Sweet potato stem nematode disease （SPSND）， caused by the Ditylenchus destructor Thorne， is a quarantine disease that seriously affects the yield and quality of sweet potato. Identifying resistance genes and breeding resistant varieties through molecular design is an effective way to control SPSND. In this study， the resistant sweet potato variety 'American Red' （male parent） was pollinated with the susceptible variety 'Xuzishu8' （female parent） to generate a segregating population of 274 F₁ progenies. The F₁ progenies were evaluated for their resistance to SPSND using an artificial inoculation method. The resistance to SPSND was observed showing continuously distribution a skewed peak. The relative incidence volume ratio of SPSND was significantly positively correlated with the expansion diameter and expansion length， but not correlated with the tuber diameter， tuber length， and length-width ratio. That indicated that the size and shape of the tuber were un-correlated with the resistance severity. The heritability of the relative incidence volume ratio of SPSND resistance was 75.7%， indicating that resistance was mainly controlled by genetic factors. Based on the previously-published genetic map， QTL mapping for resistance was performed， identifying 10 tightly linked QTLs， each of which might explain 6.6%-10.7% of the phenotypic variation. The candidate gene functional annotation revealed that pathways such as phenylpropanoid biosynthesis， plant hormone signal transduction， and plant-pathogen interactions were likely involved in disease resistance stress. Out of five key candidate genes that were analyzed for quantitative expression analysis， the expression level of the candidate gene itf13g19570 was significantly increased after inoculation with stem nematode. Collectively， this study provided a basis for future identification of SPSND resistance genes and the analysis of their resistance mechanisms.