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Biomedical subjects

B Fellström

Publications and source records attributed to B Fellström.

At least 127 records · Page 7Linked to original sources

Dietary animal protein and urinary supersaturation in renal stone disease.

Eight stone-forming patients were given diets that were high (HPD) and low (LPD) in dietary animal protein, each for two weeks. Urines were collected by the end of each diet period. Urinary calcium, phosphate, urate and acids were increased on HPD whereas citrate and urine-pH decreased. The urinary supersaturation and thereby the risk of forming crystals and stones of uric acid and ammonium urate was increased on HPD. The supersaturation of calcium oxalate was unchanged, but the inhibition of calcium oxalate crystallisation may have become unfavourably affected.

Calcium↗

Urinary excretion of urate in renal calcium stone disease and in renal tubular acidification disturbances.

The 24-hour urinary excretion of urate was investigated in 467 consecutive stone formers - 350 males and 117 females - and 89 apparently healthy controls with no history of stone disease. Males had a higher urinary excretion of urate than females but there was no difference between stone formers and controls. Urinary urate decreased with advancing age. Patients with a proximal tubular acidification defect had a lower urate clearance than patients with a normal acidification of the urine. Patients with hyperuricosuria presented a higher frequency of stone operations but a lower stone episode rate than matched normouricosuric stone formers. Hyperuricosuria in combination with renal acidification defects was associated with the highest frequency of stone operations. Hyperuricosuric patients also had a higher excretion of calcium than normouricosuric patients. Hyperuricosuria is not a common feature of calcium stone disease but when present is associated with a more severe stone disease in terms of stone operations.

Acidosis, Renal Tubular↗

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↗

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↗

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↗

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↗

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↗

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↗

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↗

Urate metabolism and renal calcium stone disease.

Both hyperuricaemia and hyperuricosuria have been considered to be common in renal calcium stone disease. Abnormalities in serum or urinary urate was not more common in 450 investigated patients than in 90 healthy controls, but when present it was often associated with a more complicated course of the disease, particularly in combination with renal acidification defects. Hyperuricosuria was not explained by a renal tubular dysfunction of urate transport. A decreased urate clearance in proximal renal acidification dysfunction was associated with a high tubular reabsorption of filtered urate. Sodium urate or uric acid crystals did not adsorb urinary macro-molecular inhibitors of crystal growth other than in calcium oxalate solution, whereby a substantial loss of the inhibitory activity was detected. A high intake of dietary animal protein had a unfavourable effect, as several urinary constituents potentially important for calcium stone formation were aggravated. The urinary excretion of calcium and urate increased, whereas urine pH and urinary citrate decreased. It was concluded that the protein content of the diet may be an important factor contributing to the increase in the renal calcium stone disease in the industrialized world.

Acute Kidney Injury↗

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↗

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↗

Initial vector rates in differentiation between supraventricular extrasystoles with aberration and ventricular extrasystoles.

A computer method was constructed for analysing vector rates. Initial vector rates of QRS of ventricular extrasystoles (VES) and of aberrant supraventricular extrasystoles were compared. Bundle branch block (BBB) was used as a model for aberration. Spontaneous VES during heart catheterization and VES found by His-bundle recording represented the VES group. The VES were found to contain a longer average "activation time," i.e. the duration from the onset to the spatial amplitude maximum, than the BBB. The maximum amplitudes were similar. A method for calculating initial vector rate distribution was also developed. This showed a significantly higher proportion of fast rate components in BBB than in VES. The calculation of vector rate distribution gave advantages over the calculation of the mean initial vector rate, when considering electrocardiographic abnormalities such as preexcitation QRS or post-infarction Q waves. With a simple discriminatory analysis using initial vector rate distribution values, a 95% precision was obtained in differentiating between VES and BBB. It is concluded that a QRS from a supraventricular impulse focus with aberration has faster initial vector rates than a QRS from a ventricular focus and that this difference is useful in distinguishing between them.

Bundle-Branch Block↗