SummaryAllometry was used to study the effect of growth hormone (GH) deficiency on compensatory renal growth (CRG) in a dwarf mouse strain (Little). Nucleic acid and protein estimations were used to assess changes in cellular hyperplasia and hypertrophy. Nephrectomy was performed at 5,15, or 35 days of age with removal of the renoprival kidney 15 days later. Controls underwent sham nephrectomies at 35 days of age. The allometric growth of the normal kidney in the homozygote dwarf (lit/lit) between 8 and 50 days of age was closely related to that of the normal heterozygote (lit/ +). A regression line for the renoprival kidneys in lit/lit animals was parallel to that of the control right kidney (P< 0.001). The interval between the regression lines was equivalent to a constant difference of approximately 40% between renoprival and control right kidneys and was similar to that found in the normal heterozygote (43%). Increases in DNA, RNA, and protein in control animals during CRG indicate that cell division and hypertrophy were occurring in similar proportions. In the GH-deficient mouse, the total amount of DNA in renoprival kidneys was 0.451 mg compared with 0.439 mg in controls (NS). This suggests that cell replication was suppressed. The protein:DNA ratio increased from 20.91 to 24.27 (P< 0.001) and the RNA:DNA ratio increased from 0.732 to 0.912 (P< 0.001), suggesting that cell size was markedly increased. These findings suggest that reduced amounts of GH may produce a dissociation between hyperplasia and hypertrophy, with CRG occurring predominantly by cellular hypertrophy.SpeculationGrowth hormone deficiency does not prevent compensatory renal growth, which occurs to the same extent in control and growth-hormone-deficient animals, both of which have undergone nephrectomy. However, the increase in kidney size is accomplished predominantly by cellular hypertrophy instead of cell replication.