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首页> 外文期刊>Clinical nephrology >The effect of calcitriol on fasting urine calcium loss and renal tubular reabsorption of calcium in patients with mild renal failure--actions of a permissive hormone.
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The effect of calcitriol on fasting urine calcium loss and renal tubular reabsorption of calcium in patients with mild renal failure--actions of a permissive hormone.

机译：骨化三醇对轻度肾功能衰竭患者禁食尿中钙丢失和肾小管重吸收钙的作用-允许激素的作用。

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AIM: Renal production of 1,25-dihydroxycholecalciferol is attenuated in early renal failure. Renal tubular reabsorption of calcium is diminished in moderate renal failure and we wished to see if this were true in the early stages and whether supplementary calcitriol would bring about correction. We were interested in the idea of 1,25-dihydroxycholecalciferol being a permissive agent, operating indirectly. METHODS: We measured calcium-related variables, including calculated ultrafiltrable serum calcium, before and after calcitriol 0.5 microg daily for six days in 34 subjects with stable mild renal failure. RESULTS: The mean serum creatinine was 0.21 (+/- 0.08) mmol/l. The mean serum Ca++ was normal (1.18 mmol/l) but nine patients had values outside the normal range and in six cases, with low-normal serum Ca++ levels, there was a diminished tubular reabsorption. In five cases, basal serum Ca++ was mildly elevated. The coefficient of variation for serum Ca++ was 4.4%. PTH (1-84) levels were mildly elevated and 1,25-dihydroxycholecalciferol levels low-normal. The urine Ca/Cr, representing net bone resorption, was elevated in six cases. After calcitriol, the mean serum Ca++ level rose slightly and the coefficient of variation decreased to 3.6%. Changes in Ca++ whether upward or downward were accounted for by minor alterations in tubular reabsorption and a tendency to less net bone resorption. The initial Ca++ predicted (negatively) the magnitude of the correction. Neither the prevailing PTH nor the 1,25-dihydroxycholecalciferol levels explained any of the observed changes. CONCLUSION: In early renal failure, there may be impaired regulation of serum Ca++. Despite elevated PTH, mild hypocalcemia may exist in the presence of increased net bone resorption relative to GFR. Hypocalcemia was accounted for by reduced renal tubular reabsorption of calcium which corrected after calcitriol. Net bone resorption tended to fall after calcitriol. Mild hypercalcemia, when present, was corrected by a reduction in tubular reabsorption. Calcitriol did not have a simple unidirectional effect but instead contributed to efficiency of the homeostatic mechanisms controlling the serum Ca++ set-point.
机译：目的：在早期肾衰竭中，肾脏的1,25-二羟基胆钙化固醇含量降低。在中度肾功能衰竭中，肾小管对钙的重吸收会减少，我们希望了解在早期阶段这是否成立以及补充钙三醇是否会带来矫正作用。我们对1,25-二羟基胆钙化固醇为间接操作的允许剂的想法很感兴趣。方法：我们测量了钙相关变量，包括计算出的超滤性血清钙，在稳定的轻度肾功能衰竭的34名受试者中，每天服用0.5毫克三钙三醇之前和之后的六天。结果：血清肌酐平均为0.21（+/- 0.08）mmol / l。平均血清Ca ++正常（1.18 mmol / l），但9例患者的血钙值超出正常范围，其中6例血清Ca ++正常值较低，肾小管重吸收减少。在五例中，基础血清Ca ++轻度升高。血清Ca ++的变异系数为4.4％。 PTH（1-84）水平轻度升高，1,25-二羟基胆钙化固醇水平低正常。尿中Ca / Cr代表净骨吸收增加了6例。骨化三醇后，平均血清Ca ++水平略有上升，变异系数降至3.6％。 Ca ++的变化（向上还是向下）是由于肾小管再吸收的微小变化和净骨吸收的减少所致。最初的Ca ++预测（否定）了校正的幅度。普遍存在的PTH和1,25-二羟基胆钙化固醇水平都不能解释任何观察到的变化。结论：在早期肾衰竭中，血清Ca ++的调节可能受损。尽管PTH升高，但相对于GFR，在净骨吸收增加的情况下可能存在轻度低钙血症。低钙血症是由于肾小管对钙的重吸收减少所致，而钙三醇可纠正这种低钙血症。骨化三醇后净骨吸收趋于下降。如果存在轻度高钙血症，可通过减少肾小管重吸收来纠正。骨化三醇没有简单的单向作用，而是有助于控制血清Ca ++设定点的稳态机制的效率。

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