Glucose-enriched, racemic lactate buffered solutions for peritoneal dialysis induce a significant reduction of cell viability as well as a hypertrophic, senescent phenotype of the exposed monolayer. The present study was designed to verify whether the aforementioned changes resulted form the buffer, from the osmotic agent, or from a combined effect of both. Mice were acutely (2 h) and long-term (15 and 30 days) exposed to daily intraperitoneal injections of a racemic lactate, heat-sterilized, low-pH (5.2), glucose-free solution. Imprints of the monolayer were taken at the end of each time interval. The glucose-free lactated buffer used in the present study did not induce significant changes in density distribution, mean cell size, mean cytoplasmic surface area, prevalence of large cells, multinucleation, proportion of observed cells in mitosis, and cell viability. So far, the previously mentioned hypertrophic phenotype appears to derive from substantial alterations in the cell cycle of mesothelium exposed to high concentrations of glucose and/or advanced glycosylation end products and unrelated to lactate.