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Background Calciphylaxis is not uniquely observed in uraemic patients, as some cases have also been reported in patients with normal renal function or moderate chronic kidney disease (CKD), in association with severe vasculopathy or systemic inflammation. A particular subset worthy of studying is represented by those patients who develop calciphylaxis after kidney transplantation (KT). Methods Analysis of the local series of calciphylaxis after KT (n = 14) along with all the other cases reported in the literature from 1969 to 2019 (n = 31), for a total population of 45 patients, is presented. Demographic data, CKD history, risk factors, immunosuppression, clinical presentation and management have been analysed both as a whole and according to the time period (before or after the year 2000). Results Calciphylaxis developed during the first year after KT in 43.2% of patients and median (interquartile range) creatinine at diagnosis was 2.4 (1.25–4.64) mg/dL. The most frequent presentation included distal purpura or ulcers in one-third of cases and 39.1% of patients were receiving vitamin K antagonists. PTH values were above 500 pg/mL and below 100 pg/mL in 50.0% and 25.0% of cases, respectively. Whole population mortality was 55.6%. As expected, clinical presentation, immunosuppression and management varied depending on the time period. Patients diagnosed after 2000 were older, with longer dialysis vintage, and treatment was usually multimodal; on the contrary, in patients diagnosed before 2000, parathyroidectomy was the treatment of choice in 61.9% of cases. Conclusions Calciphylaxis can still occur after KT, in many cases during the first year and in patients with a good renal function. Risk factors and management varied according to the time period studied.

The dialysis-based definition of Delayed Graft Function (dDGF) is not necessarily objective as it depends on the individual physician's decision. The functional definition of DGF (fDGF, the failure of serum creatinine to decrease by at least 10% daily on 3 consecutive days during the first week post-transplant), may be more sensitive to reflect recovery after the ischemia-reperfusion injury. We retrospectively analyzed both definitions in 253 deceased donor kidney transplant recipients for predicting death-censored graft failure as primary outcome, using eGFR < 25 ml/min/1.73 m2 as a surrogate end-point for graft failure. Secondary outcome was a composite outcome that included graft failure as above and also patient's death. Median follow-up was 3.22 [2.38-4.21] years. Seventy-nine patients developed dDGF (31.2%) and 127 developed fDGF (50.2%). Sixty-three patients fulfilled criteria for both definitions (24.9%). At multivariable analysis, the two definitions were significantly associated with the primary [HR (95%CI) 2.07 (1.09-3.94), P = 0.026 for fDGF and HR (95%CI) 2.41 (1.33-4.37), P = 0.004 for dDGF] and the secondary composite outcome [HR (95%CI) 1.58 (1.01-2.51), P = 0.047 for fDGF and HR (95%CI) 1.67 (1.05-2.66), P = 0.028 for dDGF]. Patients who met criteria for both definitions had the worst prognosis, with a three-year estimates (95%CI) of survival from the primary and secondary outcomes of 2.31 (2.02-2.59) and 2.20 (1.91-2.49) years for fDGF+/dDGF+, in comparison with the other groups (P < 0.01 for trend). fDGF provides supplementary information about graft outcomes on top of the dDGF definition in a modern series of kidney transplantation.

X-linked hypophosphataemia (XLH) rickets is a rare disease frequently misdiagnosed and mismanaged. Despite having clinical guidelines that offers some therapeutic recommendations based on the clinical experience of experts, physicians still have questions about some important aspects of the diagnosis and treatment of XLH, such as when the disease should be suspected, who should be in charge of the diagnosis, what should be done once the disease is diagnosed, or what therapeutic options are currently available. The objective of this paper is to answer some of the more frequent questions related to the management of patients with XLH by a group of experts participating in a scientific conference on XLH held in Madrid.

Background It is commonly believed that mTOR inhibitors (mTORi) should not be used in high-immunological risk kidney transplant recipients due to a perceived increased risk of rejection. However, almost all trials that examined the association of optimal-dose mTORi with calcineurin inhibitor (CNI) have excluded hypersensitized recipients from enrollment. Methods To shed light on this issue, we examined 71 consecutive patients with a baseline calculated panel reactive antibody (cPRA) ≥50% that underwent kidney transplantation from June 2013 to December 2016 in our unit. Immunosuppression was based on CNI (tacrolimus), steroids and alternatively mycophenolic acid (MPA; n = 38), or mTORi (either everolimus or sirolimus, n = 33, target trough levels 3-8 ng/mL). Results Demographic and immunological risk profiles were similar, and almost 90% of patients in both groups received induction with lymphocyte-depleting agents. Cox-regression analysis of rejection-free survival revealed better results for mTORi versus MPA in terms of biopsy-proven acute rejection (hazard ratio [confidence interval], 0.32 [0.11-0.90], P = 0.031 at univariable analysis and 0.34 [0.11-0.95], P = 0.040 at multivariable analysis). There were no differences in 1-year renal function, Banff chronicity score at 3- and 12-month protocol biopsy and development of de novo donor-specific antibodies. Tacrolimus trough levels along the first year were not different between groups (12-mo levels were 8.72 ± 2.93 and 7.85 ± 3.07 ng/mL for MPA and mTORi group respectively, P = 0.277). Conclusions This single-center retrospective cohort analysis suggests that in hypersensitized kidney transplant recipients receiving tacrolimus-based immunosuppressive therapy similar clinical outcomes may be obtained using mTOR inhibitors compared to mycophenolate.

Background and Aims Calciphylaxis, also known as calcific uremic arteriolopathy (CUA), is a rare and underdiagnosed condition usually associated with end-stage renal disease (ESRD), with a poor prognosis once established. Although typically related with ESRD vintage, there are some reports of CUA after kidney transplantation (KT). The development of CUA in patients with KT is uncommon, and the underlying factors for its development remain unclear. Method Revision of the factors associated with the development of CUA after KT in 37 cases, of which 8 cases were extrapolated from our local registry and 29 cases reported by the literature from 1969 to 2019. Differences between groups were analyzed with Student’s T-test and Fisher’s exact test, according to the studied variable (continuous/dichotomous). Results Demographic and baseline characteristics are displayed in Table 1. In the whole population, 52.8% of patients were men and mean age was of 46.95 ± 18.72 years. Diabetes mellitus was present in 36.4% of patients while only 5.3% were reported to be obese. Vitamin K inhibitors were used in almost half of the population (45.5%). Creatinine at diagnosis was 3.14 ± 3.63 mg/dl. Dialysis and transplant vintage were respectively 76.97 ± 141.90 and 29.54 ± 56.11 months. Mean PTH was 631.15 ± 502.64 and previous parathyroidectomy was performed in 21.6% of patients. It has to be highlighted that 28.0% of total population had PTH levels < 100 pg/ml at diagnosis. Total calcium was 9.69 ± 1.04 mg/dl and phosphorus 4.16 ± 1.51 mg/dl. Many of these factors differed greatly depending on the time period of the diagnosis (before or after 1990). Patients diagnosed before 1990 were younger than those diagnosed after 1990 (31.57 ± 10.19 years vs. 56.30 ± 16.44 years; p < 0.001). Creatinine at diagnosis was much lower in patients diagnosed before 1990 (1.44 ± 0.58 vs. 3.68 ± 4.03). Dialysis and transplant vintage were greater in cases diagnosed after 1990 (dialysis plus transplant vintage 19.87 ± 12.65 vs. 115.04 ± 174.14, p=0.02). Patients diagnosed after 1990 had higher phosphorus and lower calcium compared to the other group. The employed immunosuppression changed considerably during time, being based on azathioprine (90.9%) and prednisone (100.0%) before 1990 and on calcineurin inhibitors (76.5%), mycophenolic acid (41.2%) and/or mTOR inhibitors (41.2%) and steroids (82.4%) after 1990. The CUA treatment demonstrated great variability too. Before 1990, 76.9% of patients were submitted to therapeutic parathyroidectomy, while after 1990 it was only performed in 10.5% of patients (P Conclusion Factors associated with the development of CUA after KT varied greatly during time. Patients diagnosed before 1990 were younger, with better renal function, shorter dialysis and transplant vintage, higher calcium and lower phosphorus. Parathyroidectomy was the main therapeutic option before 1990 while after 1990 treatment was multimodal.

Background and Aims Tertiary hyperparathyroidism is a common cause of hypercalcemia after kidney transplant (KT) and has been associated with renal dysfunction, loss bone mineral density and increased risk of fracture, vascular calcification, and increased risk of cardiovascular events. Long clinical management remains controversial. The aim of this study is to evaluate the long-term effectiveness and safety of parathyroidectomy versus cinacalcet in patients with persistent hyperparathyroidism. Method A 12-month prospective, multicenter, randomized study demonstrated than subtotal parathyroidectomy is more effective than cinacalcet for controlling hypercalcemia. Now, we evaluate in the same cohort of patients if this effect is maintained after 5 years of follow-up. Laboratory assessment included serum calcium, serum phosphate, intact parathyroid hormone (iPTH), calcidiol levels, estimated glomerular filtration rate and proteinuria at 2, 3, 4 and 5 year follow-up. Therapeutic details about the use of vitamin D, calcium supplementation and phosphate binders were compiled. Fragility fractures were also collected. Results In total, 24 patients had data available at 5 years, 13 in the cinacalcet group and 11 in the parathyroidectomy group. At 5 years, six of 13 patients in the cinacalcet group and ten of 11 patients in the parathyroidectomy group (p=0.015) showed normocalcemia (Figure 1). Subtotal parathyroidectomy retained a greater reduction of iPTH compared with cinacalcet group (Figure 2). No differences were observed in kidney function and incidence of fragility fractures between both groups. In relation of treatment, 8 of 13 patients in cinacalcet group maintained treatment with cinacalcet after 5 years follow-up. Conclusion Subtotal parathyroidectomy is more effective in long term to maintain normal serum calcium and iPTH compared with cinacalcet in kidney transplant patients with tertiary hyperparathyroidism.

The TRANSFORM study demonstrated that an immunosuppression based on a combination of calcineurin inhibitors and de-novo mTOR inhibitors (mTORi) is safe and effective in kidney transplant recipients. However, data that validate this approach in clinical practice are currently missing. Analysis of 401 kidney transplant recipients transplanted from June 2013 to December 2016. All patients received tacrolimus with prednisone in combination with either mycophenolate (n = 186) or mTORi (either everolimus or sirolimus, n = 215). A propensity score to receive mTORi was calculated based on the inverse probability of treatment weighting (IPTW) from the following parameters: age and sex of donor and recipient, BMI, previous transplants, diabetes, cPRA, dialysis before transplantation, dialysis vintage, type of donor, ABO-incompatibility, HLA-mismatches, induction and ischemia time. Median follow-up was 2.6 [1.9; 3.7] years. Cox-regression analysis suggests good results for mTORi versus MPA in terms of 1-year biopsy-proven acute rejection (BPAR, P = 0.063), 1-year graft loss (P = 0.025) and patient survival (P

ResumenEl hiperparatiroidismo secundario (HPTS) es una complicación habitual en pacientes con enfermedad renal crónica que se caracteriza por unos niveles elevados de hormona paratiroidea (PTH) y una serie de anomalías en el metabolismo mineral-óseo. En pacientes con HPTS, el tratamiento con paricalcitol, un activador selectivo de los receptores de la vitamina D, ha demostrado reducir los niveles de PTH con mínimas variaciones del calcio y del fósforo séricos. El efecto clásico de paricalcitol es el de mediador en la homeostasis mineral y ósea. Sin embargo, estudios recientes han indicado que los beneficios del tratamiento con paricalcitol van más allá de la reducción de PTH, por ejemplo, ocasionando efectos positivos en la enfermedad cardiovascular y en la supervivencia. El objetivo del presente trabajo es revisar los estudios más significativos sobre los llamados efectos pleiotrópicos del tratamiento con paricalcitol en pacientes con ERC.AbstractSecondary hyperparathyroidism (SHPT) is a common complication in patients with chronic kidney disease (CKD) that is characterised by elevated parathyroid hormone (PTH) levels and a series of bone-mineral metabolism anomalies. In patients with SHPT, treatment with paricalcitol, a selective vitamin D receptor activator, has been shown to reduce PTH levels with minimal serum calcium and phosphorus variations. The classic effect of paricalcitol is that of a mediator in mineral and bone homeostasis. However, recent studies have suggested that the benefits of treatment with paricalcitol go beyond PTH reduction and, for instance, it has a positive effect on cardiovascular disease and survival. The objective of this study is to review the most significant studies on the so-called pleiotropic effects of paricalcitol treatment in patients with CKD.

In the original article, third author name has been published incorrectly.

Calciphylaxis, also known as calcific uremic arteriolopathy, is a rare syndrome that typically causes skin necrosis and usually affects dialysis patients. Its pathogenesis is multifactorial and is the consequence of many factors causing ectopic calcifications in patients with chronic kidney disease, such as calcium-phosphate metabolism disorders, hyper- or hypo-parathyroidism, diabetes, obesity, systemic inflammation and the use of vitamin K antagonists, among others. From a clinical point of view, calciphylaxis may progress from painful purpura to extensive areas of skin necrosis that can potentially lead to superinfection and the death of the patient due to sepsis. Treatment is primarily based on managing the wounds, eliminating all the possible precipitating factors of ectopic calcification and administering agents which are capable of inhibiting the process of calcification. Resumen: La calcifilaxis, también denominada arteriolopatía urémica calcificante, es un síndrome raro que causa típicamente necrosis cutánea y que afecta principalmente a los pacientes en diálisis. La patogénesis es multifactorial y depende de la suma de todos los factores que producen calcificaciones ectópicas en el paciente con enfermedad renal crónica, como las alteraciones del metabolismo calcio-fósforo, el hiper o el hipoparatiroidismo, la diabetes, la obesidad, la inflamación sistémica y el uso de inhibidores de vitamina K, entre otros. Desde un punto de vista clínico, la calcifilaxis puede evolucionar desde una púrpura dolorosa hasta extensas áreas de necrosis cutánea que pueden sobreinfectarse y llegar a causar el fallecimiento del paciente por sepsis. El tratamiento se basa fundamentalmente en el manejo de las heridas, la eliminación de todos los elementos que puedan precipitar la calcificación ectópica y el uso de agentes inhibidores del proceso de calcificación. Keywords: Calciphylaxis, Vascular calcifications, Hyperparathyroidism, Bisphosphonates, Palabras clave: Calcifilaxis, Calcificaciones vasculares, Hiperparatiroidismo, Bifosfonatos

INTRODUCTION Bisphosphonates may aid in treating and preventing bone loss promoted by chronic immunosuppressive treatment and secondary hyperparathyroidism in renal transplant (RT) patients. However, the effectiveness of bisphosphonates is compromised by poor patient compliance. The objective of the study was to compare the effects of once monthly ibandronate with those of weekly risedronate administration on bone mineral density (BMD) and renal function in RT patients. PATIENTS AND METHODS Sixty-nine patients were prospectively recruited who were at least 12 months post-RT and were treated with either oral ibandronate 150 mg monthly (n=35) or oral risedronate 35 mg weekly (n=34). At baseline and 1 year, creatinine, calcium, alkaline phosphatase, and i-parathyroid hormone were measured, and BMD was determined by dual-energy X-ray absorptiometry. RESULTS Group I consisted of 35 patients (28 women) treated with ibandronate who were of a mean age of 63±12 years. Group II consisted of 34 patients (30 women) treated with risedronate who were of a mean age of 64±10 years. Lumbar BMD was as follows: baseline T-score (group I vs. group II) of -1.7±0.8 versus -1.9±0.8 (P=NS); and annual T-score of -1.3±0.6 versus -1.4±0.8 (P=NS). After 1 year, lumbar BMD improved to reveal a T-score of -1.3±0.6 in the ibandronate group (P

Background Malignancy is one of the most common long-term complications in renal transplant patients, often related to immunosuppressive treatment although other factors could be considered. Vitamin D plays an important role in reducing cancer risk. After kidney transplantation (KT), 25-hydroxyvitamin D (25OH-D, or calcidiol) insufficiency concerns >85%. The main aim of the present study was to determine the relationship between calcidiol blood levels and cancer development in KT recipients. Methods This was a retrospective observational case-control study including patients who received transplants in our hospital from 2003 to 2009 with a follow-up period to 2015. A total of 738 patients were included; 94 of them developed malignancy process, 80 of whose tumor data were analyzed in the cancer group, and the rest composed the control group. At the moment of cancer presentation, age, sex, primary kidney disease, time after surgery, immunosuppressant schedule, and 25OH-D blood levels were collected. Results The mean patient age was 57 years. The percentages of man and women were 59.5% and 41.5%. The predominant etiology of kidney disease was chronic glomerulonephritis in 31.9%. There were no significant differences between sex, primary kidney disease, immunosuppressant schedule, or incidence of neoplasm in each group of patients. There were no significant differences in 25OH-D blood levels. The incidence of cancer was 7.1%-13.7% per year. The mean time between the graft surgery and the event was 5.6 years. Conclusions In patients with functioning KT, we found no correlation between blood levels of calcidiol and the incidence of cancer.

Persistent hyperparathyroidism (HPT) after kidney transplantation (KTx) is associated with hypercalcemia, hypophosphatemia and abnormally high levels of parathyroid hormone (PTH). In this randomized trial, cinacalcet was compared to placebo for the treatment of hypercalcemia in adult patients with persistent HPT after KTx. Subjects were randomized 1:1 to cinacalcet or placebo with randomization stratified by baseline corrected total serum calcium levels (≤11.2 mg/dL [2.80 mmol/L] or >11.2 mg/dL [2.80 mmol/L]). The primary end point was achievement of a mean corrected total serum calcium value

Aims Our aim was to evaluate the long-term effect of cinacalcet in patients with hypercalcaemic secondary hyperparathyroidism (SHPT) after renal transplantation (RT) in order to expand real-world data in this population. Methods We performed a multicentre, observational, retrospective study in 17 renal transplant units from Spain. We collected data from renal recipients with hypercalcaemic (calcium >10.2 mg/dL) SHPT (intact parathyroid hormone (iPTH) > 120 pg/mL) who initiated cinacalcet in the clinical practice. Results We included 193 patients with a mean (standard deviation (SD)) age of 52 (12) years, 58% men. Cinacalcet treatment was initiated at a median of 20 months after RT (median dose 30 mg/day). Mean calcium levels decreased from a mean (SD) of 11.1 (0.6) at baseline to 10.1 (0.8) at 6 months (9.0% reduction, P

Previous studies have examined control rates of office blood pressure (BP) in chronic kidney disease (CKD). However, recent evidence suggests major discrepancies between office and 24-hour BP values in hypertensive populations. This study examined concordance/discordance between office- and ambulatory-based BP control in a large cohort of patients with CKD.Cross-sectional.5,693 hypertensive individuals with CKD stages 1-5 from the Spanish ABPM (ambulatory BP monitoring) Registry.Thresholds of 140/90 and 130/80 mm Hg for office BP and 24-hour ambulatory BP, respectively. Age, sex, body mass index, waist circumference, hypertension duration, kidney measures, diabetes, dyslipidemia, target-organ damage, and cardiovascular comorbid conditions.Misclassification of BP control as "white-coat" hypertension (office BP ≥140/90 mm Hg, 24-hour BP130/80 mm Hg) or masked hypertension (office BP140/90 mm Hg, 24-hour BP ≥130/80 mm Hg).Standardized office-based BP and 24-hour ABPM.Mean age was 61.0 ± 13.9 (SD) years and 52.6% were men. The proportion with white-coat hypertension was 28.8% (36.8% of patients with office BP ≥140/90 mm Hg) and that of masked hypertension was 7.0% (but 32.1% of patients with office BP140/90 mm Hg). Female sex, aging, obesity, and target-organ damage were associated with white-coat hypertension; aging and obesity were associated with masked hypertension. Only 21.7% and 8.1% of the CKD population had office BP140/90 and130/80 mm Hg, respectively. In contrast, 43.5% of individuals had average 24-hour BP130/80 mm Hg.Cross-sectional design, longitudinal associations cannot be established.Misclassification of BP control at the office was observed in 1 of 3 hypertensive patients with CKD. Ambulatory-based control rates were far better than office-based rates. Nevertheless, the burden of uncontrolled ambulatory BP and misclassification of BP control at the office constitutes a call for wider use of ABPM to evaluate the success of hypertension treatment in patients with CKD.

El hiperparatiroidismo secundario (HPTS) es una complicación habitual en pacientes con enfermedad renal crónica que se caracteriza por unos niveles elevados de hormona paratiroidea (PTH) y una serie de anomalías en el metabolismo mineral-óseo. En pacientes con HPTS, el tratamiento con paricalcitol, un activador selectivo de los receptores de la vitamina D, ha demostrado reducir los niveles de PTH con mínimas variaciones del calcio y del fósforo séricos. El efecto clásico de paricalcitol es el de mediador en la homeostasis mineral y ósea. Sin embargo, estudios recientes han indicado que los beneficios del tratamiento con paricalcitol van más allá de la reducción de PTH, por ejemplo, ocasionando efectos positivos en la enfermedad cardiovascular y en la supervivencia. El objetivo del presente trabajo es revisar los estudios más significativos sobre los llamados efectos pleiotrópicos del tratamiento con paricalcitol en pacientes con ERC. Secondary hyperparathyroidism (SHPT) is a common complication in patients with chronic kidney disease (CKD) that is characterised by elevated parathyroid hormone (PTH) levels and a series of bone-mineral metabolism anomalies. In patients with SHPT, treatment with paricalcitol, a selective vitamin D receptor activator, has been shown to reduce PTH levels with minimal serum calcium and phosphorus variations. The classic effect of paricalcitol is that of a mediator in mineral and bone homeostasis. However, recent studies have suggested that the benefits of treatment with paricalcitol go beyond PTH reduction and, for instance, it has a positive effect on cardiovascular disease and survival. The objective of this study is to review the most significant studies on the so-called pleiotropic effects of paricalcitol treatment in patients with CKD.

Background:Prospective studies on the clinical progression of Alzheimer's disease (AD) and its relationship to caregiver burden are needed to improve illness management and use of resources.Methods:This national, multicenter, observational study evaluated 1235 moderate to severe AD patients under routine care in Spain. Baseline cross-sectional sociodemographic and clinical data, and changes from baseline to month 12 of various neuropsychological tests and clinical ratings, including Blessed Dementia Scale, Mini-mental State Examination (MMSE), Hughes Clinical Dementia Rating sum-of-boxes (CDR-SB), Clinical Global Impression of Change (CGIC) and Zarit Caregiver Burden scales, were recorded and comprehensively analyzed.Results:Baseline data were in accordance with characteristics consistently reported to influence AD risk regarding anthropometrics, sociocultural features and comorbidities. Significant progressive functional impairments (i.e. in routine activities and essential daily tasks) and cognitive (i.e. MMSE and CDR-SB) impairments were found at month 12. However, patients' behavior and caregivers' burden improved slightly, but significantly, corroborating the major influence of behavioral symptoms on caregivers' distress. Caregivers showed significantly lower burden with patients with higher levels of education and, to a lesser extent, when patients received AD-specific medication. Physicians accurately detected AD clinical evolution as their CGIC ratings significantly correlated with all tests.Conclusions:These findings reinforce previous AD knowledge and add data on the clinical course of advanced stages of AD. Caregiver burden depended more on patients' behavioral alterations than on their functional or cognitive declines; and it was diminished by their patients having higher levels of education and being treated with AD-specific medications. Research into unexplored factors that might reduce caregiver burden, ultimately benefiting both patients and caregivers, is encouraged.

The outcome of patients with cirrhosis and chronic kidney disease treated with combined liver-kidney transplantation (CLKT) is not well known because most series of patients treated with CLKT include not only patients with cirrhosis but also patients with inherited diseases without cirrhosis. To evaluate to what extent the combined kidney transplantation impairs posttransplantation outcome compared to liver transplantation (LT) alone, the outcome of patients with cirrhosis and chronic kidney disease treated with CLKT (n = 20) was compared to that of a group of patients with cirrhosis without chronic kidney disease treated with LT alone matched by age, sex, year of transplantation and severity of cirrhosis (n = 60). The primary end point of the study was survival, and secondary end points were outcome of renal function and complications within 6 months of transplantation. Patients with CLKT had a higher incidence of bacterial infections and transfusion requirements compared to LT patients. The incidence of acute renal failure during the first 6 months was similar, yet the severity of renal failure was greater in patients with CLKT. Hospital and intensive care unit (ICU) stays were longer in the CLKT group. One- and three-year survival probabilities in patients treated with CLKT were 80 and 75% compared to 97 and 88%, respectively, in patients treated with LT. In conclusion, CLKT for patients with cirrhosis and chronic kidney disease is associated with a relatively high frequency of postoperative complications that moderately impairs short-term survival. However, 3-year survival of patients with cirrhosis treated with CLKT is excellent.

OBJECTIVE To evaluate the effect of calcimimetics with 99mTc-methoxy-isobutyl-isonitrile (MIBI) parathyroid scintigraphy in secondary hyperparathyroidism. METHODS This prospective study included 30 consecutive haemodialysis patients with inadequately controlled secondary hyperparathyroidism despite standard medical treatment. Patients were given a single daily oral dose of 30 mg of cinacalcet. A baseline and 1-year follow-up dual-phase 99mTc-MIBI scintigraphy were performed. 99mTc-MIBI uptake in each parathyroid gland was graded on a semiquantitative scale (scoring 0-3). RESULTS Twenty-one of the 30 patients responded to cinacalcet (70%). Abnormal positive glands were identified by 99mTc-MIBI scintigraphy in 27 out of 30 patients (53 glands). The sensitivity and specificity of 99mTc-MIBI in detecting cinacalcet response were 90 and 89%, respectively. The mean baseline and posttreatment grades of 99mTc-MIBI uptake were 2.9 ± 1.8 and 1.1 ± 1.2 (P < 0.0001) in the responder group and 3.1 ± 2.1 and 3.9 ± 2.2 (P = ns) in the nonresponder group. CONCLUSION 99mTc-MIBI scintigraphy is useful in monitoring the response to calcimimetics in secondary hyperparathyroidism.

Introduccion y objetivos El sindrome metabolico agrupa alteraciones estrechamente relacionadas. El objetivo principal de este estudio es conocer la frecuencia del sindrome metabolico y de la resistencia a la insulina, y su papel como indicadores de riesgo cardiovascular en poblacion adulta asignada a consultas de Atencion Primaria en Espana. Metodos Sujetos ≥ 45 anos con glucemia basal ≥ 90 mg/dl y perimetro de cintura ≥ 94 cm (hombres) u 80 cm (mujeres). Se utilizaron los criterios del ATP III modificados para identificar el sindrome metabolico y el indice HOMA > 3,29 para la resistencia a la insulina. El riesgo cardiovascular se estimo mediante los modelos Framingham y SCORE. Resultados Se incluyeron 2.341 sujetos (62 ± 10 anos; 44,6%, varones). La frecuencia de sindrome metabolico y resistencia a la insulina fue del 54,6% (52,5; 56,8) y de 56,6% (54,5; 58,7) respectivamente. El sindrome metabolico se asocio a una mayor puntuacion de riesgo cardiovascular tanto en el modelo Framingham (16 [15; 16] frente a 11 [11; 12]; p Conclusiones El sindrome metabolico y la resistencia a la insulina son predictores de riesgo cardiovascular. La identificacion precoz del sindrome metabolico mediante la utilizacion de herramientas clinicas sencillas (glucemia basal y perimetro de cintura) posibilitaria la intervencion sobre los distintos trastornos englobados en el.

Background: Secondary hyperparathyroidism remains a serious problem in hemodialysis patients. The therapy of renal osteodystrophy is mainly based on lowering phosphate levels and administering vitamin D3 metabolites and calcimimetic agents. Methods: An observational, prospective, multicenter study was made to evaluate the efficacy of alfacalcidol in 185 chronic hemodialysis patients with secondary hyperparathyroidism (i-PTH >150 pg/ml). Patients with a Ca×P product >70 were excluded. Intermittent therapy with intravenous alfacalcidol was observed for 6 months. Results: The mean dose of alfacalcidol per week was 3.63 ± 1.71 µg. Patients previously treated with vitamin D3 metabolites needed higher doses of alfacalcidol (4.0 ± 1.7 vs. 3.2 ± 1.6; p = 0.01). Only 50.8% of the patients had received vitamin D3 metabolites prior to the start of the study and at baseline they had higher i-PTH levels (600.3 ± 360.5 vs. 489.9 ± 292.6, p = 0.02). i-PTH levels decreased from 546 ± 332.6 to 332.4 ± 274.5 pg/ml (p < 0.001). 60.5% of the patients had i-PTH < 300 pg/ml at the last observation. Serum calcium increased (9.4 ± 0.8 to 9.97 ± 1.0 mg/l, p < 0.001). Conclusion: Alfacalcidol reduced the levels of i-PTH and produced a slight increase in serum calcium and phosphate levels. In mild or moderate hyperparathyroidism the doses needed were lower than in severe hyperparathyroidism.

The aim was to evaluate feasibility and safety of calcineurin inhibitor-free immunosuppression in high-risk donor kidney transplantation with sequential sirolimus introduction. Kidney transplant patients (n=76) with a donor aged >60 years, donor with acute renal failure, or a nonheartbeating donor were included. Immunosuppression consisted of antithymocyte globulin or basiliximab, mycophenolate mofetil, prednisone, and sequential introduction of sirolimus. One-year patient survival was 96.2% and 95.8%; graft survival was 94.2% and 91.7%; acute rejection rates were 21.2% and 12.4%; delayed graft function was 21.2% and 66.7%; and creatinine clearance was 58+/-20 mL/min and 56+/-21 mL/min for the brain-dead donor group and the nonheartbeating donor group, respectively. Most adverse events were infections, but also three lymphoceles, three urinary fistulas, three wound seromas. Sequential sirolimus introduction in high-risk donor kidney transplantation was found to lead to good patient and graft survival and incidence of acute rejection and delayed graft function.

The aim of this study was to compare the group of patients receiving a new kidney transplant before starting dialysis again (pre-reTR) with a group of patients receiving a new kidney transplant after restarting dialysis (reTR).This retrospective cohort included all the kidney retransplantations (second transplantations) between 2000 and 2012 performed at our center and their follow-up until July 2014. We analysed graft and patient survival, rejection rates, and immunologic parameters of these patients.We studied 18 patients who had pre-reTR and 83 who had reTR. In the pre-reTR group no patient had panel-reactive assay (PRA)10% at any time. In the reTR group 26.5% had PRA10% at the time of transplantation (P = .014) and 54.2% had a historical highest PRA10% (P .001). The rejection rate was 11.1% in the pre-reTR group and 27.7% in the reTR group during the first year post-retransplantation (P = .227). Patient survival rate was 100% in the pre-reTR group at 5 years of follow-up, whereas in the reTR group at 1 year it was 95.2% and 85.9% at 5 years after retransplantation. Allograft survival at 1 and 5 years was 88% and 89%, respectively, in the pre-reTR group. On the other hand, in the reTR group it was 89% after the first year and 65% at 5 years post-retransplantation.Pre-emptive renal retransplantation is a feasible option that should be assessed in patients with kidney graft failure and may help to minimize the morbidity associated with dialysis reinitiation.

Vitamin D deficiency is prevalent in kidney transplant recipients (KTR) and recommendations on how to replenish vitamin D deposits are scarce. To evaluate, in KTR, the safety and efficacy of calcifediol in two different vitamin D supplementation regimens, in order to assess the most suitable dose. Prospective observational study with two calcifediol supplementation regimens randomly prescribed by clinicians in liquid form, at 266 mcg doses, monthly or biweekly. We analyzed 168 KTR with a functioning allograft for more than 6 months. Patients receiving other vitamin D forms, calcimimetics or bisphosphonates were excluded. Before calcifediol initiation (pre-treatment levels) and after at least 3 months of treatment (post-treatment levels), we measured serum levels of 25-OH vitamin D (25(OH)D), parathyroid hormone (PTH), alkaline phosphatase (ALP), calcium (sCa), phosphate (sPO4) and creatinine (sCreat). In the monthly group (n = 72), 25(OH)D levels increased from 14 ng/ml [interquartile range, IQR 9–22] at baseline to 31 [20–38] (p = 0.000), PTH decreased from 124 pg/ml [87–172] to 114 [78–163] (p = 0.006), while sCa and sPO4 remained stable. In the biweekly group (n = 96), 25(OH)D increased from 14 ng/ml [9–20] at baseline to 39 [28–52] (p = 0), PTH decreased from 141 pg/ml [95–221] to 112 [90–180] (p = 0.000), sCa remained stable and sPO4 increased from 3.3 ± 0.6 mg/dl to 3.5 ± 0.6 (p = 0.003). Renal function remained stable in both groups. Vitamin D reposition with oral calcifediol, in a biweekly or monthly regimen, is safe and effective in improving 25(OH)D blood levels and in decreasing PTH in kidney transplant recipients.

Summary Donor after cardiac death (DCD) grafts have excellent survival despite the high incidence of delayed graft function (DGF). We assessed the feasibility of a mammalian target of rapamycin inhibitor (mTOR-I) protocol in uncontrolled DCD kidney transplantation and compared it with brain-dead donor (DBD) transplantation under calcineurin inhibitor (CNI) treatment. This retrospective study (2002–2011) included 109 Maastricht category II DCD patients and 218 standard-criteria DBD as controls. Immunosuppression consisted of polyclonal antibody induction, mycophenolate mofetil, prednisone, and mTOR-I (starting on day 6) in the DCD group and tacrolimus in the DBD group. DGF occurred in 72.5% of the DCD group vs. 26.1% of the DBD group (P = 0.001). Patient survival at 1 year was 99.1% vs. 95.9% (P = 0.112), and graft survival was 89% vs. 92.2% (P = 0.253). Patient survival at 5 years was 85.3% vs. 90.1% (P = 0.340) and graft survival was 85.5% vs. 78.8% (P = 0.166). During the first year, 46.8% (n = 51) of DCD patients were converted to CNI therapy. Serum creatinine at 1 year was 1.5(1.26–2) mg/dl vs. 1.4(1.16–1.8) mg/dl (P = 0.078). At 1 year, the acute rejection rate was 7.3% vs. 12.5% (P = 0.766). mTOR-I-based therapy was not associated with inferior graft function or higher rejection rates than standard CNI therapy. DCD kidney transplantation with an mTOR-I-based protocol is feasible but is associated with a high conversion rate to CNI-based therapy.

Background and objectives Calcific uremic arteriolopathy (CUA) is a life-threatening condition almost exclusively affecting patients with end-stage renal failure. Several therapies have been employed to treat this disease with irregular results. Methods Comparison of a prospective case series with a historical cohort. Group I: 12 patients with CUA diagnosed before 2002 (5 men, 6 on dialysis and 6 with functioning allografts) treated with standard treatment. Group II: 11 patients with CUA diagnosed between 2002 and 2010 (4 men, 6 on dialysis and 5 with functioning allografts) treated with standard treatment and bisphosphonates for 6 months. The diagnosis was made by clinical suspicion and a confirmatory biopsy in both groups. Ten patients had a previous history of high calcium-phosphorus product, 9 had a history of high parathyroid hormone (> 800 pg/ml) levels, 13 had a history of high cumulative steroids and 9 patients were under dicoumarin treatment. Two patients were obese and 5 had diabetes mellitus. Results In Group I, 58.7% required amputation of the affected limb, 3 patients recovered and 2 died. In all patients of Group II the progression of the skin lesions decreased between 2 and 4 weeks after the start of bisphosphonate therapy with no changes in blood levels of calcium and phosphate. The improvement in pain and lesions was faster in the patients receiving endovenous bisphosphonates. Renal function remained stable in transplant recipients. No adverse effects were observed. Conclusions Bisphosphonates could constitute an alternative to treat CUA in addition to standard therapy.

Introduction End-stage renal disease (ESRD) is a major public health problem in the Spanish health system. Kidney transplantation is the treatment of choice, offering better survival and cost-effectiveness than other alternatives. This study aimed to compare the cost of living-donor kidney transplantation (LDKT) during the first year after transplantation with that of hemodialysis (HD). Method A prospective, descriptive study of cost and efficacy was performed in the Hospital Clinic in Barcelona from January to December 2011. We included 106 patients (57 undergoing HD and 49 receiving a LDKT). The costs of LDKT (donor and recipient) and HD were calculated based on our economic database program. Results The mean age of recipients and donors was 46 ± 15 and 52 ± 10 years, respectively, and 67% of the recipients were men. In HD patients, the mean age was 67 ± 11 years and 62% were men. The total cost of LDKT was €29,897.91 (€8,128.44 for donors and €21,769.47 for recipients). The total cost of HD was €43,000.88 (€37,917 for HD and related procedures plus €5,082 for transport). LDKT represented a savings of €13,102.97 per patient/year and the payback period was less than 1 year. Quality-adjusted life years were higher in LDKT than in HD patients. Conclusion LDKT is cost effective during the first year after transplantation and is associated with enhanced quality of life. From both the medical and economic points of view, pre-emptive LDKD should be encouraged in Spain to reduce the health budget for ESRD.

Anemia after kidney transplantation (KT) has a negative impact on graft and patient survival. Anemia management includes iron supplements and erythropoiesis-stimulating agents (ESAs). Most ESAs require short frequency of administration and conversion to ESAs with longer half-life are complex.This study was performed to assess the efficacy of continuous erythropoietin receptor activator (CERA) in hemoglobin (Hb) maintenance after conversion from shorter-acting ESAs with a simple conversion scheme in kidney transplant recipients.This is an open-label, prospective, single-arm, single-center, 12-month follow-up study including 77 anemic KT patients with stable renal function. Baseline and monthly measurements of Hb, iron, and creatinine were performed. The conversion scheme from darbepoetin alfa or epoetin was as follows:30 μg or 5000 IU/week was switched to 75 μg/mo; between 30-50 or 5000-8000 was switched to 100 μg/mo;50 μg or 8000 IU was changed to 150 μg/month of CERA. Dose adjustments were performed to maintain Hb levels between 10 g/dL and 12 g/dL.The mean age was 57 ± 19 years. The mean time of conversion after KT was 61 ± 49 months. Before conversion, 62.9% of patients were administered epoetin and 37.1% with darbepoetin alfa. Baseline Hb is noted at 10.6 ± 1.3 g/dL. Thirteen percent of patients started receiving CERA at doses of 50 μg/mo, 66% at 75 μg/mo, 13% at 100 μg/mo, and 8% at 150 μg/mo. During the first month, 21% required dose adjustment (6% were increased, 15% were decreased). The final Hb was 11.2 ± 0.8 g/dL. Iron and creatinine levels remained stable during the follow-up examination.We propose a simple scheme of conversion from short-acting ESAs to a once-monthly dose of CERA that provides sustained Hb levels within the recommended target with small dose adjustments and low CERA doses.

The aim of the present study was to evaluate the effect of hemodialysis and renal failure on serum bone markers. Serum total alkaline phosphatase (TAP), procollagen type I aminoterminal propeptide (PINP), and beta-carboxyterminal telopeptide of type I collagen (beta-CTX), as well as intact parathyroid hormone (iPTH), creatinine, and total protein were measured in 14 patients with endstage renal disease (ESRD) before and at 1, 2, and 4 h during a hemodialysis session, and at the same sampling interval in 6 renal transplant recipients. The results were compared to those obtained in 20 healthy adults. All patients showed increased baseline mean values of PINP, beta-CTX, and iPTH. Beta-CTX differed significantly between hemodialysis patients and renal transplant recipients. TAP and beta-CTX were the only markers which correlated with iPTH ( P << 0.05) and creatinine values ( P << 0.001), respectively. Renal transplant recipients did not show significant variations in the evolution of mean values of bone markers throughout the study, whereas, during the dialysis period, all the bone markers analyzed in the study showed a significant change. The change differed depending on the marker considered: beta-CTX showed a significant decrease at the end of the session, TAP increased at this time and, although PINP showed an initial increase during hemodialysis, no significant changes were observed at the end of the session. We conclude that bone markers are significantly influenced by hemodialysis, especially serum TAP and beta-CTX. ESRD is associated with an increase in these bone markers, in some cases related to iPTH values and in others to glomerular function. These findings should be taken into account when evaluating bone markers in these patients.

The major factor influencing scintigraphic detection of abnormal parathyroid glands seems to be their size. However, false-negative results have been reported in large glands while some very small adenomas have been identified. Other factors can influence 99mTc-MIBI and 99mTc-Tetrofosmin uptake and therefore the accurate detection of hyperfunctioning glands depends also on these. Increases in both perfusion and functional activity and targeting of abundant mitochondria-rich oxyphil cells seem to be relevant mechanisms of uptake. A relationship has been observed between the intensity of focal uptake in the parathyroid glands and the cell cycle phases for patients with secondary hyperparathyroidism. Higher uptake grades correlated with the active growing phase, showing that scintigraphy accurately reflects the functional status of the hyperplastic parathyroid glands. Serum calcium levels may modify radiotracer kinetics by influencing the membrane potential. In addition, P-glycoprotein or multidrug resistance (MDR) associated protein expression may play an important role in the false-negative results of parathyroid scintigraphy. If the lipophilic cationic radiotracers used in parathyroid scintigraphy are transported by the same mechanism as the anticancer drugs, they will be quickly eliminated from the parathyroid glands containing P-glycoprotein or MDR-related protein expression and the uptake in images will be negative. In parathyroid glands with no P-glycoprotein or MDR-related protein expression, the radiotracers remain in the cells, making it easier to detect them by scintigraphy.

The relationship between anticalcineurin (CNI) drugs and the development new-onset diabetes mellitus after kidney transplantation (NODAT) is well established. Among these agents cyclosporine shows lesser diabetogenicity than tacrolimus. It has been described that conversion from tacrolimus to cyclosporine improves glycemic control; however, there are no studies showing whether this reduced risk is maintained upon long-term follow-up.To evaluate whether CNI drugs conversion from tacrolimus to cyclosporine helps to maintain better glycemic control.We retrospectively evaluated the evolution of glucose metabolism at 5 years after conversion from tacrolimus to cyclosporine in eight patients (six men) with NODAT. Mean age was 42.8 ± 15 years, and time after transplantation to conversion 128 ± 40 months. We analyzed fasting serum glucose, lipid metabolism, renal function, and cyclosporine levels at 0, 6, 12, 24, 36, 48, and 60 months after conversion.At 6 months after conversion, improved glucose metabolism was observed (268 ± 161 versus 121 ± 31 mg/dL; P.01) although it was minimal in one case with persistent high blood glycemic levels. Only two patients maintained a normal glucose at the end of follow-up. Five subjects showed increased glycemia at 12 to 24 months after conversion requiring antidiabetic therapy: three patients, insulin and two oral antidiabetic agents. Two patients lost their allografts due to chronic rejection at 32 and 50 months respectively. Among the other six patients, renal function remained stable (1.9 ± 0.6 versus 2.11 ± 0.97 mg/dL; P = NS). There was no significant differences among the other variables. Cyclosporine levels remained stable during the follow-up.Conversion of renal transplant patients with NODAT from tacrolimus to cyclosporine improves glucose metabolism in the short term but glycemia increases thereafter.

Simultaneous pancreas-kidney transplant (SPKT) has been associated with an increased risk of fracture. We prospectively evaluated the long-term effects of SPKT on bone mineral density (BMD) and fracture risk. During 1998 to 1999, 29 participants were consecutively monitored, and 18 completed the 10-year follow-up. Laboratory blood parameters, lumbar-dorsal radiography, and DEXA were determined at baseline, 1 year, and 10 years. The medical record was reviewed for peripheral fragility fractures. The BMD revealed no changes between baseline and 1 or 10 years after SPKT. Lumbar-dorsal radiography showed 0% asymptomatic vertebral fractures at baseline and after 1 year with 16.7% at 10 years. Vertebral asymptomatic fractures were correlated with acute rejection episodes (P = 0.025). During the first year, no nonvertebral fractures were identified. At the end of the follow-up, 5 nonvertebral fractures in 4 patients were reported. Dorsal and lumbar spine fractures correlated with lumbar spine t score (r = -0.591, P =0.022) and peripheral fractures with femoral neck t score (r = -0.633, P = 0.013). Patients with SPKT did not show long-term significant loss of BMD. The incidence of vertebral fractures was low and related to steroid treatment; the incidence of peripheral fractures was higher and independent of clinical or biochemical parameters.

Department of Imaging, Nuclear Medicine, Radiology,NeuroRadiology, Medical Physics, Nuclear Medicine & PET/CT Centre, SantaMaria della Misericordia Hospital, Rovigo, ItalyCorrespondence to Domenico Rubello, MD, Department of Imaging, NuclearMedicine, Radiology, NeuroRadiology, Medical Physics, Nuclear Medicine& PET/CT Centre, Santa Maria della Misericordia Hospital, Via Tre Martiri 140,45100 Rovigo, ItalyTel: +39 0425 39 4428; fax: +39 0425 39 4434;e-mail: domenico.rubello@libero.itReceived 23 December 2013 Accepted 12 January 2014

Methods We analyzed all PRA-negative patients who received a first kidney transplant from an HLA-identical living donor. The patients received no antibody induction. An intraoperative bolus of 500 mg of methylprednisolone was administered. Then, steroid therapy was withdrawn within one week. Tacrolimus and mycophenolate treatment were started 3 days before transplantation with tacrolimus target levels of 4 to 8 ng/mL. In the absence of rejection, tacrolimus was withdrawn between 3 and 12 months post-transplant to reach mycophenolate mofetil monotherapy of 2 g/day or equivalent. Results Six patients were treated with the above protocol. At last follow-up, graft and patient survival were 100%. MDRD glomerular filtration rates were 54, 60, and 62 mL/min at 3 months, 12 months and last follow-up, respectively. None of the patients developed PRA post-transplant. One episode of acute rejection Banff IA occurred 9 years after transplantation due to non-adherence with good outcome after treatment. The mean number of concomitant drugs given with mycophenolate was 2.6. Four patients needed antihypertensive drugs. Conclusion Steroid-free de novo treatment and calcineurin-inhibitor weaning with mycophenolate monotherapy is feasible in first HLA-identical kidney transplantation from a living sibling. Although recipients of a first HLA-identical living-donor kidney transplant seem to need less immunosuppression, there are no guideline recommendations for these patients, and few prospective trials are available.

Persistent secondary hyperparathyroidism is common after renal transplantation (RT) [1–4]. Approximately one-third of patients show persistent PTH hypersecretion after surgery. The development of hypercalcemia correlates with the duration of dialysis and parathyroid gland hypertrophy [5], and appears to be secondary to hyperplasia of the parathyroid glands, rather than hypersecretion in individual cells [6]. Although the parathyroid glands involutes after renal transplantation, this process can take a few months (if mild) or even several years to reach completion. Another factor that can contribute to persistent hyperparathyroidism is nodular transformation by monoclonal growth [7, 8]. Persistent secondary hyperparathyroidism after RT is characterized by an autonomous pattern of PTH secretion [9] and its severity is mainly dictated by pre-existing hyperparathyroidism prior to RT. PTH secretion is modulated by extracellular ionized calcium, which interacts with a specific parathyroid cell calcium-sensing receptor [10]. The dynamics of PTH secretion in response to change in serum calcium concentration have been reported to be abnormal in hyperplastic parathyroid glands [11]. This prospective study was undertaken to investigate changes in the PTH secretion parameters of the iCa/PTH relationship curve during the first 12 months post-RT, in order to define the conditions underlying the reversibility of SHP in an homogenous group of patients with moderateto-severe biochemical SHP.

The key players of the CKD–MBD are calcium, phosphorus, PTH, FGF23, and the vitamin D hormonal system. The progressive reduction of kidney function greatly modified the tightly interrelated mechanisms controlling these parameters. As a result, important changes occurred in the bone and mineral hormonal axis leading to changes in bone turnover with consequences in relevant clinical outcomes, such as decrease in bone mass with increased bone fragility and bone fractures and increased vascular and valvular calcification with great impact in the cardiovascular outcomes.

Double-phase parathyroid MIBI (99mTc-sestamibi) was performed in 27 patients with secondary hyperparathyroidism (SPT). Focal areas of increased uptake were scored for intensity on a three-point scale. All patients underwent subtotal parathyroidectomy (SPTx), and a total of 78 glands were removed at operation. Blood was obtained from the jugular vein before and after SPTx to measure the parathyroid hormone (PTH) levels. The volume and weight of the glands were calculated. The tissue was divided, with one aliquot being used for cell cycle analysis. The nuclei were acquired by flow cytometry and analyzed using CELLEIT software. Cell viability was assessed by flow cytometry and analyzed with LYSIS II software. Positive MIBI uptake was observed in 88.8% of patients. Focal MIBI uptake of one, two, or three glands was observed in 6, 11, and 8 patients, respectively. All patients experienced an 86% decrease in PTH blood level after SPTx compared to that before excision. A correlation was found between the volume of glands and the blood levels of intact PTH (iPTH) (r= 0.5, p < 0.05). A positive correlation was observed between MIBI uptake and the iPTH levels before SPTx (p < 0.01) and between the uptake of MIBI in the parathyroid glands and the cell cycle phases; low-grade uptake correlated with the G0 phase and higher uptake with G2+S phase (r= 7, p < 0.01). No correlation was observed between MIBI uptake and the weight of the glands. MIBI scintigraphy accurately reflects the functional status of the hyperplastic parathyroid glands: Higher uptake grades correlated with the active growth phase. MIBI uptake does not reveal parathyroid enlargement; rather, it identifies the presence of hyperfunctioning autonomous glands. SPTx and total parathyroidectomy with autografting (TPTx+A) are the most widely accepted surgical approaches for patients with SPT. Reoperation for recurrence is necessary in 6% to 15% of cases. MIBI is now considered to be the radionuclide of reference for parathyroid gland scanning, although it is widely accepted that it produces poor results when trying to detect hyperplastic glands.

Background Secondary hyperparathyroidism (SHPT) is a relevant problem in patients undergoing dialysis, and cinacalcet hydrochloride seems to be the best option for controlling it. After kidney transplantation (KTx), moderate to severe SHPT may persist and cause hypercalcemia and hypophosphatemia, among other deleterious effects. The number of patients receiving cinacalcet before KTx is increasing. Objective To evaluate the evolution of calcemia, phosphatemia, and intact parathyroid hormone (iPTH) after KTx in patients with SHPT receiving cinacalcet on dialysis. Patients and Methods The study included 19 patients (15 men and 4 women; mean [SD] age, 52 [13] years) undergoing dialysis and receiving cinacalcet before KTx. Mean duration of dialysis before KTx was 33 (25) months, and cinacalcet dose was 45 (15) mg/d. Creatinine, calcium, phosphorus, alkaline phosphatase, and iPTH concentrations were evaluated at baseline (day of surgery), at 15 days after surgery, and then monthly for 6 months. In all patients, cinacalcet therapy was discontinued on the day of surgery. Results After the first month post-KTx, mean (SD) serum creatinine concentration was 1.6 (0.4) mg/dL and remained stable during follow-up. Calcium and phosphorus concentrations were normal in 13 patients after KTx; however, in 6 patients, hypercalcemia (calcium concentration, 11 [1.3] mg/dL) or hypophosphatemia (phosphorus concentration, 1.7 [0.6] mg/dL) developed, with iPTH concentration of 557 (400) pg/mL and alkaline phosphatase concentration of 307 (114) IU/mL. Treatment with cinacalcet resulted in correction of calcium and phosphorus concentrations (10.1 [0.4] mg/dL and 1.7 [0.7] mg/dL, respectively). Patients in whom hypercalcemia or hypophosphatemia developed were receiving cinacalcet, 60 mg/d or more, during dialysis therapy. Patients who received cinacalcet, 30 mg/d, before KTx did not exhibit hypercalcemia or hypophosphatemia after KTx. Conclusion In patients with HPT undergoing dialysis and receiving cinacalcet, 60 mg/d or more, this drug therapy should be continued after KTx to avert development of hypercalcemia or hypophosphatemia.

Everolimus (Eve) has shown good efficacy and safety profiles in clinical trials in combination with low doses of cyclosporine but there is limited experience in other modes, especially with calcineurin inhibitor elimination. We developed a retrospective study to analyze its clinical use after approval in Europe in 2005. Herein we have presented the results of a series of 272 patients followed for the first 6 months after Eve introduction. In 93.8% of cases Eve was introduced after the first month posttransplantation (conversion use), and 6 months after introduction, the CNI had been eliminated in 75% of cases. The main indication for Eve introduction was the diagnosis of a malignant neoplasm (42%), whereas the combined indication of prevention and/or treatment of toxicity, especially nephrotoxicity, accounted for 46.3% of cases. Initial doses were low (1.37 mg/d), but were progressively increased up to 2 mg/d at 6 months. Renal function remained unchanged during the follow-up period, whereas proteinuria moderately increased. Only 5 cases (2%) of acute rejection episodes were observed with excellent patient and graft survivals at 6 months after conversion. Further analysis of this extensive series of patients with a longer follow-up is needed.

The equation proposed by Cotes and coworkers is currently considered as the most acceptable to correct carbon monoxide diffusing capacity (DLCO) for hemoglobin concentration [Hb] by both the American Thoracic Society (ATS) and the European Respiratory Society (ERS) guidelines for standardization of DLCO. In a previous study on 24 anemic patients undergoing bone marrow transplantation (1), we found that DLCO is underestimated using the equation of Cotes and coworkers. To further explore this finding, 28 anemic patients ([Hb] = 8.2 +/- 1.0 (SD) g/dl) with chronic renal failure were prospectively studied during the recovery period of anemia (5.4 +/- 3.5 mo). In all 28 subjects, the slope deltaDLCO/delta[Hb] computed as ratio of overall change in DLCO to overall change in [Hb] throughout the study period was 1.40 +/- 0.72 ml CO/min/mm Hg/g/dl. The individual relationship between measured DLCO and [Hb] closely fitted a simple linear regression. The resulting equations for adjustment of DLCO (DLCOadj) to a standard [Hb] of 14.6 g/dl for men and 13.4 g/dl for women are: [equations: see text]. The present adjustment function for DLCO is linear and independent of the observed DLCO values, whereas the formulas previously proposed are curvilinear, DLCO correction varying with the measured DLCO values. For a measured DLCO of 15 ml CO/min/mm Hg and [Hb] ranging from 7 to 12 g/dl, the present DLCO adjustment is higher (by 2.7 ml CO/min/mm Hg, on average) than that proposed by Cotes and coworkers. This difference appears to be relevant for a precise interpretation of DLCO in patients with normocytic anemia in different clinical conditions.

The increased incidence of Kaposi’s sarcoma (KS) in organ transplantation has been related to the KS herpes virus and the permissive effect of immunosuppressive therapy. We postulated that conversion to SRL in renal recipients with KS favored regression of KS lesions without increasing the risk of graft rejection. Methods In this estudy we performed a retrospective chart review of 7 caucasian renal transplant recipients affected by KS to determine demographic data, etiology of ESRD, immunologic risk factors, immunosuppressive treatment, KS disease follow-up, and renal function before and after SRL conversion. Results All seven patients were under calcineurin inhibitor treatment at the onset of KS which was limited to the skin, without regression despite attempts to minimize immunosuppression. After conversion to SRL, six patients showed progressive regression of KS lesions, with only hyperpigmented atrophic cutaneous lesions remaining after a mean time of 8.1 months (2–18 months). The seventh patient has completed 9 months follow-up with a near complete regression of KS lesions. One patient returned to hemodialysis after 13 months following irreversible acute renal failure not directly related to SRL conversion; in the other six, renal function was stable. The mean serum creatinine was 1.87 ± 0.64 versus 1.74 ± 0.68 mg/dL, pre-conversion versus the end of follow up, respectively. Mean SRL blood level was 9.2 ± 2.0 ng/mL. Conclusion After SRL conversion, patients with KS showed progressive regression without an increased risk of acute rejection. SRL offers a promising approach to the management of posttransplantation KS and probably other malignancies in organ transplant recipients.

is directly related with the impairment of renal function, and in patients with chronic renal failure is commonly associated with increased PTH [12]. Also, after renal transplantation, secondary hyperparathyroidism remains unchanged, being difficult to control due to the development of hypercalcaemia [13]. In both groups and in patients on peritoneal dialysis the administration of intravenous calcitriol seems to be less useful than in haemodialysis patients, but may be of more value than subcutaneous administration of calcitriol [14,15]. In the present study, we prospectively evaluated the effectiveness and usefulness of subcutaneous calcitriol in the treatment of moderate secondary hyperparathyroidism in dialysis patients, and we investigated its pharmacokinetics.

Post-transplant cure tubular necrosis (ATN) represents the most frequent cause of delayed graft function in the immediate post-transplant period. Several causes have been associated with the development of post-transplant ATN such as donor and recipient ages, cold-warm ischemia times, HLA mismatches, and postoperative hypotension. In the present study, we retrospectively evaluated the role of secondary hyperparathyroidism and high parathyroid hormone (PTHi) blood levels in the development of post-transplant ATN. One hundred patients submitted to cadaveric renal transplant between January 1992 and March 1993 in our unit were included. Twenty-seven patients (27%) developed post-transplant ATN and seventy-three (73%) did not. Post-transplant ATN was significantly associated with gender (p0.01), recipient age (p0.01), number of transplantations (p0.01), time on hemodialysis (p0.001), cold ischemic time (p0.05) and PTHi levels (p0.001). The bivariate and multivariate statistical analyses demonstrated that the development of post-transplant ATN was significantly more frequent in females; retransplanted patients, patients with a time on dialysis of more than 5 years, recipients over 60 years old, patients with a PTHi blood level higher than 240 pg/ml (4 times normal level) and a cold ischemia time of more than 18 h. Based on these results, we conclude that high PTHi blood levels in the renal transplant recipients represent a relevant factor in the development of post-transplant ATN. The administration of intravenous pulsed of 1,25(OH)2D3 and/or a calcium channel blocker in the perioperative period could be useful to decrease the incidence and severity of post-transplant ATN in these patients.

Behcet's disease (BD) is a chronic, relapsing, inflammatory disorder, and the underlying histophatological lesion is vasculitis of unknown cause. Some case reports of BD with positive C-ANCA titers have been reported, but only 2 case reports have documented the association of ANCA-associated glomerulonephritis (GN) and BD, and no renal transplantation cases have been described. We report such a case. A 27-year-old male was referred for consultation due to acute renal failure. Seven years before, BD was diagnosed. At the time of consultation he suffered from uveitis and generalized arthralgias. The serum creatinine was 14 mg/dl and urinalysis showed 4+ protein and microscopic hematuria. Results of serological tests were normal. The ANCA PR 3 titer was 1:100 of cytoplasmic pattern. A renal biopsy showed a rapidly progressive type III glomerulonephritis. In spite of immunosuppressive therapy with cyclophosphamide and high steroid doses, renal function did not recover and hemodialysis therapy was initiated. One year later, the patient underwent a renal transplantation. Follow-up was absolutely normal, and 5 years after transplantation, renal function persisted to be normal, without urinary abnormalities and signs of reactivation of original disease, except for occasional arthralgias. C-ANCA titer was decreased and remained stable (