Hyperkalemia (HK) is a common electrolyte disorder in chronic kidney disease (CKD), mainly in the advanced stages. A positive potassium balance due to reduced renal excretory capacity is likely the main pathogenic mechanism of HK. Research into the relative role of each pathogenic element in the development of HK in CKD may help to implement more suitable therapies. To investigate renal potassium handling in advanced CKD patients, and to determine the differences between patients with or without HK. Cross-sectional observational study in adult patients with stage 4-5 CKD pre-dialysis. Selection criteria included clinically stable patients and the ability to collect a 24hour urine sample correctly. Blood and urinary biochemical parameters were analysed including sodium and potassium (K). Fractional excretion of K (FEK) and K load relative to glomerular filtration (Ku/GFR) were calculated. HK was defined as a serum K concentration ≥5.5mmol/l. The study group consisted of 212 patients (mean age 65±14 years, 92 females) with a mean GFR of 15.0±4.2ml/min/1.73m². 63 patients (30%) had HK. Patients with HK had lower mean bicarbonate levels with respect to patients with normal K levels (NK) (20.3±3.1 vs. 22.8±3.2 mEq/l, P<.0001), but no differences were noted in total urinary sodium and K excretion. While mean FEK values were lower in patients with HK (32.1±12.1% vs. 36.4±14.3%, P=.038), Ku/GFR values were significantly greater with respect to the NK subgroup (4.2±1.5 vs. 3.7±1.4 mmol/ml/min, P=0,049). FEK showed a strong linear correlation with Ku/GFR (R²=0.74), and partial linear regressions demonstrated that at a similar Ku/GFR level, the FEK of patients with HK was lower than that of NK patients. By multivariate linear and logistic regression analyses, both FEK and Ku/GFR were shown to be the main determinants of K serum levels and HK. Although the K load relative to glomerular filtration (Ku/GFR) is an important determinant of HK in advanced CKD, the most noteworthy characteristic associated with HK in these patients was the limitation of compensatory urinary K excretion, as indicated by lower FEK.

Objectives: Anti-glutathione S transferase T1 (GSTT1) antibodies, a type of non-HLA antibody, have been associated with chronic hepatic graft rejection. Despite the presence of this enzyme in the kidney, there are not enough studies on the development of anti-GSTT1 antibodies and their impact on renal grafts. Our objective was to evaluate the presence of anti-GSTT1 antibodies after renal transplant and their impact on graft outcomes. Materials and Methods: We conducted an ambispective cohort study. We performed real-time polymerase chain reaction to screen for GSTT1 alleles in 293 recipients and their donors. In null GSTT1 (GSTT1*0) genotype recipients of GSTT1-positive donors, the presence of anti-GSTT1 antibodies was evaluated using indirect immunofluorescence and Luminex assays, and their effects on graft function were evaluated. The median follow-up period was 54.3 months. Results: Of the 293 patients studied, 42 recipients (14.4%) with GSTT1-positive donors did not have the GSTT1 allele (GSTT1-positive donor/GSTT1*0 recipient). Using Luminex assay, we detected antibodies in 16 patients (38.1%), 12 of which were already present at the time of transplant. Of these cases, 37.5% with antibodies had undergone a previous renal transplant. Using indirect immunofluorescence, we found that only 12 patients tested positive, 4 at the time of transplant. Antibody presence did not effect graft glomerular filtration rates or graft loss at 1 year, at 2 years, or end of follow-up. Conclusions: The presence of anti-GSTT1 antibodies is frequent in renal transplant GSTT1*0 recipients of GSTT1-positive donors but has no effects on graft outcome.

Background and objective: After kidney transplantation, there is an overall increase in weight, which may increase the risk of chronic kidney disease (CKD) and graft loss. But, not all patients gain weight, and the impact on the graft of this different evolution has not been well studied. The objective was to determine the causes of this different evolution and its effect on the graft. Patients and methods: Retrospective single-center cohort study of 201 patients followed up after transplantation, analyzing the determinants of the variation in weight at one year using logistic regression, and its effect on graft survival at the end of follow-up using Cox regression. Results: Globally, there was an average weight gain of 4.5 kg in the first year, but 26.6% lost weight. 37.2% increased their BMI, while 9.5% decreased it. The determinants of the different evolution of weight were age (OR for every 10 years: 0.6, P=.002), previous dialysis modality (ref. hemodialysis) (OR 0.3, P=.003), and BMI before transplantation (OR 0.9, P=.017). The different evolution of weight did not influence the final situation of the graft. The BMI at one year did influence as a continuous variable (HR 1.3, P=.003), and obesity, with a worse evolution (HR 7.0, P=.025). Conclusions: Although not all patients gain weight after kidney transplantation, the different evolution of weight does not influence graft survival. (C) 2021 Sociedad Espanola de Nefrologia. Published by Elsevier Espana, S.L.U.