Structural and Functional Adaptation in Renal Failure

The Influence of Glomerular Filtration Rate, Solute Excretion and Hydration on the Concentrating Mechanism of the Experimentally Diseased Kidney in the Dog *

“…However, there are certain considerations which suggest that this phenomenon may have occurred. It has long been suspected that glomerular filtration rate increases in the surviving nephrons of the diseased kidney as an adaptive change (18,19) and certain of the observations in the present studies are consistent with the thesis that GFR per nephron might be greater in the diseased kidneys than in the contralateral control organs." If GFR per nephron is indeed increased, renal plasma flow per nephron must also be increased because of the fact that filtration fractions typically have been the same for the diseased kidneys as for the normal organs.…”

Quantitative Histochemistry of the Nephron. V. Alkaline Phosphatase and Lactic Dehydrogenase Activities in Lupus Nephritis*

“…By contrast, in primary renal tubular diseases, the LDH activity of the convoluted tubules was normal in the presence of mild tubular abnormalities and was significantly decreased when the tubules were severely damaged (3). The view that the tubules in lupus glomerulonephritis are capable of responding to increased metabolic demands would be consistent with the hypothesis of Platt, namely, that in chronic renal disease residual functioning nephrons may be capable of normal activities and even of functional adaptations which may result in an increase of work done per residual functioning nephron (8). The view of Platt has gained considerable support from the studies of Bricker, Morrin and Kime on the adaptive changes in residual nephrons of dogs with experimenal unilateral renal disease (9).…”

Mechanism of change in the excretion of sodium per nephron when renal mass is reduced

“…We suggest that the primary reason for this is the increased osmotic load of solutes, and especially urea, per nephron. The notion that urine formed during renal insufficiency results from osmotic diuresis through a few remaining normal nephrons is a familiar one, well articulated by Platt (13). While massive urea loads can decrease reabsorption in the proximal tubule (14), mild urea diuresis is likely to retard absorption chiefly in the lower reaches of the nephron since it is here that the concentration of urea rises highest and it is here as well that the tubular epithelium is least permeable to the back-diffusion of urea (15).…”