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Introduction: Cytokines are important immune modulator factors controlling homeostasis of the body and are involved in tissue regeneration after wound healing. The encapsulation of cytokines in liposomes has many advantages potentially useful for their transfer to the cells. Liposomes protect cytokines from neutralization, improving their pharmacokinetics or biologic activity in vivo . They are targeted to specific cell types and may delay the release of cytokines, allowing their sustained paracrine delivery. Their physicochemical characteristics such as size, shape, charge, and stability are important parameters improving bio-distribution and prolonged pharmacokinetics of encapsulated cytokines., Material and Methods: We developed an efficient protocol for the encapsulation of two types of cytokines, granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), in liposomes that can be stored long term in the active state., Results: This method allows for the encapsulation of 12-13% of the total amount of cytokines and 50% of encapsulated cytokines are entrapped in liposomes of more than ≤ 600 nm in diameter. We show that in the studied cell lines the liposome-encapsulated cytokines do not affect cell morphology, proliferation or mortality., Conclusions: The G-CSF or GM-CSF can be delivered to the cells in working concentrations through the encapsulation in the liposomes. Before the clinical application, the efficiency of these liposomes should be confirmed by an in vivo study., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2020 Termedia & Banach.)

Molecular biology and medical genetics, one of the most dynamically developing fields of medicine, nowadays is also a base for development of basic and clinical research in internal medicine. Understanding of crucial genetic pathomechanisms of many common diseases was possible due to the newest and modern molecular methods and tools. Moreover, development of genetics also made possible the discovery and understanding of the pathogenesis of many different diseases. However, not so long ago, we discovered precise pathomechanisms leading from damage of a single gene to a related pathological phenotype. Now, we have just started to explain molecular mechanisms of complex, multifactorial diseases. To achieve these goals, we need permanent development of genetic tests, genomics and proteomics. After fulfilling these conditions, we will get a chance to implement all molecular and genetic hopes, particularly their practical application in the clinic.

Introduction: Pathomechanism of HRS is still poorly understood. The aim of our study was: (1) to test whether different strains of rats could develop typical HRS, and (2) to estimate the influence of activation and inhibition of nitric oxide for development of renal failure in course of HRS., Material and Methods: First, we used 16 of Wistar and 16 of Sprague-Dawley rats in galactosamine model of HRS. Next, we used 48 of SDR rats, which received saline, N-nitro-L-arginine or L-arginine before and after liver damage. Twenty four hours urine and blood samples were collected 48 h after saline or Ga1N injection. Biochemical parameters were determined in serum or urine and then creatinine clearance and osmolality clearance were calculated. Liver and kidney tissues were collected for histopathological examination., Results: Liver failure developed in all tested groups with significant increase of bilirubin (p < 0.001), ALT (p < 0.001) and ammonia (p < 0.001). Nevertheless we did not achieve any evidence of renal failure in Wistar, but we found typical renal failure in Sprague-Dawley group with significant decrease in creatinine clearance (p < 0.0012) and increase in concentration of creatinine and urea (p < 0.001) and (p < 0.001) respectively. Inhibition of NOS prevented development of renal failure with significant improvement of GFR both before (p < 0.0017) and after (p < 0.003) Ga1N injection. Injection of L-arginine after Ga1N injection did not caused significant improvement of GFR., Conclusions: Our study showed, that genetic factors might be responsible for development of renal failure in course of HRS and nitric oxide play important role in acute model of this syndrome.

This report presents the case of a young female suffered for many years from type 1 diabetes, complicated by recurrent urinary tract infections and urosepsis with multiple abscesses which led to right nephrectomy in 2002. The patient was hospitalised in our Department in June 2009 because of urosepsis in the course of multiple left renal abscesses and subsequent acute renal failure requiring hemodialysis. A dramatic decision of removing the solitary kidney was taken, and patient was included in a long-term renal replacement therapy programme in our Centre as a preparation to kidney and pancreas transplantation.

Introduction: High blood pressure (BP) leads to target organ damage. It is suggested that regression of early organ lesions is possible on condition of BP normalization. The study objective was to assess whether permanent reduction of BP to the recommended values modifies renal vascular response to acute angiotensin II inhibition in the Doppler captopril test (DCT) in patients with essential hypertension (EH)., Material and Methods: Twenty-nine persons (58 kidneys) were found eligible for the study: 18 patients with EH and 11 healthy volunteers constituting the control group. Glomerular filtration rate estimation (eGFR), 24-h ambulatory BP monitoring (ABPM) and DCT with evaluation of renal resistive index change (ΔRI) were performed before and after a 6-month period of intensive antihypertensive therapy (IAT). Additional ABPM was performed at the end of IAT., Results: The mean IAT period was 8.5 ±2.4 months. The mean 24-h values of systolic and diastolic BP in the EH group were significantly lower in the IAT period than at the beginning and at the end of the study. Significantly lower systolic and diastolic BP (p < 0.05) and improvement of renal function (eGFR 121 ±38 vs. 139 ±40 ml/min, p < 0.001) were found after IAT as compared to initial values. Before IAT, ΔRI was significantly lower in the EH group as compared to the controls, but no such differences were found after IAT., Conclusions: In EH patients, intensive BP lowering to the recommended values was associated with improvement of renal function and normalisation of renal vascular response to acute angiotensin II inhibition.