Abstract
One of the intriguing mysteries of biologic design is why there is such redundancy in the function of the kidneys. If a single kidney is removed (as it is from a living renal-transplant donor), the remaining kidney promptly grows larger and increases its glomerular and tubular functions to approach the levels previously achieved by two kidneys. When nephrons are gradually destroyed by glomerular or tubulointerstitial diseases, as little as 10 percent of the original nephron population can maintain acceptable fluid and electrolyte balance, at a level that is certainly sufficient to sustain life. It is only when renal function falls . . .

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