Background Ankylosing spondylitis (AS) is a chronic inflammatory condition with pain, stiffness and fatigue reported as the most troubling symptoms. Early and sustained relief of these symptoms is essential for effective management. Secukinumab provided sustained relief from pain and fatigue in AS patients over 2 years in the MEASURE 2 study. We report the effect of subcutaneous secukinumab 150 mg on key clinical symptoms (pain, morning stiffness and fatigue) in AS patients over 208 weeks in MEASURE 2. Methods This post-hoc analysis of MEASURE 2 assessed mean change from baseline to Week 208 in total and nocturnal back pain scores (by VAS [0-100]; ASAS outcome component), overall level of spinal pain (neck, back or hip) from BASDAI scores, and morning stiffness (overall level; mean of question 5 and 6 of BASDAI score). Additionally, the SF-36 physical component summary score, overall level of fatigue (BASDAI question 1), FACIT-Fatigue score and patients meeting minimal clinically important difference (MCID) criteria across multiple clinical domains were assessed. Data are shown for patients originally randomised to secukinumab 150 mg and placebo. Data are reported as observed for the overall population and by prior TNF inhibitor (TNFi) therapy status (naive vs inadequate response [IR]). Results Baseline characteristics were comparable across secukinumab 150 mg (N = 72) and placebo (N = 74) groups; total mean back pain score was 67.7±17.79, nocturnal back pain score was 64.9±19.58 and morning stiffness was 6.5±2.11. Secukinumab 150 mg-treated patients reported rapid and early reductions in pain scores by Week 4, which were sustained through Week 208 (Table 1). Improvements with secukinumab 150 mg were reported for all key clinical symptoms by Week 4, which were sustained at Week 208. A higher proportion of secukinumab 150 mg-treated patients met MCID criteria at Week 16 vs placebo across multiple clinical domains, which was sustained or further improved through Week 208. Improvements were observed in TNFi-naive and -IR patients, with a greater magnitude of improvement in TNFi-naive patients. Conclusion Secukinumab 150 mg was associated with rapid and clinically meaningful improvements in total and nocturnal back pain, morning stiffness and fatigue, with improvements sustained over 4 years of treatment. Disclosures H. Marzo-Ortega: Consultancies; AbbVie, Celgene, Janssen, Lilly, Novartis, Pfizer, UCB. Member of speakers’ bureau; AbbVie, Celgene, Janssen, Lilly, Novartis, Pfizer, UCB. Grants/research support; Janssen, Novartis. C. Miceli-Richard: Consultancies; Pfizer, Roche, UCB, Wyeth, Merck. Member of speakers’ bureau; Abbott, Bristol-Myers Squibb, Merck, Pfizer, Roche, Schering-Plough, Wyeth. Grants/research support; AbbVie, Bristol-Myers Squibb, Novartis, Merck, Pfizer, Wyeth. S. Gill: Consultancies; AbbVie, Eli Lilly, Janssen, Novartis, Pfizer, UCB, Amgen, Sanofi-Genzyme. Other; AbbVie, Eli Lilly, Janssen, Novartis, Pfizer, UCB, Amgen, Sanofi-Genzyme. M. Magery: Consultancies; Eli Lilly, Novartis. Grants/research support; AbbVie, UCB, Amgen. P.G.P. Machado: Shareholder/stock ownership; Novartis. Other; Employee of Novartis. A. Shete: Shareholder/stock ownership; Novartis. Other; Employee of Novartis. J. Wang: Other; Employee of Novartis. S. Rohrer: Shareholder/stock ownership; Novartis. Other; Employee of Novartis. A. Deodhar: Consultancies; AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly, GSK, Galapagos, Janssen, Novartis, Pfizer, UCB. Grants/research support; Eli Lilly, GSK, Novartis, Pfizer, Boehringer Ingelheim, Bristol-Myers Squibb, UCB.

Non-white patients show higher tacrolimus variability and lower drug exposures after transplantation compared with W patients. Therefore, higher initial tacrolimus doses and intensive monitoring are recommended when administering tacrolimus-based immunosupressive therapy to NW patients of this transplant population.

The combination of 2 mg fixed doses of SRL, reduced cyclosporine exposure and prednisone was associated with a low incidence of acute rejection and did not result in significantly impaired graft function compared with patients receiving AZA, standard doses of cyclosporine and prednisone.

Systemic arterial hypertension is a common complication among transplanted patients. The objective of this study was to investigate the risk factors for arterial hypertension after kidney transplantation in children. A retrospective study was carried out of 70 kidney transplants performed on patients under 18 years of age at the Hospital do Rim and Hipertensão, from January 1998 to June 2001. At the end of 6 months post transplant, the patients were classified into either normotensive ( n=31) or hypertensive ( n=39) groups. The following potential risk factors for arterial hypertension were studied: (1) hypertension before transplantation; (2) the glomerular filtration rate (GFR) at 1, 3, and 6 months post transplant; (3) acute rejection episodes; (4) cumulative dose of corticosteroids; (5) the presence of native kidneys; (6) symptomatic renal artery stenosis; (7) cold ischemia time greater than 24 h; (8) age and sex of the donor; (9) age of the recipient; (10) transplant type (living related or cadaveric donor); (11) the body mass index of recipients at the end of the follow-up period; and (12) delayed graft function. The two groups were comparable in terms of the etiology of renal insufficiency, age, gender, and immunosuppressive drugs. Among the risk factors studied, the sole factor showing a statistically significant association with arterial hypertension was the GFR at 3 and 6 months after transplantation. In the group of normotensive patients, GFRs were 92+/-29 and 83+/-20 ml/min per 1.73 m(2) at 3 and 6 months, respectively, whereas in the hypertensive patients, GFRs were 74+/-23 and 70+/-21 ml/min per 1.73 m(2) respectively. Hence, only the lower GFR can be considered a risk factor for hypertension in children within our sample. However, arterial hypertension might be a risk factor for the early onset of chronic allograft nephropathy; in this case, hypertension should be considered the cause of lower glomerular filtration. Our data do not permit us to distinguish between these two hypotheses. The known risk factors for hypertension following renal transplantation in adults were not confirmed in the present study. It remains unclear to us as to whether this means the etiology of hypertension differs in children, or if this is the result of a bias in patient selection.

Our study demonstrated that patients with transplanted kidney and augmented bladder had more asymptomatic bacteriuria and urinary tract infections than those without bladder augmentation. However, the rate of graft survival was similar between the groups.

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