Urinary oxalate in summer and winter in normal subjects and in stone-forming patients with idiopathic hypercalciuria, both untreated and treated with thiazide and/or cellulose phosphate

1976 ◽  
Vol 4 (4) ◽  
pp. 169-173 ◽  
Author(s):  
P. C. Hallson ◽  
G. P. Kasidas ◽  
G. Alan Rose
Keyword(s):  
Normal Subjects ◽  
Idiopathic Hypercalciuria ◽  
Urinary Oxalate ◽  
Cellulose Phosphate

scholarly journals Sex differences in proximal and distal nephron function contribute to the mechanism of idiopathic hypercalcuria in calcium stone formers

2015 ◽  
Vol 309 (1) ◽  
pp. R85-R92 ◽  
Author(s):  
Benjamin Ko ◽  
Kristin Bergsland ◽  
Daniel L. Gillen ◽  
Andrew P. Evan ◽  
Daniel L. Clark ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Distal Tubule ◽  
Normal Subjects ◽  
Idiopathic Hypercalciuria ◽  
Distal Nephron ◽  
Stone Formers ◽  
Calcium Reabsorption ◽  
Normal Women ◽  
Normal Males ◽  
Normal Men

Idiopathic hypercalciuria (IH) is a common familial trait among patients with calcium nephrolithiasis. Previously, we have demonstrated that hypercalciuria is primarily due to reduced renal proximal and distal tubule calcium reabsorption. Here, using measurements of the clearances of sodium, calcium, and endogenous lithium taken from the General Clinical Research Center, we test the hypothesis that patterns of segmental nephron tubule calcium reabsorption differ between the sexes in IH and normal subjects. When the sexes are compared, we reconfirm the reduced proximal and distal calcium reabsorption. In IH women, distal nephron calcium reabsorption is decreased compared to normal women. In IH men, proximal tubule calcium reabsorption falls significantly, with a more modest reduction in distal calcium reabsorption compared to normal men. Additionally, we demonstrate that male IH patients have lower systolic blood pressures than normal males. We conclude that women and men differ in the way they produce the hypercalciuria of IH, with females reducing distal reabsorption and males primarily reducing proximal tubule function.

scholarly journals Evidence for increased postprandial distal nephron calcium delivery in hypercalciuric stone-forming patients

2008 ◽  
Vol 295 (5) ◽  
pp. F1286-F1294 ◽  
Author(s):  
Elaine M. Worcester ◽  
Fredric L. Coe ◽  
Andrew P. Evan ◽  
Kristin J. Bergsland ◽  
Joan H. Parks ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Stone Formation ◽  
Selective Reduction ◽  
Normal Subjects ◽  
Idiopathic Hypercalciuria ◽  
Calcium Excretion ◽  
Distal Nephron ◽  
Clinical Research Center ◽  
Calcium Reabsorption ◽  
New Finding

A main mechanism of idiopathic hypercalciuria (IH) in calcium stone-forming patients (IHSF) is postprandial reduction of renal tubule calcium reabsorption that cannot be explained by selective reduction of serum parathyroid hormone levels; the nephron site(s) responsible are not as yet defined. Using fourteen 1-h measurements of the clearances of sodium, calcium, and endogenous lithium during a three-meal day in the University of Chicago General Clinical Research Center, we found reduced postprandial proximal tubule reabsorption of sodium and calcium in IHSF vs. normal subjects. The increased distal sodium delivery is matched by increased distal reabsorption so that urine sodium excretions do not differ, but distal calcium reabsorption does not increase enough to match increased calcium delivery, so hypercalciuria results. In fact, urine calcium excretion and overall renal fractional calcium reabsorption both are high in IHSF vs. normal when adjusted for distal calcium delivery, strongly suggesting a distal as well as proximal reduction of calcium reabsorption. The combination of reduced proximal tubule and distal nephron calcium reabsorption in IHSF is a new finding and indicates that IH involves a complex, presumably genetic, variation of nephron function. The increased calcium delivery into the later nephron may play a role in stone formation via deposition of papillary interstitial apatite plaque.

Evidence that postprandial reduction of renal calcium reabsorption mediates hypercalciuria of patients with calcium nephrolithiasis

2007 ◽  
Vol 292 (1) ◽  
pp. F66-F75 ◽  
Author(s):  
Elaine M. Worcester ◽  
Daniel L. Gillen ◽  
Andrew P. Evan ◽  
Joan H. Parks ◽  
Katrina Wright ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Serum Magnesium ◽  
Normal Subjects ◽  
Urinary Calcium ◽  
Idiopathic Hypercalciuria ◽  
Calcium Excretion ◽  
Stone Formers ◽  
Calcium Reabsorption ◽  
Renal Tubular ◽  
Filtered Load

Idiopathic hypercalciuria (IH) is common among calcium stone formers (IHSF). The increased urinary calcium arises from increased intestinal absorption of calcium, but it is unclear whether increased filtered load or decreased renal tubular reabsorption of calcium is the main mechanism for the increased renal excretion. To explore this question, 10 IHSF and 7 normal subjects (N) were studied for 1 day. Urine and blood samples were collected at 30- to 60-min intervals while subjects were fasting and after they ate three meals providing known amounts of calcium, phosphorus, sodium, protein, and calories. Fasting and fed, ultrafiltrable calcium levels, and filtered load of calcium did not differ between N and IHSF. Urine calcium rose with meals, and fractional reabsorption fell in all subjects, but the change was significantly higher in IHSF. The changes in calcium excretion were independent of sodium excretion. Serum parathyroid hormone levels did not differ between N and IHSF, and they could not account for the greater fall in calcium reabsorption in IHSF. Serum magnesium and phosphorus levels in IHSF were below N throughout the day, and tubule phosphate reabsorption was lower in IHSF than N after meals. The primary mechanism by which kidneys ferry absorbed calcium into the urine after meals is via reduced tubule calcium reabsorption, and IHSF differ from N in the magnitude of the response. Parathyroid hormone is not likely to be a sufficient explanation for this difference.

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