We measured lead and calcium in multiple bone biopsies from 11 cadavers without known excessive past exposure to lead. Paired iliac crest, transiliac and tibial bone biopsies from these cadavers indicated that in bone biopsy specimens the lead/calcium ratio is more reproducible than the absolute lead concentration. There were no significant differences between the lead/calcium ratios from the iliac crest, transiliac, or tibial specimens. Transiliac bone biopsies from 35 patients (13 patients showing symptoms of slight or moderate degree of renal failure, medical history of gout and/or arterial hypertension and 22 lead workers with chelatable lead in excess of 1000 micrograms) indicated that the lead and the lead/calcium ratio in bone biopsies reflect body lead stores as estimated by the EDT A test (r = 0.87 and 0.83, respectively). Chemical and histological studies of transiliac biopsies previously obtained from 153 dialysis patients (from 8 dialysis centers from Belgium, France and Germany) for studies of aluminum-induced bone disease showed that chronic renal failure and dialysis do not cause accumulation of lead in bone and elevated bone lead does not appear to alter trabecular bone histomorphometry. We found that in 5% of the hemodialysis population studied, bone lead concentrations approximated levels found in active lead workers.

The serum ferritin (SF) level was measured in 58 chronic hemodialysis (CHD) patients (46 living and 12 deceased subjects) and compared to bone marrow iron concentrations, cytological bone marrow iron stores (BMIS), and histological BMIS. In the 12 deceased subjects, liver iron concentrations, histological liver parenchymal, and Kupffer cell iron stores were also studied. The mean SF level of the whole group was 302 +/- 251 ng/ml (mean +/- SD). No close relationship was found between transferrin saturation and cytological BMIS. A high correlation was found between SF level and cytological BMIS (Spearman rank rs = 0.74). In the deceased CHD patients a close correlation was observed between histological parenchymal liver iron stores and histological Kupffer cell iron stores, but not between liver and bone marrow iron stores. A good correlation was found between SF levels and liver iron concentrations. It is concluded that in CHD patients SF levels are higher than in healthy controls, even in the absence of iron therapy (except in the form of blood transfusions); in some of these patients iron is disproportionately stored in the bone marrow and the liver. Although the level of BMIS cannot be estimated unequivocally from an SF measurement in every CHD patient, SF levels provide useful estimates of BMIS.

The clinical relevance of regular serum aluminium monitoring in dialysis patients was investigated in a multicentre study by 6-monthly determination of the serum aluminium during 4 consecutive years. In a group totalling 1193 patients, a striking decrease of mean serum aluminium was observed the last 2 years of the study. This phenomenon was accompanied by a substantial reduction of the prescribed dose of aluminium hydroxide (Al(OH)3) and its partial replacement by calcium carbonate (CaCO3) and/or magnesium hydroxide (Mg(OH)2). Under this policy serum phosphate control remained satisfactory. In all the centres, water treatment was found to be adequate, yielding dialysate aluminium around 2 micrograms/l. Dialysis patients with clinically overt liver disease showed a significantly greater median serum aluminium concentration than that observed in a control dialysis population. Compared to the latter group, the median serum aluminium concentration of dialysis patients with diabetes mellitus did not differ significantly. Results further indicated that patients with biopsy-proven osteomalacia presented a significantly greater median serum aluminium compared to that of patients without osteomalacia. We demonstrated that a serum aluminium of 60 micrograms/l provides a relatively sensitive (82%) and specific (86%) index for the detection of aluminium-related bone disease (ARBD). Provided the aluminium determinations are performed by a qualified laboratory, serum monitoring in dialysis patients (a) allows the safer use of aluminium-containing phosphate binders, and (b) is of value in the diagnosis of overload/toxicity.

A method was developed for the determination of gadolinium (Gd) in biological material using graphite furnace atomic absorption spectrometry (GFAAS). The element is first extracted into methyl isobutyl ketone and then reextracted into hydrochloric acid. Factors influencing the recovery of extraction such as pH, choice of chelating agents, and hydrochloric acid concentration have been investigated. The element is determined under STPF (stabilized temperature platform furnace) conditions with atomization from a tantalum boat. Under optimized furnace conditions, the use of the tantalum boat improved sensitivity substantially compared to the use of pyrolytically coated graphite tubes. Around 150 measurements could be performed with 1 boat. Memory effects, being a common problem in the GFAAS determination of lanthanoids, were no longer observed after insertion of the boat. The characteristic mass and detection limit (2SD; SD = standard deviation) of the Gd determination are 1000 and 2060 pg, respectively. The precision evaluated as the relative standard deviation (RSD) of six analyses was below 10% for tissue Gd concentrations ranging from 0.92 to 72.0 micrograms g-1. The recovery of added analyte ranged between 92.0% and 99.3%. The method was found to be suitable for studying the pharmacokinetics and biodistribution of Gd in rats.

Direct measurement of lead and cadmium in blood and urine by electrothermal atomic absorption spectrometry with deuterium background correction (D2-AAS) is prone to severe matrix and spectral interferences. We overcame these effects by coating the L'vov platform with ammonium molybdate, reducing the atomization time, introducing a post-atomization cooling step, carefully selecting ashing and atomization temperatures, and using an appropriate procedure for matrix modification. To determine Pb and Cd in blood and urine, we used matrix-matched calibration curves. With the proposed procedure for sample preparation, both Pb and Cd in whole blood can be determined in the same diluted sample. Results obtained by D2-AAS correlate closely with those by Zeeman-corrected AAS. Detection limits (mean blank + 3 SDblank) for Pb in urine and blood were 4 micrograms/L. For cadmium, the detection limits were 0.4 and 0.1 micrograms/L for urine and blood analysis, respectively. Between-run CVs were less than 5.0%.