i.e., it is absorbed from the solution, while with hypertonic solutions it is less positive or even negative. Daily phosphorus removal by CAPD is insufficient to control serum phosphorus, hence CAPD patients require phosphate binders and/or phosphate restriction. Peritoneal phosphorus removal is greater with hypertonic than with isotonic solutions. In patients on CAPD, the loss of substantial amounts of D-binding protein and 25(OH)DJ into the dialysate, produces a gradual decrease in plasma 25(OH)D levels. Similarly, these patients have low 1,25(OH)D2 DJ levels and, hence, should receive vitamin D or its analogues. Unlike hemodialysis, CAPD results in a significant removal of PTH, with a peritoneal clearance of 1.5 ml/min. However, despite an estimated daily loss of 13.5% of the circulating PTH, there probably is not a significant effect on plasma PTH levels, which usually respond to changes in serum Ca. Levels of the intact PTH molecule provide a better index of hyperparathyroidism than do levels of its COOH-terminal fragment. With regard to investigation and treatment, one should measure serum ionic calcium rather than total calcium, even if the latter is corrected for total protein. The minimal dialysate calcium should be 7 mg/dl and for hypertonic solutions, perhaps it should be higher (7.5–8.0 mg%). Total serum calcium should be maintained at 10.2–10.7 mg/dl (ionized calcium of 5.1–5.5 mg/dl); adjunctive use of active forms of vitamin D and prevention of aluminum intoxication may prevent progressive bone disease in CAPD, and existing bone disease may heal. Whereas there are enough data supporting the connection of aluminum toxicity and osteomalacia in hemodialysis patients, data concerning the incidence of osteomalacia and its relationship to aluminum in CAPD patients are scarce. Apparently CAPD removes aluminum more efficiently than hemodialysis. CAPD patients are less likely to develop osteomalacia because the dialysate aluminum content is low and these patients tend to require lower doses of phosphate binder. There are no extensive studies on trace element deficiencies or excess in patients on CAPD. These patients may be more susceptible to deficiencies of trace elements which are protein bound. Desferoxamine may be effectively used for the treatment of patients with either aluminum or iron overload.

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