Biomedical subjects
G S Reusz
Publications and source records attributed to G S Reusz.
X linked hypophosphataemia: treatment, height gain, and nephrocalcinosis.
The clinical data of 18 patients with X linked hypophosphataemia were analysed retrospectively. The height data were expressed as SD scores. There was no difference in the final height of patients treated with vitamin D (or 1,25-dihydroxyvitamin D) and phosphate for at least two years (n = 12) and that of 16 hypophosphataemic family members who had never been treated. The mean final SD score (-2.07) of treated patients, however, was significantly higher than the value before treatment (-2.79), which indicated an average absolute height gain of 4-4.5 cm compared with the expected height values. Six of the treated patients developed ultrasonographically detectable nephrocalcinosis with normal renal function. The daily phosphate intake and excretion of patients with nephrocalcinosis was significantly higher than that of patients with normal renal morphology. There was no difference in the doses of vitamin D between the two groups. The average urinary calcium:creatinine ratio of the two groups was similar to and below the hypercalciuric 0.6 mmol:mmol limit. The group with nephrocalcinosis, however, had a higher incidence of hypercalciuric episodes than the group without nephrocalcinosis (12 in 130 observations compared with six in 334 observations, respectively). The benefits and risks of treatment of patients with X linked hypophosphataemia must be further evaluated. The high dose of phosphate seems to be an important factor in the development of nephrocalcinosis in this group of patients.
Data on the degree of saturation of urine with respect to calcium hydrogen phosphate in hypercalciuric children and renal stone formers.
Calcium hydrogen phosphate (CaHPO4) was considered as one of the main factors governing renal calculus formation. The degree of saturation with respect to this phase was therefore calculated in urines of 36 hypercalciuric children (20 absorptive, 16 renal subtype) with isolated hematuria, 10 renal stone patients, and 30 healthy controls. The effects of low calcium diet and hydrochlorothiazide treatment were also investigated in the patient groups. The results were compared to the widely used indicator of hypercalciuria (Ca/Cr ratio). Urines of both the hypercalciuric and the normocalciuric renal stone patients were saturated on basal conditions. On low calcium diet, 12 children of the absorptive hypercalciuric, 13 of the renal hypercalciuric and 7 of the renal stone-forming children had their urines in the saturated zone - irrespective of the evolution of Ca/Cr ratio. Thiazide normalized the activity product of CaHPO4 in all groups. The use of the Ca/Cr ratio as the sole parameter in the investigation of children with isolated hematuria and hypercalciuria or calcium nephrolithiasis seems to be insufficient; simultaneous determinations of the state of saturation of urines is recommended. This technique should also allow a quantitative assessment of the various therapeutic regimens recommended.
Effect of thiazide on urinary calcium excretion and hematuria in children with postglomerular hematuria.
The effect of short term hydrochlorothiazide therapy on urinary calcium excretion was compared to that of low calcium and a combined low calcium and low sodium diet in 30 children with postglomerular hematuria. On basal conditions 9 children were normocalciuric, 11 had absorptive, 10 renal hypercalciuria. The effect of thiazide treatment on the haematuria was also evaluated. Thiazide revealed to be more effective in reducing calcium excretion than low calcium diet alone in all groups (p less than 0.001 in normocalciuria; p less than 0.01 in both hypercalciuric groups). Combined low calcium--low sodium diet and thiazide treatment were equally effective in reducing calcium excretion in the hypercalciuric groups. On the first 3 days of thiazide treatment a slight increase of hematuria was observed; in the following period a significant decrease in the occurrence (p less than 0.01 in both hypercalciuric groups) and degree (p less than 0.01 in absorptive; p less than 0.02 in renal hypercalciuria) of hematuria was noted. These data furnish further evidence on the relation of hypercalciuria and post-glomerular hematuria.
Studies on the urinary calcium excretion in children with hematuria of postglomerular origin: effects of the variation of dietary calcium and sodium intake.
The effect of different dietary regimens and of an oral calcium (Ca) load was studied in 30 children with postglomerular hematuria, 8 of whom were renal stone formers. In addition we investigated the urinary inorganic phosphate complex composition in 12 of them, based on the principles of complex equilibria. Twenty-one of the 30 hematuric children with a urinary Ca/creatinine (Ca/cr) ratio of greater than or equal to 0.6 (mmol/mmol) were regarded as hypercalciuric. Low calcium intake normalised the ratio in 11 patients, fulfilling the definition of absorptive hypercalciuria, but not in the other 10 patients with renal hypercalciuria. Sodium restriction combined with low calcium diet induced a further significant decrease of the urinary Ca/cr ratio to a normal range in both forms of hypercalciuria (mean +/- SD: 0.325 +/- 0.112 in absorptive hypercalciuria; 0.533 +/- 235 in renal hypercalciuria). There was a significant difference in the composition of phosphate complexes between the 6 normocalciuric patients and the 6 children with renal hypercalciuria investigated. Lithogenic urinary phosphate complexes (CaHPO4, MgHPO4) were excreted by the latter group in a significantly higher amount under basal conditions. On the basis of these data sodium restriction added to low calcium diet could represent a dietary approach in preventing excessive calcium excretion in idiopathic hypercalciuria, and therefore renal stone formation.