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EN
Immunosuppression is a characteristic feature of chronic kidney disease. It may lead to the increased risk of infections and neoplastic diseases occurrence. We present an unusual case of 57-years-old women with uncommon neoplasm of the head and neck region – osteoclastoma.
EN
Objectives. Post exercise proteinuria (PEP) is found in about 20–40% of sportsmen after intensive exercise. Urinary NGAL is a new marker of tubulointerstitial kidney damage. The relationship between PEP and uNGAL has not been defined yet. In presented study a resting uNGAL as a predictor of PEP was analyzed. The changes of albuminuria after exercise were monitored to estimate a frequency and range of PEP. Methods. 40 amateur healthy runners (mean age 36.65 ±10.61 years) participating in 10-km run took part in the study. Before and after the competition urine was collected. NGAL, albumin and creatinine were subsequently measured in urine. uNGAL to creatinine ratio (NCR) and albumin to creatinine ratio (ACR) were calculated. Results. 28 participants (mean age 37.9 ±11.46, 19 M, 9 F) with uNGAL below 15 ng/ml before competition were analyzed. The increase of ACR was observed in every case. Mean post-exercise ACR was 104.55 ±123.1 mg/g and was significantly higher than pre-exercise ACR 6.33 ±5.86 mg/g (p < 0.0005). The positive correlation was found between resting NCR and post-exercise ACR (r = 0.60, p < 0.05). Conclusions. Resting uNGAL positively correlated with PEP. The possible explanation of these findings is that persons with PEP had some early, occult tubulointersitial kidney damage. It is speculated that those runners have higher risk of chronic kidney disease.
EN
Background: Analgesics can be sold following medical prescription, but also as over-the-counter (OTC) medications. In patients with chronic kidney disease (CKD), their use could potentially be associated with increased risk of side-effects, due to impaired renal elimination. The aim was to evaluate the epidemiology and indications for the use of OTC analgesics, and the knowledge of their side-effects in patients with CKD. Material and methods: A cross-sectional, controlled survey on the use of OTC analgesic drugs was conducted among 180 CKD patients (stage 1-5, dialysis, kidney transplant), compared to 60 controls. Results: The proportion of patients using OTC analgesics on a regular basis was higher in the CKD group, compared to controls (18.9% vs. 10.0%, p<0.02). The major indications included musculoskeletal issues, followed by headaches and other. Subgroup analysis revealed that analgesic use was lowest among transplanted patients, in comparison to CKD stage 1-5, and dialysis subjects (10%, 20%, 26%, respectively, p=0.06). Less than half of CKD patients and controls declared any knowledge on potential side-effects of analgesic drugs (45.6% vs. 40.0%, NS). Conclusions: The use of OTC analgesics among patients with CKD is higher than in subjects without CKD, with the exception of transplanted patients. The knowledge on the potential side-effect of analgesics is limited.
EN
Recent years, obesity is a growing health problem also in patients with chronic renal failure and end it’s end stage. This situation has a negative impact both on the extension of the waiting period for transplantation, and the survival rate of the transplanted organ and the recipient. Weight loss through lifestyle modification before transplantation is ambiguous. Its well known fact of rapid body mass gain after transplantation, and finnaly the results of transplantation are not better than those of patients who have not reduced body weight. The paper presents preliminary experience associated with bariatric operations of three chronic dialysed patients with morbid obesity BMI> 35 kg/m2, all patients had been treated by Roux-en-Y gastric by-pass (RYGB). All operated patients were classified as potential recipients were listed by Poltransplant. One of them three months after RYGB surgery underwent without complications a renal transplantation. Preliminary experiences based on operating these three caese confirmed the complete safety of this type of approach in patients with end-stage chronic kidney disease (CKD).
EN
Background Analgesics can be sold following medical prescription, but also as over-the-counter (OTC) medications. In patients with chronic kidney disease (CKD), their use could potentially be associated with increased risk of side-effects, due to impaired renal elimination. The aim was to evaluate the epidemiology and indications for the use of OTC analgesics, and the knowledge of their side-effects in patients with CKD. Material and methods A cross-sectional, controlled survey on the use of OTC analgesic drugs was conducted among 180 CKD patients (stage 1-5, dialysis, kidney transplant), compared to 60 controls. Results The proportion of patients using OTC analgesics on a regular basis was higher in the CKD group, compared to controls (18.9% vs. 10.0%, p<0.02). The major indications included musculoskeletal issues, followed by headaches and other. Subgroup analysis revealed that analgesic use was lowest among transplanted patients, in comparison to CKD stage 1-5, and dialysis subjects (10%, 20%, 26%, respectively, p=0.06). Less than half of CKD patients and controls declared any knowledge on potential side-effects of analgesic drugs (45.6% vs. 40.0%, NS). Conclusions The use of OTC analgesics among patients with CKD is higher than in subjects without CKD, with the exception of transplanted patients. The knowledge on the potential side-effect of analgesics is limited.
EN
Due to the wide use of radiocontrast agents (RCA) in modern radiology and interventional cardiology, the incidence of radiocontrast-induced nephropathy (RCIN) is increasing. The risk factors for RCIN are primarily pre-existing (even mild) renal dysfunction, diabetes mellitus, absolute or relative hypovolemia, nephrotoxic drugs, etc., particularly in elderly patients. The presence of these risk factors seems to be more important than the type of contrast agent used. To date, there are several certainties and controversies in the prevention of RCIN. Hydration with normal saline and/or bicarbonate administration pre-and post-intervention is certainly useful. Though controversial, N-Acetylcysteine administration may be still advisable. Recent investigations showed the benefits of aminophylline/theophylline administration in RCA-induced renal tubular toxicity. Conventional hemodialysis cannot prevent RCIN, but may potentially aggravate renal dysfunction through hemodynamic instability. “High-flux” hemodialysis and hemodiafiltration may contribute efficiently to RCIN prevention, but systematic use of these modern dialysis techniques is limited by high costs and availability. The authors review - in a systematic manner, and in the perspective of evidence-based medicine - the most important data from literature concerning the prevention of RCIN.
EN
Background. There is evidence that dyslipidemia is associated with chronic kidney disease (CKD) and it has been implicated in the progression of renal damage. Optimal management of dyslipidemia should therefore lead to renal benefits. A number of experimental models demonstrate a beneficial effect of statins in ameliorating renal damage. However, the exact mechanism by which statins protect against renal damage remains unclear. Methods. In a placebo-controlled, randomized, cross-over study we evaluated the influence of atorvastatin (ATO) 40 mg/day added to the renin-angiotensin-aldosterone systeme (RAAS) blockade on proteinuria and surrogate biomarkers of tubular damage or injury in 14 non-diabetic patients with proteinuria (0.4-1.8 g per 24 h) with normal or declined kidney function (eGFR 55-153 ml/min). In the eight-week run-in period, therapy using angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: ATO/washout/placebo or placebo/washout/ATO. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. The primary end point of this study was a change in proteinuria measured as 24-h urine protein excretion (DPE). Secondary end points included urine N-acetyl-β-d-glucosaminidase (NAG) and α1-microglobulin (α1m) excretion. Results. The ATO therapy significantly reduced urine excretion of α1m (p=0.033) and NAG (p=0.038) as compared to placebo. There were no differences in proteinuria, blood pressure, eGFR and serum creatinine between the ATO and placebo groups. Conclusion. Atorvastatin treatment is safe and improves biomarkers of tubular damage or injury in non-diabetic patients with CKD.
EN
INTRODUCTION: Chronic glomerulonephritis is one of the common causes of chronic kidney disease that can lead to end-stage renal failure and the need for renal replacement therapy. Understanding the aetiology of this disease and its risk factors can help develop new methods of early diagnosis and effective therapy. Uromodulin is a protein with a broad spectrum of activity, and is involved in the key pathways that regulate kidney homeostasis. AIM OF THE STUDY: The aim of the study was to analyse the relationship between three selected polymorphisms (rs13335818, rs4293393 and rs13333226) of the uromodulin gene (UMOD) and the risk of chronic kidney disease caused by chronic glomerulonephritis. MATERIAL AND METHODS: 113 patients with chronic glomerulonephritis and eGFR < 60 ml/min/1.73 m2 (experimental group) and 196 patients from the General Outpatient Clinic without a history of renal disease and eGFR > 60 ml/min/1.73 m2 (control group) were recruited for the study. The study protocol assumed a one-time blood collection for genetic testing and serum creatinine level determination. Genetic material was isolated from the peripheral blood lymphocytes of the subjects. Genotyping of the analysed polymorphisms was performed using TaqMan SNP Genotyping Assay kits. The results were processed with statistical methods using Statistica 10 and Microsoft Office Exel 2003 software, the Mann-Whitney U test and the χ2 test. Statistical significance was adopted at p < 0.05. RESULTS: No statistically significant differences in the distribution of genotypes between the experimental and control groups were found for any of the three analysed UMOD variants. CONCLUSIONS: UMOD polymorphisms rs13335818, rs4293393 and rs13333226 are not associated with the risk of chronic kidney disease caused by chronic glomerulonephritis.
PL
WSTĘP: Przewlekłe kłębuszkowe zapalenie nerek jest jedną z częstych przyczyn przewlekłej choroby nerek mogącej prowadzić do ich schyłkowej niewydolności i konieczności stosowania terapii nerkozastępczej. Poznanie etiologii tej choroby oraz czynników ryzyka daje nadzieję na wdrożenie nowych metod wczesnej diagnostyki i skutecznej terapii. Uromodulina jest białkiem prezentującym szerokie spektrum działań, włączonym w kluczowe szlaki warunkujące homeostazę nerek. CEL PRACY: Celem pracy była ocena związku wybranych trzech polimorfizmów (rs13335818, rs4293393 i rs13333226) genu uromoduliny (UMOD) z występowaniem przewlekłej choroby nerek na tle przewlekłego kłębuszkowego zapalenia nerek. MATERIAŁ I METODY: Do badania zrekrutowano 113 chorych z przewlekłym kłębuszkowym zapaleniem nerek i eGFR < 60 ml/min/1,73 m2 (grupa badana) oraz 196 pacjentów Poradni Ogólnej POZ bez chorób układu moczowego w wywiadzie, z eGFR > 60 ml/min/1,73 m2 (grupa kontrolna). Protokół badania przewidywał jednorazowe pobranie krwi do wykonania badań genetycznych oraz w celu oznaczenia stężenia kreatyniny w surowicy. Materiał genetyczny wyizolowano z limfocytów krwi obwodowej badanych. Genotypowanie badanych polimorfizmów przeprowadzono z wykorzystaniem zestawów TaqMan SNP Genotyping Assay. Uzyskane wyniki opracowano statystycznie na podstawie programów Statistica 10 i Microsoft Office Exel 2003 z wykorzystaniem: testu Manna-Whitneya i testu χ2. Za granice istotności statystycznej przyjęto wartości p < 0,05. WYNIKI: W zakresie żadnego z trzech badanych polimorfizmów UMOD nie stwierdzono znamiennych statystycznie różnic w rozkładzie genotypów pomiędzy grupami badaną a kontrolną. WNIOSKI: Nie wykazano związku polimorfizmów rs13335818, rs4293393 i rs13333226 genu UMOD z występowaniem przewlekłej choroby nerek na tle przewlekłego kłębuszkowego zapalenia nerek.
EN
Background: Numerous authors have shown that selenium (Se) concentration and glutathione peroxidase (GSH-Px) activity in plasma of chronic kidney disease (CKD) patients are lower than in healthy subjects, but there are only few publications on the level of GSH-Px protein in those patients and no reports on the effect of Se supplementation to HD patients on the level of this enzyme. Subjects and Methods: Se concentration and GSH-Px protein level in plasma were measured in a group of 30 CKD patients on hemodialysis (HD) supplemented with 200 µg Se/day for 3 months, and 28 patients on HD administered with placebo. Se concentration was measured by graphite furnace atomic absorption spectrometry and plasma GSH-Px protein level by the sandwich ELISA method using polyclonal antibody specific for human plasma GSH-Px. Results: Se concentration in patients on placebo did not change throughout the 3-month study period, but increased significantly in Se supplemented group. Se supplementation to CKD patients on HD had no effect on the level of GSH-Px protein. Conclusions: The lack of GSH-Px protein in CKD patients on HD is not linked to Se deficiency since the level of this element increased after Se supplementation while enzyme protein level did not change. The damaged kidney of HD patients is unable to synthesize GSH-Px, even after induction with selenium.
EN
Chronic kidney disease (CKD) is characterized by loss of kidney function and generally it is associated with several alterations in pulmonary functions, including restriction, obstruction, and impaired diffusion capacity. It became challenging to maintain oxygenation in a CKD patient associated with COVID 19 on non-invasive ventilation (NIV). In patients with end stage renal disease (ESRD), several factors likes, fluid overload, anaemia, immune suppression, extraosseous calcification, malnutrition, electrolyte imbalance, and acid-base disorder affecting the lungs indirectly. Here we are reporting NIV failure in two COVID 19 patients during dialysis. Both patients were stable on NIV before starting dialysis and underwent oxygen desaturation and shifted to invasive mechanical ventilation during hemodialysis. The possible mechanism of the oxygen desaturation is alveolar hypoventilation in the absence of hypercapnia, which may be due to the removal of CO2 from the body by some route (dialysate) other than the lungs.
PL
Przewlekła choroba nerek (PChN) charakteryzuje się utratą funkcji nerek i generalnie wiąże się z kilkoma zmianami w czynnościach płuc, w tym ograniczeniem, niedrożnością i upośledzeniem zdolność dyfuzyjnej. Podczas wentylacji nieinwazyjnej (NIV) u pacjenta z PChN związanego z COVID 19 wystąpiły problemy z utrzymaniem odpowiedniego utlenowania. Pacjenci ze schyłkową niewydolnością nerek wyróżniają się kilkoma czynnikami, takimi jak: przeciążenie płynami, anemia, immunosupresja, zwapnienie pozakostne, niedożywienie, zaburzenia równowagi elektrolitowej i zaburzenia kwasowo-zasadowe pośrednio oddziałujące na płuca. Zgłaszamy niepowodzenie NIV u dwóch pacjentów z COVID 19 podczas dializy. Obaj pacjenci byli stabilni na NIV przed rozpoczęciem dializy lecz ulegli desaturacji, wymagając przejścia na inwazyjną wentylację mechaniczną podczas hemodializy. Możliwym mechanizmem desaturacji jest hipowentylacja pęcherzykowa przy braku hiperkapnii, która może być spowodowane usunięciem CO2 z organizmu inną drogą (dializat) niż płuca.
EN
INTRODUCTION: Understanding the complex etiopathogenesis of chronic kidney disease (CKD) raises hopes for the development of effective methods for its early diagnosis and effective prevention and treatment. The significance of genetic predisposition in renal damage development has been proven in many studies. The objective of our study was to estimate the connections between selected VEGF polymorphisms and the incidence of chronic renal failure. MATERIALS AND METHODS: 103 families, consisting of both parents and affected offspring with CKD stage below 3, i.e. eGFR below 60 ml/min/1.73 m2, participated our study. The mean age of the children was 15.2 years and mean eGFR 28.9 ml/min/1.73 m2. The main reason for renal damage was interstitial nephropathy (71%) and the second (29%) – chronic glomerulonephritis. 45% of patients were conservatively treated, while others remained on chronic renal replacement therapy. Venous blood samples were collected for DNA isolation. Selected VEGF polymorphisms were genotyped by the TaqMan method. The obtained results were analyzed on the basis of Statistica 10 and Microsoft Office Excel 2003 software using the transmission disequilibrium test (TDT), χ2 test and the Kaplan-Meier estimator. For all the calculations, a p value below 0.05 was adopted as the limit of statistical significance. RESULTS: No differences in the estimated and observed rs699947 or rs1570360 allele transmission between the parents and their affected offspring were found. CONCLUSIONS: No relations between rs699947 and rs1570360 VEGF polymorphisms and the incidence of chronic kidney disease of at least stage 3 were established.
PL
WSTĘP: Poznanie złożonej etiopatogenezy przewlekłej choroby nerek (PChN) budzi nadzieje na rozwój skutecznych metod jej wczesnej diagnostyki oraz skutecznej profilaktyki i leczenia. Liczne badania dowodzą znaczenia predyspozycji genetycznej w rozwoju przewlekłego uszkodzenia nerek w przebiegu różnych chorób. Celem pracy była ocena związku wybranych polimorfizmów genu VEGF (vascular endothelial growth factor) z występowaniem przewlekłej choroby nerek. MATERIAŁ I METODY: Grupę badaną stanowiły 103 rodziny (trios): dwoje biologicznych rodziców i dziecko z PChN w stadium co najmniej trzecim, tj. z eGFR ≤ 60 ml/min/1,73 m2, na tle przewlekłego kłębuszkowego zapalenia nerek (29%) lub nefropatii śródmiąższowej (71%). W chwili badania średni wiek dzieci z PChN wynosił 15,2 roku, a średnia filtracja kłębuszkowa 28,9 ml/min/1,73 m2. U 45% chorych zastosowano leczenie zachowawcze, u pozostałych nerkozastępcze. U wszystkich badanych pobrano jednorazowo próbki krwi żylnej w celu wyizolowania materiału genetycznego i przeprowadzono genotypowanie wybranych polimorfizmów genu VEGF metodą TaqMan. Do opracowania statystycznego wyników posłużyły programy Statistica 10 i Microsoft Office Excel 2003 z wykorzystaniem testu nie-równowagi sprzężeń (transmission disequilibrium test – TDT), testu χ2 oraz estymatora Kaplana-Meiera. Za granicę istotności statystycznej przyjęto wartości p < 0,05. WYNIKI: Nie wykazano różnic w przekazywaniu alleli badanych polimorfizmów rs699947 i rs1570360 genu VEGF od rodziców do potomka z PChN. WNIOSKI: Nie stwierdzono związku polimorfizmów rs699947 i rs1570360 genu VEGF z występowaniem przewlek-łej choroby nerek w stadium ≥ 3.
EN
Erythropoietin (EPO) is one of the main cytokines involved in the regulation of erythropoiesis. The main site of EPO production are the kidneys. An altered EPO production leads to pathological conditions such as anemia and polycythaemia. Due to the progressive loss of renal peritubular cells, patients with chronic kidney disease (CKD) have low EPO plasma levels. This decreases erythron stimulation with the direct consequence of developing anemia. Before the introduction in the clinical practice of rHuEpo, in the late 1980s, the only solution for treating this type of anemia were blood transfusions and anabolic steroids. Even rHuEpo has proven to be safe and effective for treatment of anemias, there are some concerns about its cost, the need for frequent parenteral administration, and development of anti-EPO antibodies. These inconveniences prompted the search for novel erythropoiesis stimulating agents. Different strategies lead to isolation or chemical synthesis of such agents as darbepoetin alfa and EPO mimetics. In this review, we present some general aspects of EPO biology, with emphasis on chronic renal failure, and expose some of the alternatives to EPO used for anemia correction.
EN
Background. Dietary supplements (DS) are available over the counter, but patients with impaired renal function are specifically at risk for toxicity when consuming certain DS. The aim of this study was to evaluate the prevalence and characteristics of DS use in patients with chronic kidney disease (CKD). Material and methods. A cross-sectional, controlled DS use survey (22 questions) was conducted among 180 CKD patients (stage 1-5, dialysis, kidney transplant), with 60 patients without CKD serving as controls. Results. DS use did not differ significantly between subjects with and without CKD, unless the CKD patients were on dialysis. In the CKD group, 20% admitted to use DS regularly and 22% did not take the mat all. In the controls, DS consumption was 17% and 13%, respectively (NS). The DS use was higher among women ascompared to men (89% vs. 70%; p < 0.005), and people living in cities versus those living in the country side (81% vs. 63%; p < 0.05). DS most commonly used were: vitamins, minerals, and herbs. Major indications for DS use included: musculoskeletal issues, general health improvement and prevention of urinary tract infections. Subgroup analyses revealed that dialysis patients were characterized by a significantly higher DS use in comparison to CKD stage 1-5 subjects and renal transplant recipients. The decision to introduce DS was made by the physician in 54% of cases; by a pharmacist in 9% of cases, and by the patients themselves in 37%. Only 21% of patients with CKD, and 27% of subjects without CKD, declared knowledge of any possible side-effects associated with DS (NS). Conclusions. The use of DS among patients with CKD is similar to patients without CKD, with the exception of those on dialysis. Vitamins and minerals were the most commonly reported DS consumed. The knowledge on potential side-effectof DS was limited to approximately one-fourth of those surveyed.
EN
INTRODUCTION The aetiology of chronic kidney disease (CKD) and its progression are multifactorial in nature. A number of reports have demonstrated the nonhaematological local protective properties of erythropoietin in diff erent tissues, including those in the kidneys. The primary goal of the reported, family-based study was to assess the infl uence of rs 1617640 erythropoietin gene promoter polymorphism on the incidence and progression of CKD. MATERIAL AND METHODS For that purpose, 109 patients with CKD (72.5% with chronic interstitial nephritis and 27.5% with chronic glomerulonephritis) and their parents were examined. At the time of the study, the mean glomerular fi ltration rate was 28.2 ml/min and 53.2% patients were maintained on renal replacement therapy. Fluorescence labelled probes of the TaqMan Pre-designed SNP Genotyping Assay (Applied Biosystems Company) were used for rs1617640 polymorphism investigation. RESULTS The genome distribution of rs 1617640 polymorphism of the erythropoietin gene promoter was: 48.6% AC, 25.7% AA and 25.7% CC patients. Based on Transmission Disequilibrium Test results, the bordeline statistical signifi cance of preferential C allele transfer from parents to their aff ected children with glomerulonephritis was observed. CONCLUSIONS No infl uence of rs 1617640 promoter polymorphism of the erythropoietin gene on the incidence of CKD in the course of chronic interstitial nephritis was observed. The bordeline signifi cance of preferential C allele transfer in patients with glomerulonephritis suggests association between rs1617640 and CKD of this aethiology.
PL
WSTĘP Etiologia przewlekłego uszkodzenia nerek oraz jego progresji jest wieloczynnikowa. Prace ostatnich lat dowodzą znaczenia pozaszpikowego miejscowego działania ochronnego erytropoetyny w wielu tkankach, w tym także w nerkach. Celem pracy była ocena w modelu rodzinnym wpływu polimorfizmu rs1617640 promotora genu dla erytropoetyny na rozwój i progresję przewlekłej choroby nerek. MATERIAŁ I METODY Badania przeprowadzono w grupie 109 chorych na przewlekłą chorobę nerek w przebiegu przewlekłego śródmiąższowego zapalenia nerek (72,5%) i przewlekłego kłębuszkowego zapalenia nerek (27,5%) oraz u 218 ich biologicznych rodziców. W momencie prowadzenia badania średnia filtracja kłębuszkowa (GFR) wynosiła 28,2 ml/min, a 53,2% chorych było leczonych nerkozastępczo. Genotypowanie polimorfizmu rs1617640 w promotorze genu erytropoetyny wykonano, wykorzystując znakowane fluorescencyjnie sondy z zestawu TaqMan Pre-designed SNP Genotyping Assay firmy Applied Biosystems. WYNIKI Analizując rozkład genotypów badanego polimorfizmu, stwierdzono: u 48,6% chorych genotyp AC, a u pozostałych chorych w równym procencie (po 25,7%) genotyp AA i CC. W teście TDT (Transmission Disequilibrium Test) wykazano na granicy istotności statystycznej przekazywanie preferencyjne allelu C w grupie chorych z przewlekłym kłębuszkowym zapaleniem nerek. WNIOSKI Nie obserwowano wpływu polimorfizmu rs1617640 genu promotora dla erytropoetyny na występowanie przewlekłego uszkodzenia nerek w przebiegu przewlekłego środmiąższowego zapalenia nerek. Stwierdzone na granicy istotności statystycznej, preferencyjne przekazywanie allelu C w grupie chorych na przewlekłe kłębuszkowe zapalenie nerek, sugeruje związek rs1617640 z przewlekłą chorobą nerek o tej etiologii.
EN
Introduction: The number of patients with end-stage renal failure (ESRF) that require inclusion in the renal replacement therapy program (RRT) is steadily increasing. This fact caused an increase in vascular operations involving the production of vascular access. According to the current guidelines, the best and safest option for a patient with chronic kidney disease (CKD) is the early creation of arteriovenous fistula (AVF). An efficient vascular access to haemodialysis determines the procedure and directly affects the quality of life of a patient with CKD. Aim: The aim of this paper is to present the author’s project of the health policy program „Vascular access in renal replacement therapy – fistula first/catheter last”, the essence of which is to assess the practical effectiveness and develop an optimal model of CKD patient care organization qualified for the chronic RRT program. Material and methods: The target population of the program consists of all patients diagnosed with CKD, qualified for the RRT program. The basic measures of the program’s effectiveness include: (1) reduction in the number of re-hospitalizations related to vascular access, (2) reduction in the number of complications associated with haemofiltration surgery, (3) reduction in general mortality among patients undergoing dialysis in a 12-month perspective, (4) increasing knowledge in the field of self-care and self-care of arteriovenous anastomosis, and (5) creating a register of vascular access in Poland. Conclusions: To sum up, health policy programme “Vascular access in renal replacement therapy – fistula first/catheter last” covering health care services provided in the scope and on the conditions specified in the regulations issued on the basis of article 31d of the Act of 27 August 2004 on health care benefits financed from public funds, is to check whether planned changes in the organization and delivery of services will improve the situation of patients with CKD eligible for chronic RRT and whether it will be effective the point of view of the health care system.
EN
BACKGROUND The aim of the study was to investigate the infl uence of single nucleotide polymorphisms (SNPs) of carboxypeptidase A4, CPA4, leptin, LEP and aldo-keto reductase family 1, AKR1B1 genes located at the long arm of chromosome 7 (7q31-q35) on development and progression of chronic kidney disease (CKD). MATERIAL AND METHODS There was an association study by PCR-RFLP method of following SNPs in parent-off spring trios performed: G934T of CPA4 gene, A19G of LEP gene and C-106T of AKR1B gene. 471 subjects, 157 patients with CKD and 314 their biological parents were examined. The patients were divided into 3 groups: diabetic nephropathy due to type 1 diabetes (n = 34), chronic primary glomerulonephritis (n = 70) and chronic inter- stitial nephritis (n = 53). The mode of alleles transmission was determined using the transmission disequilibrium test (TDT). RESULTS There was no association of studied SNPs and CKD occurrence or pro- gression rate of renal function loss. Transmission of alleles of investigated SNPs did not diff er signifi cantly: G934T of CPA4 gene: P = 0.61 in whole group of CKD patients, p = 0.66 in GN group, p = 0.70 – IN group and p = 0.61 in DN one; A19G of LEP gene: p = 0.58, 0.71, 0.78 and 0.49, respectively; C-106T of ALDR1 gene: p = 0.31, 0.47, 0.12 and 0.38, respectively. No impact of examined polymorphisms on the rate of progression of renal function loss was observed. CONCLUSIONS The results, obtained in the study, suggest that the investigated SNPs: G934T of CPA4 gene, A19G of LEP gene and C-106T of AKR1B gene may not play a major role in the development and progression of chronic nephropathies.
PL
WSTĘP Celem badań było zbadanie wpływu polimorfi zmów pojedynczego nukleotydu (SNPs) genów karboksypepsydazy A4, CPA4, leptyny, LEP i reduktazy aldozy, AKR1B1, znajdujących się na długim ramieniu chromosomu 7 (7q31-q35) na rozwój i progresję przewlekłej choroby nerek (PChN). MATERIAŁ I METODY Wykorzystując metodę PCR-RFLP przebadano następujące polimorfizmy: G934T CPA4 genu, A19G LEP i C-106T genu AKR1B. Badaniami objęto 471 osoby: 157 z PChN i 314 ich biologicznych rodziców. Pacjentów podzielono na 3 grupy: z nefropatią cukrzycową w przebiegu cukrzycy typu 1 (DN, n = 34), z przewlekłym pierwotnym kłębuszkowym zapaleniem nerek (GN, n = 70) oraz z przewlekłym śródmiąższowym zapaleniem nerek (IN, n = 53). Tryb przekazywania alleli został oceniony testem nierównowagi przekazywania (Transmission-Disequilibrium Test, TDT). WYNIKI Częstość przekazywania alleli analizowanych SNPs nie odbiegała znacząco od oczekiwanej: G934T CPA4: p = 0,61 w całej grupie badanej, p = 0,66 w grupie GN, p = 0,70 – w grupie IN oraz p = 0,61 w grupie DN; A19G LEP: p = 0,58; 0,71; 0,78 i 0,49, odpowiednio; C-106T genu ALDR1: p = 0,31; 0,47; 0,12 i 0,38, odpowiednio. Nie zaobserwowano żadnego wpływu badanych polimorfi zmów na szybkość utraty funkcji nerek. WNIOSKI Uzyskane w badaniu wyniki wskazują, że badane SNPs: G934T genu CPA4, A19G LEP i C-106T genu AKR1B nie odgrywają istotnej roli w rozwoju i progresji przewlekłych nefropatii.
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Nefronoftyza (NPH) jest genetycznie heterogenną chorobą nerek dziedziczoną autosomalnie recesywnie. Najczęściej (u 20% chorych) wykrywana jest mutacja w genie NPHP1. W obrazie klinicznym dominują zaburzenia zdolności zagęszczania moczu, obecność torbielek na granicy korowo-rdzeniowej i utrata funkcji nerek przed 30 r.ż. Wyróżnia się trzy podtypy kliniczne choroby: niemowlęcą, młodzieńczą i dorosłych. Pozanerkowe manifestacje nefronoftyzy, występujące u 10–20% chorych, to m.in. retinopatia barwnikowa, włóknienie wątroby i deformacje kostne. W pracy opisano troje dzieci z rozpoznaniem nefronoftyzy potwierdzonej badaniem genetycznym. Pierwszymi objawami choroby były niedokrwistość i moczenie nocne. Ze względu na pierwsze niespecyficzne objawy kliniczne, brak zmian w badaniu ogólnym moczu lub zmiany łagodne (zmniejszenie ciężaru właściwego moczu) oraz początkowo prawidłowy obraz nerek w badaniu ultrasonograficznym NPH zostało rozpoznane późno.
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Nephronophthisis (NPHP) is an autosomal recessive, genetically heterogenic kidney disorder. Most commonly (in 20% of cases) a mutation in the NPHP1 gene is detected. The phenotype is characterized by a reduced urinary concentrating ability, corticomedullary cysts and kidney failure, with progression to end-stage renal disease before the age of 30. Three clinical cases of nephronophthisis are distinguished: infantile, juvenile and adult. Extrarenal manifestations occur in 10–20% of cases of nephronophthisis and include i.a. retinitis pigmentosa, hepatic fibrosis and bone deformities. The article comprises the cases of three children with nephronophthisis confirmed by a genetic test. The initial medical signs of the disease were anaemia and nocturnal enuresis. As a result of initial nonspecific medical signs, no or minor abnormalities detected in urine tests (a reduced urinary concentrating ability), as well as an initially normal ultrasonography examination, NPHP was diagnosed late.
EN
Background: Inhibition of the renin-angiotensin-aldosterone system (RAAS) with angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) is a common strategy used in the management of patients with chronic kidney disease (CKD). However, there is no universal therapy that can stop progression of CKD. Pentoxifylline (PTE) is a non-specific phosphodiesterase inhibitor with anti-inflammatory properties. It has been reported to have promising effects in CKD treatment. Methods: In a placebo-controlled, randomized, cross-over study we evaluated the influence of PTE (1200 mg/day) added to RAAS blockade on proteinuria, surrogate markers of tubular injury and oxidative stress-dependent products in 22 non-diabetic patients with proteinuria (0.4-4.3 g per 24h) with normal or declined kidney function [eGFR 37-178 mL/min]. In an eight-week run-in period, therapy using ACEI and/or ARB was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: PTE/washout/placebo or placebo/washout/PTE. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. Results: The PTE therapy reduced proteinuria (by 26%) as compared to placebo. There were no differences in α1-microglobulin, urine excretion of N-acetyl-β-d-glucosaminidase (NAG), hsCRP, the urinary excretion of 15-F2t-isoprostane, blood pressure (BP), eGFR and serum creatinine between the PTE and placebo groups. Conclusion: Pentoxifylline may decrease proteinuria in non-diabetic patients with CKD.
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Identifying anxio-depressive disorders, evaluating their prevalence and determining the different factors that can intervene in their hap- pening to the patients suffering from hemodialysis. Transversal descriptive and analytical study over 70 patients, real- ized at the dialysis unit of the Idrissi regional hospital’s department of medicine at Kenitra, Morocco, over a period of three months starting from 27 March to 26 June 2015. The data were acquired from a survey and psychiatric evaluation scales: The scale HADS (Hospital Anxiety and Depression Scale ) to evaluate anxiety and depression and the scale of « Big Five French Inventory to evaluate the treats of personality» (BF-Fr). Average age was from 54,66±15,96 years. The seniority of the hemodialysis was on average 5,20±3,23 years. The studied traits of personality show a decrease regard to the average score of dimen- sion O (overture of sense) and of the dimension E score (extraversion) versus an evaluation of the dimension N score (Neu ro ticism). The prevalence of anxio-depressive troubles were as the following; 74,29% presented an anxious state (suspected or proven) and 70% had a depressive state (suspected or proven). The anxious troubles were correlated to age and to N and O characters of personality traits BFI-Fr. the depressive troubles were correlated to N charac- ters traits of personality BFI-Fr, and the anxious troubles were pos- itively correlated to depressive troubles. The prevalence of anxio-depressive troubles among hemodialysis subjects was elevated with repercussions on the personality. The involvement of a psychologist in the processes of taking charge is obligatory.
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Chronic kidney disease (CKD) is unquestionably a problem of social significance because it affects about 10% of the population. There is a search for biomarkers which could help select persons out of such a large group of patients with a high risk of disease progression and of its complications. The major cause of death in patients with end-stage renal disease are cardiovascular diseases. Accelerated atherosclerosis in this group of patients is associated with a chronic inflammatory state. The new biological marker of inflammation suPAR (soluble urokinase-type plasminogen activator receptor), is the focus of attention of the authors of this report. The relationship of suPAR with urinary tract infections and focal segmental glomerulosclerosis is also very interesting from the clinical perspective. The perception of suPAR as a blood circulating factor, inducing FSGS, throws new light on the pathomechanism of this medical condition, while unveiling promising therapeutic perspectives. A better understanding of the pathogenesis of the diseases discussed will help to reduce the unacceptably high mortality rate in patients with CKD. At present, common assaying of suPAR is not yet possible in the context of the above-mentioned issues. Nevertheless, studies are ongoing which may explain the still unclear issues concerning the relationship of the biomarker with the mentioned kidney diseases. Perhaps, follo-wing their results suPAR assays may in the near future become routine diagnostics means in selected kidney diseases.
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Przewlekła choroba nerek (PChN) to niewątpliwie problem o znaczeniu społecznym, dotyczy bowiem około 10% populacji. Poszukiwane są biomarkery, dzięki którym spośród tak dużej liczby pacjentów udałoby się wyselekcjonować osoby z dużym ryzykiem progresji choroby i jej powikłań. Główną przyczyną zgonów u pacjentów ze schyłkową niewydolnością nerek są choroby układu sercowo-naczyniowego. Przyspieszony rozwój miażdżycy w tej grupie chorych wiąże się z przewlekłym stanem zapalnym. Przedmiotem zainteresowania autorów pracy jest nowy biomarker stanu zapalnego suPAR (soluble urokinase-type plazminogen activator receptor – rozpuszczalna forma receptora aktywatora plazminogenu typu urokinazy). Z klinicznego punktu widzenia interesujący jest również związek suPAR z zakażeniami układu moczowego oraz ogniskowym segmentalnym stwardnieniem kłębuszków nerkowych (focal segmental glomerulosclerosis – FSGS). Identyfikacja suPAR, jako krążącego we krwi czynnika wywołującego FSGS, rzuca nowe światło na patomechanizm choroby i stwarza obiecujące możliwości lecznicze. Lepsze zrozumienie patogenezy omawianych schorzeń pomogłoby zredukować nieakceptowalnie wysoką śmiertelność pacjentów z PChN. Na dzień dzisiejszy nie można zlecać powszechnego oznaczania suPAR w kontekście omawianych zagadnień. Niemniej trwają badania, które pozwolą wyjaśnić niejasne kwestie dotyczące związku biomarkera z omawianymi schorzeniami nerek. Być może na podstawie ich wyników w najbliższych latach oznaczanie suPAR w wybranych chorobach nerek będzie rutynowe.
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