Biomedical subjects

J G Heaf

Publications and source records attributed to J G Heaf.

At least 19 recordsLinked to original sources

PubMed1998

The effect of acute rejection on long-term renal graft survival is mainly related to initial renal damage.

It has been suggested that poor long-term prognosis of acute rejection is due to hyperfiltration-mediated injury secondary to the initial renal damage, rather than to ongoing immunological mechanisms. A total of 953 renal transplant recipients was reviewed to examine the effect of acute rejection episodes on graft function and survival; 40% had no rejections, 45% one, 12% two and 3% three. Rejection episodes adversely affected short- and long-term prognosis (5-year survival for no rejections, 62%; one, 34%; two, 26%; three, 19%, P < 0.001) and creatinine clearance at one year (cl 1) (none, 56.7 ml/ min; one, 51.1; two, 52.9; three, 35.2, P < 0.01). This was mainly due to increased graft loss, but patient survival was also reduced (5-year survival for no rejections, 77%; one, 76%; two, 63%; three, 53%, P < 0.05). There was no overall effect of rejection number, independently of cl 1. However, subgroup analysis showed a detrimental effect of rejection number on grafts with high residual function, i.e. cl 1 > 60 ml/min (5-year graft survival none and one, 87%; two and three, 71%, P < 0.01). Late initial rejection episodes adversely affected prognosis (5-year survival 1-7 days, 34%; 8-60, 31%; 60-300, 21%, P < 0.05) and residual graft function (cl 1 1-7 days, 56.2 ml/min; 8-60, 48.7; 60-300, 44.6, P < 0.01). In conclusion, the poor long-term prognostic effect of rejection episodes is mainly, but not entirely, related to initial graft destruction. Late (> 2 months after transplantation) initial rejection is an important independent risk factor for graft loss.

Acute Disease↗

PubMed1998

The cellular clearance theory does not explain the post-dialytic small molecule rebound.

AIM: (a) To determine the normalized cellular clearance (Kcn) of urea, creatinine and phosphate in patients undergoing maintenance hemodialysis; (b) To identify the factors, particularly circulatory, which determine Kcn; (c) To evaluate whether intra-dialytic blood sampling can predict the size of the post-dialytic solute concentration rebound. METHODS: Kinetic modelling of urea, creatinine and phosphate, using a two-pool variable volume computer simulation, was performed on two occasions on 34 patients undergoing maintenance dialysis. The cellular clearance was determined (a) from the size of the rebound 50 min after the end of dialysis; (b) from a mid-dialytic blood sample. Conventional two-dimensional M-mode echocardiography and Doppler peripheral blood pressure measurement were performed. RESULTS: The model produced accurate measurements of rebound Kc for urea in 93% of measurements, creatinine in 49% and phosphate in 13%. The corresponding figures for mid-dialysis Kcn were 76%, 39% and 0%. The rebound Kcn was, for urea, 8.31 +/- 4.31 ml/kg/min, and for creatinine 4.07 +/- 2.98. The mid-dialysis Kcn was, for urea, 8.57 +/- 4.25 ml/kg/min, and for creatinine 5.06 +/- 3.36. High post-dialytic rebounds (and low Kcn values) were associated with erythropoietin use (p < 0.05) and occurrence of end-dialytic hypotension (p < 0.02). Patients treated with calcium antagonists had a significantly (p < 0.001) higher Kcn. There was no correlation between mid-dialysis and rebound Kcn. Circulatory indices had no influence on Kcn. CONCLUSIONS: The two-pool cellular clearance model is compatible with urea kinetics, but not creatinine or phosphate. It is therefore unlikely that it is the correct model for small molecule kinetics. The post-dialytic solute rebound may be partly an iatrogenic phenomenon and can be reduced by preventing post-dialytic hypotension and by calcium antagonist treatment, both of which improve regional blood flow. The size of the rebound cannot be predicted by intra-dialytic blood sampling.

Blood Urea Nitrogen↗

PubMed1998

Hyperfiltration, creatinine clearance and chronic graft loss.

Chronic graft loss (CGL) may be caused by immunological- or hyperfiltration-mediated tissue destruction. If the hyperfiltration theory is correct, grafts from female donors given to heavy recipients, and having a relatively poor initial function, should suffer an accelerated rate of loss of function. 590 renal transplantations surviving more than 1 yr, including 171 cases of (CGL), were reviewed to identify causes of CGL. No overall influence of recipient or donor sex was found, but female donation resulted in lower acute graft loss and higher CGL. Warm ischemia affected CGL marginally, but cold ischemia < 12 h (excluding living donors) reduced CGL (35 vs. 53% at 10 yr, p < 0.05) and delayed function increased CGL (38% vs. 56% p < 0.001). Patients with a high urea production had high CGL (43% vs. 77%, p < 0.02). No overall effect of recipient weight was found; however 7 patients weighing > 90 kg all had CGL within 10 yr. Creatinine clearance was increasingly correlated to recipient weight (r = 0.23 at 1 yr, 0.38 at 10 yr, p < 0.001). For all years, change in creatinine clearance correlated with change in weight (p < 0.001). The most important factor predicting CGL was creatinine clearance, (> 80 ml/min: 6% at 10 yr; 20-40 ml/min 53%). However, at any level of creatinine clearance, patients with late CGL had a slower loss of renal function. Rate of change of renal function was proportional to creatinine clearance, but only for grafts surviving > 6 yr. Creatinine clearance rose between 3 mths and 2 yr; this rise indicated a good prognosis, was related to recipient weight and weight increase, and was reduced in older donors and cyclosporine treated patients. For patients with low clearance (< 60 ml/min), the increased CGL seen in patients with previous rejection episodes could be explained by their consequent lower clearance, but above this level, rejection episodes had an independent deleterious effect. These findings are compatible with hyperfiltration being the major cause of CGL after 6 yr. Before this immunological factors dominate. Good quality grafts respond to the increased protein load of heavy recipients with an increased GFR. Thus at any time, graft GFR is a function of protein-induced hyperfiltration, immunological graft destruction and hyperfiltration-mediated damage. Hyperfiltration-mediated renal damage is not a problem if the creatinine clearance is greater than 60 ml/min.

Adolescent↗

PubMed1996

Can bone histomorphometry be predicted by clinical assessment and noninvasive techniques in peritoneal dialysis?

In an attempt to evaluate whether bone histology could be predicted by clinical assessment and noninvasive techniques in patients on peritoneal dialysis, bone histomorphometry was correlated with symptoms of renal osteodystrophy, serum bone markers and parathyroid hormone (PTH) as well as radiographs and forearm osteodensitometry (bone mineral content, BMC). No correlations were found between clinical symptoms, biochemical markers, radiographic bone surveys, BMC measurements, and bone diagnosis. Serum 1,25-(OH)2D3 correlated negatively with the intracortical resorption and the degree of osteoporosis. No other correlations were seen between the serum markers measured, PTH and the radiographic parameters. Alkaline phosphatase correlated negatively with mineralization lag time and positively with eroded surface, mineral appositional rate, tetracycline-labelled surface and bone formation rates. HCO-3 correlated negatively with osteoid thickness and osteoid surface. Ca2+ correlated with osteoid surface, osteoid volume and cortical thickness. Mg correlated with the duration of azotemia, cortical porosity and bone aluminum content, while serum phosphate correlated with the mineral appositional rate. Osteocalcin and PTH correlated with osteoid thickness, the mineral appositional rate, tetracycline-labelled surface, the adjusted apposition rate, mineralization lag time and the bone formation rates. BMC measurements correlated with PTH and Ca2+ and inversely with sex and trabecular bone volume, osteoid thickness, osteoid surface, osteoid volume, eroded surface, osteoclast surface, tetracycline-labelled surface and the bone formation rates. Seven of the histomorphometric parameters correlated significantly with the radiological bone features. However, the clinical assessment and the serum markers of bone metabolism were of limited value. Thus, bone histology cannot be comprehensively predicted by non-invasive methods, although radiographs and forearm osteodensitometry provided some valuable information.

Adult↗

PubMed1995

Consistent absorption of cyclosporine from a microemulsion formulation assessed in stable renal transplant recipients over a one-year study period.

To evaluate the pharmacokinetic properties of the new microemulsion formulation of cyclosporine (Sandimmun Neoral), a double-blind, prospective study in stable renal transplant recipients was performed. The patients were randomized on a 4:1 basis either to receive Sandimmun Neoral (n = 45) or continue on regular Sandimmun (n = 12). Before randomization, a steady-state pharmacokinetic profile study was performed in all patients while they were still on regular Sandimmun. Pharmacokinetic assessments were then performed after 8 and 12 weeks and after 1 year. A milligram-to-milligram dose conversion was shown to be adequate to maintain the patients within a predefined target therapeutic window. Changes in pharmacokinetic parameters after conversion to Sandimmun Neoral were consistent with an increased rate and extent of cyclosporine absorption from the Neoral formulation. This was reflected by a shorter time to reach peak concentration and also by a mean increase in peak concentration by 67%, and an overall mean increase in drug exposure (area under the curve) by 34%. These findings were also confirmed 1 year after conversion. Furthermore, significantly reduced intraindividual variability in pharmacokinetic parameters was found, as well as improvements in the correlation between trough concentrations and area under the curve after conversion to Sandimmun Neoral. In conclusion, our results indicate an improved and consistent absorption of cyclosporine from the Neoral formulation, which should make clinical management easier and safer.

Absorption↗

PubMed1995

Type I procollagen propeptide in patients on CAPD: its relationships with bone histology, osteocalcin, and parathyroid hormone.

Serum procollagen type I carboxyterminal propeptide (PICP) has been shown to be a useful marker of bone formation in patients undergoing haemodialysis. However, PICP levels has not been evaluated in depth in patients maintained on continuous ambulatory peritoneal dialysis (CAPD). Therefore serum and dialysate levels of PICP, its peritoneal clearance (Clp), mass transfer (MTp), and its possible relationship with osteocalcin, parathyroid hormone (PTH), and bone histomorphometry were studied in a group of CAPD patients. Serum PICP was just above the normal range with significant amounts detected in the dialysate but no correlations were found between levels of serum PICP, dialysate PICP, and Clp-PICP. One patient with systemic lupus and osteitis fibrosa had extraordinarily high serum and dialysate levels of PICP. The patient later developed sclerosing peritonitis. No associations were seen between serum PICP and Clp-PICP and any of the 18 bone histomorphometric parameters evaluated. Dialysate level of PICP correlated negatively with mineral appositional rate (r = -0.62, P < 0.01) and mineralization lag time (r = 0.64, P < 0.01). MTp-PICP correlated positively with mineral appositional rate (r = 0.65, P < 0.01). Serum osteocalcin and serum PTH levels did not correlate to serum, dialysate, Clp or MTp measurements of PICP. These results suggest that measurements of PICP in CAPD patients do not give substantial information as an non-invasive marker of bone histology.

Adult↗

PubMed1994

Osteocalcin: a non-invasive index of metabolic bone disease in patients treated by CAPD.

Serum osteocalcin has been found to correlate with bone formation. However, present literature gives only limited data on osteocalcin and bone histomorphometry in patients undergoing peritoneal dialysis. This study assessed serum osteocalcin, dialysate osteocalcin, peritoneal clearance of osteocalcin (Clp-osteocalcin) and mass transfer of osteocalcin (MTp-osteocalcin), and evaluated relationships between these values and bone histomorphometry. Eighteen patients were treated by continuous ambulatory peritoneal dialysis (CAPD). Bone biopsies, serum and dialysate osteocalcin, serum levels of parathyroid hormone, alkaline phosphatase, aluminum, phosphate, Ca2+ and vitamin D3 metabolites were measured at the start and in 10 of the patients a year later. Serum osteocalcin was found to be elevated. Osteocalcin was detected in the dialysate resulting in significant values of Clp-osteocalcin and MTp-osteocalcin. Serum and dialysate levels of osteocalcin correlated significantly (r = 0.66, P < 0.001) and like MTp-osteocalcin with serum levels of alkaline phosphatase and PTH. Histomorphometry showed that osteitis fibrosa was the predominant bone disease detected. Serum concentration of osteocalcin correlated with osteoid thickness, eroded and osteoclast surfaces, aluminum staining, and some of the bone dynamic parameters. Dialysate osteocalcin, MTp-osteocalcin, PTH and alkaline phosphatase correlated with practically the same histomorphometric parameters as serum osteocalcin. No correlations were seen between Clp-osteocalcin and any histomorphometric parameters. Serum osteocalcin was elevated above the normal range, and significant positive correlations between serum osteocalcin and bone formation parameters were found. Serum osteocalcin correlated with almost the same histomorphometric parameters as PTH. Thus, serum levels of PTH and osteocalcin gave additional information to one another as non-invasive parameters in this group of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

The reliability and representativity of non-dynamic bone histomorphometry in uremic osteodystrophy.

In order to evaluate the reliability and representativity of iliac crest bone biopsy in uremic osteodystrophy, non-dynamic bone histomorphometry was performed post-mortem on the right and left iliac crests and the 3rd lumbar vertebra in 20 patients with chronic uremia. High (> 0.8) right-left correlation coefficients were found for bone volume, osteoid volume, osteoid surface, osteoid thickness, eroded surface, osteoclast surface and aluminium labelling intensity; moderate (0.7-0.8) for trabecular thickness, and low (< 0.7) for cortical thickness, porosity and aluminium bone concentration. High iliac crest-vertebra correlations were found for trabecular thickness, osteoid volume, osteoid surface, eroded surface, osteoclast surface and aluminium labelling intensity, and low correlations for bone volume, osteoid thickness and bone aluminium concentration. In conclusion, non-dynamic iliac trabecular bone indices are reliable variables and, with the possible exception of bone mass determination, indicative of systemic bone disease. Bone aluminium concentration and cortical bone indices are unreliable measures of uremic bone disease. These reservations apply to the diagnostic use of biopsy in individuals, but not necessarily its research use in groups of patients.

Aged↗

PubMed1992

[Analysis of phenprocoumon dose regulation based on measurement of coagulation factors II, VII and X].

One hundred anticoagulation treatment records were reviewed retrospectively using stepwise regression analysis to determine the influence of phenprocoumaron on the levels of coagulation factors 2, 7 and 10 (KF) measured relative to normal. The phenprocoumaron dose was expressed relative to the correct maintenance dose determined from the entire record ("overdose", OD measured in mg). Phenprocoumaron treatment influenced the KF over two days, approximately 50% on each day, the total change being -0.03 x OD. Continuous incorrect dosage resulted in KF change, equilibrating at a new level after about four weeks at -0.47 x OD. Similarly, continuous correct dosage in patients with a non-therapeutic FK resulted in equilibration within the therapeutic range after four weeks. For long-term treatment, the dosage was likely to be inaccurate under the following circumstances: 1) if the KF was outside the therapeutic range and moving away from it; 2) if the KF was inside the therapeutic range and the change was greater than 0.05. Algorithms for calculation of phenprocoumaron therapy are presented.

Adolescent↗

PubMed1992

Bisphosphonate kinetics in patients undergoing continuous ambulatory peritoneal dialysis: relations to dynamic bone histomorphometry, osteocalcin and parathyroid hormone.

In the evaluation of renal osteodystrophy bone biopsy is often performed. However, a reliable noninvasive test could be very useful, and recently the estimation of osseous tracer uptake as an index of bone formation has been introduced-the bone bisphosphonate clearance (BBC). The aim of the present investigation therefore was to compare BBC with parameters of bone histology, serum levels of osteocalcin, alkaline phosphatase, and parathyroid hormone in patients (n = 8) undergoing continuous ambulatory peritoneal dialysis (CAPD). No significant correlations were found between BBC values and the bone histomorphometrical variables measured. A positive correlation was seen between serum osteocalcin and resorption and active resorption surface (p < 0.05), as well as tetracycline-labelled surface, bone formation rate, surfaces, volume and tissue referents, respectively (p < 0.01). Furthermore, levels of alkaline phosphatase showed significant correlations to mineral appositional rate, tetracycline-labelled surface and bone formation rate, volume referent (p < 0.05). Values of parathyroid hormone were significantly correlated to resorption surface (p < 0.02), active resorption surface, mineral appositional rate and mineralization lag time (p < 0.05). In conclusion, BBC was of no use in patients treated with CAPD as a noninvasive test for evaluation of bone histomorphometry. However, osteocalcin correlated best with resorption and bone dynamics indices. Levels of alkaline phosphatase and parathyroid hormone were of a more limited value.

Adult↗

PubMed1991

[Hyperlipidemia in nephrotic syndrome].

Hyperlipidemia is common in patients with the nephrotic syndrome. The main cause is probably increased hepatic lipogenesis, a non-specific reaction to falling oncotic pressure secondary to hypoalbuminemia. Cardiovascular morbidity and mortality are increased in patients with the nephrotic syndrome, with the exception of patients with minimal change disease. It is not clear whether this is caused by the hypercholesterolemia or secondary to uremia or medical treatment. Experiments suggest that hypercholesterolemia may cause glomerulosclerosis, a common complication of the nephrotic syndrome. The hypercholesterolemia of the nephrotic syndrome can now be treated effectively with HMG coenzyme A reductase inhibitors.

Cardiovascular Diseases↗

PubMed1989

Vitamin D and vitamin-D-binding protein kinetics in patients treated with continuous ambulatory peritoneal dialysis (CAPD).

Serum and dialysate levels of 25-hydroxycholecalciferol (25-OHD3), 1,25 dihydroxycholecalciferol (1,25-(OH)2D3), and vitamin-D-binding protein (DBP) were measured in 14 patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Serum levels of 25-OHD3 and DBP were within normal range (29.1 +/- 22.9 nmol/L and 5.9 +/- 1.1 mumol/L, respectively). Serum levels of 1,25-(OH)2D3 were subnormal in all (less than 16 pmol/L) but one. In 5 patients, dialysate concentrations of 25-OHD3 were 2.3 +/- 0.9 nmol/L, the rest had levels less than 1.0 nmol/L. Small quantities of 1,25-(OH)2D3 were found in the dialysate effluents. DBP could be detected in the dialysate in all patients (0.24 +/- 0.06 mumol/L). Mass transfer (MT) of 25-OHD3 and DBP were respectively -10.4 +/- 8.3 nmol/24 h and -1.46 +/- 0.46 0.46 mumol/24 h. Peritoneal clearances of 25-OHD3 and DBP were low (0.40 +/- 0.37 mL/min and 0.18 +/- 0.06 mL/min, respectively. We conclude that CAPD leads to losses of 25-OHD3 and DBP. However, the peritoneal loss of DBP is well compensated and does not result in serum deficiency. Serum 25-OHD3 levels did not correlate with time on CAPD.

Calcifediol↗

PubMed1989

Bone histology in CAPD patients: a comparison with hemodialysis and conservatively treated chronic uremics.

Thirteen patients treated with CAPD, 22 patients maintained on hemodialysis (HD) using aluminium-free water and matched for duration of treatment and 15 conservatively treated uremic patients (CONS) were evaluated by iliac bone biopsy to analyse the influence of CAPD on bone histomorphometry. CAPD patients were significantly (p less than 0.05) older (63.1 +/- 14.0, HD 52.7 +/- 13.3, CONS 53.3 +/- 11.7). Compared to HD the results were as follows: CAPD patients required significantly less aluminium to control hyperphosphatemia (0.16 vs. 0.49 g, p less than 0.005). They had a significantly lower incidence of symptomatic bone disease (p less than 0.05). Histomorphometry showed significantly lower osteoid volume (4.3 + 2.8% vs. 8.6 + 5.5%, p less than 0.05) and aluminium labelling intensity (0.15 vs. 1.0, p less than 0.05). Apart from bone mass indices, other histomorphometric variables showed an insignificantly more favourable trend in CAPD patients compared to HD. CONS patients had a significantly lower bone formation rate than CAPD (p less than 0.05), but otherwise no histomorphometric differences were observed. We conclude that CAPD patients require less aluminium therapy, have a lower risk of aluminium bone contamination, and may have a lower risk of developing uremic osteodystrophy.

Aluminum↗

PubMed1989

Aluminum concentrations in serum, dialysate, urine and bone among patients undergoing continuous ambulatory peritoneal dialysis (CAPD).

Aluminum (Al) concentration in serum, urine, and dialysate was estimated in 21 patients undergoing continuous ambulatory peritoneal dialysis (CAPD). In 12 of the patients bone Al concentration was measured as well. Mean serum Al level was 32.4 +/- 21.0 micrograms/l. The Al concentrations in the dialysate and urine were 9.1 +/- 4.1 micrograms/l and 52.5 +/- 47.3 micrograms/l, respectively. Bone Al concentration was 21.0 +/- 14.9 ppm and correlated significantly with concentrations of Al in serum (p less than 0.01) and dialysate (p less than 0.01). A mass transfer (MT) from the patients to the dialysate was observed in all patients (-44.0 +/- 28.8 micrograms/24 h). There was a highly significant correlation between peritoneal Al MT and serum Al (p less than 0.001), actual Al consumption (p less than 0.05) and bone Al concentration (p less than 0.005) supporting the existence of an overflow phenomenon. Despite very low Al levels in the dialysate, patients are at risk of elevated Al levels in the serum, dialysate, urine and bone because of consumption of Al-containing phosphate binders.

Adult↗

PubMed1988

Treatment of refractory cancer-associated hypercalcemia with aminohydroxypropylidene diphosphonate.

The case history is presented of a 45-year-old woman who was receiving chemotherapy for a pulmonary adenocarcinoma and who developed severe symptomatic hypercalcemia. Despite intensive treatment with fluids, loop diuretics, prednisone, calcitonin and repeated doses of mithramycin, she remained hypercalcemic. She was then treated with aminohydroxypropylidene diphosphonate (APD) with consequent rapid normalization of the serum calcium and disappearance of symptoms. We conclude that APD is a valuable supplement to the treatment of malignant hypercalcemia in that it may be effective when traditional therapies have failed.

Adenocarcinoma↗

PubMed1987

Noninvasive diagnosis of uremic osteodystrophy: uses and limitations.

45 bone biopsies from patients with chronic uremia were reviewed to define which noninvasive investigations were of value in predicting the histological diagnosis and to quantify the spectrum of uremic bone disease at a center that has consistently used an aluminum-free dialysis bath. 17 biopsies were taken postmortem. 15 patients received conservative treatment, the rest were on maintenance dialysis. 13 patients had symptomatic bone disease. Virtually all patients with a uremia duration greater than 3 years had uremic osteodystrophy. All patients with clinical bone disease, hypercalcemia or raised alkaline phosphatase activity had osteodystrophy, but the specific histology was not indicated. Greatly raised parathyroid levels suggested secondary hyperparathyroidism, but the test was only 100% specific when 20 times normal. Total aluminum consumption was highly indicative of bone aluminum concentration (p less than 0.0001) and aluminum-related osteomalacia (5 cases), suggesting that a considerable proportion of uremic bone disease is iatrogenic. Serum aluminum was of some use in the diagnosis of aluminum-related osteomalacia, but was not wholly reliable. Bone mineral content (BMC) using both forearm measurements and total body bone mineral levels (TBBM) were assessed in 32 patients and were found to be reduced in 12, with a preponderance of secondary hyperparathyroidism. BMC and TBBM were negatively correlated to resorbing surfaces and bone formation rate, suggesting that secondary hyperparathyroidism is the uremic bone disease that represents the greatest threat to bone mass. It is concluded that while noninvasive investigations give considerable information, reliable diagnosis requires the use of histological methods.

Adolescent↗

PubMed1987

The effect of oral aluminium salts on the bone of non-dialysed uremic patients.

12 patients with conservatively treated uremia were investigated using bone histomorphometry, bone aluminium concentration determination and total body bone mineral content (TBBM). The bone aluminum was raised in 10 patients and was significantly related to oral aluminium salt consumption (p less than 0.01). Two of four patients who had not received aluminium also had raised levels but the difference was not significant from nonuremic patients. The two patients with the highest levels had a mineralisation defect despite normal levels of 1,25-dihydroxyvitamin D. Three patients had significant bone loss of whom one had osteomalacia (OM) while two had secondary hyperparathyroidism (2HP). It is concluded that 1) aluminium salt consumption results in bone aluminium accumulation, and may contribute to the mineralisation defect; 2) uremic patients not treated ith aluminium salts may have slightly raised levels, but this seems not to be clinically important; 3) secondary hyperparathyroidism causes greater destruction of bone mass than other uremic bone diseases; 4) atomic absorption spectrometry is a more sensitive method for detecting aluminium bone deposition than histochemical methods.

Acetates↗

PubMed1986

Metabolic bone disease and aluminium contamination in 38 uremic patients. A bone histomorphometric study.

Iliac crest biopsies from 38 uremic patients, 26 hemodialysis, and 12 chronic uremics from a nephrology department with verified aluminium free dialysis water were investigated with histomorphometric method and aluminium-specific staining. For both the uremic and the dialysed group the results showed a high incidence of both metabolic bone disease (75%, 69% respectively) and aluminium contamination (25%, 62%).

Aluminum↗