A STABLE ANIMAL-MODEL OF DIET-INDUCED CALCIUM-OXALATE CRYSTALLURIA

Citation
C. Hennequin et al., A STABLE ANIMAL-MODEL OF DIET-INDUCED CALCIUM-OXALATE CRYSTALLURIA, Urological research, 26(1), 1998, pp. 57-63
Citations number
32
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
03005623
Volume
26
Issue
1
Year of publication
1998
Pages
57 - 63
Database
ISI
SICI code
0300-5623(1998)26:1<57:ASAODC>2.0.ZU;2-5
Abstract
Twenty male Wistar rats, weighing 150 g, were placed in metabolic cage s on a 30% sucrose diet for 7 days, before allocation to two groups: a control group (n = 5) and a lactose group (n = 15). They received res pectively a 30% sucrose diet or a 30% lactose diet for 8 weeks, each c ontaining 0.67% calcium and 0.38% phosphorus. After 4 (T1) and 8 (T2) weeks, the serum calcium (Ca) and citrate levels were significantly (P < 0.01) higher in rats fed the lactose diet. Serum alkaline phosphata se activity was increased in the lactose group (P < 0.01) at T1 and T2 . The lactose-rich diet induced an increase in urinary Ca excretion at T1 and T2; citrate excretion was only enhanced at T2 (P < 0.001). No difference between the two groups was observed in urinary oxalate (Ox) excretion or creatinine clearance. Crystalluria analysis revealed a m arked number (>300/mm(3) at T1 and T2) of calcium oxalate dihydrate cr ystals (GOD) in rats fed the lactose-rich diet, whereas no COD crystal s were observed in sucrose-fed control rats at any time point. The for mation of COD crystals in lactose-fed rats was related to an increase in calcium oxalate (CaOx) product (pCaOx), which was respectively 12.6 vs 3.9 at T1 and 10.5 vs 1.8 at T2, and an increase in CaOx ratio (Ca /Ox), which was 99.1 vs 7.5 and 67.5 vs 18.5 at T1 and T2, respectivel y. The high pCaOx and Ca/Ox ratios in the lactose group were due to hy percalciuria, in agreement with the number and the type of crystals. T he present experimental model confirms that the ingestion of a 30% lac tose diet increases urinary Ca excretion without changing urinary Ox e xcretion and shows for the first time that it induces a stable and mar ked crystalluria composed of GOD. Such a non-nephrotoxic and stable mo del is of interest for the study of CaOx crystal formation secondary t o hypercalciuria, and thus afterwards eventually for CaOx nephrolithia sis.