Chronic metabolic acidosis stimulates renal acid secretion in part through remodelling of the collecting duct resulting in an increased number of acid-secretory type A intercalated cells A-IC) and a reduced number of bicarbonate secretory type B intercalated cells (B-IC). This process, termed plasticity, has been thought to occur through interconversion of type B to type A cells. We used markers of proliferation (PCNA, BrdU incorporation) and cell-specific markers for A-IC (AE1) and B-IC (pendrin) to investigate if proliferation of A-IC could provide an additional or alternative explanation for plasticity. Induction of remodelling in rats with metabolic acidosis (with NH4Cl for 12 hrs, 4 and 7 days) or treatment with acetazolamide for 10 days resulted in a larger portion of AE1 positive cells in the cortical collecting duct. A large number of AE1 expressing A-IC was labelled with proliferative markers in the cortical and outer medullary collecting duct whereas no staining was found in B-IC. Thus, during chronic acidosis proliferation of AE1 containing acid-secretory cells occurs and may underlie the remodelling of the collecting duct.