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1.  Hepatoprotective effect of nitric oxide in experimental model of acute hepatic failure 
World Journal of Gastroenterology : WJG  2014;20(46):17407-17415.
AIM: To evaluate the effect of nitric oxide (NO) on the development and degree of liver failure in an animal model of acute hepatic failure (AHF).
METHODS: An experimental rat model of galactosamine-induced AHF was used. An inhibitor of NO synthase, nitroarginine methyl ester, or an NO donor, arginine, were administered at various doses prior to or after the induction of AHF.
RESULTS: All tested groups developed AHF. Following inhibition of the endogenous NO pathway, most liver parameters improved, regardless of the inhibitor dose before the induction of liver damage, and depending on the inhibitor dose after liver damage. Prophylactic administration of the inhibitor was more effective in improving liver function parameters than administration of the inhibitor after liver damage. An attempt to activate the endogenous NO pathway prior to the induction of liver damage did not change the observed liver function parameters. Stimulation of the endogenous NO pathway after liver damage, regardless of the NO donor dose used, improved most liver function parameters.
CONCLUSION: The endogenous NO pathway plays an important role in the development of experimental galactosamine-induced AHF.
PMCID: PMC4265599  PMID: 25516652
Nitric oxide; Acute hepatic failure; Nitric oxide synthase; Rat model; Galactosamine
2.  Effect of Nitric Oxide Pathway Regulation on Water/Sodium Balance and Renal Function in a Rodent Model of Acute Liver and Renal Failure 
The pathomechanism of acute hepatorenal syndrome (HRS), a particular form of acute renal failure that occurs in the course of acute liver injury, is still poorly understood. The aim of our study was to estimate the influence of the activation and inhibition of the nitric oxide pathway on the water/sodium balance and development of acute renal failure in the course of HRS.
We used male Sprague-Dawley rats in the acute galactosamine (Ga1N) model of HRS. The nitric oxide synthase (NOS) inhibitors L-NAME and L-arginine were administered intraperitoneally before and after liver damage.
HRS developed in all tested groups. L-NAME increased osmotic clearance and urine volume more effectively before liver injury. Furthermore, administration of L-NAME increased creatinine clearance both before and after Ga1N injection. A double dose of L-NAME did not yield further improvement before Ga1N injection, but improved creatinine clearance after Ga1N intoxication. Injection of L-arginine increased sodium excretion and urine volume, but only after liver injury. Moreover, L-arginine injected after Ga1N caused significant improvement of the creatinine clearance in a dose-dependent manner.
Our study shows that inhibition of the nitric oxide pathway improves parameters of water and sodium balance and prevents development of acute renal failure in the course of acute liver injury and liver failure. Activation of the nitric oxide system also has a favorable influence on water/sodium balance and renal failure, but only after liver injury.
PMCID: PMC4186324  PMID: 25270512
Hepatorenal Syndrome; Liver Failure; Acute; Nitric Oxide; Renal Insufficiency; Water-Electrolyte Balance
3.  Oral Anticoagulant Therapy in Patients Receiving Haemodialysis: Is It Time to Abandon It? 
The Scientific World Journal  2013;2013:170576.
Oral anticoagulant (OAC) therapy in haemodialysis patients causes a great deal of controversy. This is because a number of pro- and anticoagulant factors play an important role in end-stage renal failure due to the nature of the disease itself. In these conditions, the pharmacokinetic and pharmacodynamic properties of the OACs used change as well. In the case of the treatment of venous thromboembolism, the only remaining option is OAC treatment according to regimens used for the general population. Prevention of HD vascular access thrombosis with the use of OACs is not very effective and can be dangerous. However, OAC treatment in patients with atrial fibrillation in dialysis population may be associated with an increase in the incidence of stroke and mortality. Doubts should be dispelled by prospective, randomised studies; at the moment, there is no justification for routine use of OACs in the above-mentioned indications. In selected cases of OAC therapy in this group of patients, it is absolutely necessary to control and monitor the applied treatment thoroughly. Indications for the use of OACs in patients with end-stage renal disease, including haemodialysis patients, should be currently limited.
PMCID: PMC3863463  PMID: 24379737
4.  Contemporary role of medical genetics in internal medicine 
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.
PMCID: PMC3776171  PMID: 24049516
medical genetics; genetic testing; internal medicine
5.  Strain of experimental animals and modulation of nitric oxide pathway: their influence on development of renal failure in an experimental model of hepatorenal syndrome 
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.
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.
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.
PMCID: PMC3400905  PMID: 22852015
hepatorenal syndrome; experimental studies; nitric oxide
6.  Multiple renal abscesses leading to nephrectomy of the solitary kidney in a young female with type 1 diabetes and history of recurrent urinary tract infections 
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.
PMCID: PMC3258731  PMID: 22291780
urinary tract infections; renal abscesses; nephrectomy
7.  Renal vascular response to angiotensin II inhibition in intensive antihypertensive treatment of essential hypertension 
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.
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.
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.
PMCID: PMC3284067  PMID: 22371796
renal resistive index; Doppler captopril test

Results 1-7 (7)