Inflammation on the Waiting List Is a Risk Factor for New-Onset Prediabetes and Post-Transplant Diabetes Mellitus: A Prospective Study.

INTRODUCTION: Inflammation is a risk factor for diabetes in the general population. The role of inflammation in prediabetes or post-transplant diabetes mellitus (PTDM) is not clear. We evaluated the association between inflammatory markers in patients on the waiting list for renal transplantation and the onset of prediabetes and PTDM 12 months after transplantation. METHODS: This is a post hoc analysis of a prospective study that included nondiabetic patients on the waiting list for kidney transplantation who underwent an oral glucose tolerance test (OGTT) and were followed up to 12 months after transplantation. At this time, those patients without PTDM underwent another OGTT. At pre-transplantation, five cytokines: TNFα, IL6, IL1ß, CRP, MCP1 were determined. The association between inflammation and prediabetes/PTDM was evaluated using multiple regression models. RESULTS: 110 patients on the waiting list were enrolled: 74 had normal glucose metabolism and 36 had prediabetes or occult diabetes. At 12 months, 53 patients had normal glucose metabolism, 25 prediabetes, and 32 PTDM. In multiple regression analysis, pre-transplant inflammation was not a risk factor for prediabetes or PTDM. This was attributed to the high interrelation between obesity, prediabetes, and inflammation: about 75% of the cases had these conditions. In a sub-analysis, we analyzed only patients without prediabetes and occult diabetes on the waiting list and found that TNFα levels and BMI at pre-transplantation were independently associated with the onset of prediabetes or PTDM 1 year after transplantation. CONCLUSIONS: Pre-transplant inflammation and BMI are risk factors for prediabetes and PTDM in patients without glucose metabolism alterations.

Hiperparatiroidismo terciario como presentación de enfermedad ósea metabólica en trasplante renal: un reto diagnóstico-terapéutico. Presentación de un caso clínico / Tertiaryhyperparathyroidism as a manifestation of bone mineral metabolismdisease in kidneytransplantrecipient: a diagnostic and therapeuticchallenge. Presentation of a clinical case

RESUMEN El hiperparatiroidismo terciario se caracteriza por hipercalcemia e hiperparatiroidismo autónomo en el contexto de hiperparatiroidismo secundario persistente. El HPT3 se relaciona con calcificaciones extraesqueléticas o calcifilaxis, fracturas, dolor óseo, pérdida progresiva de la densidad mineral ósea, nefrocalcinosis, litiasis, disfunción o rechazo del aloinjerto, alteraciones neuropsiquiátricas, enfermedad cardiovascular y aumento de la morbimortalidad. La paratiroidectomía subtotal es el tratamiento de elección, con altas tasas de curación. Presentamos el caso de una paciente con hiperparatiroidismo terciario como enfermedad ósea metabólica después de un trasplante renal exitoso, con evolución insidiosa y daño óseo severo, con adecuada respuesta al tratamiento oportuno con paratiroidectomía subtotal. El diagnóstico y tratamiento oportuno del hiperparatiroidismo terciario en el paciente con trasplante renal es fundamental para disminuir la incidencia de comorbilidades, mejorar el pronóstico del paciente y optimizar recursos de salud.

ABSTRACT Tertiary hyperparathyroidism (THPT) is characterized by hypercalcemia and autonomous hyperparathyroidism in the context of persistent secondary hyperparathyroidism (SHPT). THPT is related with extraskeletal calcifications, calciphylaxis, fractures, bone pain, progressive loss of bone mineral density, nephrocalcinosis, lithiasis, kidney allograft dysfunction and rejection, neuropsychiatric alterations, cardiovascular disease, and high morbimortality. Subtotal parathyroidectomy is the gold standard for treatment, with high cure rates. We described a case of THPT as a manifestation of Bone Mineral Metabolism Disease after a successful kidney transplant, with an insidious evolution and severe bone damage, with an adequate response to subtotal parathyroidectomy. We evidenced that early diagnosis and treatment of THPT in kidney transplant recipients is essential to the diminution of comorbidities, the improvement of prognosis and the optimization of health resources.

Role of inflammatory cytokines in peripheral nerve injury.

Inflammatory events occurring in the distal part of an injured peripheral nerve have, nowadays, a great resonance. Investigating the timing of action of the several cytokines in the important stages of Wallerian degeneration helps to understand the regenerative process and design pharmacologic intervention that promotes and expedites recovery. The complex and synergistic action of inflammatory cytokines finally promotes axonal regeneration. Cytokines can be divided into pro- and anti-inflammatory cytokines that upregulate and downregulate, respectively, the production of inflammatory mediators. While pro-inflammatory cytokines are expressed in the first phase of Wallerian degeneration and promote the recruitment of macrophages, anti-inflammatory cytokines are expressed after this recruitment and downregulate the production of all cytokines, thus determining the end of the process. In this review, we describe the major inflammatory cytokines involved in Wallerian degeneration and the early phases of nerve regeneration. In particular, we focus on interleukin-1, interleukin-2, interleukin-6, tumor necrosis factor-ß, interleukin-10 and transforming growth factor-ß.