Biomedical subjects
Publications and source records attributed to E S Moore.
Pediatricians frequently have faced one or more of an array of lower urinary tract symptoms without obvious cause. Now, with increasing recognition, many of these diagnostic enigmas have been ascribed to idiopathic hypercalciuria. This article reviews this "new" clinical syndrome, attempts to clarify pathophysiology, and selects patients for therapeutic intervention.
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During intrauterine life, fetal mineral accretion depends on active transfer from mother to fetus by the placenta. To evaluate the role of fetal production of 1,25-dihydroxyvitamin D in regulation of fetal phosphorus, calcium, and parathyroid homeostasis, studies were performed in ewes and their fetal lambs. Fetal nephrectomy caused a rise in fetal serum phosphorus and a fall in total calcium 5 days after nephrectomy. Fetal blood ionized calcium also fell and serum parathyroid hormone rose. In sham-nephrectomized fetuses, all four measurements were unchanged compared to control values. Simultaneous maternal values of ionized calcium were normal in control and nephrectomized fetuses. Fetal ureteral severance and drainage of urine into the fetal peritoneal cavity produced none of the effects of fetal nephrectomy. Daily intravenous injection of 1,25-dihydroxyvitamin D into fetuses after nephrectomy prevented the rise in serum phosphate, and serum calcium did not fall. The results suggest that fetal 1,25-dihydroxyvitamin D regulates fetal phosphate homeostasis, perhaps by the placenta, which in turn regulates blood-ionized calcium concentration.
Idiopathic hypercalciuria is a cause of a variety of urinary tract complaints in clinical pediatrics. These include gross or microscopic hematuria, enuresis, urinary frequency or urgency, dysuria, sterile pyuria, and proteinuria in addition to renal calculi. A random urine calcium-creatinine concentration ratio can be used to initially screen for hypercalciuria. Patients with indeterminate results should have the test repeated, while those with abnormal values should receive a complete metabolic workup to determine the cause of hypercalciuria. Identifiable causes of hypercalciuria should be treated specifically, and thiazide diuretics are the preferred treatment for uncomplicated renal calculi. Pharmacotherapy in children with idiopathic hypercalciuria and symptomatology other than renal stones is controversial and should be limited to patients with severe clinical manifestations.
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The frequency of hypercalciuria was determined in the families of nine hypercalciuric patients with idiopathic hypercaliuria who formed recurrent calcium oxalate renal stones. Idiopathic hypercalciuria occurred in 26 of 73 relatives, in three consecutive generations of two families and in two successive generations of four other families. Multiple siblings or children of the probands were affected in three families. Nineteen of 44 first-degree relatives (43 per cent) had idiopathic hypercalciuria, as compared to seven of 29 (29 per cent) other relatives; there was no relation to age or sex. Renal stones were formed by 19 of the 44 first-degree relatives but by none of the others; nine of the 19 were women. We conclude that there is a familial form of hypercalciuria, which appears to be transmitted as an autosomal dominant trait. Stone disease is frequent in first-degree relatives, and affects both sexes equally.
Compensatory renal hypertrophy was studied in fetal lambs during midgestation. Functional adaptation was correlated with anatomica and biochemical changes by measuring glomerular filtration and clearance of para-amino hippurate (PAH). Normal intrauterine body growth and kidney growth by changes in RNA and DNA over a 72-hr period were studied in twin fetuses. Seventy-two hr after left uninephrectomy in single fetuses, there was a significant increase in weight of the renoprival right kidney as well as a significant increase in renal cortical content of RNA and DNA. The rate of increase in RNA was greater than the increase in DNA. Preliminary studies suggest that an increase in renal function parallels renal hypertrophy in fetal lambs.
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A group of 273 children with minor complaints was screened for idiopathic hypercalciuria by measurement of the urine Ca/Cr. Borderline or definitely high levels were noted in 17 of these children, 11 of whom were boys. More intensive metabolic studies were completed on four of these children and on three children who were noted to have symptomatic renal stones associated with idiopathic hypercalciuria. These studies suggest that IH, well recognized in adults, may have its origins in childhood and that appropriate management, if initiated in childhood, may have significant long-term benefits.
The purpose of this study was to investigate the possible role of diminished phosphate clearance by the fetal kidney in production of relative fetal hyperphosphatemia. Stimuli known to affect renal phosphate clearance in adults were investigated in young fetal lambs. Our studies confirm that the fetal lamb kidney responds to exogenous and endogenous parathyroid hormone (PTH) with inhibition of tubular phosphate reabsorption. Renal tubular phosphate reabsorption in the fetus is in part related to sodium reabsorption. These studies indicate that so-called "immaturity" of renal phosphate clearance in utero is not a significant factor in production of fetal hyperphosphatemia.
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