oxalates and Atrophy

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.

Topics: Animals; Atrophy; Blood Pressure; Enalapril; Hyperoxaluria; Kidney Tubules; Male; Nephritis, Interstitial; Oxalates; Rats; Rats, Sprague-Dawley; Time Factors

The clinical features of a newly recognised inherited disease, primary hyperoxaluria in the cat, are reported. Affected cats developed acute renal failure between five and nine months old owing to the deposition of oxalate crystals in the tubules of the kidney. In addition to the signs attributable to kidney failure the affected animals became profoundly weak; there was evidence of denervation atrophy in skeletal muscle, and accumulations of neurofilaments were found in the proximal axons of the ventral horn cells and dorsal root ganglion cells of the spinal cord. Examination of urine from affected cats revealed L-glyceric aciduria and intermittent hyperoxaluria suggesting that the disease is a feline analogue of the human disorder, primary hyperoxaluria type 2. This supposition was confirmed by liver enzyme studies.

Topics: Acute Kidney Injury; Animals; Atrophy; Cat Diseases; Cats; Electromyography; Female; Hyperoxaluria; Hyperoxaluria, Primary; Kidney; Male; Muscles; Oxalates; Pedigree; Spinal Cord

Topics: Aged; Atrophy; Cicatrix; Electroretinography; Fluorescein Angiography; Fundus Oculi; Humans; Hyalin; Light Coagulation; Macular Degeneration; Middle Aged; Oxalates; Pigment Epithelium of Eye; Retinal Detachment; Retinal Diseases; Retinal Hemorrhage; Retinal Vessels; Retinitis; Vascular Diseases; Vitamin A Deficiency

Topics: Adult; Aged; Atrophy; Cholelithiasis; Clinical Enzyme Tests; Diagnosis, Differential; Female; Hepatitis A; Humans; Isoenzymes; L-Lactate Dehydrogenase; Liver; Liver Cirrhosis; Liver Diseases; Liver Neoplasms; Male; Middle Aged; Oxalates; Potassium; Urea