LRRK2 mutations underlie some forms of familial and sporadic Parkinson disease. LRRK2 is expressed in many organs including the CNS, kidney, and intestine, and its exact role and targets have not been identified. Here we found that mice lacking Lrrk2 excrete more phosphate in urine with normal serum phosphate levels, a difference that was abolished when mice were placed on low phosphate diet. Expression of the major renal phosphate cotransporters NaPi-IIa and NaPi-IIc was decreased in KO mice on protein level but not mRNA. The difference in renal phosphate excretion was maintained when mice were injected with agonists for D1 or D2 dopamine receptors. Serum levels of Parathyroid hormone were similar in WT and KO mice, whereas FGF23 levels were significantly elevated in Lrrk2 KO mice along with a 80% reduction in renal 1alpha-hydroxylase expression (the enzyme responsible for activation of 1,25-(OH)₂-vitamin D₃). We further examined the expression of the intestinal NaPi-IIb phosphate transporter which was found to be increased approximately two-fold. Thus, Lrrk2 deficiency in mice stimulates intestinal phosphate absorption which in turn increases FGF23 inhibiting renal phosphate absorption and suppresses expression of 1alpha OHase.