Dietary Protein Manipulation in Experimental Nephrotic Syndrome

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Abstract
Evidence that glomerulosclerosis may be accelerated by high-protein diet and ameliorated by low-protein diet has led to debate concerning appropriate dietary recommendations in nephrotic syndrome. In this study, dietary protein was manipulated in a chronic, non-uraemic experimental model of nephrotic syndrome. Groups of 12 AS rats received 12, 24 or 48% protein diet after nephrotic syndrome was induced by adriamycin. Animals were sacrificed 8 weeks after change of diet when all were normotensive and none were uraemic. Animals on 24 and 48% maintained initial body weight and had persistent nephrosis. There was renal hypertrophy and histology showed tubular casts, focal tubulo-interstitial injury and glomerulosclerosis. Animals on 48% diet had more renal hypertrophy and worse histological damage but no differences in other parameters compared to 24% diet. On a 12% protein diet animals lost 15 ± 3% of initial body weight (from 221 ± 6 to 188 ± 6 g; p < 0.001). There was less proteinuria (p < 0.0001), and lower serum cholesterol (p < 0.0001) and triglyceride (p < 0.01). Serum albumin was not different but total protein was lower than on 24 and 48% diet (p < 0.01). Renal histological damage, although less severe than on 48% diet, did not differ from 24% diet. There was fatty infiltration of the liver. In view of the effects of low-protein diet in this model of nephrotic syndrome, dietary protein restriction should be applied with caution in human nephrotic syndrome.