Studies from our laboratory have revealed an important role for the maternal diet as well as the dietary protein source in the development of hypertension and renal injury in Dahl Salt-Sensitive (SS) rats. The current study sought to compare salt-induced hypertension, renal damage, and immune cell infiltration in the offspring of breeders fed either a casein-or gluten-based diet, with the hypothesis that offspring from gluten-fed breeders would fail to develop these salt-sensitive phenotypes. When fed identical diets postweaning, the F1 generation gluten offspring demonstrated lower mean arterial pressure (MAP, 149.1±3.1 vs 162.5±5.8 mmHg), albuminuria (166.2±34.6 vs 250.9±27.8 mg/day) and outer medullary protein casting (7.4±0.8% vs 13.1±1.3%) in response to high salt compared to the casein offspring (n=9-11). The gluten offspring also had fewer CD45+ leukocytes, CD11b/c+ monocytes/macrophages, CD3+ T-cells, and CD45R+ B-cells infiltrating the kidney. Analysis of the F2 generation gluten offspring also exhibited lower MAP and renal damage compared to rats born from casein breeders (n=7-9), with no difference in renal immune cell infiltration. CMKLR1 (chemokine like receptor 1), receptor for the novel prohypertensive adipokine chemerin, was found via PCR array to be significantly upregulated (2.99fold) in renal T-cells isolated from F2 offspring of casein-fed versus gluten-fed parents. Furthermore, CMKLR1 inhibition via 2-(α-naphthoyl) ethyltrimethylammonium iodide (α-NETA) treatment significantly attenuated renal immune cell infiltration, hypertension, and renal damage in SS rats fed high salt. Together these data demonstrate the influence of the parental diet in determining the salt-induced hypertensive, renal damage, and inflammatory phenotype of the offspring.