Pain management, supportive and palliative care in patients with renal cell carcinoma.

molecules or antibodies for each of these factors are currently under development in clinical trials for kidney cancer [6]. However, at present, speciﬁc targeted therapy for cachexia is not available. Several drugs with more general metabolic effects are available and potentially useful. Progestins were long thought to have antitumour activity in kidney cancer but have since been shown to lack signiﬁcant effects on progression or overall survival. The commonly used progestins, medroxyprogesterone acetate and megestrol acetate, have shown beneﬁt in decreasing loss of lean body mass and improving appetite in patients with advanced human immune virus infection [7,8]. In RCC, and many other cancers, progestins improve appetite and reduce or reverse cancer cachexia in some patients. Some patients beneﬁt from a subsequent dose-escalation. Recent meta-analyses of studies using megestrol acetate in cancer showed an improvement in appetite and body weight [9,10]. The optimum dose of megestrol acetate varies among patients, but a starting dose of 160 mg/day is well tolerated and increases or stabilizes weight over the subsequent 2 weeks [11,12]. Corticosteroids are used in managing cachexia in a proportion of patients, as well as being useful for treating anorexia, lethargy, spinal cord compression and pain from bone and liver metastases, in part through decreasing the amount of oedema present in and around tumour deposits. When studied in a formal phase III setting, dexamethasone 0.75 mg/day was equivalent in improving or maintaining weight gain and appetite to megestrol acetate 800 mg/day in patients with cancer-related anorexia–cachexia syndrome [13]. However, the two medications result in different side-effect proﬁles, which generally favour megestrol acetate except for the increased incidence of deep vein thrombosis (5% for megestrol vs 1% for dexamethasone) [13].Anaemia is a classic presenting symptom of RCC [14]. On occasion, RCC can also produce polycythaemia through erythropoietin production, which might be mediated through certain point mutations in the von Hippel-Lindau gene and loss of the feedback-loop effect in the erythropoietin pathway [15–18]. Anaemia can occur for various reasons in RCC and it is important to clinically evaluate the patient for signs of haematuria or alternative sites of bleeding, as well as potential iron, vitamin B12 or folate deﬁciency, before assuming they have paraneoplastic anaemia of malignancy. Similarly, not all lethargy is due to anaemia. A clinical evaluation for the contribution of side-effects from therapy, renal impairment and/or infection is important. The underlying cause of anaemia in patients with malignancy is complex, but in those with RCC it might relate to tumour production of IL-6 [19], once again suggesting it might be fruitful to target this and other similar molecules as part of the supportive therapy of patients with RCC. Anaemia of malignancy responds to erythropoietin in appropriately selected patients with an increase of 1–2 g/dL in haemoglobin over 6–12 weeks. Patients with a need for more rapid increase in haemoglobin need to consider red-cell transfusion.Hypercalcaemia can produce symptoms of confusion, constipation, somnolence and dehydration. Paraneoplastic production of PTHrp is the major underlying mechanism for hypercalcaemia in RCC, although some hypercalcaemic patients might have underlying osteolytic or prostaglandin-mediated increases in serum calcium [20–22]. The precise mechanisms by which PTHrp overproduction occurs in RCC are being elucidated, but patients with hypercalcaemia most likely have a distinct molecular signature that might include K-ras overexpression, among other molecular aberrations [23]. The incidence of hypercalcaemia in patients with RCC increases with stage [24]. The required treatment involves adequate hydration, either orally or i.v., and institution of therapy with i.v. bisphosphonates such as pamidronate or