Chronic kidney disease and vascular risk - what's new?

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Magnesium: An old player revisited in the context of CKD-MBD.

Chronic kidney disease (CKD) is associated with a wide number of abnormalities in mineral metabolism. Often, these alterations are the leading players in the development of comorbidities associated with CKD, which are risk factors of mortality. In this context, mineral and bone disorder associated with CKD (CKD-MBD) are highlighted, connecting bone, renal, and cardiovascular disorders. Many studies have been led to propose strategies to avoid, reduce, or slow down CKD-MBD progression using different compositions of metallic elements-based P binders such as aluminum, magnesium, or calcium. Magnesium, the aim of this review, has been used by nephrologists to treat CKD-MBD with a variable acceptation due mainly to different results on bone homeostasis. Nowadays, we have new evidence about the efficacy of magnesium supplementation on vascular calcification, renal function, and bone disorders, suggesting potential beneficial effects of Magnesium in the management of CKD-MBD.

24-Hour Proteinuria Versus Spot Protein-Creatinine Ratio for Kidney Transplant Management in Clinical Practice.

BACKGROUND: 24-hour proteinuria (24h-P) has been the most widespread test for clinical follow-up of proteinuria after kidney transplantation (KT), but urine collection is often not properly collected. Spot protein-creatinine ratio (P/Cr) has become the alternative to 24h-P for proteinuria evaluation in many KT units. However, its reliability, equivalence to 24h-P, and prognostic value regarding allograft outcome remain unknown. Therefore, the aim of this study was to evaluate the correlation and agreement between both methods for assessing proteinuria and to analyze which of them is a better predictor of graft survival. METHODS: We collected proteinuria measurements from KT patients in our center. 24h-P was adjusted for body surface area. Pearson correlation test and the Bland-Altman method were used to analyze correlation and agreement. Survival analysis was performed with the use of the Kaplan-Meier method and multivariate Cox proportional hazard model. RESULTS: A total of 8,549 urine samples were analyzed from 472 patients in whom 24h-P and P/Cr were simultaneously measured. A significant correlation was observed between 24h-P and P/Cr (r = .76; P < .001); however, the agreement between methods showed that P/Cr overestimated proteinuria compared with 24h-P, particularly when the latter was >1 g/24 h. The Cox regression multivariate model showed an increased risk of graft loss associated with proteinuria when assessed by either 24h-P (hazard ratio [HR] 6.53, 95% confidence interval [CI] 2.49-17.1) or P/Cr (HR 3.34, 95% CI 1.04-10.7). CONCLUSIONS: P/Cr is an method interchangeable with 24h-P for detecting proteinuria after KT. When proteinuria increases, the P/Cr overestimates 24h-P, even though it also has a significant and similar prognostic value for predicting graft survival.

Factors related to the development of CMV-specific CD8+ T cell response in CMV-seropositive solid organ transplant candidates.

This cross-sectional study analyzes factors associated with the development of CMV-specific CD8+ response, measured by IFNg production after cytomegalovirus (CMV) peptide stimulation, in CMV-seropositive solid organ transplantation candidates. A total of 114 candidates were enrolled, of whom 22.8% (26/114) were nonreactive (IFNγ < 0.2 IU/mL). Multivariate logistic regression analysis showed that age, HLA alleles and organ to be transplanted were associated with developing CMV-specific CD8+ immunity (reactive; IFNγ ≥ 0.2 IU/mL). The probability of being reactive was higher in candidates over 50 than in those under 50 (OR 6.33, 95%CI 1.93-20.74). Candidates with HLA-A1 and/or HLA-A2 alleles had a higher probability of being reactive than those with non-HLA-A1/non-HLA-A2 alleles (OR 10.97, 95%CI 3.36-35.83). Renal candidates had a higher probability of being reactive than lung (adjusted OR 8.85, 95%CI 2.24-34.92) and liver candidates (OR 4.87, 95%CI 1.12-21.19). The AUC of this model was 0.84 (p < 0.001). Positive and negative predictive values were 84.8% and 76.9%, respectively. In renal candidates longer dialysis was associated with an increased frequency of reactive individuals (p = 0.040). Therefore, although the assessment of CMV-specific CD8+ response is recommended in all R+ candidates, it is essential in those with a lower probability of being reactive, such as non-renal candidates, candidates under 50 or those with non-HLA-A1/non-HLA-A2 alleles.

Tyrosine-phosphatase and glutamate-decarboxylase antibodies after simultaneous pancreas kidney transplantation: do they have an impact on pancreas graft survival?

INTRODUCTION: The pathogenesis of type 1 diabetes mellitus (T1DM) is associated with auto-antibodies. These auto-antibodies contribute to pancreatic ß-cell destruction. Tyrosine-phosphatases (IA-2) and glutamic acid decarboxylase (GAD65) are the most frequently used by clinicians. When T1DM patients develops advanced chronic kidney disease, simultaneous pancreas-kidney (SPK) transplantation becomes the best option. However, pancreatic graft survival is limited. The role of the auto-antibodies on pancreas graft survival remains controversial. OBJECTIVE: The aim of this study was to assess pancreas graft survival according to the presence of GAD65 and IA-2 auto-antibodies after SPK transplantation. METHODS: We analyzed all SPK transplantations performed in our hospital since January 1990 to December 2013 with at least 30 days of pancreas graft survival. We collected demographic and clinical variables from donors and recipients. Graft failure was defined as complete insulin independence after transplantation. Pancreatic graft survival was analyzed using the Kaplan-Meier method. RESULTS: Overall, 152 SPK transplantations were performed during the period. One hundred sixteen were accessed for de novo post-transplantation auto-antibodies. Also, 17.8% (n = 27) were positive for anti-GAD65, 13.8% (n = 20) for IA-2, 3.9% (n = 6) were positive for both, and the rest were negative for any auto-antibody (n = 63). Kaplan-Meier survival curves estimated a worst pancreas graft survival for patients with positive IA-2 antibodies versus those patients with negative auto-antibodies and GAD65+auto-antibodies (P = .003 and .022, respectively, by log-rank). Mean pancreas graft survival rates at first and fifth year were 72% and 64%, respectively, for those patients with positive IA-2. CONCLUSIONS: IA-2 antibodies after SPK transplantation are associated with long-term graft lost compared with the rest of the groups. Monitoring of these auto-antibodies after SPK may help to identify patients with a higher risk of graft failure.

Associated characteristics and impact on survival of post renal-transplantation lymphoproliferative disease: case-control study from a regional registry.

BACKGROUND: Lymphoproliferative disease (LPD) after renal transplantation (RT) is an unusual complication but one that impacts greatly on survival. We examined possible predisposing factors and their effect on survival using data from the Andalusian Transplant Co-ordination Information System (SICATA) regional computerized database of patients on renal replacement therapy due to chronic kidney disease (CKD). METHODS: The study population comprised all RT undertaken at adult centers in Andalusia from January 1, 1990 to December 31, 2009 (N = 5577). We retrospectively analyzed cases at December 31, 2011 (N = 60). A control group comprised the 2 closest RT in time done at the same center and with equal or greater graft survival at the time of diagnosis of LPD in the associated case (N = 120). The basic variables were obtained from the general register (1990-2009) and widened from the specific register (2000-2009). Case-control comparison of survival was done with Kaplan-Meier from diagnosis to death or organ loss censored for death. Cox univariate and multivariate (LPD plus available covariables of demonstrated effect) analyses were done. RESULTS: We found no significant differences between cases and controls regarding the characteristics of the recipient or of the donor/organ, initial immunosuppression by intention to treat, or post-RT course. The impact on recipient survival 5 years after diagnosis was as follows: LPD, 35%; controls, 90% (P < .000). Cox univariate analysis showed the relative risk (RR) of death for LPD was 11.36 (95% confidence interval [CI], 6.2-20.9; P < .000) and the multivariate analysis showed relative risk (RR) = 13.87 (7.45-25.3; P < .000). The impact on death-censored graft survival 5 years after diagnosis was as follows: LPD, 65%; controls, 87% (P = .007). Cox univariate analysis was as follows: RR of failure for LPD, 2.70 (95% CI, 1.3-5.7; P = .009). CONCLUSIONS: We found no significant differences between LPD cases and contemporary controls regarding the basic characteristics of the recipient, donor/organ, initial immunosuppression, or initial graft evolution. There was an enormous impact on both patient and graft survival.