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Objective: we aim to illustrate step by step the technique of enucleoresection of renal mass during robot-assisted partial nephrectomy (RAPN). Patient and surgical procedure: 72-year-old man affected by asymptomatic and incidental small renal mass in the middle third of the left kidney. The diameter of the renal mass was 3 cm on preoperative imaging, with a PADUA score of 7. We performed left transperitoneal RAPN with selective clamping. After the enucleoresection, medullary and cortical sutures were performed. A hemostatic agent was applied at the end of the procedure. Results: Intraoperative blood loss was 50 ml, with an ischemia time of 15 min. Postoperative hemoglobin was 14.8 g/dL and the creatinine was 0.69 mg/dL. On the third post-operative day, the drain was removed and the patient was discharged on the same day. No postoperative complications or recurrences were found during the 6-month follow-up. Conclusion: partial nephrectomy maximizes the amount of healthy renal parenchyma spared. Evidence supports the adoption of this technique whenever feasible.

Renal cell carcinoma (RCC) comprises various histologically distinct subtypes, each characterized by specific genetic alterations, necessitating individualized management and treatment strategies for each subtype. An exhaustive search of the PubMed database was conducted without any filters or restrictions. Inclusion criteria encompassed original English articles focusing on molecular mechanisms of kidney cancer. On the other hand, all non-original articles and articles published in any language other than English were excluded. Hereditary kidney cancer represents 5–8% of all kidney cancer cases and is associated with syndromes such as von Hippel–Lindau syndrome, Birt–Hogg–Dubè syndrome, succinate dehydrogenase-deficient renal cell cancer syndrome, tuberous sclerosis complex, hereditary papillary renal cell carcinoma, fumarate hydratase deficiency syndrome, BAP1 tumor predisposition syndrome, and other uncommon hereditary cancer syndromes. These conditions are characterized by distinct genetic mutations and related extra-renal symptoms. The majority of renal cell carcinoma predispositions stem from loss-of-function mutations in tumor suppressor genes. These mutations promote malignant advancement through the somatic inactivation of the remaining allele. This review aims to elucidate the main molecular mechanisms underlying the pathophysiology of major syndromes associated with renal cell carcinoma. By providing a comprehensive overview, it aims to facilitate early diagnosis and to highlight the principal therapeutic options available.

Kidney stone disease (KSD) is one of the most common urological diseases. The incidence of kidney stones has increased dramatically in the last few decades. Kidney stones are mineral deposits in the calyces or the pelvis, free or attached to the renal papillae. They contain crystals and organic components, and they are made when urine is supersaturated with minerals. Calcium-containing stones are the most common, with calcium oxalate as the main component of most stones. However, many of these form on a calcium phosphate matrix called Randall’s plaque, which is found on the surface of the kidney papilla. The etiology is multifactorial, and the recurrence rate is as high as 50% within 5 years after the first stone onset. There is a great need for recurrence prevention that requires a better understanding of the mechanisms involved in stone formation to facilitate the development of more effective drugs. This review aims to understand the pathophysiology and the main molecular mechanisms known to date to prevent recurrences, which requires behavioral and nutritional interventions, as well as pharmacological treatments that are specific to the type of stone.