Kidney Wet Weight Research Articles

Acute renal failure after folate: NaK ATPase in isolated rat renal tubule. Ultramicrochemical and clinical studies.

Abstract. Using refinements of quantitative histochemistry, i.e. oil‐well technique, enzymatic Pi analysis and NADP/ NADPH cycling, the activity of NaKATPase (E.C. 3.6.1.3), an enzyme involved in transmembrane ion transport, was measured in single dissected segments of the proximal and distal tubule of male rats 10 min., 30 min., 60 h and 14 days after folate administration (250 mg/kg body weight). 10 min. after injection the onset of acute renal failure was already apparent by an increase in blood urea of 45 per cent and cessation of urine flow. 60 h after folate the rats became polyuric. The kidney wet weight rose by 40 per cent in a few minutes after the injection due to universal tubular dilatation. During the first hours numerous folate casts were localized, mainly in the thick ascending iimb of Henle's loops. In addition precipitates were found intracellularly in the distal part of the proximal convoluted tubules. The straight portion of the proximal tubules was free of precipitates. 10 min. after the injection tubular segments containing folate material did not show Na K ATPase activity, whereas the folate free tubular segments revealed a residual activity of 30 per cent. Only 15 per cent of the tubules within one lyophilized section had collapsed proximal portions with control activity values. However, the less collapsed segments of the distal tubules revealed a loss of Na K ATPase activity of 55 per cent. Thus folate seems to affect the distal tubule first of all. 60 h after folate administration, when kidney growth reached its maximum, the whole nephron lost its Na K ATPase activity. No tubular cell degeneration or necrosis could be detected during the development stage or the sustained phase of renal failure. After addition of folate to renal homogenate, Na K ATPase exhibited activation (+ 35 per cent) and inhibition (–42 per cent and more) of activity plotted against folate concentration. A careful evaluation of the available evidence led to the conclusion that the acute renal failure induced by folate differs markedly from other models by a directly altered tubular cell metabolism in the development stage of oliguria. Acute tubular obstruction may initiate oliguria. However it seems unlikely that tubular obstruction will be the unique pathogenic factor for this syndrome, especially for the development of the tremendous kidney growth. The inhibition of tubular Na K ATPase activity after folate may indicate an impaired tubular active reabsorption capacity which would be involved in the acute renal failure. The most important finding is that glomerular filtration does not seem to be a primary factor in the development of oliguria after folate administration.

The influence of dactinomycin on compensatory renal hypertrophy

Compensatory renal hypertrophy in the renoprival kidney of Charles River mice and the effect of dactinomycin on this process were studied. Increases in animal weight, wet kidney weight, total protein, and bulk nucleic acid occurred as early as 12 hr postnephrectomy and continued throughout the 28-day period. Dactinomycin inhibited compensatory renal hypertrophy for 7 days. This effect was transient and after an initial lag, accelerated growth rates were observed. By 28 days growth parameters in the dactinomycin-treated animals equaled those of control animals undergoing compensatory renal hypertrophy.

Syndromes of "Minimal Cerebral Damage"

Long-Evans rats intubated daily from 3 to 21 days of age with 0, 10, 30, or 90 mg/kg of lead acetate in aqueous solution were tested postweaning on eight behavioral measures. The three levels of lead exposure had no effect on growth and all animals were overtly free of signs of poisoning. However, neonatal lead exposure produced subtle behavioral effects including increased motor activity (jiggle cages) and impairment of motor coordination (rotarod test), response inhibition ability (operant delayed response), and reversal learning of a tactually cued conditional discrimination. The lead treatment had no effect on simple learning (turning response in E-maze), complex visually cued learning (conditional discrimination in E-maze), and visual acuity (optokinetic test). Acquisition and extinction of passive shock avoidance were not affected by lead exposure, but both acquisition and extinction of active avoidance were affected. Lead treatment also decreased hematocrit, increased blood lead concentration, and increased adrenal and kidney wet weights.

Biochemical studies on the Chinese hamster (22 chromosomes) and the Syrian hamster (44 chromosomes)

The DNA content, transaminase, succinoxidase, cytochrome oxidase, and free amino acid patterns of tissues of the Chinese hamster (2N = 22) and the Syrian hamster (2N = 44) were compared. The DNA concentration per cell of liver and spleen and the DNA concentration per gram wet weight of liver, kidney, and lung were of the same order of magnitude for the two species. Transaminase activity per gamma DNA was also about the same but succinoxidase and cytochrome oxidase activity per gamma DNA of the Chinese hamster was about twice that of the Syrian hamster. The free amino acid pattern of the Chinese hamster tissue resembled that of the analogous Syrian hamster tissue more than it resembled other tissues of the Chinese hamster. Some free amino acids were present at approximately the same concentration per gamma DNA in the corresponding tissues of the two hamster species. However, in other cases, an amino acid was present at two times the concentration in the Chinese hamster as in the Syrian hamster tissue. The reverse of this was also observed.