Abstract
One hundred and ninety-five outpatients in pre-dialysis period served as subjects. The mean age of subjects was 58.0±11.2 (range: 29-82) years. The subjects were divided into 8 groups according to their serum creatinine (Cr) levels (Cr≤1.0, 1.0<Cr≤2.0, 2.0<Cr≤3.0, 3.0<Cr≤4.0, 4.0<Cr≤5.0, 5.0<Cr≤6.0, 6.0<Cr≤8.0, and Cr>8.0 mg/100 ml). The levels of 1,25-dihydroxyvitamin D (1,25(OH)2D) decreased in accordance with the progression of chronic renal failure (CRF). Even in subjects with 1.0<Cr≤2.0 mg/100 ml, the levels of 1,25(OH)2D were significantly lower than those in subjects with Cr≤1.0 mg/100 ml. The levels of calcium adjusted by serum albumin levels (adjusted Ca) were relatively maintained within the normal range until Cr>8.0 mg/100 ml. The levels of inorganic phosphate (IP) were significantly lower in subjects with 1.0<Cr≤2.0 mg/100 ml, but significantly higher in subjects with Cr>4.0 mg/100 ml than those in subjects with Cr≤1.0 mg/100 ml. The levels of immunoreactive high-sensitive parathyroid hormone (HS-PTH) were greatly increased and the levels of intact PTH were significantly increased even in subjects with 1.0<Cr≤2.0 mg/100 ml, in association with a decrease in levels of 1,25(OH)2D, suggesting that a decline in 1,25(OH)2D production due to a decrease in renal mass contributes to the acceleration of secondary hyperparathyroidism. When the levels of adjusted Ca, intact PTH and 1,25(OH)2D of subjects with hypophosphatemia (IP<2.8 mg/100 ml), normophosphatemia and hyperphosphatemia (IP>4.4 mg/100 ml) were compared, there were not any significant differences in the levels of adjusted Ca among these subjects in each group. But, the levels of 1,25(OH)2D in subjects with hypophosphatemia were significantly higher than those with normophosphatemia in groups with Cr≤2.0 mg/100 ml, and those with hyperphosphatemia were significantly lower than those with normophosphatemia in groups with 3.0<Cr≤4.0, 5.0<Cr≤6.0 and Cr>8.0 mg/100 ml. These results suggest that increased secretion of PTH might compensate the decreased production of 1,25(OH)2D3 by lowering phosphate in the early phase of CRF, and phosphate retention inhibits the activity of 1α-hydroxylase and contributes to the decrease in 1,25(OH)2D3 in the advanced stage of CRF. Monitoring of 1,25(OH)2D is considered to be vitally important for diagnosing the 1,25(OH)2D3 deficiency in CRF.
