In this population-based study, 21 % of the patients had metastatic disease at presentation, with a decreasing trend over the study period. During 5-year follow-up, 20 % of the primary non-metastatic patients had recurrent disease. Of the patients with recurrence, half were given systemic oncological treatment and 17 % underwent metastasectomy.

No abstract

Background:This retrospective register study assessed overall survival (OS) and influential factors on OS in Swedish renal cell carcinoma (RCC) patients.Methods:Using three merged national health registers, Cox proportional-hazards analysis was conducted and, in three models, it was used to assess the impact of cytokine (interferon-α and tyrosine kinase inhibitor (TKI; sunitinib or sorafenib) treatment on OS in metastatic (m)RCC.Results:From 2000 to 2008, 8009 patients were diagnosed with RCC and 2753 with mRCC (2002–2008). Median OS in RCC patients diagnosed from 2006 to 2008 compared with 2000–2005 was not reached vs 47.9 months (P<0.001), and in mRCC patients diagnosed from 2006 to 2008 compared with 2002–2005, was 12.4 vs 9.6 months, respectively (P=0.004). Factors associated with significantly improved OS in RCC were female gender, lower age, and previous nephrectomy, and, in mRCC female gender, previous nephrectomy, and any TKI prescription (Model 1: median-adjusted OS, 19.4 months (TKI patients) vs 9.7 months (non-TKI patients); hazard ratio, 0.621; P<0.001).Conclusion:OS was improved in Swedish patients diagnosed with RCC and mRCC in the period 2006–2008 compared with 2000–2005 (RCC) and 2002–2005 (mRCC). Although multifactorial in origin, results suggest that increased nephrectomy rates and the use of TKIs contributed to the improvement seen in mRCC patients.

The NSKCR explores population-based data on the clinical handling of patients with RCC. This study, between 2005 and 2010, shows significant decrease in tumour size and metastatic RCC at presentation, a more complete preoperative work-up, and significantly increased use of PN and laparoscopic nephrectomy in Sweden.

The intrarenal erythrocyte distribution, total renal blood flow and renal vascular resistance were studied before and during recirculation after 60 min of warm ischaemia in three groups of rabbits. One group was pretreated with superoxide dismutase, another with catalase and the third group was not pretreated at all. In non-pretreated ischaemic kidneys there was a significant trapping of labelled erythrocytes in the outer stripe of the medulla. This trapping was not seen in non-ischaemic control kidneys and was completely prevented by pretreatment with either superoxide dismutase or catalase. In non-pretreated ischaemic kidneys there was a transient increase in total renal blood flow during the first 5 min of recirculation, after which it returned to preischaemic values. After pretreatment with catalase the postischaemic increase in blood flow was more pronounced but again the blood flow returned to preischaemic values within 30 min. Pretreatment with superoxide dismutase resulted in a rapid postischaemic increase in blood flow which remained high throughout the 30 min period studied. The renal vascular resistance decreased initially during recirculation after ischaemia in both pretreated and non-pretreated kidneys. In the latter it returned to pre-ischaemic values within 10 min whereas a slower increase was observed after catalase pretreatment. After pretreatment with superoxide dismutase the resistance remained low during the 30 min recorded.

Metabolic reprogramming is a hallmark of clear cell renal cell carcinoma (ccRCC) progression. Here, we used genome-scale metabolic modeling to elucidate metabolic reprogramming in 481 ccRCC samples and discovered strongly coordinated regulation of glycosaminoglycan (GAG) biosynthesis at the transcript and protein levels. Extracellular GAGs are implicated in metastasis, so we speculated that such regulation might translate into a non-invasive biomarker for metastatic ccRCC (mccRCC). We measured 18 GAG properties in 34 mccRCC samples versus 16 healthy plasma and/or urine samples. The GAG profiles were distinctively altered in mccRCC. We derived three GAG scores that distinguished mccRCC patients with 93.1%-100% accuracy. We validated the score accuracies in an independent cohort (up to 18 mccRCC versus nine healthy) and verified that the scores normalized in eight patients with no evidence of disease. In conclusion, coordinated regulation of GAG biosynthesis occurs in ccRCC, and non-invasive GAG profiling is suitable for mccRCC diagnosis.

An early decrease in the mean glucose uptake was found in both soft and skeletal lesions after treatment with sorafenib. FDG-PET thus seems to be advantageous, compared with RECIST evaluation, which is limited to soft lesions.

The mechanism for the high lactate production during hypothermic kidney perfusion has not been clarified previously. The metabolism of lactate and acetate was studied in 23 dog kidneys during continuous hypothermic perfusion. The perfusions were performed in a Gambro machine with a perfusate based on human serum albumin. With a perfusate containing fatty acid extracted albumin, which was almost free of fatty acids, the glucose uptake of the kidney was more pronounced than during perfusion with a fatty acid-rich perfusate. The high glucose uptake under this perfusion condition was associated with a lower lactate production and a higher glucose oxidation rate. In perfusions with a perfusate containing lactate at a concentration of 2.5 mmol/l a considerable lactate uptake of the kidney was shown. By isotope dilution technique the production and uptake rate of lactate was estimated at 4.4 and 8.0 µmol/g kidney and day in two experiments. The labeled lactate carbon was recovered in CO₂, and glucose in the perfusate indicating a continuous oxidation and gluconeogenesis. Acetate was used by the kidney both for oxidation and for gluconeogenesis. Addition of acetate to the ordinary fatty acid-rich perfusate caused an enhanced lactate production from the perfused kidney. The results indicate that the high lactate production during hypothermic perfusion of kidneys is mainly dependent on a metabolic blockade at the level of pyruvate dehydrogenase.