Intratumor heterogeneity (ITH) and tumor evolution have been described for clear cell renal cell carcinomas (ccRCC), but only limited data are available for other kidney cancer subtypes. Moreover, previous ITH studies predominately focused on single nucleotide variants (SNVs); little is known of the stepwise process in which additional genomic alterations such as copy number alterations (SCNAs) or structural variants (SV) are acquired. We investigated ITH and clonal evolution of papillary renal cell carcinoma (pRCC) and rarer kidney cancer subtypes using whole-genome sequencing and multi-omics analyses in 124 samples from 29 subjects. We collected multiple samples from the center of the tumor to the periphery and matched metastatic lesions to capture changes occurring along the physical tumor expansion. We used phylogenetic analysis to order the impact of SCNAs, SNVs, and SVs along the evolutionary trajectory of these tumors. While the few mutations in cancer driver genes were clonal, pRCC ITH was lowest for SCNAs, intermediate for SNVs, and highest for SVs. The phylogenetic analysis confirmed a clonal expansion cascade along these genomic alteration types. Moreover, while SNVs and SCNAs were similar, SVs were >20 times more frequent in pRCC type 2 than pRCC type 1, suggesting a role for SVs in pRCC type 2 aggressive behavior. Unlike ccRCC or other cancer types, pRCCs tumorigenesis appears to begin from SCNAs and/or rare mutations in cancer driver genes. No effective treatment is available for this tumor. Our work highlights the need for tailored intervention against large-scale somatic alterations beyond SNVs.