Metabolic aspects of phosphate replacement therapy for hypophosphatemia after renal transplantation: Impact on muscular phosphate content, mineral metabolism and acid/base homeostasis

Hypophosphatemia caused by renal phosphate loss occurs frequently after kid ney transplantation. In assumption of systemic phosphorus depletion, the pr esumed deficit commonly is replaced by oral phosphate supplements. However, such treatment is debatable, because intracellular phosphorus stores have not been assessed in this setting and may not be accurately reflected by se rum phosphate concentrations. Moreover, disturbances in mineral metabolism from chronic renal failure, such as hypocalcemia and hyperparathyroidism, m ay be prolonged with oral phosphate supplements. Conversely, a neutral phos phate salt might improve renal acid excretion and systemic acid/base homeos tasis for its properties as a urinary buffer and a poorly reabsorbable anio n. Twenty eight patients with mild early posttransplantation hypophosphatem ia (0.3-0.75 mmol/L) were randomly assigned to receive either neutral sodiu m phosphate (Na2HPO4) or sodium chloride (NaCl) for 12 weeks and examined w ith regard to (1)correction of serum phosphate concentration and urinary ph osphate handling; (2) muscular phosphate content; (3) serum calcium and par athyroid hormone (PTH); and, (4) renal acid handling and systemic acid/base homeostasis. Mean serum phosphate concentrations were similar and normal i n both groups after 12 weeks of treatment; however, more patients in the Na Cl group remained hypophosphatemic (93% versus 67%). Total muscular phospho rus content did not correlate with serum phosphate concentrations and was 2 5% below normophosphatemic controls but was completely restored after 12 we eks with and without phosphate supplementation. However, the percentage of the energy-rich phosphorus compound adenosine triphosphate (ATP) was signif icantly higher in the Na2HPO4 group, as was the relative content of phospho diesters. Also, compensated metabolic acidosis (hypobicarbonatemia with res piratory stimulation) was detected in most patients, which was significantl y improved by neutral phosphate supplements through increased urinary titra table acidity, These benefits of added phosphate intake were not associated with any adverse effects on serum calcium and PTH concentrations. In concl usion, oral supplementation with a neutral phosphate salt effectively corre cts posttransplantation hypophosphatemia, increases muscular ATP and phosph odiester content without affecting mineral metabolism, and improves renal a cid excretion and systemic acid/base status. (C) 1999 by the National Kidne y Foundation, Inc.