Serum Phosphate, Parathyroid Hormone and Vitamin D Metabolites in Patients with Chronic Renal Failure: Effect of Aluminum Hydroxide Administration

Abstract

Patients with chronic renal failure showed the existence of phosphate retention, secondary hyperparathyroidism, and reduced production of 1,25-(OH)₂D. In order to determine the effect of correction of hyperphosphatemia on secondary hyperparathyroidism and vitamin D metabolism in those patients, 7 nondiaiyzed patients with chronic renal failure were treated with large doses of Al(OH)₃ (15–18 g/day) to correct their high levels of serum phosphate. After treatment with A1(OH)₃, serum phosphate fell significantly (p < 0.005) from 6.3 ± 1.3 (mean ± SD) to 3.7 ± 0.5 mg/dl. Serum parathyroid hormone decreased significantly (p < 0.02) from 2.87 ± 1.64 to 1.85 ± 1.26 ngEq/ ml. Serum l,25-(OH)₂D was low compared to the normal mean level before A1(OH)₃ administration and decreased significantly (p > 0.02) from 19.4 ± 6.1 to 11.4 ± 4.3 pg/ml after the treatment. Aluminum levels increased significantly (p > 0.02) from 1.7 ± 1.0 to 3.6 ± 1.5 μg/dl. Serum calcium, calcitonin, and 25-(OH)D showed no significant change. Our data suggested that the suppression of secondary hyperparathyroidism by A1(OH)₃ treatment results in a decrease of the 1,25-(OH)₂D level in patients with chronic renal failure, even though their hyperphosphatemia has been corrected. We speculate that aluminum loading might play a role in diminishing the secretion of parathyroid hormone and the production of 1,25-(OH)₂D in humans.

VITAMIN D IN HEALTH AND DISEASE: Vitamin D for Health and in Chronic Kidney Disease

“…In the early 1970s it was demonstrated that anephric rats that received 3 H-25(OH)D 3 had no detectable amounts of 3 H-1,25(OH) 2 D 3 in their circulation (1,26). This was confirmed by the observation that patients with CKD had little if any detectable levels of 1,25(OH) 2 D in their circulation (2,26,(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42). Thus it has always been assumed that the kidney is the sole source for the production of 1,25(OH) 2 D 3.…”

“…Patients with mild to moderate kidney disease often have low or undetectable circulating concentrations of 1,25(OH) 2 D (32–34). The major cause of 1,25(OH) 2 D deficiency is hyperphosphatemia, which can markedly reduce or completely shut down the renal production of 1,25(OH) 2 D (Fig.…”

“…Thus in these patients it is imperative to maintain serum phosphorus levels in the normal range using a phosphate binder and decreasing dietary phosphorus intake (33). When the glomerular filtration rate (GFR) is approximately 33% of normal, the renal reserve of 1‐OHase is inadequate, thereby resulting in reduced concentrations of 1,25(OH) 2 D (26,32–35). These patients develop severe secondary hyperparathyroidism because there is an inadequate amount of 1,25(OH) 2 D to sustain intestinal calcium absorption, resulting in a decrease in serum ionized calcium concentrations.…”

Slowing the Progression of Vascular Calcification in Hemodialysis

“…Hyperphosphatemia and secondary hyperparathyroidism (HPT) are common complications of end-stage renal disease (ESRD) (1). Untreated secondary HPT can lead to significant morbidity as a result of pain, pruritus, bone loss, increased fracture risk, and anemia (2,3) and can contribute to heart disease and hypertension (4,5).…”

Immunoreactive Serum Calcitonin and Skeletal Histology in Chronic Renal Failure

“…The effect of administered aluminium hydroxide on serum calcitonin was studied in non-dialysed patients with chronic renal failure by Takamoto et al [35]. Serum calcitonin did not change, whereas serum inorganic phosphate, and serum PTH fell.…”