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available at https://pubmed.ncbi.nlm.nih.gov/32464217/ Editorial Comment: Type 1 primary hyperoxaluria is a devastating autosomal recessive disease in which those afflicted have nephrocalcinosis, kidney stones and deposition of oxalate in other tissues (oxalosis), with the majority progressing to renal failure. It is due to a deficit in the hepatic peroxisomal enzyme, alanine glyoxylate aminotransferase type 1, which diverts glyoxylate away from oxalate synthesis. The majority of models with this disease have been developed in mice. These investigators used a CRISPR/Cas9 approach to develop a model in rats. They were able to prevent the severe renal crystal deposition in these animals that occurs with an ethylene glycol challenge as well as a reduction in urinary oxalate excretion by knocking out hydroxyacid oxidase 1 (glycolate oxidase) using a similar approach. Glycolate oxidase is the enzyme that catalyzes the oxidation of glycolate to glyoxylate, the immediate precursor of oxalate. A liver targeted si-RNA knockdown of glycolate oxidase has recently been shown to dramatically reduce urinary and plasma oxalate excretion in patients with type 1 primary hyperoxaluria. A potential disadvantage of the CRISPR/Cas9 approach is that it could be difficult to reverse it as compared to si-RNA effects, which are transient. Dean G. Assimos, MD Suggested Reading Levin-Iaina N, Dinour D, Romero L et al: Late diagnosis of primary hyperoxaluria type 2 in the adult: effect of a novel mutation in GRHPR gene on enzymatic activity and molecular modeling. J Urol 2009; 181: 2146. Holmes RP and Assimos DG: Glyoxylate synthesis, and its modulation and influence on oxalate synthesis. J Urol 1998; 160: 1617. Lieske JC, Spargo BH and Toback FG: Endocytosis of calcium oxalate crystals and proliferation of renal tubular epithelial cells in a patient with type 1 primary hyperoxaluria. J Urol 1992; 148: 1517. Urological Oncology: Adrenal, Renal, Ureteral and Retroperitoneal Tumors Re: Impact of Hospital Nephrectomy Volume on Intermediateto Long-Term Survival in Renal Cell Carcinoma R. Hsu, M. Barclay, M. Loughran, G. Lyratzopoulos, V. Gnanapragasam and J. Armitage Academic Urology Group, Department of Surgery, Cambridge Biomedical Campus, University of Cambridge, Department of Urology, Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation Trust and The Healthcare Improvement Studies (THIS) Institute, University of Cambridge, Cambridge and Transforming Cancer Services Team, National Health Service, National Cancer Registration and Analysis Service, Public Health England, and Epidemiology of Cancer Healthcare and Outcomes (ECHO) Group, Department of Behavioural Science and Health, University College London, London, United Kingdom BJU Int 2020; 125: 56e63. doi:10.1111/bju.14848 Abstract available at https://pubmed.ncbi.nlm.nih.gov/31206987/available at https://pubmed.ncbi.nlm.nih.gov/31206987/ Editorial Comment: The authors explore the relationship between hospital volume and survival of patients undergoing nephrectomy for renal cell carcinoma (RCC). They evaluated 12,912 patients with solitary nonmetastatic RCC from the English Hospital Episode Statistics database and the National Cancer Data Repository (United Kingdom) treated between 2000 and 2010. Hospitals were categorized as low volume (LV, fewer than 20 cases), medium volume (MV, 20 to 39) or high volume 1092 ADRENAL, RENAL, URETERAL AND RETROPERITONEAL TUMORS Copyright © 2020 American Urological Association Education and Research, Inc. Unauthorized reproduction of this article is prohibited.