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Biomedical subjects

C G Elinder

Publications and source records attributed to C G Elinder.

At least 19 recordsLinked to original sources
PubMed1997

Kidney donors live longer.

BACKGROUND: A very important issue in living kidney donor transplantation is whether the donation is safe for the donor. The aim of this study was to examine survival and causes of death in kidney donors and to assess the renal function in those who had donated a kidney more than 20 years ago. METHODS: A total of 459 living donor nephrectomies were performed in Stockholm from 1964 until the end of 1994. By using national registers, all 430 donors living in Sweden were traced. Donor survival was analysed using the Kaplan-Meier method. Expected survival was computed using the Hakulinens method and was based on national mortality rates. RESULTS: Forty-one subjects had died between 15 months and 31 years after the donation. The mortality pattern was similar to that in the general population, the majority dying of cardiovascular diseases and malignancies. After 20 years of follow-up, 85% of the donors were alive, whereas the expected survival rate was 66%. Survival was thus 29% better in the donor group. One third of the donors (aged 46-91 years) who had donated >20 years ago had hypertension. There was a deterioration in the renal function with increasing age, similar to what is seen among normal healthy subjects. The average glomerular filtration rate in donors aged 75 years and over was 48 ml/min/1.73 m2. CONCLUSIONS: To donate a kidney does not seem to constitute any long-term risk. The better survival among donors is probably due to the fact that only healthy persons are accepted for living kidney donation.

Adult↗
PubMed1997

In vivo analysis of cadmium in battery workers versus measurements of blood, urine, and workplace air.

OBJECTIVES: To measure in vivo the cadmium concentrations in kidney cortex (kidney-Cd) and in superficial liver tissue (liver-Cd) of nickel cadmium battery workers, and to compare the results with other commonly used estimates of cadmium exposure (current concentrations of cadmium in blood (B-Cd) and urine (U-Cd)) or repeated measurements of cadmium in workplace air (CumAir-Cd). METHODS: The study comprised 30 workers with a range of duration of exposure of 11-51 years. 13 subjects were currently employed, whereas the other 17 had a median period without occupational exposure of eight years before the measurements. The in vivo measurements were made with an x ray fluorescence technique permitting average detection limits of 30 and 3 micrograms cadmium per g tissue in kidney and liver, respectively. RESULTS: 19 of 30 (63%) people had kidney-Cd and 13 of 27 (48%) had liver-Cd above the detection limits. Kidney-Cd ranged from non-detectable to 350 micrograms/g and liver-Cd from non-detectable to 80 micrograms/g. The median kidney-Cd and liver-Cd were 55 micrograms/g and 3 micrograms/g, respectively. Kidney-Cd correlated significantly with B-Cd (r, 0.49) and U-Cd (r, 0.70), whereas liver-Cd correlated significantly with U-Cd (r, 0.58). Neither kidney-Cd nor liver-Cd correlated with the CumAir-Cd. The prevalence of beta 2-microglobulinurea increased with increased liver-Cd. CONCLUSIONS: Current U-Cd can be used to predict the kidney-Cd and liver-Cd measured in vivo. In vivo measurements of kidney-Cd and liver-Cd were not shown to correlate with the individual cadmium exposure estimates, obtained by integration of the cadmium concentration in workplace air. There may be several reasons for this, including uncertainties in the estimate of the individual cumulative exposures as well as in the in vivo measurements. There was a suggestion of a relation between liver-Cd and tubular proteinuria.

Aged↗
PubMed1997

Blood cadmium as an indicator of dose in a long-term follow-up of workers previously exposed to cadmium.

OBJECTIVES: This investigation attempted to follow the tubular function of 46 workers initially examined in 1984 and heavily exposed to cadmium from 1955 to 1978 and the occurrence of renal stones among these workers. Three different markers of tubular dysfunction were also studied, and blood cadmium was evaluated as an estimate of dose after the cessation of cadmium exposure. METHODS: Cadmium in blood (B-Cd) and urine (U-Cd) and the urinary excretion of beta 2-microglobulin (U-beta 2-microglobulin), protein HC (alpha 1-microglobulin) and N-Acetyl-beta-D-glucosaminidase (NAG) were determined. RESULTS: Although cadmium exposure ceased in 1978, 40% of the workers showed signs of tubular dysfunction both in 1984 and in 1993. The current B-Cd was the best dose indicator. Dose-response relationships were found for B-Cd and various tubular markers (U-beta 2-microglobulin, protein HC and NAG). Protein HC appeared to be the most sensitive, as well as an early, indicator of cadmium-induced tubular dysfunction. The levels of U-Cd had an average decrease of 48% for persons with a normal tubular function, 56% for those with slight tubular dysfunction, and 62% for workers with severe tubular damage. A history of renal stones was significantly more common for workers with high B-Cd levels. CONCLUSIONS: Cadmium-induced tubular dysfunction is irreversible and best assessed in an analysis of protein HC (alpha 1-microglobulin) in urine. B-Cd is the best dose estimate several years after the cessation of exposure, whereas U-Cd is less suitable for dose assessment in follow-up studies of persons with persistent tubular damage.

Acetylglucosaminidase↗
PubMed1997

[Cadmium--a pubic health problem?].

Exposure to cadmium has long been associated with the risk of renal damage and skeletal effects. Research has shown early renal damage to occur at much lower exposure levels than formerly believed, though the clinical significance of such damage has not been fully determined. The effect of cadmium on bone metabolism and mineralisation might be a contributory cause of the increasing prevalence of osteoporosis in the elderly.

Age Factors↗
PubMed1996

Report on management of renale failure in Europe, XXVI, 1995. Rare diseases in renal replacement therapy in the ERA-EDTA Registry.

The proportion of centres returning the ERA-EDTA Registry questionnaires has decreased considerably in recent years. Demographic information, based on the response rate of centres in 1994 (44%), does not allow reasonable projections for management of renal failure in Europe. To encourage the participation of non-responding centres, the timing was right to show the powerful impact of the ERA-EDTA Registry as a supra-national registry, by studying patients in renal replacement therapy (RRT) suffering from rare diseases. Four such diseases, Fabry's disease, nephropathy due to cyclosporin (CsA), nephropathy due to cisplatin and scleroderma, were studied using the records of 440665 patients on file up to 31 December 1993. There were 83 patients with Fabry's disease (0.0188%), 85 patients with CsA nephropathy (0.0193%), 120 patients with cisplatin nephropathy (0.0272%) and 625 patients with scleroderma (0.142%). Scleroderma was introduced as a primary renal disease (PRD) in the ERA-EDTA Registry in 1977. Seven patients were accepted for RRT in that year, whereas the number increased to over 50 new patients per year after 1986. More than half of the patients were aged over 55 years, and 68% of them were women. Survival rate of dialysis patients suffering from scleroderma was 22% at 5 years, compared to 51% in patients with standard primary renal diseases. The main causes of death were cardiovascular complications (41%), cachexia (15%) and infection (10%). Survival of first graft in a small number of 28 patients was 44% at 3 years, compared to 60% in standard PRD. Patient survival after first transplant, however, was higher by 32% at 3 years compared to that of dialysis patients. Cisplatin nephropathy was introduced as a PRD in the ERA-EDTA Registry in 1985, and since then six to 19 new patients have been accepted for RRT each year. The main reason for undergoing cisplatin treatment was ovarian (32%) and testicular cancer (21%), and the mean interval from treatment to RRT was 21.5 months, ranging widely from 0.1 to 131 months. Patient survival on dialysis was 22% at 5 years, compared to 51% in patients with standard PRD. Malignancy and cachexia accounted for over 60% of the total number of deaths. CsA nephropathy was introduced as a PRD in the ERA-EDTA Registry in 1985 and, despite its rarity, is of particular interest as a new iatrogenic entity resulting from CsA administration, mainly in solid organ transplantation. In 1985, two new patients commenced RRT in Europe, and the number increased to 59 in 1991-93. The main reason for undergoing CsA treatment was heart (68%) and liver transplant (22%), and the mean interval from treatment to RRT was 50.2 months, ranging from 5 to 90 months. Patient survival on dialysis was 46% at 4 years, compared to 58% in patients with standard primary nephropathies. Cardiovascular causes (48%) and infection (17%) were the main causes of death. Fabry's disease was introduced as a PRD in the ERA-EDTA Registry in 1985, and since the four to 13 new patients per year have commenced RRT in Europe. It is a sex-linked recessive disorder primarily affecting males (87%), and the mean age at start of RRT was 38 years. Proteinuria, skin lesions and painful paresthesiae were the most common presenting symptoms, and over 70% of the patients were hypertensive and had significant cardiovascular problems at RRT. Patient survival on dialysis was 41% at 5 years, compared to 68% in patients with standard primary nephropathies. Cardiovascular complications (48%) and cachexia (17%) were the main causes of death. Graft survival at 3 years in 33 patients was not inferior to that of patients with standard nephropathies (72% vs 69%), and patient survival after transplantation was comparable to that of patients under 55 years of age with standard PRD. (ABSTRACT TRUNCATED)

Adolescent↗
PubMed1996

No evidence of renal toxicity from amalgam fillings.

Dental amalgam continuously releases mercury. Studies of sheep [Boyd et al., Am. J. Physiol. 261 (Regulatory Integrative Comp. Physiol. 30): R1010-R1014, 1991] showed decreased renal function after placement of amalgam fillings. In this study, renal function was investigated in 10 healthy volunteers before and after amalgam removal. The subjects had an average of 18 tooth surfaces filled with amalgam, which was removed during one dental session. One week before and sixty days after removal, the glomerular filtration rate (GFR) was determined by 51Cr-EDTA clearance technique. Blood and urine samples were collected for analysis of mercury, creatinine, beta 2-microglobulin, N-acetyl-beta-glucosaminidase (NAG), and albumin 1 wk before and 1, 2, and 60 days after amalgam removal. The plasma mercury concentration increased significantly 1 day after removal. Sixty days later, significantly lower mercury levels were found in blood, plasma, and urine. The GFR values were similar before and after mercury exposure (mean 94 and 94 ml/min per 1.73 m2, respectively). No detectable effects occurred on excretion of NAG, beta 2-microglobulin, or albumin. It is concluded that no signs of renal toxicity could be found in conjunction with mercury released from amalgam fillings.

Acetylglucosaminidase↗
PubMed1996

Bone demineralization after renal transplantation: contribution of secondary hyperparathyroidism manifested by hypercalcaemia.

BACKGROUND: Renal transplantation patients often present signs and symptoms of bone disease. METHODS: In a cross-sectional study, dual-energy X-ray absorptiometry was used to examine bone mineralization in kidney transplantation patients. The contribution of secondary hyperparathyroidism manifested by hypercalcaemia was assessed. Twenty transplantation patients with long-standing (> 6 months) hypercalcaemia (> 2.6 Ca mmol/l) after transplantation, 21 normocalcaemic transplantation patients, and 20 healthy controls were examined. RESULTS: Bone mass density (BMD) was significantly less in the hypercalcaemic (1.00 +/- 0.1 g/cm2) and in the normocalcaemic groups (1.11 +/- 0.15 g/cm2) compared to the healthy controls (1.17 +/- 0.11 g/cm2). Decreased bone mineralization was evident shortly after transplantation and may well have been present before surgery. Females had less BMD compared to males and their BMD decreased further with age. CONCLUSION: Kidney transplantation patients with persistent hypercalcaemia comprise a risk group with regard to bone demineralization.

Adult↗
PubMed1995

Enzymuria in a population living near a cadmium battery plant.

OBJECTIVES: To study the body burden of cadmium and signs of tubular dysfunction in a rural population living near a closed nickel cadmium battery plant. METHODS: Cadmium and N-acetyl-beta-glucosaminidase (NAG) in urine were measured in 72 subjects who lived close to the plant. RESULTS: Residents living close to the plant had higher median urinary cadmium concentrations than those living farther away (1.01 v 0.46 nmol/mmol creatinine) and than a control group (0.2 nmol/mmol creatinine). There was a significant correlation between urinary cadmium and the excretion of NAG in urine as well as signs of tubular dysfunction in residents who excreted urinary cadmium above 0.5 nmol/mmol creatinine. CONCLUSION: Tubular dysfunction may appear in environmentally exposed subjects at lower cadmium body burdens than previously anticipated.

Acetylglucosaminidase↗
PubMed1995

Decreased glomerular filtration rate in solderers exposed to cadmium.

OBJECTIVES: to evaluate the degree of cadmium induced glomerular impairment and to assess the dose-response relation between cadmium dose and the prevalence of glomerular dysfunction. METHODS: A comparison of glomerular filtration rates (GFR) assessed by Cr-EDTA clearance was made in 42 solderers previously exposed to cadmium for at least five years. Blood and urine data were collected at health examinations in 1984, 1989, and 1993. Individual doses of cadmium were estimated by analysing cadmium in blood. RESULTS: Glomerular lesions induced by cadmium are irreversible and the GFR decreases with the degree of tubular damage. The GFR also decreases with cadmium dose and there is a dose-response relation between blood cadmium and prevalence of glomerular damage with 3.4% prevalence at blood cadmium concentrations below 50 nmol/l, 33% at blood cadmium concentrations between 50 and 75 nmol/l and 100% prevalence of glomerular damage when cadmium in blood exceeds 75 nmol/l. CONCLUSIONS: The kidney lesions induced by cadmium are irreversible and the prevalence of those lesions are dose dependent. There is also evidence of a dose related decrease in GFR even a long time after the end of exposure. Exposure to cadmium should therefore be minimised and workers exposed to cadmium should be examined regularly for many years after the end of exposure.

Cadmium↗
PubMed1994

Dose-response relations between urinary cadmium and tubular proteinuria in cadmium-exposed workers.

Cadmium in urine reflects the body burden in cadmium-exposed individuals. Urinary beta 2-microglobulin is frequently used as a marker of tubular proteinuria with an arbitrarily chosen value (34 micrograms/mmole creatinine) as the cut-off limit. Both this cut-off level and a lower limit (25 micrograms/mmole creatinine) were used in a study of the relationship between urinary cadmium and beta 2-microglobulin in 561 cadmium-exposed battery workers. There was a clear dose-response relation between the urinary cadmium level and the prevalence of tubular proteinuria ranging from 0.8% in the lowest exposure group, excreting less than 1 nmole cadmium/mmole creatinine, to 46.4% (50.0 for the lower cut-off level) in the highest exposure group with a mean urinary cadmium of 15 nmole/mmole creatinine. The relation between urinary cadmium and tubular proteinuria was also assessed using probit analysis. There was a 10% response at a urinary cadmium of 3 nmole/mmole creatinine. The impact of age on the dose-response relation was explored in two age groups with the cut-off point at 60 years of age, showing a 10% prevalence of tubular proteinuria at urinary cadmium levels of 1.5 nmole/mmole creatinine in this older age group and 5.0 nmole/mmole creatinine in the category under 60 years of age. The study thus indicates that the present health-based limit (10 nmole/mmole creatinine) proposed by the World Health Organization (WHO) is too high and it is suggested that a new limit should be set to 3 nmole/mmole creatinine.

Aged↗
PubMed1993

Incidence of renal stones among cadmium exposed battery workers.

The health effects of occupational exposure to cadmium were studied in a group of 902 workers employed for at least one year in a Swedish battery factory between 1931 and 1982. Data on air cadmium concentrations for different periods were combined with company employment records to obtain individual cumulative exposure estimates. A questionnaire including questions on the occurrence of kidney stones was sent to all 601 living workers and to the next of kin of 267 of the deceased workers. The response rate was 88%. 73 workers reported renal calculi that appeared after initial employment. A dose-response relation was found between cumulative exposure to cadmium and age standardised cumulative incidence. Incidence rate ratios (IRRs) were then computed for three exposure categories (< 250, 250- < 5000, and 5000 micrograms/m3 x years) standardised for calendar time, age, and smoking with the low exposure group as reference level. The IRRs were 1.0, 1.6 [95% confidence interval (95% CI) 0.7-3.4], and 3.0 (95% CI 1.3-6.8) respectively. beta 2 Microglobulin measurements were available for 33 workers who formed stones; 13 of these workers had tubular proteinuria (beta 2 microglobulin > or = 34 micrograms/mmole creatinine)--that is, a prevalence of 39%. There was also an indication of a steeper dose-response relation among workers with tubular proteinuria.

Age Factors↗
PubMed1993

Renal function impairment in workers previously exposed to cadmium.

Cadmium-induced renal effects were followed (1989) in 16 workers previously exposed to cadmium, who had been shown 5 years earlier to have had tubular damage; all but 1 worker had persistent tubular damage (beta 2-microglobulin > 60 micrograms/mmol creatinine). The mean glomerular filtration rate (GFR) decreased from 77.3 to 71.7 ml/min/1.73 m2, which is 2.0 ml/min more than would have been expected from aging only. There was a negative correlation between loss of tubular function (relative clearance of beta 2-microglobulin) and the ratio of observed versus reference GFRs in accordance with a 1984 study. The results confirm that cadmium-induced tubular damage is irreversible. They also suggest that the glomerular dysfunction after cadmium exposure is irreversible and progressive also after exposure stops. A nonsignificant correlation was found between cumulative cadmium exposure and decreased GFR.

Adult↗
PubMed1993

Fatal cadmium-induced pneumonitis.

A previously relatively healthy 78-year-old man was exposed to cadmium fumes during brazing with cadmium-containing silver solder. He developed severe chemical pneumonitis and died 25 d after exposure.

Aged↗