Immunoglobulin A (IgA) is the most abundant antibody isotype produced in humans, predominantly present in the mucosal areas where its main functions are the neutralization of toxins, prevention of microbial invasion across the mucosal epithelial barrier, and simultaneous maintenance of a physiologically indispensable symbiotic relationship with commensal bacteria. The process of IgA biosynthesis, interaction with receptors, and clearance can be disrupted in certain pathologies, like IgA nephropathy, which is the most common form of glomerulonephritis worldwide. This review summarizes the latest findings in the complex characteristics of the molecular structure and biological functions of IgA antibodies, offering an in-depth overview of recent advances in the understanding of biochemical, immunologic, and genetic factors important in the pathogenesis of IgA nephropathy.
COBISS.SI-ID: 6761388
Plant-based diets (PBDs) are associated with decreased risk of morbidity and mortality associated with important noncommunicable chronic diseases. Similar to animal-based food sources (e.g., meat, fish, and animal visceral organs), some plant-based food sources (e.g., certain soy legume products, sea vegetables, and brassica vegetables) also contain a high purine load. Suboptimally designed PBDs might consequently be associated with increased uric acid levels and gout development. Here, we review the available data on this topic, with a great majority of studies showing reduced risk of hyperuricemia and gout with vegetarian (especially lacto-vegetarian) PBDs. Additionally, type of ingested purines, fiber, vitamin C, and certain lifestyle factors work in concordance to reduce uric acid generation in PBDs. Recent limited data show that even with an exclusive PBD, uric acid concentrations remain in the normal range in short- and long-term dieters. The reasonable consumption of plant foods with a higher purine content as a part of PBDs may therefore be safely tolerated in normouricemic individuals, but additional data is needed in hyperuricemic individuals, especially those with chronic kidney disease.
COBISS.SI-ID: 6381484
Aim: The use of glomerular filtration rate (GFR) estimating equations is not always reliable, especially in specific populations, such as patients with transplanted kidney. The purpose of this study was to improve the performance of GFR equations by taking into account dry lean body mass. Materials and methods: A prospective clinical study included 100 patients with kidney graft. Estimated GFR (eGFR) with Chronic Kidney Disease Epidemiology Collaboration equations with serum creatinine concentration (CKD-EPI Cr), serum cystatin C concentration (CKD-EPI CysC), or both (CKD-EPI Cr-CysC) were compared with measured GFR with 51Cr-EDTA clearance (mGFR 51Cr-EDTA). Dry lean body mass (body mass without fat mass and water) was measured with bioimpedance analysis. Results: All of the eGFRs overestimated mGFR 51Cr-EDTA by a significant degree (shown as bias ± SD in mL/min/1.73m2 with 30% accuracy in parentheses): CKD-EPI Cr 15.1 ± 15.3 (50%), CKD-EPI CysC 8.0 ± 16.6 (56%), CKD-EPI Cr-CysC 10.3 ± 13.4 (55%). Dry lean body mass significantly correlated with mGFR 51Cr-EDTA (R = 0.241; p = 0.016) and all biases except the bias of CKD-EPI CysC. Considering the dry lean body mass and preexisting equations with creatinine, we developed two new equations with better performance and statistically insignificant bias: Corrected CKD-EPI Cr -1.43 ± 13.6 (67%) and Corrected CKD-EPI Cr-CysC -1.64 ± 13.4 (77%). Conclusion: Dry lean body mass improves the performance of GFR equations in our kidney transplant cohort.
COBISS.SI-ID: 6739628
Opportunistic infections commonly occur during the first 6 months after kidney transplant, including cytomegalovirus (CMV) and polyomaviruses. Viral pathogens such as CMV and polyomaviruses, JC or BK virus (BKV), are able to replicate in the kidney and/or cause systemic disease, and symptomatic infection with these agents can be associated with significant morbidity and mortality in immunocompromised host. While BK virus usually replicates in kidney transplant causing BK virus nephropathy (BKN) with characteristic decoy cells in the urine, CMV infection more often leads to systemic infection involving the gastrointestinal tract (GIT), lungs, or liver and can only sporadically be detected in renal transplant. In both cases, the disease is most often due to reactivation of a latent virus. Prevention and early treatment of posttransplant infection are therefore crucial with kidney transplant recipients. Since BKV viruria and viremia can be seen without renal injury and viral nephropathy, a diagnosis of BKN must be confirmed by renal biopsy. To date, preemptive treatment is the best strategy for CMV infection, while no available standard therapy, except for reduction of immunosuppression, is available for BKV infection.
COBISS.SI-ID: 34542297