Grosso S, Douthat W, Garay G, de Arteaga J, Boccardo G, Fernández Martín J L, Canteros A, Cannata Andía J, Massari P
Renal Service, Hospital Privado Centro-Médico de Cordoba, Argentina.
Nephrol Dial Transplant. 1998;13 Suppl 3:98-102. doi: 10.1093/ndt/13.suppl_3.98.
Urinary excretion of aluminium after a successful transplant can reverse pre-transplant aluminium intoxication. We have evaluated the time course of urinary aluminium excretion and its correlation with several parameters of renal function and mineral metabolism in 49 patients (33 men and 16 women) with a wide range of pre-transplant serum aluminium concentrations, performing sequential determinations at pre-transplant time and at 7, 30, 60, and 90 post-transplant days. Mean serum aluminium at pre-transplant was 54.5+/-46.8 microg/l decreasing progressively to 28.7+/-24.4 microg/l at 90 days (P<0.0002), paralleling the decrease in serum creatinine. Urinary aluminium decreased from 63.0+/-77.9 to 52.4+/-55.9 microg/l at 90 days (P<0.0001). The maximum urinary aluminium/creatinine was 1.8+/-2.7 at 7 days and was associated with the greatest fractional excretion of sodium (4.7+/-5.1%), and the lowest tubular reabsorption of phosphate (55.7+/-25.1%). The fractional excretion of aluminium was also greatest at day 7 (1.1+/-0.9%) when serum creatinine was still elevated (3.6+/-2.3 mg/dl). At each period of time after transplantation fractional excretion of aluminium was similar in all patients despite disparate serum aluminium concentrations. Fractional excretion of aluminium was highest in those patients who developed post-Tx acute tubular necrosis (0.7+/-0.5 vs 1.5+/-1.0%, P=0.008). We found a direct positive correlation (r=0.43; P<0.002) between urinary aluminium and urinary phosphate. Basal levels and sequential changes in serum PTH, calcium, and phosphate did not correlated with fractional excretion of aluminium. These findings suggest: (i) urinary aluminium remains elevated during prolonged periods after transplant and is probably a marker of pre-transplant tissue aluminium accumulation; (ii) post-transplant fractional excretion of aluminium seems to correlated positively with other evidences of renal tubular dysfunction. Early post-transplant tubular malfunction could significantly enhance urinary aluminium elimination.
成功移植后铝的尿排泄可逆转移植前的铝中毒。我们评估了49例患者(33例男性和16例女性)移植前血清铝浓度范围广泛,在移植前以及移植后7天、30天、60天和90天进行连续测定,尿铝排泄的时间进程及其与肾功能和矿物质代谢的几个参数的相关性。移植前血清铝的平均值为54.5±46.8μg/l,在90天时逐渐降至28.7±24.4μg/l(P<0.0002),与血清肌酐的下降平行。尿铝在90天时从63.0±77.9降至52.4±55.9μg/l(P<0.0001)。尿铝/肌酐的最大值在7天时为1.8±2.7,与最大的钠分数排泄(4.7±5.1%)相关,且与最低的磷酸盐肾小管重吸收(55.7±25.1%)相关。铝的分数排泄在第7天也最大(1.1±0.9%),此时血清肌酐仍升高(3.6±2.3mg/dl)。尽管血清铝浓度不同,但在移植后的每个时间段,所有患者的铝分数排泄相似。移植后发生急性肾小管坏死的患者铝分数排泄最高(0.7±0.5对1.5±1.0%,P=0.008)。我们发现尿铝与尿磷酸盐之间存在直接正相关(r=0.43;P<0.002)。血清甲状旁腺激素、钙和磷酸盐的基础水平及连续变化与铝的分数排泄无关。这些发现表明:(i)移植后长时间内尿铝仍升高,可能是移植前组织铝蓄积的标志物;(ii)移植后铝的分数排泄似乎与肾小管功能障碍的其他证据呈正相关。移植后早期肾小管功能异常可能显著增强尿铝的排泄。