KPD is readily diagnosible because it presents a single characteristic, ketoacidosis, which if present, confirms it as ketosis-prone diabetes. KPD comes in four forms depending upon the presence or absence of β-cell autoantibodies (A+ or A−) and β-cell functional reserve (β+ or β−).
^There is clearly a spectrum of clinical phenotypes among patients with islet autoantibodies who do not present with ketosis, including those termed “latent autoimmune diabetes in adults” (LADA) (30), “type 1.5 diabetes” (31,32,33), and “slowly progressing type 1 diabetes” (34). A similar spectrum exists in KPD that includes the very different phenotypes of A+β− and A+β+ KPD. A+β− KPD is synonymous with classic, early onset autoimmune type 1 diabetes; A+β+ KPD may overlap with LADA. However, there are differences between LADA, as recently defined by the Immunology of Diabetes Society, and A+β+ KPD patients; most importantly, the definition of LADA excludes patients who require insulin within the first 6 months after diagnosis, whereas the majority (90%) of A+β+ KPD patients present with DKA as the first manifestation of diabetes and therefore require insulin at the start. Balasubramanyam, A.; Nalini, R.; Hampe, C. S.; Maldonado, M. (2008). "Syndromes of ketosis-prone diabetes mellitus". Endocrinology Review. 29 (3): 292–302. doi:10.1210/er.2007-0026. PMC2528854. PMID18292467.
^Leslie, R. D. G.; et al. (2008). "Diabetes classification: grey zones, sound and smoke: Action LADA 1". Diabetes/metabolism research and reviews. 24 (7): 511–519. doi:10.1002/dmrr.877.
^Nalini, Ramaswami; et al. (2008). "HLA class II alleles specify phenotypes of ketosis-prone diabetes". Diabetes Care. 31 (6): 1195–1200. doi:10.2337/dc07-1971.