Evolution of secondary hyperparathyroidism in patients following return to hemodialysis after kidney transplant failure.

INTRODUCTION: Severe uncontrolled secondary hyperparathyroidism and kidney transplantation history are both risk factors for fractures in hemodialyzed patients. Moreover, patients who return to dialysis after transplant failure have more severe infections/anemia and higher mortality risk than transplant-naive patients starting dialysis with native kidneys. In this context, our aim was to test the hypothesis that transplant failure patients have more secondary hyperparathyroidism than transplant-naive patients. METHODS: We retrospectively compared 29 transplant failure patients to 58 transplant-naive patients matched for age, sex, chronic kidney disease duration and diabetes condition (1 transplant failure/2 transplant-naive ratio), who started dialysis between 2010 and 2014. Clinical and biological data were collected at baseline, 6 and 12 months. FINDINGS: At baseline, neither serum parathyroid hormone (transplant-naive: 386±286pg/mL; transplant failure: 547±652pg/mL) nor serum 25-hydroxyvitamin D (transplant-naive: 27.8±17.0µg/L, transplant failure: 31.1±14.9µg/L) differed between groups. However, serum parathyroid hormone at 12 months and the proportion of patients with uncontrolled secondary hyperparathyroidism (parathyroid hormone>540pg/mL, KDIGO criteria) were significantly higher in transplant failure than in transplant-naive (parathyroid hormone: 286±205 vs. 462±449, P<0.01; uncontrolled secondary hyperparathyroidism: 30% vs. 13%, P<0.01, respectively). Within the transplant failure group, patients with uncontrolled secondary hyperparathyroidism at 12 months were younger than patients with normal or low parathyroid hormone. DISCUSSION: This retrospective and monocentric study suggests that transplant failure patients are more likely to develop secondary hyperparathyroidism. Thus, finding high serum parathyroid hormone in young transplant failure patients, who are expected to undergo further transplantations, should incite physicians to treat early and more aggressively this complication.

The use of the Oxford classification of IgA nephropathy to predict renal survival.

BACKGROUND AND OBJECTIVES: A new classification for IgA nephropathy was recently proposed, namely the Oxford classification. It established specific pathologic features that predict the risk of progression of renal disease. This classification needs validation in different patient populations. We propose a retrospective study to evaluate the predictive value of the Oxford classification on renal survival defined by doubling creatinine or end-stage renal disease in patients with IgA nephropathy. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: We included 183 patients with primary IgA nephropathy diagnosed between 1994 and 2005. Mean follow-up time was 77 months. Doubling creatinine occurred in 20% of the patients, and end-stage renal disease occurred in 16%. The biopsies were revisited to apply the Oxford classification. The influence of pathologic features on renal survival was analyzed in univariate and multivariate models. RESULTS: In univariate time-dependent analyses, tubular atrophy/interstitial fibrosis, segmental glomerulosclerosis, and endocapillary hypercellularity strongly impacted doubling creatinine or end-stage renal disease. On the contrary, mesangial hypercellularity was not associated with renal outcome. In the multivariate model, only estimated GFR at baseline was a risk factor, pathologic lesions having no independent influence. CONCLUSIONS: We confirm the usefulness of the Oxford classification to establish the renal prognosis of patients with IgA nephropathy, although renal function at baseline seems to be of a greater importance than pathologic lesions.