tendency to fewer damaged kidneys in animals 

 surviving more than 800 days of age. When 

 growth was retarded throughout life, nephrosis was 

 almost nonexistent. 



Berg and Harmison (20) and Simms and Berg 

 (172), investigating a stock colony from which 

 respiratory infections had practically been elimi- 

 nated, reported that chronic nephrosis, the 

 commonest pathological condition observed, was 

 present in 80 percent of the animals by 700 days. 

 Kennedy (102) also observed severe renal damage 

 in rats surviving 2 years or longer with little 

 evidence of renal abnormalities before they reached 

 an age of 21 months. Kenal damage appeared 

 earlier, between 12 and 15 months, in obese rats. 

 Overfeeding or unilateral nephrectomy resulted 

 in the premature appearance of a type of kidney 

 lesion common to senile rats. Andrew and Pruett 

 (10) compared normal kidneys of rats in age groups 

 300 days and younger with kidneys from rats over 

 800 days of age. The greatest differences ob- 

 served were in the tubules rather than in the 

 glomeruli. Blatherwick and Medlar (SO) pre- 

 sented evidence that functional impairment of 

 the kidney may exist for some time before 

 histologic changes indicative of nephritis become 

 apparent. Gover (77) reported differences in the 

 type of renal lesions observed in three strains of 

 mice. 



Dietary studies in relation to kidney damage 

 have dealt chiefly with the influence of protein 

 level and have yielded somewhat controversial 

 results. Bischoff (29) reviewed the results of the 

 early investigations in this field. Casein has been 

 studied most frequently in experiments dealing 

 with high levels of dietary protein. There seems 

 to be considerable evidence that rats under many 

 conditions can consume relatively high levels of 

 casein for the greater part of the normal lifespan 

 without suffering renal lesions characteristic of 

 nephritis. Saxton and Kimball (168), however, 

 observed chronic nephrosis more often in animals 

 receiving casein than in those receiving liver. 

 Nephrosis was frequently greater in rats that re- 

 ceived diets high in protein than in those on low 

 protein diets. Although chronic nephrosis was 

 more common in animals on high levels of protein 

 there appeared to be no correlation of lifespan 

 with the level of dietary protein. 



A few reports have also dealt with the possible 

 role of magnesium in the production of renal dam- 

 age. A diet containing cholesterol and cholic acid 

 and producing atherosclerosis in the rat increases 

 markedly the magnesium requirement of the ani- 

 mal (187). Vitale, Hellerstein, Hegsted, and 

 others (186), in reviewing the present knowledge 

 of the interrelationship between dietary magne- 

 sium and calcium in atherosclerosis and renal le- 

 sions, reported that additional magnesium decreases 

 or eliminates calcium deposition in the kidney, 

 regardless of other variables. 



Summary. — Gross examinations of the tissues 

 at the time of necropsy indicated that the kidney 



721-631—64 4 



was the organ most frequently abnormal. Kidney 

 damage was observed in rats showing no obvious 

 signs of ill health as well as in sick animals, but 

 the extent of the damage was considerably greater 

 in the moribund rats. 



Microscopic examination revealed three types 

 of kidney damage. The most prevalent finding 

 was the presence of eosinophilic albuminous mate- 

 rial or hyalin casts in dilated tubules. As evidence 

 of degenerative changes increased, glomerular 

 damage became apparent, and in the large, exces- 

 sively damaged kidneys, extreme dilation of the 

 tubules resembling cystic degeneration was ob- 

 served. Calcium deposits were found chiefly in 

 the kidneys of moribund rats and were rarely seen 

 except in kidneys showing extensive damage. 



The BHE strain of rats seemed to be particularly 

 susceptible to kidney damage regardless of the diet, 

 and the results suggest that several factors may 

 accelerate an inherent weakness in this strain of 

 rats. Some diets obviously hastened the onset of 

 lesions and appeared to influence the type and 

 extent of the degenerative changes observed. The 

 levels of protein in the stock and experimental 

 diets were moderate and were similar except for 

 those diets consisting of 100 percent whole egg or 

 egg yolk. Level of protein, therefore, does not 

 explain the excessive kidney damage observed with 

 rats fed SPE or SPPB diets. Level of dietary fat 

 also provides no explanation for the results 

 observed. 



The tendency for kidney damage to be less 

 when the diet consisted solely of whole egg or egg 

 yolk supplemented with a mineral mixture than 

 when it contained 25 percent whole egg indicates 

 that the undesirable effect of this latter diet was 

 due to the interaction of the various dietary 

 ingredients rather than to egg alone. The results 

 with the mineral-supplemented egg-yolk diet 

 suggest the possibility of a mineral imbalance. 



The enlarged and damaged kidneys observed 

 in some extremely heavy animals, particularly 

 those fed the diet containing peanut butter, may 

 be due to an acceleration of degenerative changes 

 in the kidneys, associated with the stress of 

 obesity. 



The results provide no answer as to why calcium 

 deposits were present with certain diets but were 

 absent in equally damaged kidneys from rats fed 

 other experimental diets. The diets were designed 

 to supply the animal with adequate amounts of 

 vitamins and minerals, but the possibility that 

 certain dietary stresses may increase the need for 

 some of these nutrients has not been excluded. 



Wistar rats proved much less susceptible to 

 kidney damage than did BHE rats and responded 

 very differently to the diet containing 25 percent 

 egg. These results provide further evidence of 

 the importance of considering inherent charac- 

 teristics of the strain of animal under investiga- 

 tion when interpreting the results of nutritional 

 investigations, and of the need for further research 

 to discover the biochemical mechanisms involved. 



35 



