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Biomedical subjects

U Backman

Publications and source records attributed to U Backman.

At least 55 records · Page 3Linked to original sources
PubMed1982

Effects of bendroflumethiazide on urate metabolism during treatment of patients with renal stones.

Treatment with bendroflumethiazide (2.5 mg, twice daily with potassium supplements) in 63 patients with calcium-containing renal stones for a minimum period of 1 year (average duration of treatment 2.6 years) increased the serum urate values in all patients with an average of 90 mumol./l. (conversion factor: 1 mmol. urate = 183 mg.). Despite this the mean urinary urate excretion was unchanged. In the individual patient a systematic effect of therapy was evident since in patients with low pretreatment values the thiazide increased the urate output while in those with the highest levels before therapy it caused a reduction. In most patients there was a reduction of the urate clearance during therapy, which was most evident in those with the highest pretreatment clearance values. In patients with incomplete types of renal acidification defects the same effects were seen on urate metabolism during thiazide treatment as in the other, idiopathic, stone formers. Although the possible role of urate in calcium stone formation has not been definitely settled this study shows that thiazides do not cause hyperuricosuria and hence their beneficial effects on calcium excretion are not counteracted.

Adult↗
PubMed1982

Inhibitory activity of human urine on calcium oxalate crystal growth: effects of sodium urate and uric acid.

1. Freshly voided urine from healthy subjects was pooled and ultrafiltered (10,000 daltons). The ultrafiltrable and the macromolecular portions were preincubated with calcium oxalate, uric acid and sodium urate crystals and the effects on the inhibitory activity of calcium oxalate crystal growth assessed by monitoring the disappearance of [14C]oxalate from the solution. 2. The inhibitory activity of the ultrafiltrate was higher than that of the urinary macromolecular fraction. Both uninhibited and inhibited crystal growth processes followed second-order kinetics. 3. Calcium oxalate crystals adsorbed almost all the urinary macromolecular inhibitors whereas sodium urate or uric acid crystals adsorbed only 10-20%. 4. In the presence of a metastable solution of calcium oxalate, the incubation of the urinary macromolecular fraction with sodium urate crystals caused a pronounced reduction in the inhibitory activity. A similar effect was seen with uric acid crystals, but to a lesser degree. 5. We conclude that the effect of sodium urate or uric acid crystals alone on naturally occurring urinary macromolecular inhibitors of calcium oxalate crystal growth is weak, but that in the presence of metastable calcium oxalate this is greatly enhanced. A substantial adsorption of the inhibitors on to the crystals is suggested, possibly secondary to epitaxial growth of calcium oxalate on the surface of the urate crystals.

Calcium Oxalate↗
PubMed1982

Effects of magnesium hydroxide in renal stone disease.

Magnesium is a known inhibitor of the formation of calcium oxalate crystals in the urine and was proposed for prophylactic treatment in renal stone disease as early as the 17th and 18th centuries. We have treated 55 patients with recurrent renal calcium stone disease without signs of magnesium deficiency (normal serum magnesium, urinary magnesium, intracellular magnesium in muscle biopsies, gastrointestinal absorption of 28Mg, and magnesium loading test) from our outpatient stone clinic for up to four years with 500 mg Mg2+, in the form of Mg(OH)2, daily. The mean stone episode rate before therapy was 0.8 stones/year/patient. Forty-three recurrent renal calcium stone-formers without medical therapy served as controls. Serum magnesium increased initially but after one year returned to the pretreatment level. Urinary magnesium excretion increased promptly and remained elevated during the follow-up period. The urinary calcium excretion remained unchanged. The magnesium/calcium ratio in the urine increased and approached a value earlier found in healthy subjects without stone disease. Urinary citrate increased on therapy when analysed after three years of treatment. The mean stone episode rate decreased from 0.8 to 0.08 stones/year on treatment and 85% of the patients remained free of recurrence during follow-up, whereas 59% of the patients in the control group continued their stone formation. Side effects were few. Magnesium treatment in renal calcium stone disease is effective with few side effects. No clinical signs of magnesium excess were observed.

Adult↗
PubMed1982

Renal handling of urate in patients with calcium stone disease.

The renal handling of urate was investigated in 28 recurrent calcium stone formers and 12 healthy controls. 12 patients were hyperuricosuric and 16 patients had incomplete proximal or distal acidification defects. Measurements of the glomerular filtration and the tubular reabsorption of filtered urate were made through the pyrazinamide (PZA)-suppression test of urate secretion. Hyperuricosuria could not be explained by defects in the renal handling of urate. Patients with proximal acidification defects had a higher tubular reabsorption of filtered urate than the other subjects. Tubular reabsorption of filtered urate was inversely correlated, and filtered urate escaping reabsorption positively correlated to the 24-hour excretion of urate. In contrast, the PZA-suppressible fraction of urate excretion, which is the net effect of tubular secretion and post-secretory reabsorption and thought to be the main regulator of urate excretion, was not correlated to the 24-hour excretion of urate. It is concluded that the renal handling of urate is basically normal in calcium stone disease, whereas minor deviations may co-exist with renal tubular acidification dysfunction.

Calcium↗
PubMed1981

Calcium and magnesium metabolism during long-term treatment with thiazides.

The effects of treatment with bendroflumethiazide (2.5 mg twice daily with potassium supplements) on mineral metabolism were evaluated in 111 patients followed for a minimum period of one year. The urinary calcium decreased with approximately 30% irrespective of the pretreatment levels and remained on this lower level during follow-up. This reduction of urinary calcium was associated with a reduction of the intestinal calcium absorption. The serum calcium increased slightly in most of the patients and in 10% of them hypercalcaemia could be demonstrated at some time. In most of these cases the hypercalcaemia was slight and temporary and when sustained rapidly reversed upon withdrawal of therapy. Initially the urinary magnesium excretion increased but after two years' treatment the values were no longer raised. The serum magnesium levels showed a continued decrease during follow-up but in muscle biopsies, performed after three years treatment, no magnesium deficiency was evident. During treatment also the fasting urinary calcium was reduced, suggesting reduced bone resorption, but urinary hydroxyproline was unchanged. The serum PTH levels appeared unchanged during follow-up. Thiazides appear to cause a persisting reduction of calcium excretion, which is compensated by reduced intestinal uptake, whereas parathyroid function is unaffected. Although there was a gradual decline of serum magnesium, magnesium deficiency was not demonstrated.

Adult↗
PubMed1981

Phosphate metabolism in renal stone formers. (II): Relation to renal tubular functions and calcium metabolism.

Patients with idiopathic recurrent calcium nephrolithiasis (n = 57) and controls (n = 16) were investigated regarding the relationship between renal phosphate handling, other renal tubular functions and calcium metabolism. Incomplete renal tubular acidosis (RTA) was disclosed in 13 patients. RTA patients together with stone formers with normal renal acidification capacity (SF) exhibited low values for serum phosphate and renal threshold phosphate concentration (TmP/GFR) compared with controls. TmP/GFR was lower in RTA patients than in stone formers with normal renal acidification. Hypercalciuria of the absorptive type with normal serum PTH and urinary cAMP concentrations was a common finding in both stone patient groups, whereas no patient displayed unequivocal evidence of parathyroid hyperfunction. Fractional excretion of sodium was raised in both SF and RTA patients compared with controls. There was a positive relationship between the fractional excretion of phosphate and sodium in all subjects as a group. TmP/GFR was negatively correlated to fractional excretion of sodium. Twenty-three percent of RTA patients and 8% of SF displayed tubular proteinuria which often was associated with low TmP/GFR levels and enhanced natriuresis. It is concluded that a defective renal tubular phosphate handling is common in calcium stone formers and often associated with signs of other tubular dysfunctions. The altered phosphate handling seems to be unrelated to hypercalciuria.

Adolescent↗
PubMed1981

Phosphate metabolism in renal stone formers. (I): Indices of phosphate handling in calcium stone patients and healthy subjects.

Healthy subjects (n = 112) and patients with recurrent idiopathic calcium nephrolithiasis (n = 44) were evaluated regarding various indices of phosphate handling: serum phosphate concentration, renal tubular reabsorption of phosphate, index of phosphate excretion and renal threshold concentration for phosphate (TmP/GFR). The 24 hour and fasting 2 hour urinary phosphate excretions were similar in the two groups and the index of phosphate excretion was higher in stone formers, but for all the other variables lower mean values were found in the group of stone formers than in the group of normal subjects. The renal tubular capacity for reabsorption of phosphate (as evaluated by the different indices) appeared to decrease with advancing age concomitant with a reduction of the serum phosphate concentration. When age- and sex-matched subjects from the two groups were compared with regard to the phosphate variables lower values were still found in the group of stone forming subjects. This study gives support to earlier observations that renal stone formers tend to waste phosphate by and altered renal handling.

Absorption↗
PubMed1980

Biochemical and clinical effects of the prophylactic treatment of renal calcium stones with magnesium hydroxide.

Prophylactic treatment with magnesium hydroxide ws instituted in 56 consecutive cases with renal calcium stones. The patients had been investigated previously with regard to the magnesium metabolism. The urinary magnesium excretion increased promptly and remained on a higher level during treatment. No changes were observed in the serum or urinary calcium concentrations. Most patients have undergone treatment for at least 2 years and 45 have been free of recurrences of formations of new stones. The mean stone episode rate during treatment was 0.03 stones per year compared to 0.8 stones per year before treatment was instituted. The natural history of stone disease also was followed in 34 patients with stones who had received no prophylactic therapy and 15 have experienced recurrences after 2 years. Therefore, in comparison, treatment with magnesium hydroxide appeared to reduce the recurrence rate. Apart from minor gastrointestinal discomfort no adverse effects were observed during treatment.

Adult↗
PubMed1980

Treatment of recurrent calcium stone formation with cellulose phosphate.

Sodium cellulose phosphate was given to 35 patients for recurrent formation of calcium-containing stones. During therapy urinary calcium decreased by 40% in the first month and remained at this lower level. In addition, urinary magnesium excretion was reduced and the urinary magnesium/calcium ratio remained unaffected. In these patients, who mostly had had calcium oxalate stones, the prophylactic effects of sodium cellulose phosphate was poor, with a 47% recurrence rate after 2 years. This lack of prevention, despite the significant reduction of the urinary calcium, is assumed to be owing to the effects of treatment on magnesium and oxalate metabolism. Side effects were common, mainly consisting of moderate gastrointestinal discomfort, and caused withdrawal of treatment in 8 patients. This fact contributes further to our opinion that sodium cellulose phosphate is not the drug of choice in cases of calcium oxalate stone formation.

Adult↗
PubMed1980

Incidence and clinical importance of renal tubular defects in recurrent renal stone formers.

Renal tubular function was studied in 318 consecutive recurrent renal stone formers. Impaired acidification capacity was found in 19% of the patients, and tubular proteinuria in 13% of the patients. Most of the patients with defective acidification of the urine had the incomplete form of renal tubular acidosis (RTA), rpoximal and distal defects being equally common. The incidence of impaired acidification was much higher in the female (38%) than in the male (13%) stone formers. A further analysis of the clinical picture in patients with acidification defects revealed a more severe stone disease than among other stone formers. Characteristic findings were an early onset, multiple recurrences were an increased need for surgery. Stone analyses showed a high frequency of calcium phosphate stones. Investigations of renal tubular functions appear to be a valuable adjunct in the evaluation of recurrent renal stone disease.

Acid-Base Equilibrium↗
PubMed1980

Kidney stone disease. Experiences from Uppsala, Sweden.

In summary, several biochemical investigations give valuable information about a possible etiological explanation for the stone formation but to get a more complete picture of the individual stone former, some clinical aspects should be considered such as heredity for stone disease and the age of onset. All these factors are relevant when considering prophylactic treatment to stone formers.

Adult↗
PubMed1980

Magnesium metabolism in renal stone disease.

Magnesium metabolism in 70 consecutive patients with renal stone disease was evaluated and compared with that of a control group matched for age and sex. Serum and urinary magnesium values were not different in the two groups, but magnesium output was greater in males than in females. Stone-formers excreted more calcium in their urine than did controls, and the urinary calcium and magnesium values for both groups were positively correlated. For both groups, the magnesium/calcium ratio in the urine declined with increasing calcium values but was lower in stone-formers than in controls for corresponding calcium values. Intestinal magnesium uptake was the same in both groups. Magnesium deficiency was not evident among stone-formers as assessed by the determination of the magnesium content in muscle specimens or by the retention of an intravenously administered magnesium load. Although stone-formers were not found to display any features of magnesium metabolism that were different from those in the control group, their lower urinary excretion of magnesium in relation to calcium may be a factor in their increased stone-forming propensity.

Adult↗