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Several experiments have shown that deterioration of renal parenchyma after reduction of functional mass is affected by the protein content of the diet. The respective role of proteins and that of other nutrients that vary with proteins were never clearly separated. Three groups of 9 uremic rats received diets differing exclusively in protein (casein) content, which was 8% (group 1), 16% (group 2), and 32% (group 3). Energy and minerals were maintained identical. Food intake was similar in groups 1 and 2 and was lower in group 3. Mortality rate remained closely related to protein intake. Of group 3 rats, 78% died within 10 weeks and 100% within 15 weeks. Of group 2 rats, 56% were dead at week 15, and 100% at week 30. Mortality occurred significantly later in group-1 rats fed the lowest protein diet. Histology of remnant kidneys showed severe glomerular and tubular damage, with no or little calcium deposits despite normal phosphorus diet and frequent hyperphosphatemia. These data suggest that protein intake, independent of any other nutrient, influences survival by accelerating the renal damage in rats with reduced kidney mass.

Six infants, 4.5 to 19 months old, whose creatinine clearance was less than 6 ml/min/1.73 m2 received, successively, three low-nitrogen diets. Diet A contained 9.3 g of human milk protein; and diet B, 4.2 g of human milk protein plus synthetic essential amino acids. Diet C was the same as B except that five essential amino acids were replaced by alpha-keto and hydroxy analogs. Serum urea decreased as the infants were transferred from diet A to diets B and C, and the serum urea/creatinine ratio decreased from diet A to diet B and from diet B to diet C. Urea appearance was 14.8 +/- 4.5, 9.1 +/- 4.3, and 6.9 +/- 1.7 mmoles/day, with diets A, B, and C, respectively. Weight gain was also lowest with diet C, as was the difference between nitrogen intake and urea nitrogen appearance, an indicator of nitrogen balance. Plasma free amino acids were not modified by diets A and B, but valine, leucine, and the plasma free essential amino acid pool decreased significantly with diet C.

Thirty-four children with severe kidney disease, either congenital (32 cases) or developing at birth, were followed until age 5 to 19 years. Overall growth retardation corresponded to -2.5 SD below the mean normal values. The retardation occurred almost exclusively before therapy for it was started. Fifteen children were first treated during infancy. In all of them except one, growth was dramatically improved following the first visit to our center, growth changing from slowed to normal rate, although catch-up growth was rare: the average change from normal mean height was -1.68 SD (or -5 SD per year) calculated for the infantile period up to the first visit to our clinic, followed by a change of +0.18 SD per year between first presentation and age 12 months, and +0.01 SD per year between first presentation and last observation at a mean age of 8.3 years. In the 19 patients who were treated after the first year of life, the mean change of height from birth to first presentation was -0.33 SD per year followed by a mean change of -0.04 SD per year up to the last observation (mean period, 7.3 years). Catch-up growth was exceptional. Five children entered puberty with a normal growth spurt. When GFR deteriorated, growth velocity was unchanged. Height calculated for corresponding bone maturity was reduced in half of the patients when first seen, but progressed to the same degree as height during follow-up, except in one patient. Mental development was normal in 31 of 34 patients. Conclusion. Normal growth rate and normal development is possible in children and even in infants with CRF chronic renal failure. The importance of instituting early conservative treatment to prevent height loss must be emphasized.