Time course and functional correlates of post-transplant aluminium elimination

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 pretransplant time and at 7, 30, 60, and 90 post-transplant days. Mean serum aluminium at pre-transplant was 54.5 ± 46.8 μg/l decreasing progressively to 28.7 ± 24.4 μg/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 μg/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.