Renal counterbalance.

Unilateral renal injury, whether caused by ureteral obstruction or ischemia, is followed by an increase in RVR, a decrease in RBF, and eventual tubular atrophy. Each of these abnormalities can be modified by a reduction in the function of the contralateral kidney. Whether this occurs as a result of increases in vasodilatory substances or decreases in vasoconstrictor compounds is unknown. Equally uncertain is the possibility that the response is mediated by the accumulation of naturally occurring cytoprotective agents. In either case, a stimulus for growth of the previously damaged kidney seems to be necessary for full recovery to occur. It appears that this response primarily involves the regeneration of tubular epithelial cells and differs from that associated with compensatory hypertrophy. This may require adjustments in the action of other growth factors or inhibitors. Hinman believed that counterbalance described a relationship between a hypertrophic kidney and an injured kidney and required the presence of both. However, it is quite possible that a similar relationship may exist in instances of bilateral disease when the injury does not involve all nephrons to the same extent. If so, a vicious circle may be established in which the least-damaged nephrons, which are first to recover, later hypertrophy. This internal redistribution of function may not only suppress the recovery of the most severely injured nephrons but also promote their eventual atrophy. Ultimately, the continued hypertrophy and hyperfusion of the functioning nephrons may lead to sclerotic changes within their glomeruli.(ABSTRACT TRUNCATED AT 250 WORDS)