The use of intravascular contrast media in patients with impaired kidney function - joint clinical practice position statement of the Polish Society of Nephrology and the Polish Medical Society of Radiology.

Radiological procedures utilising intravascular contrast media (ICM) are fundamental to modern medicine, enhancing diagnostics and treatment in diverse medical fields. However, the application of ICM has been constrained in patients with compromised kidney function due to perceived nephrotoxic risks, called contrast-induced nephropathy or contrastinduced acute kidney injury. Historical evidence marked ICM as a possible contributor to kidney damage. This led to restrictive guidelines advocating limited ICM use in patients with impaired renal function, preventing crucial radiographic interventions in patients with acute kidney injury (AKI) and chronic kidney disease. Recent advances challenge these traditional views. In particular, no direct causal relationship has been confirmed between contrast admi-nistration and elevated serum creatinine concentrations in humans. Furthermore, contemporary research models and meta-analyses do not associate AKI with contrast usage. This paper, prepared by a cross-disciplinary team of nephrologists and radiologists, presents updated guidelines for ICM application amid renal function impairments, emphasising the reduced nephrotoxic risks currently understood and loosening the previous restrictive approach in patients with renal dysfunction.

Difficulties in the diagnostics of chronic hyponatremia based on the case study of a 66-year old female patient during antihypertensive therapy.

Clinical consequences of hyponatremia might be serious. It is often related to the administration of diuretics, especially thiazide and thiazide-like diuretics. It is known that elderly subjects are prone to thiazide induced hyponatremia (TIH). A CASE REPORT: A 66-year old female patient was admitted to our Department. The aim of the admission was to complete a differential diagnosis of chronic hyponatremia. For about two years the patient had suffered from the following symptoms: severe headaches, fatigue, episodic mental confusions, stomachaches, and diarrhea. Before admission to the hospital, the patient was treated with bisoprolol, amlodipine, telmisartan, indapamide, furosemide, acetylsalicylic acid, thiamazole, and zolpidem. The general clinical picture might suggest that the cause of hyponatremia was the indapamide diuretic therapy. However, only moderate hyponatremia, normokalemia, as well as, an increased antidiuretic hormone serum concentration were observed. These findings are not typical for TIH. Despite those findings, natremia improved after the cessation of indapamide therapy. CONCLUSIONS: This case report described the atypical presentation of TIH resembling SIADH. TIH diagnosis should be primarily based on the improvement of hyponatremia after the termination of thiazide or thiazide-like diuretic treatment.

Food Products That May Cause an Increase in Blood Pressure.

PURPOSE OF REVIEW: To review latest reports of the food products which might increase blood pressure and therefore might participate in the pathogenesis of hypertension. RECENT FINDINGS: Results of clinical study suggest that consumption of high-sodium food leads to transient increase in plasma sodium concentration. This is accompanied by blood pressure increase. Results of both clinical and experimental studies suggest direct vasculotoxic effects of sodium. Increased plasma sodium concentration could mediate its effects on blood pressure by changes in endothelial cell stiffness and glycocalyx integrity. Energy drinks are non-alcoholic beverages with increasing popularity. Clinical, interventional, randomized, placebo controlled, and cross-sectional studies showed that energy drinks may increase arterial blood pressure. Blood pressure increase after exposure for the energy drinks is mainly related to the caffeine content in these drinks. Many case reports were published concerning the clinically significant increase in blood pressure caused by the consumption of liquorice root or food products containing liquorice, such as candies, tea, Pontefract cookies, and chewing gum. Liquorice contains a precursor of glycyrrhetic acid. Glycyrrhetic acid reduces the activity of the 11ß-hydroxysteroid dehydrogenase type 2 (11ß-HSD2) isoenzyme, which leads to activation of the mineralocorticoid receptor by cortisol in the distal convoluted tubule resulting in hypertension, hypokalemia, and metabolic alkalosis. The relationship between chronic alcohol intake and blood pressure is well established on the basis of a diverse body of evidence including animal experiments, epidemiological studies, mendelian randomization studies, and interventional studies. Results of recent studies suggested that binge drinking (i.e., episodic consumption of a very high amount of alcohol beverages) has pronounced hypertensinogenic effects. Recently, it was documented that also low doses of alcohol may increase the risk of cardiovascular complications. Therefore, the amount of alcohol consumption that is safe is zero. High-salt food products, energy drinks, food products containing liquorice, and alcoholic beverages have hypertensinogenic properties. Patients with hypertension and other cardiovascular diseases should avoid even accidental consumption of these food products.

Vitamin D and Arterial Hypertension: Facts and Myths.

PURPOSE OF REVIEW: Vitamin D and its derivatives are biologically active fat-soluble steroid hormones, which are transcription factors for numerous genes. The results of several observational studies suggest the relationship between plasma concentration of vitamin D and the risk of arterial hypertension, as well as between the intensity of insolation and the risk of arterial hypertension. RECENT FINDINGS: Based on the results of the abovementioned studies, it was hypothesized that vitamin D is characterized by the antihypertensive properties. Animal experiments have shown that vitamin D reduces activity of the renin-angiotensin-aldosterone system and improves vasorelaxation of blood vessels. Results of clinical studies did not confirm these results. Moreover in interventional clinical trials, it was documented that supplementation of vitamin D did not reduce blood pressure. The influence of exposure to sunshine at different wave lengths on blood pressure was examined in clinical studies and it was found that ultraviolet A radiation (UVA) lead to the release of nitric oxide from the skin. This might explain lower level of blood pressure in subjects from the regions with a higher rate of insolation. The aim of this review is to summarize current knowledge concerning the relationship between vitamin D and arterial hypertension based on both observational and interventional studies.

Is Metabolic Acidosis a Novel Risk Factor for a Long-Term Graft Survival in Patients after Kidney Transplantation?

BACKGROUND: Results of both experimental and clinical studies suggest that metabolic acidosis (MA) contributes to the progression of chronic kidney disease (CKD) and mortality in CKD patients. It is unknown whether the same relationship exists in kidney transplantation (KTx) patients. The aim of this observational study was to examine this relationship between MA and both mortality and renal outcomes in patients after KTx. METHODS: Four hundred eighty-six (290 male; 196 female) patients aged 48 ± 12 years, at least 1 year after KTx, were analyzed. Blood HCO3- was measured, and patients were then observed over 3 years. MA was defined as the blood HCO3- concentration <22 mmol/L. The end points of survival analysis were death and initiation of dialysis therapy. In patients who did not reach the above-mentioned end points, the difference between final (after 3 years of follow-up) and initial estimated glomerular filtration rate (eGFR) was calculated. RESULTS: MA was initially diagnosed in 57 (12%) patients after KTx. Three-year patient survival was 89.5% in the MA group and 97.4% in the non-MA group (p = 0.001). Three-year graft survival was 73.7% for patients with MA and 93.0% for patients without MA (p < 0.001). In patients with MA who did not reach study end points, blood bicarbonate concentration at baseline correlated positively with a change in eGFR (R = 0.48, p = 0.002, n = 36). Such a correlation was not found in patients without MA (n = 388). CONCLUSIONS: (1) MA significantly increases the risk of mortality in patients after KTx. (2) The intensity of MA may be associated with progression of transplanted kidney dysfunction in KTx patients.

The Prevalence of Metabolic Acidosis in Patients with Different Stages of Chronic Kidney Disease: Single-Centre Study.

BACKGROUND: Metabolic acidosis (MA) is one of the most common consequences of CKD. MA is also a risk factor of CKD progression and increased mortality in these patients. AIM: The aim of this retrospective, cross-sectional study was to assess the prevalence of MA in different stages of CKD and renal replacement therapy (RRT) modalities - haemodialysis (HD) and peritoneal dialysis (PD). Additionally, the relationship between the prevalence of MA and aetiology of kidney disease was analysed. METHODS: One thousand five patients in different stages of CKD, or modalities of RRT were enrolled into this single-centre cross-sectional study. Forty-one patients were ruled out because of oral bicarbonate supplementation. In the remaining 964 patients (698 CKD stages 1-5, 226 HD, 40 PD), venous blood HCO3- concentration, as well as serum Cr and urea concentrations were assessed. MA was diagnosed when blood HCO3- concentration was below 22 mmol/L. RESULTS: The prevalence of MA increased among all stages of CKD. Patients on HD had lower prevalence of MA in comparison with CKD 5 patients with no RRT (38.5 vs. 56.0%; p = 0.02) In PD patients, the prevalence of MA was significantly lower than in HD patients (2.5 vs. 38.5%; p < 0.001). In the whole study group, there were no significant differences in the prevalence of MA between different aetiologies of CKD (glomerulonephritis 24%, hypertension 23%, diabetes 25%, and tubule-interstitial diseases 24%). Also, when only patients in stages CKD 3-5 were compared, no significant differences in the prevalence of acidosis were found (glomerulonephritis 28%, hypertension 22%, diabetes 24%, and tubule-interstitial 21%). CONCLUSIONS: (1) MA is more frequent in patients with more advanced stages of CKD. (2) RRT reduces the prevalence of MA. (3) In PD patients, MA is rare. (4) Aetiology of CKD seems not to have a significant impact on MA prevalence.

Diagnosis and Treatment of Metabolic Acidosis in Patients with Chronic Kidney Disease - Position Statement of the Working Group of the Polish Society of Nephrology.

Metabolic acidosis is commonly found in patients with chronic kidney disease (CKD), and its causes are: impaired ammonia excretion, reduced tubular bicarbonate reabsorption and insufficient renal bicarbonate production in relation to the amount of acids synthesised by the body and ingested with food. As the consequence, numerous metabolic abnormalities develop, which may lead to dysfunction of several organs. In observational studies, it has been found that CKD patients with metabolic acidosis are characterised by faster progression of kidney disease towards end stage kidney failure, and by increased mortality. Results of interventional studies suggest that alkali therapy in CKD patients slows progression of kidney disease. In view of these facts, the members of "The Working Group of the Polish Society of Nephrology on Metabolic and Endocrine Abnormalities in Kidney Diseases" have prepared the following statement and guidelines for the diagnosis and treatment of metabolic acidosis in CKD patients. Measurement of bicarbonate concentration in venous plasma or venous blood to check for metabolic acidosis should be performed in all CKD patients and metabolic acidosis in these patients should be diagnosed when the venous plasma or venous blood bicarbonate concentration is lower than 22 mmol/l. In patients with metabolic acidosis and CKD, oral sodium bicarbonate administration is recommended. The goal of such a treatment is to achieve a plasma or blood bicarbonate concentration equal to or greater than 22 mmol/l.

Different Relevance of Peripheral, Central or Nighttime Blood Pressure Measurements in the Prediction of Chronic Kidney Disease Progression in Patients with Mild or No-Proteinuria.

BACKGROUND/AIMS: Arterial hypertension is one of the leading factors aggravating the course of chronic kidney disease (CKD). It seems that the novel parameters used in the assessment of the blood pressure (BP) load (i.e. central blood pressure, nighttime blood pressure) may be more precise in predicting the cardiovascular risk and the progression of CKD in comparison with the traditional peripheral blood pressure measurements in the office conditions. The aim of the study was to assess the impact of the central, or nighttime blood pressure on the progression of CKD in patients with mild or no-proteinuria (autosomal, dominant polycystic kidney disease or IgA nephropathy). METHODS: In each of the enrolled 46 patients with CKD stage 3 or 4, serum creatinine concentration was assessed, eGFR (MDRD) was calculated, also central blood pressure and pulse wave velocity (PWV) was assessed and the 24-hour ambulatory blood pressure monitoring (ABPM) was conducted at the beginning of the study and then repeated after one-year observation period. RESULTS: During the observation period mean eGFR decreased from 44.1 (33.2-50.6) mL/min to 36.7 (29.7-46.3) mL/min. No significant differences were observed in the peripheral blood pressure or central blood pressure parameters. After one-year observation period the values of diastolic blood pressure dipping during the night significantly decreased from 16 (13-19) mmHg to 12 (10-15) mmHg; p< 0.05. The values of systolic dipping during the night or the mean BP values recorded in ABPM did not change significantly. Additionally, no significant differences in the PWV values were found. In the multivariate regression model the change of serum creatinine concentration was explained by the initial diastolic dipping values. CONCLUSION: 1. In patients with CKD stages 3 or 4 and mild or no- proteinuria, peripheral and central blood pressure did not change significantly during a one-year observation period despite the significant decline of eGFR and seems not to participate in the CKD progression. 2. Reduced magnitude of the diastolic dipping, which reflects the increase of diastolic blood pressure load during the nighttime, may play an important role in the pathogenesis of deterioration of kidney function in these patients.

Clostridium Difficile Infection in the Nephrology Ward.

Clostridium difficile is currently the most frequently identified pathogen causing antibiotic-associated diarrhea and the main cause of nosocomial diarrhea. In recent years, increases incidence of infection, severe infection, recurrent infection and mortality from Clostridium difficile infection (CDI) have been observed. This may be a consequence of excessive antibiotic use and spread of the hypervirulent epidemic BI/NAP1/027 strain of Clostridium difficile. The main risk factors for CDI are: antibiotic therapy, previous hospitalizations and number of comorbid conditions. Prevention of CDI mainly is focused in two directions: reducing the exposure of patients to the disease pathogen by intensifying hygiene measures, and reducing the impact of risk factors. A meta-analyses of clinical studies (observational, cohort and case control) showed significantly higher risk of CDI and CDI recurrence in patients with chronic kidney disease and increased mortality risk in chronic kidney disease patients with CDI comparing those without CDI. Increased risk of CDI in patients with chronic kidney disease can be caused by: frequent antibiotic therapy associated with numerous infections resulting in intestinal microflora dysfunction, frequent hospitalizations, older age of the patients and an impaired immune system. Among preventative measures against CDI, the use of probiotics were also studied. In patients hospitalized in nephrology ward highly significant reduction of the CDI incidence was observed after the introduction of Lactobacillus plantarum 299v as CDI prophylaxis. Therefore, the use of Lactobacillus plantarum 299v seems to be a promising method of CDI prevention in chronic kidney disease patients hospitalized in nephrology ward.

Changes of Serum Total and Free Testosterone Concentrations in Male Chronic Hemodialysis Patients with Secondary Hyperparathyroidism in Response to Cinacalcet Treatment.

BACKGROUND/AIMS: Calcium sensing receptor (CaSR) is expressed, among others also in testis. Cinacalcet binds to the CaSR, increases sensitivity of CaSR to serum calcium and is used in the treatment of secondary hyperparathyroidism (sHPT) in chronic hemodialysis patients (HDP). In most of male HDP, serum testosterone concentration is lower than in healthy males. The aim of this study was to assess the influence of six-month treatment with cinacalcet on the serum total and free testosterone concentration in male HDP with sHPT. METHODS: 38 male, hemodialysed CKD patients with sHPT (PTH>300 pg/ml) were enrolled into the study. In each patient serum PTH, total testosterone (TT) and free testosterone (FT) concentrations were assessed before the first dose of cinacalcet and then after 3 and 6 months of treatment. The results are presented as means with 95% confidence interval. RESULTS: In 33 patients who completed the study cinacalcet treatment caused significant decrease of serum PTH from 1143 pg/ml (828 - 1458 pg/ml) at the baseline, to 809 pg/ml (487 - 1132 pg/ml) after 3 month of treatment (p = 0.002), and to 607 pg/ml (281 - 934 pg/ml; p < 0.0001) after 6 months of treatment. Serum TT concentration also decreased from 4.95 ng/ml (4.23 - 5.67 ng/ml) to 4.45 ng/ml (3.85 - 5.06 ng/ml) and to 4.39 ng/ml (3.75 - 5.03 ng/ml), respectively (p for trend = 0.009). Moreover, serum FT concentration decreased from 6.95 pg/ml (5.54 - 8.36 pg/ml) to 5.98 pg/ml (5.00-6.94 pg/ml); p = 0.14 and to 5.60 pg/ml (4.63 - 6.57 pg/ml); p = 0.034, respectively (p for trend = 0.012). CONCLUSION: Treatment with cinacalcet decreases serum total and free testosterone concentration in male hemodialysed patients with chronic kidney disease and secondary hyperparathyroidism.

Serum Anti-Müllerian Hormone Concentration in Young Women with Chronic Kidney Disease on Hemodialysis, and After Successful Kidney Transplantation.

BACKGROUND/AIMS: In women with chronic kidney disease (CKD) fertility abnormalities occur frequently. Anti-Müllerian hormone (AMH) inhibits excessive recruitment of primordial follicles. The aim of the study was to evaluate the serum AMH concentration in women on hemodialysis and after kidney transplantation (KTx). METHODS: 46 hemodialysed women and 14 with CKD about to undergo kidney transplantation were enrolled into the study. The control group consisted of 40 healthy women. In all subjects serum concentration of AMH was determined (in chronic hemodialysis women and in control group once, and in women after KTx immediately before surgery, and 3 times after the transplantation). RESULTS: Serum AMH concentration in hemodialysed women and in the control group did not differ significantly, while in hemodialysed women with regular menstrual cycles it was significantly lower than in the control group: 2.20 (1.08-3.55ng/ml) and 3.30 (1.80-6.10ng/ml) respectively, (p=0.02). In the KTx group, a significant decrease in serum AMH concentration was found from 3.30ng/ml (2.20-6.50ng/ml) at baseline to 1.90ng/ml (1.30-2.40ng/ml) at 6 months after KTx (p=0.007). CONCLUSIONS: 1. Significantly lower serum AMH concentration was found in the regularly menstruating CKD women on hemodialysis in comparison with the healthy controls. 2. Serum AMH decreased significantly after successful KTx.

Treatment with cinacalcet increases plasma sclerostin concentration in hemodialysis patients with secondary hyperparathyroidism.

BACKGROUND: Sclerostin is a paracrine acting factor, which is expressed in the osteocytes and articular chondrocytes. Sclerostin decreases the osteoblast-related bone formation through the inhibition of the Wnt/ß-catenin pathway. Osteocytes also express the Calcium sensing receptor which is a target for cinacalcet. The aim of this study was to assess the influence of six-month cinacalcet treatment on plasma sclerostin concentration in hemodialysed patients with secondary hyperparathyroidism (sHPT). METHODS: In 58 hemodialysed patients with sHPT (PTH > 300 pg/ml) plasma sclerostin and serum PTH, calcium and phosphate concentrations were assessed before the first dose of cinacalcet and after 3 and 6 months of treatment. RESULTS: Serum PTH concentration decreased after 3 and 6 month of treatment from 1138 (931-1345) pg/ml to 772 (551-992) pg/ml and to 635 (430-839) pg/ml, respectively. Mean serum calcium and phosphate concentrations remained stable. Plasma sclerostin concentration increased after 3 and 6 months of treatment from 1.66 (1.35-1.96) ng/ml, to 1.77 (1.43-2.12) ng/ml and to 1.87 (1.50-2.25) ng/ml, respectively. In 42 patients with cinacalcet induced serum PTH decrease plasma sclerostin concentration increased after 3 and 6 months of treatment from 1.51 (1.19-1.84) ng/ml to 1.59 (1.29-1.89) ng/ml and to 1.75 (1.42-2.01) ng/ml, respectively. Contrary, in the 16 patients without cinacalcet induced serum PTH decrease plasma sclerostin concentration was stable. Plasma sclerostin concentrations correlated inversely with serum PTH concentrations at the baseline and also after 6 months of treatment. CONCLUSIONS: 1. In hemodialysed patients with secondary hyperparathyroidism treatment with cinacalcet increases plasma sclerostin concentration 2. This effect seems to be related to decrease of serum PTH concentration.

Analysis of Clostridium difficile infections in patients hospitalized at the nephrological ward in Poland.

BACKGROUND: Few studies have evaluated the incidence and risk factors of Clostridium difficile infection (CDI) in the adult Polish population, in particular in solid organ recipients hospitalized at the nephrological ward. AIM: The aim of this study was to analyze Clostridium difficile infections (CDI) among patients hospitalized in the Department of Nephrology, Transplantation and Internal Medicine, Medical University of Silesia in Katowice. MATERIAL/METHODS: Thirty-seven patients with Clostridium difficile infection diagnosed between October 2011 and November 2013 (26 months), identified among a total of 3728 patients hospitalized in this department during this period, were included in this retrospective, single-center study. The CDI definition was based on the current recommendations of the European Society of Clinical Microbiology and Infectious Diseases. RESULTS: The observation period was divided into two 13-month intervals. Increased incidence (of borderline significance) of CDI in the second period compared to the first period was observed (1.33% vs 0.65% respectively; p=0.057). Patients after kidney (n=11), kidney and pancreas (n=2) and liver (n=5) transplantation represented 48% of the analyzed CDI patients, and in half of these patients (50%) CDI symptoms occurred within the first 3 months after transplantation. Clostridium difficile infection leads to irreversible deterioration of graft function in 38% of kidney recipients. Most incidents of CDI (70%) were identified as nosocomial infection. CONCLUSIONS: 1. Clostridium difficile infection is particularly common among patients in the early period after solid organ transplantation. 2. Clostridium difficile infection may lead to irreversible deterioration of transplanted kidney function.

Smaller caliber renal arteries are a novel feature of uromodulin-associated kidney disease.

Hyperuricemia is very common in industrialized countries and known to promote vascular smooth muscle cell proliferation. Juvenile hyperuricemia is a hallmark of uromodulin-associated kidney disease characterized by progressive interstitial renal fibrosis leading to end-stage renal disease within decades. Here we describe a member of a Polish-German family with a history of familial background of chronic kidney disease, hyperuricemia, and gout. This patient had hypertension because of bilateral small renal arteries, hyperuricemia, and chronic kidney disease. Clinical and molecular studies were subsequently performed in 39 family members, which included a physical examination, Duplex ultrasound of the kidneys, laboratory tests for renal function, and urine analysis. In eight family members contrast-enhanced renal artery imaging by computed tomography-angiography or magnetic resonance imaging was conducted and showed that bilateral non-arteriosclerotic small caliber renal arteries were associated with hyperuricemia and chronic kidney disease. Of the 26 family members who underwent genotyping, 11 possessed the P236R mutation (c.707C>G) of the uromodulin gene. All family members with a small caliber renal artery carried the uromodulin P236R mutation. Statistical analysis showed a strong correlation between reduced renal artery lumen and decreased estimated glomerular filtration rate. Thus, bilateral small caliber renal arteries are a new clinical phenotype associated with an uromodulin mutation.

Administration of Cyclosporine A in Pregnant Rats - the Effect on Blood Pressure and on the Glomerular Number in Their Offspring.

BACKGROUND/AIMS: Cyclosporine A (CsA) is a commonly used immunosuppressive agent. In some patients treatment with CsA has to be continued during pregnancy. The aim of the study was to assess in an experimental model whether the exposure to CsA during fetal life influences the number and volume of glomeruli, kidney function and blood pressure in the offspring. METHODS: Eight pregnant female Sprague-Dawley rats were allocated to 2 treatment regimens: with CsA or solvent. Blood pressure was measured in the offspring at 7 and 11 weeks of age and albuminuria was determined at 11 weeks of age. In the kidney the number and mean volume of glomeruli was assessed using stereological methods. RESULTS: In the offspring of pregnant rats treated with CsA the number of glomeruli was significantly lower and the mean volume of glomeruli was higher when compared to the offspring of pregnant rats receiving solvent. Systolic and diastolic blood pressures as well as albuminuria were significantly higher in the offspring of mothers treated with CsA during gestation compared to the offspring from the control group. CONCLUSIONS: Exposure of rats to CsA during fetal life impairs kidney development, thus potentially predisposing to chronic kidney disease and hypertension in the adult life.

TREATMENT WITH CINACALCET INCREASES PLASMA ADIPONECTIN CONCENTRATION IN HEMODIALYZED PATIENTS WITH CHRONIC KIDNEY DISEASE AND SECONDARY HYPERPARATHYROIDISM.

OBJECTIVE: Cinacalcet increases calcium-sensing receptor (CaSR) sensitivity to serum calcium. CaSR is expressed by adipocytes, and adiponectin is an adipokine with antiatherogenic and insulin-sensitizing properties. The aim of this study was to assess the influence of a 3-month cinacalcet regimen on plasma adiponectin concentration in hemodialyzed patients (HDP) with chronic kidney disease (CKD) and secondary hyperparathyroidism (sHPT). METHODS: Plasma adiponectin, advanced oxidation protein products (AOPP), serum interleukin-6 (IL-6) and C-reactive protein (CRP) concentrations were assessed in 65 HDP with sHPT treated with cinacalcet (30-120 mg/day) before the first dose and after 3 months of treatment. RESULTS: There was a significant decrease in serum parathyroid hormone (PTH) concentration: from 1,089 (891-1,286) pg/mL to 775 (574-976) pg/mL after 3 months of treatment (P<.0001). The treatment was associated with a significant (P = .048) increase in plasma adiponectin concentration from 16.9 (14.4-19.5) µg/mL to 17.8 (15.0-20.6) µg/mL. Significant (P = .03) reduction of plasma AOPP concentration was observed from 186.7 (156.7-216.7) pg/mL to 162.6 (141.2-183.9) pg/mL. CONCLUSIONS: A 3-month cinacalcet regimen increased plasma adiponectin concentrations in HDP with sHPT. Increased adiponectinemia in these patients may be related to reduced oxidative stress.

Relationship between hemodynamic parameters of renal artery stenosis and the changes of kidney function after renal artery stenting in patients with hypertension and preserved renal function.

INTRODUCTION: The role of physiological assessment of renal artery stenosis (RAS) using renal fractional flow reserve (rFFR) and resting translesional pressures ratio (Pd/Pa ratio) in the prediction of benefit from revascularization is still unknown. OBJECTIVES: The aim of the study was to assess the relationship between hemodynamic data and the change in kidney function after renal artery stenting in secondary hypertension. PATIENTS AND METHODS: 34 hypertensive patients (50% males, median age 65 years) with at least 60% RAS, underwent stenting and were followed up for 6 months. Pd/Pa ratio (ratio of mean distal to lesion to proximal pressure) and hyperemic rFFR (after papaverine) were measured before the procedure. At baseline and after 6 months, the glomerular filtration rate (eGFR), serum cystatin C and albuminuria were determined. In receiver operating characteristic curves, two previously established cut-off values with the highest accuracy of identifying severe RAS were used: 0.93 for the Pd/Pa ratio and 0.8 for the rFFR. RESULTS: No significant difference in eGFR was found between patients with decreased and normal Pd/Pa ratio (1.4 vs 7.9 ml/min, p = ns). Similarly, minor changes in eGFR were observed in patients with decreased vs normal rFFR (2.4 vs 4.1 ml/min, p = ns). In patients with decreased Pd/Pa ratio, albuminuria remained stable (change 1.4 mg/24 h) compared with an increase of 12.6 mg/24 h in the subgroup with Pd/Pa ≥ 0.93(p < 0.05). However, after exclusion of two outliers with significant baseline proteinuria (425 and 1095 mg/24 h, respectively), the difference in albuminuria change according to the baseline Pd/Pa ratio was no longer maintained. CONCLUSIONS: Hemodynamic parameters of RAS do not distinguish the patients who may benefit from renal artery stenting in terms of kidney function improvement in short-term follow-up.

Cinacalcet treatment decreases plasma fibroblast growth factor 23 concentration in haemodialysed patients with chronic kidney disease and secondary hyperparathyroidism.

OBJECTIVE: Recent clinical studies suggest that fibroblast growth factor 23 (FGF23) is important in the pathogenesis of calcium-phosphate abnormalities in patients with chronic kidney disease and that increased plasma FGF23 concentration is a cardiovascular risk factor in these patients. The aim of this prospective, single-arm, open-label clinical study was to assess the influence of 6-month cinacalcet treatment on plasma FGF23 concentration in haemodialysed patients with secondary hyperparathyroidism (sHPT). DESIGN, PATIENTS AND MEASUREMENTS: In 58 haemodialysed patients with sHPT (parathormone PTH > 300 ng/l), serum PTH, FGF23, calcium and phosphate concentrations were assessed before the first dose of cinacalcet and after 3 and 6 months of treatment. RESULTS: Serum PTH concentration decreased significantly after 3 and 6 months of treatment, and the mean serum calcium and phosphate concentrations remained stable during the treatment period. Plasma FGF23 concentration (geometric mean with 95% confidence index) decreased after 3 and 6 months of treatment from 354 (261-481) ng/l to 295 (204-428) ng/l; P = 0·099 and to 183 (117-285) ng/l; P = 0·015, respectively. FGF23 concentration decreased in 52% of patients. In multivariate regression analysis, plasma FGF23 concentration changes were explained by the changes in serum phosphate, but not by serum PTH or calcium changes or by the dose of cinacalcet. CONCLUSIONS: 1. Cinacalcet treatment decreases plasma FGF23 concentration in haemodialysed patients with secondary hyperparathyroidism. 2. The decrease in plasma FGF23 concentration seems to be related to the decrease in serum phosphate concentration.

The Role of Probiotics in the Prevention of Clostridioides difficile Infection in Patients with Chronic Kidney Disease.

In patients suffering from chronic kidney disease (CKD), substantial unfavourable alterations in the intestinal microbiota composition, i.e., dysbiosis, have been noted. The main causes of such dysbiosis among others are insufficient dietary fibre content in the diet, fluid restrictions, medications used, and physical activity limitation. One clinically important consequence of dysbiosis in CKD patients is high risk of Clostridioides difficile infection (CDI). In observational studies, it was found that CDI is more frequent in CKD patients than in the general population. This appears to be related to high hospitalization rate and more often antibiotic therapy use, leading up to the occurrence of dysbiosis. Therefore, the use of probiotics in CKD patients may avert changes in the intestinal microbiota, which is the major risk factor of CDI. The aim of this review paper is to summarize the actual knowledge concerning the use of probiotics in CDI prevention in CKD patients in the context of CDI prevention in the general population.

The effect of sodium restricted diet on plasma visfatin levels in hypertensive patients with visceral obesity.

AIM/BACKGROUND: Experimental and clinical studies revealed contradictory data concerning the influence of renin-angiotensin-aldosterone (RAA) system activation on visfatin release. The aim of the present study was the assessment of the effect of dietary sodium restriction with RAA system activation on visfatin level in hypertensive and normotensive patients with visceral obesity. METHODS: The study included 24 hypertensive patients with visceral obesity (12 women) and 22 normotensive subjects with visceral obesity (11 women) constituting the control group. Plasma renin activity, plasma insulin, aldosterone and visfatin levels were determined twice, on normal-salt diet after 6-8 h in recumbent position and the second time after 3 days of dietary sodium restriction and upright position for 2 h. Dietary compliance was controlled by 24 h natriuresis measurement. RESULTS: Hypertensive patients had significantly higher plasma visfatin level than the control group [11.0 (8.5-13.5) vs. 6.8 (6.0-7.6) ng/ml, p=0.003]. Dietary sodium restriction and upright position caused significant increase in PRA and plasma aldosterone level in both groups. While, plasma visfatin level remained unaffected. In the combined group plasma visfatin levels correlated with BMI (r=0.398), waist circumference (r=0.391), glucose (r=0.328), insulin (r=0.663), HOMA-IR (r=0.698), triglycerides (r=0.500) and CRP (r=0.546) but not with percentage of fat mass, percentage of trunk fat, and blood pressure values. CONCLUSIONS: 1) Increased plasma visfatin concentration may play a significant role in the pathogenesis of hypertension in patients with visceral obesity. 2) RAA system activation by dietary sodium restriction and upright position has no effect on plasma visfatin levels in subjects with visceral obesity.