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Acquired pure red cell aplasia (PRCA) is characterized by severe normocytic (rarely macrocytic) and normochromic anemia, a low reticulocytes count in peripheral blood, and near absence of erythroid precursors in the bone marrow, with a normal level of erythropoietin. We describe a case of the kidney transplant recipient, diagnosed with PRCA induced with parvovirus B19 infection. Our case demonstrates that although this complication is rare, it should be considered in a differential diagnosis of anemia diagnostics in immunocompromised patients. In our case reduced immune response resulted from post-transplant immunosuppressive therapy. In our patient, apart from infection by parvovirus B19, graft dysfunction due to polyomavirus BK virus infection was also detected together with histologic and serologic features of antibody-mediated renal graft rejection. Considering the entire clinical picture, intravenous immunoglobulin therapy (IVIg) was successfully introduced. [ABSTRACT FROM AUTHOR]

The incidence of type 2 diabetes (T2D) has been increasing worldwide, and diabetic kidney disease (DKD) remains one of the leading long-term complications of T2D. Several lines of evidence indicate that glucose-lowering agents prevent the onset and progression of DKD in its early stages but are of limited efficacy in later stages of DKD. However, sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor (GLP-1R) antagonists were shown to exert nephroprotective effects in patients with established DKD, i.e., those who had a reduced glomerular filtration rate. These effects cannot be solely attributed to the improved metabolic control of diabetes. In our review, we attempted to discuss the interactions of both groups of agents with inflammation and oxidative stress—the key pathways contributing to organ damage in the course of diabetes. SGLT2i and GLP-1R antagonists attenuate inflammation and oxidative stress in experimental in vitro and in vivo models of DKD in several ways. In addition, we have described experiments showing the same protective mechanisms as found in DKD in non-diabetic kidney injury models as well as in some tissues and organs other than the kidney. The interaction between both drug groups, inflammation and oxidative stress appears to have a universal mechanism of organ protection in diabetes and other diseases. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) affects more than 10% of the world population and leads to excess morbidity and mortality (with cardiovascular disease as a leading cause of death). Vascular calcification (VC) is a phenomenon of disseminated deposition of mineral content within the media layer of arteries preceded by phenotypic changes in vascular smooth muscle cells (VSMC) and/or accumulation of mineral content within the atherosclerotic lesions. Medial VC results in vascular stiffness and significantly contributes to increased cardio-vascular (CV) morbidity, whereas VC of plaques may rather increase their stability. Mineral and bone disorders of CKD (CKD-MBD) contribute to VC, which is further aggravated by accumulation of uremic toxins. Both CKD-MBD and uremic toxin accumulation affect not only patients with advanced CKD (glomerular filtration rate (GFR) less than 15 mL/min/1.72 m2, end-stage kidney disease) but also those on earlier stages of a disease. The key uremic toxins that contribute to VC, i.e., p-cresyl sulphate (PCS), indoxyl sulphate (IS) and trimethylamine-N-oxide (TMAO) originate from bacterial metabolism of gut microbiota. All mentioned toxins promote VC by several mechanisms, including: Transdifferentiation and apoptosis of VSMC, dysfunction of endothelial cells, oxidative stress, interaction with local renin–angiotensin–aldosterone system or miRNA profile modification. Several attractive methods of gut microbiota manipulations have been proposed in order to modify their metabolism and to limit vascular damage (and VC) triggered by uremic toxins. Unfortunately, to date no such method was demonstrated to be effective at the level of "hard" patient-oriented or even clinically relevant surrogate endpoints. [ABSTRACT FROM AUTHOR]

Phosphorus is an essential nutrient that is critically important in the control of cell and tissue function and body homeostasis. Phosphorus excess may result in severe adverse medical consequences. The most apparent is an impact on cardiovascular (CV) disease, mainly through the ability of phosphate to change the phenotype of vascular smooth muscle cells and its contribution to pathologic vascular, valvular and other soft tissue calcification. Chronic kidney disease (CKD) is the most prevalent chronic disease manifesting with the persistent derangement of phosphate homeostasis. Diabetes and resulting diabetic kidney disease (DKD) remain the leading causes of CKD and end-stage kidney disease (ESRD) worldwide. Mineral and bone disorders of CKD (CKD-MBD), profound derangement of mineral metabolism, develop in the course of the disease and adversely impact on bone health and the CV system. In this review we aimed to discuss the data concerning CKD-MBD in patients with diabetes and to analyze the possible link between hyperphosphatemia, certain biomarkers of CKD-MBD and high dietary phosphate intake on prognosis in patients with diabetes and DKD. We also attempted to clarify if hyperphosphatemia and high phosphorus intake may impact the onset and progression of DKD. Careful analysis of the available literature brings us to the conclusion that, as for today, no clear recommendations based on the firm clinical data can be provided in terms of phosphorus intake aiming to prevent the incidence or progression of diabetic kidney disease. [ABSTRACT FROM AUTHOR]

Introduction of the definition and classification of chronic kidney disease (CKD) according to the KDOQI guidelines in 2002 served as a turning point in nephrology. On one hand, the new definition has allowed for the standardization of terminology, on the other hand, however, it has led to a rapid growth in CKD diagnoses. Another issue is the strengthening of the assumption, that diagnosis of CKD is associated with further progressive kidney dysfunction until reaching the end stage renal disease (ESRD). Clinical practice, however, provides evidence that not all patients diagnosed with CKD reach ESRD and eventually require renal replacement therapy (RRT), and in many cases CKD does not progress., Aim: The aim of the study was to assess practical information for a clinician provided by eGFR and its changes during the follow-up of a patient as regards the RRT prognosis and mortality risk., Materials and Methods: The study group consisted of patients with CKD treated in the regional outpatient clinic. Progression was assessed by determining a linear trend line for eGFR results. Based on its course and the value of the coefficient of determination R2, four types of eGFR trajectories were identified: linear progression type (G2), nonlinear progression type (G1), improvement type (G3), undetermined eGFR change type (G4)., Results: The study group consisted of 65 patients 58.5% females, age mean 69 ± 12.8 years. The mean annual eGFR change in the entire group was -1.67±11.7 ml/min/1.73m2/year. During the study, 6.2% of patients began RRT (hemodialysis), and 9.2% died. Despite the evident tendency towards higher mortality in the group characterized by progression (G1+G2) as compared to the group without progression (G3+G4), the difference did not reach statistical significance (p=0.617). However, the comparison of groups with the baseline eGFR value above and below 45 ml/min/1.73 m2 differentiated the two groups that statistically differed in mortality (p=0.044)., Conclusions: The baseline eGFR was not a significant predictor of future renal outcomes (ESRD, RRT). However, eGFR below 45 ml/min/ 1.73m2 was associated with a significantly higher mortality risk (p=0.036). Moreover, the groups with the fastest and with improved eGFR were characterized by the highest mortality., (© 2021 MEDPRESS.)