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Kidney cancer (KC) is a disease with a rising worldwide incidence estimated at 400 000 new cases annually, and a worldwide mortality rate approaching 175 000 deaths per year. Current projections suggest incidence continuing to increase over the next decade, emphasizing the urgency of addressing this significant global health trend. Despite the overall increases in incidence and mortality, striking social disparities are evident. Low- and middle-income countries bear a disproportionate burden of the disease, with higher mortality rates and later-stage diagnoses, underscoring the critical role of socioeconomic factors in disease prevalence and outcomes. The major risk factors for KC, including smoking, obesity, hypertension and occupational exposure to harmful substances, must be taken into account. Importantly, these risk factors also often contribute to kidney injury, a condition that the review identifies as a significant, yet under-recognized, precursor to KC. Finally, the indispensable role of nephrologists is underscored in managing this complex disease landscape. Nephrologists are at the forefront of detecting and managing kidney injuries, and their role in mitigating the risk of KC is becoming increasingly apparent. Through this comprehensive analysis, we aim to facilitate a more nuanced understanding of KC's epidemiology and determinants providing valuable insights for researchers, clinicians and policymakers alike., (© The Author(s) 2024. Published by Oxford University Press on behalf of the ERA.)

Often the cause of refractory lupus nephritis (RLN) remains unclear. We performed next-generation sequencing for podocyte genes in an RLN patient and identified compound heterozygosity for APOL1 risk alleles G1 and G2 and a novel homozygous c.[1049C>T]+[1049C>T] NPHS1 gene variant of unknown significance. To test for causality renal progenitor cells isolated from urine of this patient were differentiated into podocytes in vitro. Podocytes revealed aberrant nephrin trafficking, cytoskeletal structure and lysosomal leakage, and increased detachment as compared with podocytes isolated from controls. Thus, lupus podocytopathy can be confirmed as a cause of RLN by functional genetics on patient-derived podocytes., (© The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

The tubular compartment of the kidney is the primary site of a wide range of insults that can result in acute kidney injury (AKI), a condition associated with high mortality and an increased risk to develop end-stage renal disease. Nevertheless, kidney function is often quickly recovered after tubular injury. How this happens has only partially been unveiled. Indeed, although it has clearly been demonstrated that regenerated epithelial cells arise from survived intratubular cells, the true entity, as well as the cellular source of this regenerative process, remains mostly unknown. Is whichever proximal tubular epithelial cell able to dedifferentiate and divide to replace neighboring lost tubular cells, thus suggesting an extreme regenerative ability of residual tubular epithelium, or is the regenerative potential of tubular epithelium limited, and mostly related to a preexisting population of intratubular scattered progenitor cells which are more resistant to death? Gaining insights on how this process takes place is essential for developing new therapeutic strategies to prevent AKI, as well as AKI-related chronic kidney disease. The aim of this review is to discuss why the answers to these questions are still open, and how further investigations are needed to understand which is the true regenerative potential of the tubule and who are the players that allow functional recovery after AKI., (© The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA.)