The aim of the study was to investigate the prevalence and aetiology of chronic kidney disease (CKD) and trends in estimated glomerular filtration rate (eGFR) in HIV-infected patients. MethodsAscertainment and review of CKD cases among patients attending King's College and Brighton Hospitals, UK were carried out. CKD was defined as eGFR o60 mL/min for ! 3 months. Longitudinal eGFR slopes were produced to examine trends in renal function before, during and after exposure to indinavir (IDV) or tenofovir (TFV). ResultsCKD prevalence was 2.4%. While HIV-associated nephropathy accounted for 62% of CKD in black patients, 95% of CKD in white/other patients was associated with diabetes mellitus, hypertension, atherosclerosis and/or drug toxicity. Exposure to IDV or TFV was associated with an accelerated decline in renal function (4.6-fold and 3.7-fold, respectively) in patients with CKD. In patients initiating IDV, age ! 50 years increased the odds of CKD [odds ratio (OR) 4.9], while in patients initiating TFV, age ! 50 years (OR 5.4) and eGFR 60-75 mL/min (OR 17.2) were associated with developing CKD. ConclusionThis study highlights the importance of metabolic and vascular disease to the burden of CKD in an ageing HIV-infected cohort. In patients who developed CKD, treatment with IDV or TFV was associated with an accelerated decline in renal function.Keywords: glomerular filtration rate, HIV, indinavir, kidney, tenofovir Accepted 20 November 2008 Introduction Acute renal failure (ARF) and chronic kidney disease (CKD) are important complications of HIV infection [1]. Approximately 6% of HIV-infected patients develop one or multiple episodes of ARF [2], and 15% of patients have evidence of CKD [3,4]. ARF usually occurs in the setting of severe (opportunistic) infections, malignancy or liver disease [2,5], and both ARF and CKD are associated with advanced immunodeficiency [2][3][4][5][6]. Black HIV-infected patients are at risk of developing HIV-associated nephropathy (HIVAN), which is characterized by heavy proteinuria and rapid progression to end-stage renal disease (ESRD) [7][8][9]. HIVAN, idiopathic noncollapsing focal and segmental glomerulonephritis (FSGS), immune complex kidney disease and other glomerulopathies predominate in biopsy series and among black patients with ESRD [7,[10][11][12][13].In the general, HIV-uninfected population, the prevalence of CKD increases dramatically in those aged 50 years and over [14]. CKD in these patients is associated with diabetes mellitus, hypertension and atherosclerosis [15], and is an independent risk factor for coronary heart disease [16]. CKD in this setting is often insidious in onset and may take decades to become clinically manifest. The objectives of this study were to describe the prevalence and aetiology of CKD in HIV-infected patients receiving care in the UK, and to examine trends in renal function before, during and after exposure to IDV or TFV in patients with CKD. Methods Case ascertainmentAll HIV-infected adults with CKD who attended King's College Hospital ...

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Risk of type 1 diabetes at 3 years is high for initially multiple and single Ab+ IT and multiple Ab+ NT. Genetic predisposition, age, and male sex are significant risk factors for development of Ab+ in twins.

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The leukocyte Na/H antiporter has been studied in patients with end-stage renal failure on maintenance haemodialysis. Thirteen non-diabetic haemodialysis patients (CRF group) and eight haemodialysis patients with diabetic nephropathy (CRF-DM group) were investigated. Measurements were made using the pH-sensitive fluorescent dye bis (carboxyethyl) carboxyfluorescein (BCECF). The initial intracellular pH (pHi), intracellular buffering capacity, and Na/H antiporter Vmax (at pHi = 6.0) have been recorded in bicarbonate-free solutions. The mean initial intracellular pH in the CRF group was 7.34 (SD 0.05, P less than 0.004) and this was significantly less than the CRF-DM group (7.42, SD 0.07) and normal controls (7.43, SD 0.09, n = 25). The mean intracellular buffering capacity was normal in the CRF and CRF-DM groups. The mean Na/H antiporter Vmax was also normal in the CRF and CRF-DM groups (56.5, SD 9.9; and 56.8, SD 12.8, mmol/l per min respectively compared to 55.2, SD 8.8, mmol/l per min in controls). These data are discussed with reference to the reported high values of Na/H antiporter Vmax in diabetic patients with early nephropathy. This abnormality does not appear to be present in end-stage diabetic nephropathy.