Time course and functional correlates of post-transplant aluminium elimination

Abstract

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.

Treatment of refractory secondary hyperparathyroidism with ethanol injection: The importance of glandular volume

“…higher than 300 pg/mL, lack of responsiveness to calcitriol pulse therapy (either oral or intravenous), discontinuation of calcitriol due to hypercalcemia (serum Ca One of the main problems nephrologists face when Ͼ11 mg/dL), hyperphosphatemia (serum P Ͼ6 mg/dL), treating chronic renal failure patients is to control the or a calcium x phosphorous product higher than 65. The increased secretion of parathyroid hormone during dialpossibility of aluminum overload was ruled out by bone ysis and after renal transplantation [1][2][3][4][5]. Great progress biopsy, serum aluminum levels lower than 20 g/L, lack has been achieved in this field in terms of medical therof recent exposure to aluminum-containing phosphate apy.…”

Renal Handling of Aluminium

“…C Al /GFR (GFR being assessed as creatinine clearance) has been reported to increase in renal failure [14] and values in renal transplant patients undergoing immunosuppressive therapy are higher than those in healthy subjects [19, 20], but in no case was Al filterability measured. C Al /GFR was also high (∼30%) in a group of dialysis patients in whom creatinine clearance values were extremely low [21].…”