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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperoxaluria is a recognized cause of tubulointerstitial lesions, and this could contribute to development of hypertension and chronic renal failure. Enalapril has been effective against the progression of tubulointerstitial lesions in various animal models. The aim of the present study was to evaluate the usefulness of enalapril on the tubulointerstitial damage produced by oxalates. Two-month-old male Sprague-Dawley rats were separated into 4 groups, control with tap water (G1), hyperoxaluric (G2), hyperoxaluric+enalapril (G3), enalapril (G4), for 4 weeks. G2 and G3 rats were given 1% ethyleneglycol (ETG, precursor for oxalates), and G3 and G4 rats were given enalapril 20 mg/L in drinking water. At the end of the study, we evaluated renal tubulointerstitial lesions by a semiquantitative score. Urine albumin excretion, serum and urine nitric oxide production, tubulointerstitial immunostaining by alpha-smooth muscle actin, transforming growth factor-beta1, and collagen type III were measured. Rats belonging to the hyperoxaluric group treated with enalapril (G3) showed fewer tubulointerstitial lesions (1.3+/-0.2 versus 3+/-0.2; P<0.01), lower urine albumin excretion (8+/-2 mg/d versus 25+/-2 mg/d; P<0.01), less percentage of alpha-smooth muscle actin in renal interstitium (2+/-0.4% versus 13.5+/-2.4%; P<0.01), less percentage of transforming growth factor-beta1 in tubulointerstitial area (3.3+/-1% versus 13.3+/-2. 1%; P<0.01), less percentage of collagen type III interstitial deposition (0.7+/-0.5% versus 7+/-2.6%; P<0.01), and increased NO production in serum as well as urine (both P<0.01), when compared with the hyperoxaluric group not treated with enalapril (G2). Considering these data, we believe that enalapril, by several mechanisms of action, could provide an important benefit in the prevention of inflammatory response, transforming growth factor-beta1 tubulointerstitial production, collagen type III interstitial deposition, and finally, the progressive tubulointerstitial fibrosis caused by oxalates.
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PMID:Enalapril prevents tubulointerstitial lesions by hyperoxaluria. 993 Nov 9

A number of studies have demonstrated that the urinary ion activity product (IAP) of calcium oxalate (CaOx), as an index of urinary CaOx supersaturation (SS), is higher in renal stone formers than in normal subjects. Besides, the relation between CaOx SS and lithogenesis, crystal CaOx exposition can produce tubular cell as well as renal interstitial lesions. The aim of our study was to evaluate the possible relationship between CaOx SS and tubulointerstitial (TI) damage in an animal model of hyperoxaluria. During four weeks, male Sprague-Dawley rats received: G1 (n = 8) control regular water, and G2 (n = 8) 1% ethylene glycol (ETG) (precursor for oxalates) in drinking water. In order to evaluate urinary CaOx SS, IAP assessed by Tisselius formula was performed. At the end of the study, renal lesions were evaluated by light microscopy and immunohistochemistry. Animals from G2 (ETG) presented higher (p < 0.01) values of: a) urinary oxalate excretion; b) urinary CaOx SS; c) crystalluria score; d) proteinuria; and lower (p < 0.01) creatinine clearance, with respect to the control group (G1). Moreover, pathology studies showed that rats from G2 (ETG), presented significant TI lesions characterized by a higher (p < 0.01) score of: a) tubular atrophy; inflammatory infiltrates (monocyte/macrophage); c) crystal deposits; d) intersticial fibrosis; e) interstitial alpha-smooth muscle actin; f) collagen type III; g) TI TGF beta 1 compared with G1 (control). Rats from G2 (ETG) presented a high correlation between urinary CaOx SS and most of the TI damage parameters evaluated, in especial with interstitial fibrosis. Both, inflammatory infiltrates and urinary CaOx SS were the most significant variables related to interstitial fibrosis. Finally, since hyperoxaluric animals showed higher urinary CaOx SS associated with higher renal TI damage, the results from this study suggest the presence of a tight link between urinary CaOx SS and renal TI damage. Considering these findings we think that urinary CaOx SS control rises in importance beyond nephrolithiasis.
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PMID:[Urinary calcium oxalate supersaturation beyond nephrolithiasis. Relationship with tubulointerstitial damage]. 1279 76