While patient care, kidney replacement therapy, and transplantation techniques for chronic kidney disease (CKD) have continued to progress, the incidence of malnutrition disorders in CKD appears to have remained unchanged over time. However, there is now a better understanding of the underlying pathophysiology according to the disease background, disease stage, and the treatment received. In CKD patients, the increased production of proinflammatory cytokines and oxidative stress lead to a proinflammatory milieu that is at least partially responsible for the increased morbidity and mortality in this patient population. New insights into the pathogenic role of innate immunity and the proinflammatory cytokine profile, characterized, for instance, by higher levels of IL-6 and TNF-α, explain some of the clinical and laboratory abnormalities observed in these patients. In this article, we will explore currently available nutritional–inflammatory biomarkers in distinct CKD populations (hemodialysis, peritoneal dialysis, transplantation) with a view to evaluating their efficacy as predictors of malnutrition and their involvement in the common proinflammatory process. Although there is a direct relationship between inflammatory-nutritional status, signs and symptoms [e.g., protein-energy wasting (PEW), anorexia], and comorbidities (e.g., atheromatosis, atherosclerosis), we are in need of clearly standardized markers for nutritional-inflammatory assessment to improve their performance and design appropriate bidirectional interventions.

Uncontrolled donation after circulatory death (uDCD) increases organ availability for kidney transplantation (KT) with short‐term outcomes similar to those obtained from donation after brain death (DBD) donors. However, heterogeneous results in the long term have been reported. We compared 10‐year outcomes between 237 KT recipients from uDCD donors maintained by normothermic extracorporeal membrane oxygenation (nECMO) and 237 patients undergoing KT from standard criteria DBD donors during the same period at our institution. We further analyzed risk factors for death‐censored graft survival in the uDCD group. Delayed graft function (DGF) was more common in the uDCD group (73.4% versus 46.4%; P‐value 50 years was associated with graft loss in the uDCD group (hazard ratio: 1.91; P‐value = 0.058), whereas the occurrence of DGF showed no significant effect. uDCD KT under nECMO support resulted in similar graft function and long‐term outcomes compared with KT from standard criteria DBD donors. Increased donor age could negatively impact graft survival after uDCD donation.

SARS‐CoV‐2 infection has produced high mortality in kidney transplant (KT) recipients, especially in the elderly. Until December‐2020, 1011 KT with COVID‐19 have been prospectively included in the Spanish Registry and followed until recovery or death. In multivariable analysis, age, pneumonia and KT performed ≤6 months before COVID‐19 were predictors of death, whereas gastrointestinal symptoms were protective. Survival analysis showed significant increasing mortality risk in four subgroups according to recipient age and time after KT (age 6 months, age 6 and age ≥65 and time ≤6): mortality rates were, respectively, 11.3%, 24.5%, 35.4% and 54.5% (p<.001). Patients were significantly younger, presented less pneumonia and received less frequently specific anti‐COVID‐19 treatment in the second wave (July‐December) than in the first one (March‐June). Overall mortality was lower in the second wave (15.1 vs. 27.4%, p<.001), but similar in critical patients (66.7% vs. 58.1%, p=.29). The interaction between age and time post‐KT should be considered when selecting recipients for transplantation in the COVID‐19 pandemic. Advanced age and a recent KT should foster strict protective measures, including vaccination.

Background and objectives: Mortality of patients on haemodialysis (HD) remains very high despite recent improvements in HD techniques. Cardiovascular (CV) complications and infections are the main causes of death. Some studies suggest that disturbances in the immune system could play a role in this disproportionate mortality, through the links of immunity with inflammation and propensity to infections. However, few studies have addressed the role of lymphocyte populations and the global and CV mortality of HD patients. Aim: To analyze the relationship of Peripheral Blood Lymphocyte Populations (PBLP) and all-cause and CV mortality of HD patients. Design, setting, participants and measurements: We design a prospective observational single center study in a cohort of HD prevalent patients. PBLP were analyzed at baseline and after 1-year and patients were followed for a 5-year period. Main outcomes were all-cause and CV mortality. Results: One hundred and four patients (51% male, mean age 64.8 ± 15 years) were included. Follow-up was 18 (7-47) months. Fifty-five patients (52.8%) died, main causes of death being CVD (40%) and infections (29.1%). Low total lymphocyte counts were found in 47 patients (45.2%). 45.2% of patients had total lymphopenia, and the most frequency lymphopenias were CD19+ B-cell (57.7%), CD3+ (40.4%) and CD4+ (36.5%). After 1 year, all determinations were lower except CD56+CD16+CD3- Natural Killer. Patient survival was significantly lower in patients with a CD19+ B-cell count 100 cells/µL counts at the end of follow-up (16.5% vs 54%, p=0.003). By multivariable analysis, age, history of CV disease, Charlson index, a KT/V <1.2, and a CD19+ B-cell count <100 cells/μL at baseline and after 1-year were factors associated with of all-cause mortality. A CD19+ B-cell count < 100 cells/µL at baseline was associated with CV mortality. Conclusions: CD19+ B-cell lymphopenia is very common among HD patients and it could be an independent predictor of all-cause and CV mortality. More studies are needed to confirm these findings.

Some patients with thin basement membrane disease (TBMD) develop proteinuria, hypertension and different degrees of CKD, besides the persistent microhaematuria characteristic of the disease. Little is known about factors associated with this unfavourable outcome. We reviewed clinical, pathological and radiological features of 32 patients with biopsy-proven TBMD. Patients were divided in two groups: those with persistent normal kidney function and negative or minimal proteinuria (n = 16) and those with persistent proteinuria >0.5 g/day (n = 16). Patients with proteinuria had a worse kidney function at baseline than those with negative proteinuria. Global or segmental glomerulosclerosis, together with interstitial fibrosis, was found in 37% of patients with proteinuria. All proteinuric patients were treated with renin–angiotensin system blockers. At the end of follow-up (198 months in proteinuric patients and 210 months in patients with negative proteinuria) the prevalence of hypertension was 68% in proteinuric patients (12% at baseline), compared with 12 and 6%, respectively, in non-proteinuric patients. A slow decline of renal function was observed in proteinuric patients, although no patient developed end-stage kidney disease. Ultrasound studies showed bilateral kidney cysts in nine patients (56%) with proteinuria. Cysts were bilateral and countless in six patients, and bilateral but with a limited number of cysts in the three remaining patients. No cysts were found in patients with negative proteinuria. Some patients with TBMD develop hypertension, proteinuria and CKD. Multiple bilateral kidney cysts were found in a majority (56%) of these patients. Further studies are needed to investigate the pathogenesis and the influence on long-term outcome of this TBMD-associated multiple kidney cysts.