Hypercalciurias

Pak, Charles Y.C.

doi:10.1007/978-1-4684-2451-5_3

Cited by 10 publications

(9 citation statements)

References 86 publications

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“…However, in response to marked reduction in diet Ca from 0.6 to 0.03%, Ca excretion fell far less in the hypercalciuric male (-11 vs. -35%) and female (-30 vs. -51%), which argues against AH (see Results). Furthermore, the associated increases in urinary excretion of cAMP in the SH rats are inconsistent with an absorptive etiology according to current concepts of hypercalciuria (1)(2)(3)(4)(5)(6)(7)9).…”

Section: Discussionmentioning

confidence: 93%

“…INTRODUCTION The pathogenesis of idiopathic hypercalciuria (IH)l in man is incompletely understood (1). Potential mechanisms postulated include primary intestinal hyper-absorption (1-3) and diminished renal Ca reabsorption, or "renal leak" (1)(2)(3)(4). Because increased Ca absorption is also observed, though, as a secondary or compensatory event in those patients considered to have renal leak, the mere presence of intestinal hyperabsorption is nonspecific.…”

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confidence: 99%

“…Evidence for these postulates is largely derived from the observed increase in plasma parathyroid hormone (PTH) and/or urinary cyclic AMP (cAMP) in the renal hypercalciurics (RH) (1)(2)(3)(4)(5)(6) and decreases in the same parameters in the absorptive hypercalciurics (AH) (1)(2)(3)(4)(5)(6). However, documentation for RH as vigorously defined above is scant (3,5,7), save for the original description of a few patients (2) and the recent larger series from France (6). The latter unfortunately included an indeterminable number of patients with simultaneously high serum Ca and PTH, making it impossible to exclude the so-called resorptive hypercalciuria (2).…”

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confidence: 99%

“…However, documentation for RH as vigorously defined above is scant (3,5,7), save for the original description of a few patients (2) and the recent larger series from France (6). The latter unfortunately included an indeterminable number of patients with simultaneously high serum Ca and PTH, making it impossible to exclude the so-called resorptive hypercalciuria (2). Studies by Lau et al.…”

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confidence: 99%

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Tubular Mechanism for the Spontaneous Hypercalciuria in Laboratory Rat

Lau¹,

Eby²

1982

J. Clin. Invest.

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A B S T R A C T Recently it has been observed that Ca excretion in laboratory rats does not follow a Gaussian distribution, with -10% of them excreting Ca at a rate of 2 SD above the group mean. This phenomenon has been described as spontaneous hypercalciuria (SH). Our studies were designed to define its mechanism. 48 Wistar rats were subjected to metabolic studies to identify SH, prospectively defined as Ca excretion 2 SD above the group mean during 7 d of dietary Ca deprivation (<0.03% by analysis), in the absence of hypercalcemia, P04 depletion, or exaggerated natriuresis.Progenies from SH rats were found to have significantly higher urine Ca/creatinine (micrograms per milligram) (male = 38 vs. 23, P < 0.05; female = 79 vs. 60, P < 0.005) with 7/20 males and 9/26 females having values 2 SD above the means of normal. After a 12-h fast and during 10% volume expansion with saline, clearance and micropuncture studies were performed on three groups of acutely parathyroidectomized female rats; (a) normocalciuric (N) progenies from the normal, (b) normocalciuric (NC) progenies from SH, and (c) hypercalciuric (HC) progenies from SH rats. Among these groups, there was no significant difference in body weights, glomerular filtration rate, plasma ultrafiltrable Ca (4.5, 4.6 vs. 4.7 mg/100 g), P04, and the fractional excretion (FE) late distal tubule (6.9 vs. 6.9 and 7.6%, P = NS). Although FECa exceeded late distal FDCa in all three groups, the increment was significantly greater in HC rats (7.02%) than both N (3.4, P < 0.05) and NC rats (3.05, P < 0.02).The effects of chlorothiazide (27.5 mg/kg/d, i.p. X 7 d) were evaluated in the female offsprings of the SH rats. Before chlorothiazide, average urine Ca/creatinine (253 vs. 77.2) and cyclic AMP (26.6 vs. 13.4 jAmol/mg creatinine, P < 0.001) on days 7 and 8 of the Ca-deprived diet were higher than the normal. On days 6 and 7 of chlorothiazide, average cyclic AMP (cAMP) excretion fell to normal range (11.7 vs. 12.7 ,umol/mg creatinine) as Ca excretion was reduced to normal (62 vs. 59.4 tsg Ca/mg creatinine).We conclude: (a) SH, as defined in this study, is an inheritable biochemical marker and renal in origin. (b) The hypercalciuria is independent of parathyroid hormone, changes in plasma Ca and tubular handling of Na. (c) As studied in the PTX and volume expanded conditions of our experiments, decreased Ca reabsorption in superficial proximal convoluted tubule is demonstrable, but the hypercalciuria is probably mediated by diminished Ca transport by the deep nephron. The unlikely possibility of increased secretion by the terminal nephron, however, remains to be excluded. (d) In normal rats, there is internephron heterogeneity in regard to Ca transport during saline loading.

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Section: Discussionmentioning

confidence: 93%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Tubular Mechanism for the Spontaneous Hypercalciuria in Laboratory Rat

Lau¹,

Eby²

1982

J. Clin. Invest.

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“…Studies on pathogenesis of urolithiasis have mainly been performed on the metabolism of calcium [1] and other urinary constituents [2][3][4], crystallization [5] and so forth. Although recurrent stone formers are most ap propriate subjects in such studies, the stone formation in these patients is frequently unable to be explained only by metabolic disorder.…”

Section: Introductionmentioning

confidence: 99%

Influence of Morphologic Factors on Calcium-Containing Stone Formation

et al. 1992

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Pathogenesis of urolithiasis cannot be explained only by metabolic disorder. In the present study, morphologic differences of the renal pelvic-caliceal system (PCS) were examined on both the stone and normal sides in calcium-containing stone formers. The results indicated that as compared to the normal side, the urine flow in the PCS was stagnant or not straight on the stone side even in the same individual, showing unfavorable conditions for stone formation. It is therefore considered that morphologic disorders of the urinary tract may be one of the causes for stone formation.

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The Role of Urate in Idiopathic Calcium Urolithiasis

Silcock

1980

Advances in Experimental Medicine and Biology

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Hypercalciurias

Cited by 10 publications

References 86 publications

Tubular Mechanism for the Spontaneous Hypercalciuria in Laboratory Rat

Tubular Mechanism for the Spontaneous Hypercalciuria in Laboratory Rat

Influence of Morphologic Factors on Calcium-Containing Stone Formation

The Role of Urate in Idiopathic Calcium Urolithiasis

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