Growth of residual renal tissue in response to loss of other renal tissue is usually termed compensatory hypertrophy. This process occurs not only when unilateral nephrectomy is performed with the contralateral organ increasing its mass but also when undamaged nephrons within a kidney undergo enlargement as other nephron units in that same kidney are destroyed either by natural disease or experimentally (34, 41, 49, 51). Allhough compensatory hypertro phy is a standard term for this phenomenon, it deserves some further clarifi cation. Hyperplasia (often experimentally defined as an increase in DNA content) as well as hypertrophy (often defined as an increase of proteinIDNA ratio) underlie compensatory hypertrophy. Although the compensatory nature of the response seems obvious, the exact physiologic functions of the kidney targeted for compensation are undefined. Furthermore, it is possible that com pensatory growth and associated functional alterations, despite mitigating the fall in renal function for the organism, have long-term deleterious conse quences for these residual nephrons. Along with structural enlargement, the residual nephrons take on a large number of functional adaptations, most notably, an increase in single-nephron filtration rate and net reabsorption of solutes and water (32). Other metabolic processes presumably associated with heightened transport, such as oxygen consumption, increase in remaining nephrons as do synthetic pathways such as ammoniagenesis (32, 40, 56). Undoubtedly, structural growth and functional