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Biomedical subjects

B Fellström

Publications and source records attributed to B Fellström.

At least 109 records · Page 6Linked to original sources
PubMed1987

Ceftazidime as prophylactic treatment in renal stone surgery. Clinical evaluation and pharmacokinetics in renal tissue.

The effect of ceftazidime in surgery of renal stones associated with urinary tract infection was investigated and its pharmacokinetics in serum and renal tissue was compared in 14 patients (15 kidneys) operated on for renal calculi associated with multiple urinary tract infection. Two to four days preoperatively ureteric catheterization was performed to localize the level of the infection and 2 g of ceftazidime was given intravenously twice daily for 10 days. Renal biopsy, serum samples and in one patient renal lymphatic fluid were taken simultaneously for antibiotic assay. Urine cultures were performed at regular intervals pre- and postoperatively. Ten patients had bacterial growth in the stone-carrying renal pelvis. The same strain was found in the bladder as in the pelvis. Nine patients had sterile urine after 3-5 days of treatment. One patient with bilateral stones did not get sterile urine until after seven days of treatment. Bacterial growth was found in two out of six cultured stones obtained from patients with bacterial growth in the pelvis. The decreases in concentration of ceftazidime in serum and renal tissue seemed to be parallel. Slight reversible elevation of liver transaminases was noted in 5/14 patients. It is concluded that the concentration of ceftazidime in serum parallels that in renal tissue. Ceftazidime seems to be an effective prophylactic in renal stone surgery and the preoperative dose should be given close to the operation.

Adult↗
PubMed1986

Crystal inhibition: the effects of polyanions on calcium oxalate crystal growth.

The inhibition of calcium oxalate crystal growth by the glycosaminoglycans, chondroitin sulphates and heparin, by the low-molecular-weight heparin analogue pentosan polysulphate and by Tamm-Horsfall glycoprotein extracted from human urine, was measured by using a seeded crystal procedure and compared with the inhibition by pyrophosphate. It was found that the most pronounced inhibition was obtained with the polyanions with the highest charge density, i.e., heparin and pentosan polysulphate. Tamm-Horsfall glycoprotein caused an inhibition of a similar magnitude as urinary chondroitin sulphates. Urinary polyanions with a high affinity to Sepharose 4B were more efficient inhibitors than those with a low or no affinity to the gel. It is concluded that urinary polyanions are important inhibitors of calcium oxalate crystal growth and that the potency of inhibition increases with the charge density.

Anions↗
PubMed1986

Binding of glycosaminoglycans to sodium urate and uric acid crystals.

The binding of heparin, chondroitin sulphate and the low molecular weight heparin analogue pentosan polysulphate to sodium urate and uric acid crystals was studied by the use of radioactively labelled glycosaminoglycans were used in the binding step, and varying amounts of unlabelled glycosaminoglycans for the competition experiments. The experiments were carried out in 140 mmol/l NaCl at pH 6, with or without 5 mmol/l CaCl2 in the solution. A reversible and almost complete binding of heparin and chondroitin sulphate to sodium urate crystals did occur in the presence of calcium, whereas pentosan polysulphate bound incompletely. The binding was much less pronounced in the calcium-free conditions. Uric acid crystals did not bind any of the three inhibitors, not even with calcium present. The clinical relevance depends on whether sodium urate microcrystals are present in the urine of calcium stone patients, to cause a binding and thereby a masking or inactivation of these inhibitors in the urine, which seems to be possible in the presence of calcium. However, the potential of pentosan polysulphate for the treatment of calcium stone patients does not seem to be at risk from this effect.

Binding, Competitive↗
PubMed1986

Enzymatic determination of urinary chondroitin sulphate: applications in renal stone disease and acromegaly.

A method was developed for the determination of urinary chondroitin sulphate (CS), including dermatan sulphate and chondroitin 4 and 6-sulphates, using an enzymatic degradation with chondroitinase-ABC followed by precipitation with Alcian blue, whereby CS was determined as the difference between undigested and chondroitinase digested material. The method was linear in the range 0-100 mg l-1 with a detection limit of 1 mg l-1 and allowed determinations on small urine volumes without pretreatment of the urine. It could be demonstrated that males excreted more CS than females, and growing children had the highest urinary content of CS. Renal calcium stone formers did not differ from healthy controls in urinary CS. Patients with acromegaly had a higher excretion of CS compared with controls. There was also, in these patients, a positive correlation between the serum growth hormone levels and the urinary CS, indicating that CS-excretion may be an estimate of the activity of the pituitary disorder.

Acromegaly↗
PubMed1985

Family history of renal stones in recurrent stone patients.

A survey was carried out on the family history of renal stones among 380 patients in an out-patient stone clinic, most of whom had experienced frequent recurrences. In 55.4% of patients at least one first-degree relative had experienced renal stones. A positive family history was more common in females (64.7%) than in males (51.0%) and was particularly apparent in those who had multiple recurrences. It was also significantly more common in female patients with evidence of renal tubular defects (incomplete forms of renal tubular acidosis). Among the ordinary stone patients 18% of the fathers and 8% of the mothers had also formed renal stones. The corresponding figures for female stone patients with renal tubular defects were 40 and 33% respectively. These findings indicate that tubular dysfunction could be an inherited trait that predisposes to the formation of renal stones. Hypercalciuria or hyperuricosuria was not over-represented among stone formers with a positive family history.

Acidosis, Renal Tubular↗
PubMed1985

Allopurinol treatment of renal calcium stone disease.

Thirty-one calcium stone patients were treated with 300 mg allopurinol daily during a mean follow-up period of 2 years. They were also given advice on diet and fluid intake. The effects on the recurrence rate of stones were compared with the effects on the recurrence rate in 43 calcium stone patients who were given similar advice on diet and fluid intake but were not treated with allopurinol. In both groups there was a reduction in the recurrence rate but no difference between patients treated with allopurinol and the control group. Some patients with only hyperuricosuria prior to treatment seemed to benefit from allopurinol treatment, whereas those with hypercalciuria continued to form stones with the same frequency. Allopurinol treatment in calcium stone disease appears less effective than treatment with thiazides, magnesium hydroxide or orthophosphate.

Adolescent↗
PubMed1985

The effects of methenamine-hippurate upon urinary risk factors for renal stone formation.

Among the various treatments for renal calcium stone disease, none has been documented to reduce urinary oxalate. Methenamine-hippurate (Hiprex) has been used extensively in the treatment of urinary tract infections and from micropuncture studies in the rat, using para-aminohippurate, it could be expected to reduce the renal secretion of oxalate. A daily dose of 3 g was given orally to 15 healthy subjects for 2 weeks. However, there was no net decrease in the urinary excretion of oxalate, but a risk index based on the urinary content of calcium, magnesium, oxalate, citrate and urine became reduced during treatment. The urinary inhibition of calcium oxalate crystal growth was unaffected. It is concluded that there may be a potential in methenamine-hippurate for the treatment of calcium stone disease, which can only be evaluated, however, by a clinical trial in stone patients.

Anti-Infective Agents, Urinary↗
PubMed1985

Tubular proteinuria in renal calcium stone formers.

The incidence of tubular proteinuria measured as urinary excretion of beta 2-microglobulin was evaluated in 68 consecutive renal calcium stone formers, 14 of whom had impaired urinary acidification capacity. During normal conditions 13% of these stone formers had tubular proteinuria. There was no statistical difference in the incidence of tubular proteinuria between subgroups with proximal or distal acidification defects. During transient metabolic acidosis induced by an ammonium chloride load a pronounced increase in beta 2-microglobulin excretion was noticed in all patient groups but especially in those with urinary acidification defects. In stone formers with normal acidification capacity the degree of acidosis-induced beta 2-microglobulinuria was moderate but a small group of patients exhibited a large urine excretion of beta 2-microglobulin. This finding may reflect a latent tubular defect of importance for stone genesis.

Acidosis↗
PubMed1985

Is muscle lipoprotein lipase inactivated by ordinary amounts of dietary carbohydrates?

Lipoprotein metabolism was investigated in 12 patients, healthy except for renal stone disease, who received a high-protein experimental diet for 2 weeks under metabolic ward conditions. The results were compared with those after 2 weeks on a control diet of ordinary composition. The patients were randomly allocated to begin with the control or experimental diet. The energy contributions from protein, carbohydrate and fat were 12, 48 and 41 per cent in the control diet and 29, 31 and 41 per cent in the experimental diet, respectively. Fasting concentrations of very-low-density lipoprotein (VLDL) triglycerides and cholesterol were lower with the high-protein than with the control diet (0.69 vs 1.4 mmol/l, P less than 0.0001, and 0.33 vs 0.47 mmol/l P less than 0.01, respectively). High-density lipoprotein cholesterol tended to be higher (0.05 less than P less than 0.10) with the high-protein diet. Lipoprotein-lipase (LPL) activity in skeletal muscle and the fractional catabolic rate constant of an intravenous fat tolerance test were higher with the high-protein than with the control diet (38 vs 21 mU/l, P less than 0.01, and 5.1 vs 3.6 mU/l, P less than 0.001, respectively). Neither fasting blood glucose, intravenous glucose tolerance nor insulin concentrations differed between the two dietary periods. These findings indicate that an 'ordinary' intake of refined carbohydrates has an inhibitory effect on the muscle LPL activity, thereby increasing the VLDL level and slightly decreasing the level of high-density lipoproteins, which may be of relevance for the atherosclerotic process.

Adult↗
PubMed1984

Endemic goitre in the Darfur region (Sudan). Epidemiology and aetiology.

In the Darfur region of Sudan, 85.5% of 7134 subjects examined, mainly school children, had goitre and in 23.9% the goitre was large (stage II or III). The prevalence of goitre was high in prepubertal children of both sexes and in adult females. There was a higher frequency of large goitre in the rural than in the urban areas (40.9 and 11.4%, respectively). In Port Sudan on the Red Sea Coast the goitre rate was 13.5% among 7697 schoolchildren, but here visible goitre was extremely rare. Of the subjects from Darfur, 54.5% excreted less than 50 micrograms of iodine/g creatinine, while all except one subject in Port Sudan excreted more than that. The median urinary excretion of iodine was 45.3 micrograms/g in subjects from Darfur and 171.2 in those from Port Sudan, the mean value being significantly lower in the former than in the latter (p less than 0.001). The iodine content of all water samples was very low, and the contents of calcium and fluoride were not high. Other goitrogenic factors could not be excluded. However, iodine deficiency is the major cause of goitre in the Darfur region and a prophylactic programme is urgently needed.

Adolescent↗
PubMed1984

Effects of physical exercise on serum calcium and parathyroid hormone.

The effects of physical exercise on plasma ionized calcium, total serum calcium and parathyroid hormone (PTH) concentrations were evaluated in healthy subjects submitted to work on an ergometer bicycle. When the workload was increased stepwise there was a significant increase (P less than 0.001) in the calcium concentrations (ionized calcium from 1.13 +/- 0.03 (SD) to 1.24 +/- 0.03 mmol 1(-1) and total calcium from 2.35 +/- 0.07 to 2.48 +/- 0.07 mmol 1(-1] when the workload exceeded approximately 65% of the estimated maximum--i.e. a load that caused accumulation in blood of lactic acid. The rise in plasma ionized calcium was, therefore, presumably largely attributed to the acidosis but reduction of plasma volume and influx from extracellular sources might also have contributed. Beta blockade (with oral intake of propranolol) reduced physical capacity, shortened the duration of work and caused less acidosis. These factors were probably responsible for a smaller rise in ionized calcium during beta blockade (7 +/- 4%) than in control studies (21 +/- 5%) without medication in subjects examined during short-term maximal exercise. Long-term (1 h) steady-state work which caused fatigue without producing lactic acidosis did not affect the calcium concentrations. Despite the effects of work on calcium levels there was no discernible suppression of the PTH concentrations. This might have been due to a concomitant stimulation of PTH secretion by work.

Adult↗
PubMed1984

Effects of high intake of dietary animal protein on mineral metabolism and urinary supersaturation of calcium oxalate in renal stone formers.

The metabolic effects of a high protein diet (HPD) were studied in eight patients with idiopathic recurrent calcium oxalate stones. On the HPD there was a 35% increase in urinary calcium concomitant with increased excretion of cyclic AMP and hydroxyproline. These findings point to an enhanced resorption of bone, possibly secondary to increased renal loss of calcium. The urinary citrate decreased by 25% along with reduced serum standard bicarbonate and urinary pH. The high formation of acid metabolites might also have adverse effects on calcium balance and bone. Urinary oxalate excretion was not affected nor were there any significant changes in the calculated urinary supersaturation of calcium oxalate, if changes in urinary citrate, pH, sulphate, sodium, phosphate and volume were also considered. This study suggests that the possible negative influence on the propensity to form renal stones of a diet rich in animal protein is probably due to reduced urinary inhibitory activity.

Adult↗
PubMed1983

Ambulatory diagnostic evaluation of 389 recurrent renal stone formers. A proposal for clinical classification and investigation.

389 consecutive renal stone formers (275 males, 114 females) were investigated in an out-patient stone clinic. Renal tubular acidosis (RTA) was found in 83 patients (22%). Proximal RTA was twice as common as the distal tubular type. The acidification defects were exclusively of the incomplete form with normal basal blood acidbase status. Main diagnoses besides RTA were primary hyperparathyroidism (3.5%), medullary sponge kidney (3.5%), infection induced stones (3%), urate stones (2%), intestinal disorder (1.5%) and cystinuria (0.5%). The metabolic evaluation was mainly based on 24 h urine sampling on a free diet. In 248 patients (64%) no distinct abnormality was considered to be primarily responsible for stone formation. Clinical and biochemical analysis of these so-called idiopathic stone formers disclosed a male preponderance (80%) and, compared to a non-stone-forming control group, a higher urinary calcium excretion, yet with a considerable overlap between the two groups. Hyperuricosuria and hyperoxaluria were rare findings. The conclusion of the study is given as a proposal for clinical classification and ambulatory investigation of renal stone formers.

Adolescent↗
PubMed1983

Uricemia and urinary acidification in renal calcium stone disease.

Serum urate concentrations were determined in 487 consecutive patients with stone disease and in 89 controls. Male controls had higher concentrations than female controls but men and women with stones had lower concentrations than controls. Renal acidification defects, incomplete and complete forms, were found in 25 per cent of the patients with stones, with the highest frequency in patients with hyperuricemia. Patients with proximal renal acidification defects had a higher serum urate concentration than patients with normal acidification of the urine. The urinary excretion of urate was higher in hyperuricemic than in normouricemic patients but lower in patients with hyperuricemia and renal acidification defects than in those with hyperuricemia and normal acidification of the urine. This finding indicates that underexcretion rather than overproduction contributes to the higher serum urate concentration in patients with renal acidification defects. Stone patients with high serum urate levels, especially in combination with renal acidification defects, had more severe stone disease and underwent more operations than other patients with stones. Thus, hyperuricemia does not appear to be a common feature in patients with calcium stone disease, although it is associated with formation of large stones for unknown reasons.

Adult↗
PubMed1983

The influence of a high dietary intake of purine-rich animal protein on urinary urate excretion and supersaturation in renal stone disease.

1. Eight recurrent renal stone-forming patients were housed in a metabolic ward and fed on a low (LPD) and a high (HPD) animal protein diet, which were isoenergetic. Metabolic studies were made after 2 weeks on each diet. 2. There was a 90% increase in urinary urate on HPD compared with LPD, whereas serum urate did not change consistently. 3. The urinary acid excretion increased by 200%, including a 100% increase in ammonium ion excretion. A fall in urine pH by 0.9 unit was also seen. 4. The calculated ion activities of the urines revealed a profound increase in the uric acid supersaturation, from undersaturation to supersaturation, and in some cases even surpassing the formation product ratio. The ammonium urate supersaturation also increased. The sodium urate supersaturation was unchanged, despite an induced natriuresis. 5. The risk of forming uric acid or ammonium urate crystals or stones in the urine was increased on a high protein diet, whereas the risk of forming sodium urate crystals was no greater than on a low protein diet. 6. As uric acid and ammonium urate crystals under certain conditions may adsorb a macromolecular fraction of the human urine, which inhibits calcium oxalate crystal growth, it is proposed that this mechanism, along with a decrease in urine pH, may also interfere with the inhibitory activity of calcium oxalate crystal growth and aggregation.

Adult↗