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The authors briefly describe the history of gout, mainly focusing their attention on the renal involvement. They report some works and theories on gout of great ancient physicians, such as Paracelsus, Sydenham, Boerhaave, Van Swieten and Morgagni.

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Kidney transplant from a living donor is known to be the best renal replacement therapy. While not as common as in northern Europe and the USA, living donor transplants are on the rise in Italy. Although there is a large body of evidence in the literature about the safety of the surgical procedure, the risk of long-term complications for the donor has not been clearly defined because of the lack of studies with adequate follow-up and a sufficient number of subjects involved. The main questions concern the development of chronic kidney disease in the donor, expressed as a GFR decline or the presence of microalbuminuria. The physiopathological basis of GFR decline and proteinuria development may differ from the model of nephropathy in patients with two kidneys, and this could involve prognostic differences too, particularly with regard to the cardiovascular risk. Detailed and prolonged follow-up programs are needed to monitor and, if necessary, treat long-term complications in kidney donors.

We report a case of Kaposi's sarcoma in a patient who received a double kidney transplant in 2005. Immunosuppression was induced with rapamycin and antilymphocyte serum while maintenance therapy consisted of rapamycin, corticosteroids and mycophenolic acid. The patient developed delayed graft function but no rejection. In November 2006 and March 2007 two graft biopsies were taken because of a significant rise in serum creatinine; they revealed chronic allograft nephropathy and polyomavirus infection. Meanwhile a skin biopsy of the leg was performed to determine the nature of a discolored lesion. The morphohistological diagnosis was Kaposi's sarcoma. For this reason rapamycin was stopped and steroid treatment gradually reduced. Specific therapy with doxorubicin was started; radiological and endoscopic examination excluded disseminated disease while serological tests were positive for antibodies to HHV-8, a virus known to cause Kaposi's sarcoma. Unfortunately, withdrawal of antirejection therapy caused loss of the graft, so the patient had to start dialysis. In this report we stress the possible development of malignancy in transplanted patients who are given rapamycin. Rapamycin is known to be an antirejection drug and to have antineoplastic activity; the major risk of malignancy is probably related to immunosuppression rather than the type of drugs used to obtain it.

Cyclosporin-induced hypertension and endothelial dysfunction have been attributed to the effects of cyclosporin on factors controlling vasomotor tone. Endothelial nitric oxide (NO) regulates basal vasodilation, and an NO-mediated protective mechanism from cyclosporin-induced vasoconstriction has been proposed. In transplanted patients with cyclosporin-induced hypertension, we have recently demonstrated upregulation of the NO system and superoxide and free radical overproduction, which, by increasing NO metabolism, could induce hypertension, vascular remodeling and chronic rejection. In the present work, we have evaluated endothelial constitutive NO synthase (ecNOS), transforming growth factor beta and heme oxygenase-1 (protective against oxidative stress), mRNA production and plasma NO metabolites, peroxynitrite and antioxidant power in 15 kidney transplanted patients before and after 4 months of treatment with carvedilol alpha 1-beta-blocker and potent antioxidant. Our aim was to study the efficacy of the reduction of oxidative stress on complications such as endothelial dysfunction and fibrogenesis. Monocyte ecNOS and plasma NO metabolites remained higher versus those of control subjects and were unchanged by carvedilol, while antioxidant power and heme oxygenase-1 mRNA production increased. Peroxynitrite, as well as transforming growth factor beta mRNA, were reduced by carvedilol. It also normalized blood pressure. In conclusion, carvedilol reduces oxidative stress and normalizes blood pressure; ecNOS remains upregulated while mRNA for transforming growth factor beta, a key fibrogenic cytokine, is reduced by carvedilol, which seems to preserve protective mechanisms such as NO and heme oxygenase-1 against long-term complications of oxidative stress, e.g., endothelial dysfunction, fibrogenesis and chronic rejection.

A group od 129 patients with persistent asymptomatic microhematuria was studied for 7 years (1987-1994). At the beginning of the study, 31 patients showed mild proteinuria (less than 1 g/day) and in the rest of 98 patients, 21 showed microalbuminuria. At the end of the study none of the patients developed renal failure, urological disease, hypertension. Six patients out of 31 with mild proteinuria (less than 1 g/day), developed an increase of proteinuria over 2 and 3/day and underwent a renal biopsy while 2 out of 21 patients with altered microalbuminuria completely recovered after the follow-up period. The rest of 77 patients at the end of the study still showed isolated microhematuria. The results of this study support the hypothesis that in a population with age range between 16 and 28 years, the presence of persistent microhematuria, also associated with mild proteinuria, even for a long time, does not seem to lead to changes of renal function or to urological diseases.