Hypertension and chronic kidney disease (CKD) are closely linked conditions and represent common global health problems. Hypertension is a leading risk factor for cardiovascular disease, which is the main cause of mortality in CKD. Endothelial injury underlies the etiopathogenesis of both hypertension and CKD. The endothelial glycocalyx (eGC) is a dynamic, negatively charged, carbohydrate-rich layer that covers the luminal surface of endothelial cells. Its primary physiological function is to protect the endothelium, including the regulation of vascular permeability and homeostasis. Damage to the eGC, known as “shedding”, is an early predictor of endothelial dysfunction and is driven by oxidative stress and low-grade inflammation. In hypertension, loss of eGC integrity—often impaired by a high-salt diet—can reduce the bioavailability of nitric oxide (NO) and increase arterial stiffness. Similarly, in CKD, uremic toxicity, hypertension, and inflammation damage the eGC, resulting in increased permeability, albuminuria, and higher cardiovascular risk. This review summarizes current evidence and underscores the potential of eGC shedding markers, especially syndecan 1 (SDC-1) and hyaluronic acid (HA), as early predictors of vascular risk and disease progression in hypertension and CKD.

Cerebral toxoplasmosis is a rare but potentially fatal opportunistic infection in renal transplant recipients receiving long-term immunosuppressive therapy. It may result from donor-derived transmission or reactivation of latent infection. We report the case of a 70-year-old female who underwent kidney transplantation from a deceased donor in 2004 for end-stage renal disease due to glomerulonephritis. She was maintained on cyclosporine, mycophenolate mofetil, and prednisone. In September 2024, she presented with headache, mood changes, and right-sided hemiparesis. Brain multislice computed tomography revealed a large temporoparietal lesion initially suspected to be glioblastoma. Craniotomy and histopathological analysis demonstrated encysted Toxoplasma gondii bradyzoites within gliotic tissue. Polymerase chain reaction testing confirmed the presence of T. gondii DNA, while human immunodeficiency virus testing was negative. The patient reported frequent contact with domestic cats. Treatment with pyrimethamine, sulfadiazine, and leucovorin, alongside adjustment of immunosuppressive therapy, led to marked neurological improvement and radiological regression of the lesion. However, nine months later, she succumbed to multidrug-resistant urosepsis. This case highlights the diagnostic challenges of cerebral toxoplasmosis in transplant recipients, as radiological findings are often nonspecific and can mimic neoplastic or lymphoproliferative lesions. Polymerase chain reaction and histopathological analysis remain essential for definitive diagnosis. Awareness of this rare complication is critical for early recognition and prompt initiation of anti-toxoplasma therapy, which can significantly improve outcomes. Although cerebral toxoplasmosis is uncommon after kidney transplantation, it should be considered in immunosuppressed patients presenting with neurological symptoms. Early detection and targeted therapy are key to reducing morbidity and mortality in this population.

Chronic kidney disease (CKD) is an initially asymptomatic, but chronic condition characterized by a progressive loss of kidney function over the time. Etiology of CKD includes diabetes, hypertension, autoimmune diseases, polycystic kidney disease and other genetic diseases, nephrotic syndrome, etc. The development of complications such as hypertension, anemia, bone diseases, and cardiovascular complications (like heart failure, coronary artery disease, arrhythmias, valvular heart disease, cardiac arrest etc.) with an increased risk of death and hospitalization is common. Due to the significant rate of morbidity and mortality from CKD, early detection and primary prevention are extremely important. Oxidative stress affects microvascular reactivity and is considered to be one of the most important causes of endothelial dysfunction, underlying CKD. Recently, the role of miRNA, a non-coding approximately 22 nucleotides long RNA molecules which mediate post-transcriptional gene silencing, in oxidative stress has also been investigated. Individual miRNA molecules, such as miRNA-335-5p, miR-92a, miR-92a-3p relate to endothelial dysfunction. This opens new diagnostic and therapeutic possibilities and requires further research in the field of CKD. The aim of this review article is to systemize recent knowledge on the role of miRNA in the regulation of oxidative stress and microvascular reactivity in CKD.

Cerebral toxoplasmosis is a rare but potentially fatal opportunistic infection in renal transplant recipients receiving long-term immunosuppressive therapy. It may result from donor-derived transmission or reactivation of latent infection. We report the case of a 70-year-old female who underwent cadaveric kidney transplantation in 2004 for end-stage renal disease due to glomerulonephritis. She was maintained on cyclosporine, mycophenolate mofetil, and prednisone. In September 2024, she presented with headache, mood changes, and right-sided hemiparesis. Brain multislice computed tomography revealed a large temporoparietal lesion initially suspected to be glioblastoma. Craniotomy and histopathological analysis demonstrated encysted Toxoplasma gondii bradyzoites within gliotic tissue. Polymerase chain reaction testing confirmed the presence of T. gondii DNA, while human immunodeficiency virus testing was negative. The patient reported frequent contact with domestic cats. Treatment with pyrimethamine, sulfadiazine, and leucovorin, alongside adjustment of immunosuppressive therapy, led to marked neurological improvement and radiological regression of the lesion. However, nine months later, she succumbed to multidrug-resistant urosepsis. This case highlights the diagnostic challenges of cerebral toxoplasmosis in transplant recipients, as radiological findings are often nonspecific and can mimic neoplastic or lymphoproliferative lesions. Polymerase chain reaction and histopathological analysis remain essential for definitive diagnosis. Awareness of this rare complication is critical for early recognition and prompt initiation of anti-toxoplasma therapy, which can significantly improve outcomes. Although cerebral toxoplasmosis is uncommon after kidney transplantation, it should be considered in immunosuppressed patients presenting with neurological symptoms. Early detection and targeted therapy are key to reducing morbidity and mortality in this population.