Scielo RSS http://scielo.pt/rss.php?pid=0872-016920120002&lang=en vol. 26 num. 2 lang. en http://scielo.pt/img/en/fbpelogp.gif http://scielo.pt http://scielo.pt/scielo.php?script=sci_arttext&pid=S0872-01692012000200001&lng=en&nrm=iso&tlng=en http://scielo.pt/scielo.php?script=sci_arttext&pid=S0872-01692012000200002&lng=en&nrm=iso&tlng=en The outcome of human immunodeficiency virus (HIV)-positive patients has improved dramatically with the advent of combined antiretroviral therapy. The mortality rate for HIV-positive patients with chronic kidney disease stage 5 is now similar to those without HIV infection, making kidney transplantation an increasingly considered alternative treatment for end-stage renal disease in this population. Knowledge of the pharmacokinetics of antiretroviral medications and potential drug-drug interactions between antiretroviral and immunosuppressive medications are critical to the success of transplantation in this setting. The aim of this article is to present the state of the art kidney transplant therapy in HIV-positive patients. http://scielo.pt/scielo.php?script=sci_arttext&pid=S0872-01692012000200003&lng=en&nrm=iso&tlng=en In chronic kidney disease patients there are three main stimuli for parathyroid hormone (PTH) secretion by the chief cell in the parathyroid glands: hypocalcaemia, low 1,25(OH)2D3 levels and hyperphosphataemia. FGF23 is a regulator of phosphate and vitamin D metabolism. The discovery of FGF23 actions enlightened our understanding of the development of secondary hyperparathyroidism in CKD patients. The main systemic factors that stimulate FGF23 secretion by the osteocyte in the bone appear to be phosphate load and 1,25(OH)2D3. In the kidney, FGF23 decreases the number of Na/Pi co-transporters IIa and IIc in the tubular cell and promotes phosphaturia. FGF23 also reduces 1,25(OH)2D3 levels by inhibiting, in the kidney, its production by 1-alpha-hydroxylase and stimulating its degradation by 24-hydroxylase. Increase in FGF23 levels has been described in early 2 and 3 CKD stages preceding the decrease of 1,25(OH)2D3 levels and hyperphosphatemia. In this sequence of events, increase of FGF23 in CKD patients seems to be a novel mechanism for the early decline of 1,25(OH)2D3 levels observed in these patients. It was hypothesised that klotho deficiency creates a tissue resistance to FGF23 which is responsible for the increase of FGF23 levels. Reduced renal expression of klotho has been demonstrated in CKD patients preceding FGF23 increase. Chronic kidney disease may be considered a state of klotho deficiency with increase of FGF23 levels. Klotho deficiency may be the initial alteration for the development of phosphate retention and secondary hyperparathyroidism in CKD patients. In this article we review the classic and new pathways involved in the development of secondary hyperparathyroidism in chronic kidney disease and the subsequent actions ensuing from this knowledge. It is possible that, in 3 and 4 CKD stages, an early therapeutic intervention consisting of a low phosphate diet and/or phosphate binders, even in the presence of normophosphataemia, might retard the development of secondary hyperparathyroidism http://scielo.pt/scielo.php?script=sci_arttext&pid=S0872-01692012000200004&lng=en&nrm=iso&tlng=en Introduction. IgA nephropathy is the dominant primary glomerular disease found throughout the majority of the world’s developed countries. Accurately identifying patients who are at risk of progressive disease is challenging. We aimed to characterise clinical and histological features that predict poor prognosis in adults. Patient and Methods. We performed a single-centre retrospective observational study of biopsy-proven IgA nephropathy. The primary outcome was renal survival and death from any cause, and the secondary outcome was proteinuria remission. Results.Data from 49 cases were available for analysis with a median follow-up of 4 years. There were no deaths. Univariableanalyses identified acute renal failure, low estimated glomerular filtration rate for ≥3 months (low eGFR), arterial hypertension, baseline proteinuria, glomerular sclerosis >50% and interstitial fibrosis >50% as poor prognostic markers. Low eGFR persisted significant by multivariable model that used only clinical parameters. Multivariable models with histopathologic parameters observed that tubular atrophy/interstitial fibrosis >50% was independently associated with the primary outcome. Proteinuria remission throughout follow-up had no prognostic value in our revision. Conclusions.Two independent predictors of poor renal survival at time of biopsy were found: low eGFR and tubular atrophy/interstitial fibrosis >50%. http://scielo.pt/scielo.php?script=sci_arttext&pid=S0872-01692012000200005&lng=en&nrm=iso&tlng=en Sirolimus, a mammalian target of rapamycin inhibitor, is an increasingly used immunosuppressant in solid-organ transplantation. There are an increasing number of reports of unusual oedematous adverse effects associated with this drug, including lymphoedema, ascites and pleural effusions, and a few reports of pericardial effusions. No pathophysiological explanation for these phenomena has been disclosed. We report a 33-year-old sirolimus-treated kidney transplant recipient with chronic pericardial and pleural effusions identified nine years after transplantation. He was initially treated for a presumed tuberculous pericarditis, even though cultures for Mycobacterium tuberculosis were negative. After 12 months of antitubercular therapy, visceral effusions persisted. Pericardial effusion was drained and stabilised. After exclusion of other causes, sirolimus toxicity was considered the most likely cause. Two months after discontinuation of sirolimus, visceral effusions disappeared. Interaction of mammalian target of rapamycin inhibitors with mediators of lymphangiogenesis may be a common link in oedematous states associated with sirolimus. http://scielo.pt/scielo.php?script=sci_arttext&pid=S0872-01692012000200006&lng=en&nrm=iso&tlng=en Tenofovirrenal toxicity, particularly when associated with other antiretrovirals, has been reported in the adult HIV-positive population. Reports in HIVpositive children are very rare. The authors report a paediatric case of nephrotoxicity associated with tenofovir and didanosine, emtricitabine and lopinavirritonavir coadministration. A 12-year-old girl with AIDS (clinical stage C) with a multidrug-resistant virus and several treatment failures initiated emtricitabine, tenofovir, didanosine and lopinavir-ritonavir in 2008 with good tolerance. Her viral load became undetectable and CD4 count normal. Two years later she presented generalized weakness, polydipsia and polyuria. On physical examination dehydration was evident. Her vital signs were stable. She had lost 5% of her body weight in the previous week. Urinalysis revealed a urine gravity of 1000, osmolality 150 mOsm/Kg and no proteinuria or glucosuria. Blood analysis showed osmolality 289 mOsm/Kg, normal values of glucose, creatinine, urea, sodium, potassium, chloride and calcium. A water restriction test followed by desmopressin administration confirmed the diagnosis of nephrogenic diabetes insipidus. Tenofovir and didanosine were stopped and abacavir was added. The patient was treated with a thiazide diuretic and salt restriction. There was good clinical evolution and no relapses. This case highlights important possible side effects of tenofovir and emphasises the need for further studies into the renal safety of this agent in paediatric patients. http://scielo.pt/scielo.php?script=sci_arttext&pid=S0872-01692012000200007&lng=en&nrm=iso&tlng=en The improvement of combined antiretroviral therapy regimens has made solid organ transplantation a therapeutic option for patients with human immunodeficiency virus (HIV) infection. Generally, HIV-2 infectionpresents a slower clinical progression and immunological degradation than HIV-1. HIV-2 infection treatment can be challenging when a complex immunosuppressive regimen is combined with antiretroviraltherapy. The authors report the first case in Portugal of renal transplantation in an HIV-2 patient. A 54-year-old man from Guinea-Bissau was diagnosed with HIV-2 infection on starting haemodialysis in Portugal in 1998. At diagnosis, HIV infection staging revealed undetectable plasma HIV- 2 RNA and T-cell CD4 counts of 808 cells/μl, with no need for combined antiretroviral therapy during follow-up. The patient underwent renal transplantation from a deceased donor in March 2011. He developed delayed graft function and started therapy with methylprednisolone and thymoglobulin. The patient gradually recovered renal function and was discharged after two weeks with serum creatinine of 2.3 mg/dL. The HIV-2 RNA levels remained undetectable, but T-cell CD4count decreased to less than 200 cells/μl and combined antiretroviral therapy with abacavir, lamivudine and raltegravir was started. Nine months after transplantation, the patient has a serum creatinine of 1.5 mg/dL and a nonreplicating HIV status