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Titolo:
Acid and mineral balances and bone in familial proximal renal tubular acidosis
Autore:
Lemann, J; Adams, ND; Wilz, DR; Brenes, LG;
Indirizzi:
Med Coll Wisconsin, Dept Med, Div Nephrol, Milwaukee, WI 53226 USA Med Coll Wisconsin Milwaukee WI USA 53226 ephrol, Milwaukee, WI 53226 USA Med Coll Wisconsin, Clin Res Ctr, Milwaukee, WI 53226 USA Med Coll Wisconsin Milwaukee WI USA 53226 es Ctr, Milwaukee, WI 53226 USA Hosp San Juan Dios, San Jose, Costa Rica Hosp San Juan Dios San Jose Costa Rica Juan Dios, San Jose, Costa Rica
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 3, volume: 58, anno: 2000,
pagine: 1267 - 1277
SICI:
0085-2538(200009)58:3<1267:AAMBAB>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
URINARY CALCIUM EXCRETION; METABOLIC-ACIDOSIS; PARATHYROID-HORMONE; SODIUM-BICARBONATE; HEALTHY-ADULTS; POTASSIUM; TRANSPORT; PROTEIN; NEPHROLITHIASIS; RESORPTION;
Keywords:
metabolic acidosis; growth of bone; chronic renal failure; urinary calcium; radial bone density; iliac cortices; hypercalciuria;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
71
Recensione:
Indirizzi per estratti:
Indirizzo: Lemann, J 2601 St Charles Ave, New Orleans, LA 70130 USA 2601 St Charles Ave New Orleans LA USA 70130 eans, LA 70130 USA
Citazione:
J. Lemann et al., "Acid and mineral balances and bone in familial proximal renal tubular acidosis", KIDNEY INT, 58(3), 2000, pp. 1267-1277

Abstract

Background. Metabolic acidosis caused by increased rates of fixed acid production is associated with increased urinary excretion of Ca and negative Ca balances. Metabolic acidosis caused by a reduced capacity of the kidneys to excrete acid contributes to the development of bone disease in the course of chronic renal failure and may be associated with bone disease among some patients with renal tubular acidosis. Methods. To assess the effects of life-long metabolic acidosis alone in the absence of other physiological disturbances, we measured the net balancesof fixed acid and minerals in two brothers in a Costa Rican family with hereditary proximal renal tubular acidosis. Bone radiographs were assessed, and radial bone densities were measured. On a subsequent occasion, transiliac bone biopsies, following double-tetracycline labeling, were obtained fromthese two patients and an unaffected brother. Results. During the balance studies, serum [HCO3-] concentrations of the two affected patients were stable at 12.5 +/- 0.9 and 19.2 +/- 0.7 mmol/L, respectively. Their rates of net fixed acid production were normal and appropriate for their body weights, averaging 0.90 and 1.02 mEq/kg/day. Because their distal renal tubular function was normal, they were capable of acidifying their urine maximally, allowing sufficient urinary excretion of titratable acid and ammonium to maintain net acid excretion at a level that matched acid production. Thus, their acid balances were near zero, as observed among healthy subjects, at -1.9 +/- 2.3 and -2.2 +/- 2.2 mEq/day respectively. Their rates of urinary Ca excretion were normal at 1.6 +/- 0.3 and 2.7 +/- 2.4 mmol/day, and the their balances of Ca and other minerals were closeto zero so that ongoing bone loss was not occurring despite the acidosis. Nevertheless, their heights, relative to their ages, were shorter than the heights of their unaffected relatives. Their radial bone densities were lower than normal for their age and sex, and their iliac cortices were thinnerthan that of their unaffected brother. However, they had no histomorphometric evidence of osteomalacia or osteitis fibrosa, and their rates of bone mineralization were normal. Conclusions. The results indicate that this chronic metabolic acidosis reduces growth, including that of bone. We speculate, without direct supporting evidence, that bone stores of HCO3-/CO3= are reduced, as has been observed in patients with the metabolic acidosis of chronic renal failure and in experimental metabolic acidosis in animals.

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Documento generato il 29/11/20 alle ore 00:32:26