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Biomedical subjects

U Backman

Publications and source records attributed to U Backman.

69 records · Page 4Linked to original sources
PubMed1980

Clinical effects of parathyroid surgery in normocalcaemic patients with recurrent renal stones.

Among 52 patients with recurrent renal calcium stones submitted for neck exploration 12 had adenomas, 23 hyperplasia and only 17 histologically normal parathyroid glands. These patients were selected for surgery despite a normal mean value of the total serum calcium concentration because they had, in most cases, indirect evidence of parathyroid hyperfunction such as intermittent hypercalcaemia (in 25 of the patients), hypercalciuria or a pathological response to calcium infusion. It is suggested that the patients with adenomas suffered from primary hyperparathyroidism (HPT), which however did not cause persisting hypercalcaemia. It seems likely that parathyroid hyperplasia either was a mild or an early form of primary HPT or secondary to increased calcium losses. In this study, no single laboratory feature could clearly separate the different groups. None of the patients with adenomas formed any new stone during follow-up (2-7 years) and also 40% of those with hyperplasia appeared to experience benefit from surgery. This benefit was more common in those with occasionally raised serum calcium values. In cases with borderline hypercalcaemia HPT is common and is cured by parathyroidectomy. However, in clinical practice the differential diagnosis may be difficult. In cases without firm evidence of HPT a conservative approach is favoured. Thiazides appear to reduce the stone recurrence rate in most euparathyroid patients and will probably help to unmask borderline HPT in recurrent renal stone formers.

Adenoma↗
PubMed1979

Effects of therapy with bendroflumethiazide in patients with recurrent renal calcium stones.

Forty-four patients with recurrent formation of calcium-containing renal stones were treated with bendroflumethiazide for at least 2 years. Prior to treatment each patient had formed, on average, one stone per year for 8 years; during treatment only 4 patients formed new stones. A reduction in urinary calcium excretion was seen in almost all patients irrespective of their initial urinary calcium level. The apparent clinical benefit was not related to pre-treatment urinary electrolyte levels. Side effects were slight: one patient developed symptomatic hyperuricaemia and in one case sustained hypercalcaemia was found. Long-term treatment with thiazides appears to be a safe and effective method for the prevention of recurrent calcium stones.

Bendroflumethiazide↗
PubMed1978

HLA and kidney stone disease.

Normocalcemic patients with recurring kidney stones were HLA typed. 54 patients with an idiopathic high urinary excretion of calcium but without signs of renal tubular defect showed a B27 phenotype frequency which was more than twice that of the controls and a CW1 frequency that was doubled. After correction for the number of tested HLA specificities the increase was not significant. 35 patients with renal tubular acidosis and 16 patients with no metabolic diagnosis had no deviant HLA antigen distribution.

Acidosis, Renal Tubular↗
PubMed1978

Tubular defects in patients forming calcium-containing stones.

The study of renal function, primarily the tubular function, in 55 patients with idiopathic, recurrent renal stones showed a large number of abnormalities. 49% of the patients, especially the women were affected. The most common defect was a reduced acidification capacity of varying degrees of severity in 64% of the woman and in 20% of the men. Impairment of the acidification capacity of the distal tubule was found in 18% and of the proximal tubule in 11% of the patients. Inability to dilute the urine after water loading was found in 17% and tubular proteinuria also in 17% of the patients. Most patients with an impaired tubular function had a severe stone disease. The defects in acidification and dilution capacity ought to be of pathogenetic importance for stone formation and should be considered in the selection of preventive therapy.

Adult↗
PubMed1976

Kidney function during hydropenia nad water diuresis in patients with idiopathic recurring nephrolithiasis.

The kidney function of 41 patients with idiopathic recurring kidney stones was investigated by inulin- and PAH-clearances and by measuring the excretion of electrolytes during hydropenia and water diuresis. All patients had normal inulin- and PAH-clearances and normal concentrating capacity as indicated by free water reabsorption (Tc H2O). Seven patients, all of whom had previously been found to have low excretion of magnesium in urine, were unable to dilute their urine. During water diuresis these patients also had lower osmolar clearance and lower excretion of sodium than the other patients. A defective dilution capacity may be of pathogenetic significance for stone formation; the causes of the defect, however, are not clear.

Adult↗
PubMed1976

A short duration renal acidification test.

As earlier investigations of renal acidification capacity were poorly standardized it was considered important to develop a clinically useful method. The ability of the kidneys to acidify urine was studied in 19 normal persons by short ammonium chloride loading. Ammonium chloride was given in a dose of 150 mmol/m2 body surface in one of four different ways: whole tablets, crushed tablets, capsules and in solution. The degree of acidosis developed in each subject was measured in arterialized capillary blood samples. Urine was analysed for pH, titratable acid, ammonium ions (TA and NH4+) and phosphate. The excretion of TA, NH4+ and phosphate increased with the degree of acidosis in blood whilst urine pH decreased. The critical level appeared to lie around a base excess of -6 mmol/l below which all subjects could acidify their urine to a pH below 5.0. For clinical applications a frame of reference with tolerance limits is given for acidification capacity related to the degree of acidosis expressed as base excess.

Acidosis, Renal Tubular↗
PubMed1976

Urine acidification capacity in renal stone formers.

A short ammonium chloride loading test was used in the investigation of renal acidification capacity of 51 patients with idiopathic recurrent renal stones containing calcium. Many of these patients had suffered from prolonged and severe stone disease. In 31% of the patients an impaired acidification with varying degrees of severity was found. Eight patients had defects suggesting distal renal tubular acidosis (RTA). One case with the complete and two cases with the incomplete form of RTA were found. A further five patients, who were all able to acidify their urine to an acid pH, had milder defects in the excretion of titratable acid and/or ammonium ions which may indicate an early stage of distal tubular acidosis. Six patients were suspected of having a proximal acidification defect, as they showed delayed responses to the ammonium chloride induced acidosis.

Acidosis↗
PubMed1976

Bicarbonate re-absorption in renal stone patients with acidification defects.

A pathological renal response to ammonium chloride loading was found to be common in renal stone formers. In order to elicit further information about the impaired acidification capacity eight patients were investigated by bicarbonate loading. One patient with a mild acidification defect had normal tubular re-absorption of bicarbonate. Five of these eight patients with suspected proximal acidification defect and two patients with impaired distal acidification were found to have a low bicarbonate threshold and an increased, fractionated, bicarbonate excretion at a normal plasma bicarbonate level. Four of the patients with suspected, proximal, acidification defect reached a maximal re-absorption of bicarbonate (Tm) that was low, while three patients did not reach a Tm. These three factors indicate increased bicarbonate wastage from the kidneys. A constantly alkaline urine, such as exists in patients with proximal acidification defect may give rise to an increased risk of the precipitation of renal stones - primarily calcium-phosphate stones.

Acidosis, Renal Tubular↗
PubMed1976

Urinary excretion of beta2-microglobulin in renal stone patients under normal conditions and during acidosis and alkalosis.

The urinary excretion of beta2-microglobulin was studied under normal conditions and during acidosis and alkalosis in 65 patients with renal stones. Eleven patients were studied under two of these conditions. Four out of 51 patients examined under normal conditions had an increased excretion of beta2-microglobulin in their urine. Four out of five patients with distal acidification defects were found to have an increased excretion of beta2-microglobulin during induced acidosis. During alkalosis, four out of eight patients with acidification defects increased their excretion of the protein. The tubular proteinuria that could be provoked during acute acidosis and alkalosis was considered to be secondary to changes in the acid-base status and may indicate a renal tubular defect.

Acidosis↗