Hypoxia-inducible factors in arteriovenous fistula maturation: A prospective cohort study.

BACKGROUND: Neointimal hyperplasia is the main cause of arteriovenous fistula (AVF) failure. Hypoxia-inducible factors (HIFs) factors are associated with neointimal hyperplasia. Thus, we investigated the association between HIF-2 alpha (HIF-2α) and AVF maturation in end-stage kidney disease (ESKD) patients. METHODS: This prospective cohort study was conducted in 21 voluntary healthy subjects and 50 patients with ESKD who were eligible for AVF creation. Inclusion criteria were being ESKD patients without a history of AVF surgery and dialysis. Eight patients excluded from the study due to having unavailable veins six patients were excluded due to acute thrombosis after surgery. One patient lost to follow-up. A total of 35 patients were included in final analysis. The blood samples were collected a day before the AVF surgery for biochemical parameters and HIF-2α measurement. HIF-2α levels were measured by the ELISA method. RESULTS: Compared with healthy subjects, ESKD patients had a significantly higher level of HIF-2α. [1.3 (1.0-1.9) vs 2.2 (1.6-3.0)] (P = .002). Patients were divided into two groups after the evaluation of AVF maturation, as the mature group (n = 19) and the failure group (n = 16). Serum HIF-2α level was 1.7 (1.1-1.8) in the mature group; however, it was 3.1 (2.8-3.3 in failure group (P < .001). Multiple logistic regression analyses showed that HIF-2α independently predicted AVF maturation. The ROC curve analysis showed that HIF-2α > 2.65 predicted AVF maturation failure with the 87% sensitivity and 94% specificity [AUC:0.947, 95% CI (0.815-0.994), P < .001]. CONCLUSIONS: HIF-2-α levels were higher in ESKD patients than healthy subjects. HIF-2-α could be a marker of AVF maturation failure.

A rare complication following internal jugular vein catheterization to malposition: acute Budd Chiari syndrome.

BACKGROUND: Tunneled catheters can be used as an alternative vascular access in patients with limited health expectancy,vascular access problems and several comorbidities. We aimed to present a patient with venous stenosis related- reversible acute Budd-Chiari syndrome after catheter malposition. CASE PRESENTATION: After changing of tunneled catheter insertion, 36-year old man was admitted to our hospital with sudden onset of nausea, fever, chills and worsening general condition In computed tomography (CT) imaging, a hypodense thrombus was observed in which the distal end of the catheter is at the level of drainage of the hepatic veins in the inferior vena cava and that blocked hepatic vein drainage around the catheter. The catheter was removed and a new catheter was inserted in the same session. Because patient's general condition was good and without fever, he was discharged with advices on the 9th day of hospitalization. CONCLUSION: Although catheter malposition and thrombosis are not a common complication, clinicians should be alert of these complications.

Multiple urinary tract infections are associated with genotype and phenotype in adult polycystic kidney disease.

BACKGROUND: Urinary tract infections (UTI) are one of the important clinical presentations in patients with autosomal dominant polycystic kidney disease (ADPKD). The association between UTI among genotypic and phonotypic properties of ADPKD patients is still obscure. Thus, we investigated the relationship between UTI and polycystin gene mutation with total kidney volume. METHODS: Forty patients with ADPKD patients with a history of more than two UTI and age-gender-matched 40 ADPKD patients without UTI history enrolled in the study. Ambulatory blood pressure monitoring was performed in all participants. Magnetic resonance imaging (MRI) was performed with a 1.5-T system, and total kidney volumes were calculated using mid-slice technique. To determine PKD1 and PKD2 genotype, we performed molecular and genetic tests involving the following steps: DNA isolation, next-generation sequencing (NGS) and data analysis. RESULTS: ADPKD patients with UTI had lower eGFR values than those without UTI [64.9 (32.2-100.8) vs 89.5 (59.0-110.0) (p = 0.041)]. In addition, patients with UTI had significantly increased height-adjusted total kidney volume than patients without UTI [950 (290-1350) vs 345 (243-780.0) (p = 0.005)]. Multiple logistic regression analysis showed that the PKD1-truncating mutation and hTKV independently predicted UTI. The sensitivity and specificity of hTKV were 65% and 77% (cutoff > 727 cm3) with an area of under the ROC curve of 0.70 (95% CI 0.56-0.85, p = 005). CONCLUSIONS: ADPKD patients with larger kidneys and PKD1 mutation are susceptible to increased risk of multiple UTI. Additionally, renal function decreased in ADPKD patients with multiple UTI history.

Dysmetabolic markers predict outcomes in autosomal dominant polycystic kidney disease.

BACKGROUND: Overweight and obesity were recently associated with a poor prognosis in patients with autosomal dominant polycystic kidney disease (ADPKD). Whether the metabolic consequences of obesity as defined by the metabolic syndrome (MS) are also linked with disease progression remains untested. METHODS: Eligible ADPKD patients with different stages of CKD (n = 105) and 105 non-diabetic controls matched for CKD stage were enrolled in the study. Groups were evaluated at baseline for presence of MS, blood markers of metabolism, homeostasis model assessment of insulin resistance (HOMA-IR) score, and biochemical markers of inflammation (hs-CRP, IL-1ß, IL-6, TNF-α and PON-1). MS was defined according to the National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III). Patients were followed for 12 months and progression defined as a decrease in baseline eGFR > 10%. RESULTS: MS and hypertension were more prevalent amongst ADPKD patients than in the control group. Meanwhile, markers of inflammation such as hs-CRP (3.63 [3.45-5.17] vs. 4.2 [3.45-8.99] mg/dL; p = 0.014), IL-6 (21.65 [14.1-27.49] vs. 24.9 [16.23-39.4] pg/mL; p = 0.004) and IL-1ß (21.33 [15.8-26.4] vs. 26.78 [18.22-35] pg/mL; p < 0.001) levels were all more elevated in ADPKD patients than in non-diabetic CKD subjects. In multivariate analysis having a truncating PKD1 mutation predicted (OR 1.25 [1.09-1.43]; p = 0.002) fulfilling the MS criteria. Finally, ADPKD patients fulfilling MS criteria had a significantly more rapid progression during 12 months of follow-up than did those that did not (OR 3.28 [1.09-9.87]; p = 0.035). CONCLUSIONS: Our data supports the notion that dysmetabolisms part of the ADPKD phenotype and associated with a poor outcome, especially in patients with a truncating PKD1 mutation.

Cutaneous ulcerations caused by Paecilomyces variotii in a renal transplant recipient.

Skin infections caused by Paecilomyces species have been rarely described in patients with solid organ transplantation. Cutaneous manifestations are highly variable and include erythematous macules, nodules, pustules, and vesicular and necrotic lesions. The diagnosis of these infections is generally made by examination of a skin biopsy. Management of these fungal infections is difficult due to the immunocompromised state of the patients. Moreover, antifungal therapy and immunosuppressive drug interactions should be considered during treatment management. Herein, we reported a case of cellulitis caused by Paecilomyces variotii in a 56-year-old man who had undergone a kidney transplantation. Erythematous macular and nodular lesions on the left hand and left foot appeared first; within 2 months the skin lesions became ulcerated, hemorrhagic, and progressively painful and the patient was admitted to our hospital. The diagnosis was made by skin biopsy and tissue culture. The skin lesions resolved by the sixth week of the treatment with voriconazole.

Serum micro-rna profiles in patients with autosomal dominant polycystic kidney disease according to hypertension and renal function.

BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is a common hereditary disorder with unclear disease mechanism. Currently, overt hypertension and increased renal volume are the best predictors of renal function. In this study, we assessed the usefulness of selected circulating microRNAs (miRs) to predict disease progress in a cohort with ADPKD. METHODS: Eighty ADPKD patients (44.6 ± 12.7 years, 40% female, 65% hypertensive) and 50 healthy subjects (HS; 45.4 ± 12.7, 44% female) were enrolled in the study. Serum levels of 384 miRs were determined by Biomark Real Time PCR. Groups were compared using the limma method with multiple-testing correction as proposed by Smyth (corrected p < 0.01 considered significant). RESULTS: Comparing ADPKD to HS, we found significant differences in blood levels of 18 miRs (3 more and 15 less abundant). Of these, miR-3907, miR-92a-3p, miR-25-3p and miR-21-5p all rose while miR-1587 and miR-3911 decreased as renal function declined in both cross-sectional and longitudinal analysis. Using ROC analysis, an increased baseline miR-3907 in the circulation predicted a > 10% loss of GFR over the following 12 months (cut-off >2.2 AU, sensitivity 83%, specificity 78%, area 0.872 [95% CI: 0.790-0.953, p < 0.001]). Adjusting for age and starting CKD stage using multiple binary logistic regression analysis did not abrogate the predictive value. CONCLUSION: Increased copy numbers of miR-3907 in the circulation may predict ADPKD progression and suggest pathophysiological pathways worthy of further study.

Vasopressin-related copeptin is a novel predictor of early endothelial dysfunction in patients with adult polycystic kidney disease.

BACKGROUND: In this study, we examined the relative usefulness of serum copeptin levels as a surrogate marker of vasopressin (AVP) in adult polycystic kidney disease (ADPKD) by correlating it with baseline and longitudinal changes in markers of both renal function and common CVD manifestations (hypertensive vascular disease, atherosclerosis and endothelial dysfunction) that accompany the progression of this disease. METHODS: We studied a cohort of young and otherwise healthy ADPKD patients (n = 235) and measured cardiovascular function using flow-mediation dilatation (FMD), carotid intima media thickness (cIMT) and pulse wave velocity (PWV), as well as serum copeptin (commercial ELISA, a stable marker of AVP activity). The same analyses were carried out at baseline and after 3 years of follow-up. RESULTS: At baseline, median eGFR was 69 mL/min./1.73 m2, mean FMD 6.9 ± 0.9%, cIMT 0.7 ± 0.1 mm, and PWV 8.1 ± 1.2 m/s. At follow-up, equivalent values were 65 (44-75) mL/min./1.73 m2, 5.8 ± 0.9%, 0.8 ± 0.1 mm. and 8.2 ± 1.3 m/s. with all changes statistically significant. Plasma copeptin also rose from 0.62 ± 0.12 to 0.94 ± 0.19 ng/mL and this change correlated with ΔeGFR (-0.33, p < 0.001), ΔFMD (0.599, p < 0.001), ΔcIMT (0.562, p < 0.001) and ΔPWV (0.27, p < 0.001) also after linear regression modeling to correct for confounders. Finally, ROC analysis was done for a high baseline copeptin with ΔeGFR [cut-off:≤59], ΔFMD [cut-off: ≤7.08], ΔcIMT [cut-off:>0.76], and ΔPWV [cut-off:≤7.80]. CONCLUSIONS: Vascular dysfunction as reflected by FMD and cIMT, but not PWV or an altered cardiac geometry, precede most other signs of disease in ADPKD but is predicted by elevated levels of the circulating AVP-marker copeptin.

Risk factor(s) related to high membrane permeability in peritoneal dialysis.

AIM: Peritoneal dialysis (PD) patients have different peritoneal membrane permeability (transport) characteristics. High peritoneal membrane permeability is associated with increased mortality risk in the patient population. In this study, we aimed to investigate possible risk factor(s) related to high peritoneal membrane permeability. PATIENTS AND METHOD: The study included 475 PD patients (46.1 ± 14.5 years of mean age; 198 female and 277 male). The patients were divided two groups according to peritoneal equilibration test (PET) result: high-permeability group (high and high-average) and low- permeability group (low-average and low). RESULTS: In both the univariate and multivariate logistic regression analyses, it was found that diabetes mellitus and hypoalbuminemia was significantly associated with high peritoneal membrane permeability [relative risk (RR): 1.90, 95% confidence interval (CI): 1.26-2.86, p: 0.002 and RR: 2.14, 95% CI: 1.44-3.18, p<0.001, respectively]. CONCLUSION: Diabetes mellitus and hypoalbuminemia were closely associated with high peritoneal membrane permeability. Diabetic patients had 1.9 times the likelihood of having high permeability. However, the relationship between hypoalbuminemia and high peritoneal permeability appears to be a result rather than cause.

The efficacy of theophylline in preventing cisplatin-related nephrotoxicity in patients with cancer.

OBJECTIVE: Cisplatin is a potent antineoplastic agent used and its major limiting side effect is nephrotoxicity. The aims of the study are early detection of acute kidney injury (AKI) with biomarkers and investigation of the potential nephron-protective effects of theophylline. METHODS: Glomerular filtration rates (GFR), neutrophil gelatinase-associated lipocalin (NGAL), cystatin C were measured at 5th day of treatment in all of the patients. In addition, these parameters were measured repeatedly after the administration of cisplatin, at 2nd hour, 5th and 20th days. PATIENTS: Sixty patients who are planned to receive cisplatin for the first time were included in the study. Patients were divided into two groups as Group 1 (n = 30) (standard treatment arm) and Group II (n = 30) (theophylline arm). RESULTS: In both groups after the administration of cisplatin, GFR showed a significant decrease within time (p = 0.006). Urine NGAL levels were significantly high after 2 h of cisplatin administration (p < 0.001), no significant difference was observed between groups. However, when the time*group effects were considered together, higher NGAL levels were detected in the group not receiving theophylline (p = 0.025). After 5 days of cisplatin administration, urine protein levels were significantly higher in both groups (p < 0.001). CONCLUSION: Results showed that urine NGAL level is a superior biomarker compared to serum creatinine and serum cystatin C in the detection of early AKI. Theophylline was found not to bring a complete protection for the kidneys, but less nephrotoxicity was developed when compared to the group not receiving theophylline.

Preventing amikacin related ototoxicity with N-acetylcysteine in patients undergoing peritoneal dialysis.

Amikacin is a frequently used antibiotic in the treatment of peritoneal dialysis (PD)-related peritonitis. Ototoxicity is a well-known complication of amikacin for which increased oxidative stress and free oxygen radicals are thought to be responsible. In this study, the effect of N-acetyl-cysteine (NAC) on cochlear function and oxidant situation in the amikacin related ototoxicity in PD-related peritonitis patients are investigated. Forty-six patients who had their first PD-related peritonitis attacks receiving empirical amikacin treatment were enrolled in the study. The patients were randomized into two groups; the first group (n = 23) as NAC receiving and the second group (n = 23) as a placebo receiving, control group. Otoacoustic emissions were measured before, 1 week after and 4 weeks after the treatment. Oxidative stress measurements were performed concurrently in order to evaluate the effectiveness of NAC. The results of screening with otoacoustic emission testing after amikacin treatment showed that cochlear function is protected especially in higher frequencies in NAC group when compared with the control group. Evaluation of the antioxidant status of the two groups showed no differences in the basal values, but at the first week there was an increase in the NAC group compared with the control group, and this increase became significant at the fourth week. NAC is found to be safe and effective in amikacin-related ototoxicity in patients with PD-related peritonitis. We suggest a close monitoring of the patients receiving amikacin containing treatment protocols and if amikacin is administrated supplementing the treatment with NAC.

Inflammation is associated to volume status in peritoneal dialysis patients.

AIM: The aim of this study is to investigate whether there is a relationship between inflammation and volume status in patients underwent peritoneal dialysis (PD). PATIENTS AND METHOD: This cross-sectional study included 159 PD patients. The median duration of PD was 17 (range, 1-151) months. All patients were examined using bioelectrical impedance analysis to estimate the ratio of extracellular water to total body water (ECW/TBW), which was used to assess their volume status. The patients were categorized as having one of the following three volume statuses: hypervolemic (above +2 SD from the mean, which was obtained from healthy controls), normovolemic (between +2 SD and -2 SD), or hypovolemic (below -2 SD from the mean). Five patients with hypovolemia were excluded from the study. Fifty-six patients were hypervolemic whereas 98 patients were euvolemic. High-sensitive C-reactive protein (hs-CRP) levels were measured to evaluate inflammation in all patients. RESULTS: hs-CRP value levels were significantly higher in hypervolemic patients compared with euvolemic patients [7.1 (3.1-44.0) mg/L vs. 4.3 (3.1-39.6), p: 0.015, respectively]. Left ventricular hypertrophy was more frequent in hypervolemic patients compared with euvolemic patients (53.6% vs. 30.6%, p: 0.004, respectively). ECW/TBW ratio positively correlated with hs-CRP (r: 0.166, p: 0.039). Gender, hs-CRP, and residual Kt/V urea were found to be independent risk factors for hypervolemia in multivariate analysis. CONCLUSION: Inflammation is associated with hypervolemia in PD patients. Residual renal functions play an important role to maintain euvolemia in PD patients.

The effect of strict volume control on cardiac biomarker and arterial stiffness in peritoneal dialysis patients.

INTRODUCTION: Arterial stiffness is a risk marker for cardiovascular events in peritoneal dialysis (PD) patients. Strict volume control strategy has been shown to result in better cardiac functions and control of hypertension in these patients. The aim of the study was to identify the determinants of arterial stiffness and evaluate the changes in cardiac biomarkers in PD patients under strict volume control strategy. METHODS: 58 PD patients were enrolled into this prospective observational study. Arterial stiffness determined by aortic pulse wave velocity (PWV), echocardiography, ambulatory blood pressure and NT-pro-BNP levels were measured at baseline and at first year. RESULTS: The mean age of the patients was 46.4 ± 14 years. 30 patients were on automated PD (APD) and 28 on continuous ambulatory PD (CAPD) group. In both groups, there were significant differences in PWV values at baseline and at the end of the study. A similar decrease was observed with NT-proBNP and PWV levels. In addition, a significant improvement was found in echocardiographic parameters in all patients. Comparison of APD and CAPD groups with respect to change in one year, showed no difference in echocardiographic findings, while the reduction in PWV, NTproBNP and blood pressure values was higher in the CAPD group. CONCLUSIONS: In PD patients, strict volume control leads to a reduction in NT-pro-BNP levels, better control of blood pressure and significant improvements in cardiac functions and arterial stiffness.

Does body mass index affect survival and technique failure in patients undergoing peritoneal dialysis?

OBJECTIVE: To investigate effect of body mass index (BMI) on survival and technique failure in patients undergoing peritoneal dialysis (PD). METHODS: In this retrospective study three hundred ninety-two consecutive patients undergoing peritoneal dialysis from September 1995 to January 2013 were included. Median PD duration was 53 (range: 4-189) months. Clinical outcomes were mortality and technique failure. Technique failure was defined as transfer to hemodialysis (HD) due to peritonitis, ultrafiltration failure, inadequate dialysis, exit-site and/or tunnel infection, and mechanical problems. Deaths within 3 months after transferring to HD were accepted as PD-related mortalities. The patient and technique survival rates were estimated using the Kaplan-Meier method. Mortality risks were analyzed using the multivariate Cox regression model in which we included (in a backward-wald manner) all the significant variables from the univariate analysis. RESULTS: There were 164 (41.8%) deaths. Forty-six (11.7%) patients underwent renal transplantation whereas 132 (33.7%) patients were transferred to HD. The multivariate Cox regression analysis found that the patient survival rates were significantly associated with age, BMI, baseline serum creatinine and albumin levels, and total Kt/Vurea. All variables as potential risk factors for the patient survival were also assessed for technique survival in univariate analysis and technique survival rates were significantly associated only with BMI (p: 0.015). CONCLUSION: BMI was associated with unfavorable patient survival in PD patients.

A link between the intrarenal renin angiotensin system and hypertension in autosomal dominant polycystic kidney disease.

BACKGROUND/AIMS: Early onset of hypertension and its consequences account for the great majority of deaths in patients with autosomal dominant polycystic kidney disease (ADPKD). Renin-angiotensin system (RAS) components have been shown in ADPKD kidneys independent of systemic RAS. Thus, we examined the urinary angiotensinogen (UAGT) levels as a biomarker of intrarenal RAS status in ADPKD patients with/without hypertension and healthy subjects. METHODS: Eighty-four ADPKD patients (43 with hypertension and 41 without hypertension) and 40 healthy controls were studied cross-sectionally. Patients with glomerular filtration rate <60 ml/min were excluded from the study. Hypertension was diagnosed with ambulatory blood pressure monitoring. Urinary and plasma concentration of angiotensinogen, spot urine microprotein and creatinine (UCre) levels were recorded for each participant. RESULTS: UAGT/UCre levels were higher in hypertensive ADPKD patients (23.7 ± 8.4) compared with normotensive ADPKD patients (16.6 ± 5.2) and healthy controls (6.9 ± 3.3; p < 0.001). In univariate analysis, UAGT correlated with systolic blood pressure, diastolic blood pressure (DBP) and proteinuria. The independence of these correlations was analyzed in a regression model, and UAGT was shown to be significantly predicted by proteinuria and DBP. CONCLUSION: Intrarenal RAS activation which is monitored by UAGT levels clinically may be a harbinger of hypertension and kidney disease in ADPKD patients.

Serum uric acid levels and endothelial dysfunction in patients with autosomal dominant polycystic kidney disease.

BACKGROUND/AIMS: Patients with autosomal dominant polycystic kidney disease (ADPKD) exhibit endothelial dysfunction (ED) despite normal levels of renal function. Hyperuricemia occurs in these patients and has been postulated to affect ED through the generation of oxidative stress. We therefore investigated the prevalence of ED and its association with serum uric acid levels in early-stage ADPKD. METHODS: A cross-sectional design was used for the assessment of prevalent patients with early-stage (normal renal function) ADPKD (n = 91) from two academic medical centers. ED was assessed using ischemia-induced forearm flow-mediated vasodilation (FMD). Serum uric acid levels were evaluated using an Olympus AU2700 autoanalyzer. RESULTS: ADPKD patients with higher serum uric acid levels had a higher asymmetric dimethylarginine (ADMA) level (1.19 ± 0.2 vs. 1.47 ± 0.3, p < 0.001) and lower FMD rates (8.1 ± 1.3 vs. 6.8 ± 0.7, p < 0.001). In multiple regression analysis for predictors of cohort FMD, uric acid (ß = -0.32, p < 0.001), ADMA (ß = -0.36, p < 0.001), high-sensitivity C reactive protein (CRP; ß = -0.32, p < 0.001) and estimated glomerular filtration rate (eGFR; ß = 0.33, p < 0.001) all predicted FMD. CONCLUSIONS: In early-stage ADPKD patients, uric acid levels, serum ADMA and eGFR all independently predict ED in a similar manner. Future studies are needed to investigate the causes of elevated serum uric acid, ADMA and CRP in these patients.

The role of platelet activation in determining response to therapy in patients with primary nephrotic syndrome.

To test the role of platelet activation in the prognosis of nephrotic syndrome (NS), we evaluated the mean platelet volume (MPV) in patients with NS undergoing treatment. In this prospective, multicenter clinical study 156 patients with primary NS under treatment were assigned and followed for one year. Patients were divided into three groups for complete remission, partial remission, and resistance. Biochemical parameters, estimated glomerular filtration rate, proteinuria level, and MPV levels were compared at baseline and 12 months after treatment. MPV, proteinuria, total cholesterol, triglyceride, LDL cholesterol, HDL cholesterol, total protein, albumin, and hs-CRP levels significantly decreased in partial and complete remission group after 12 months compared to the baseline (p < 0.05). However, MPV levels significantly increased and only LDL cholesterol significantly decreased in the resistance group (p < 0.05). Univariate analyses demonstrated that ΔMPV was significantly associated with Δproteinuria (r = 0.41, p < 0.001), Δhs-CRP (r = 0.39, p < 0.001), and ΔAlbumin (r = -0.30, p < 0.001). We found that ΔAlbumin (ß = -0.33, p < 0.001), ΔTotal cholesterol (ß = -0.20, p = 0.011), and Δhs-CRP (ß = 0.19, p = 0.018) were statistically significant predictors of the Δproteinuria in multiple regression analysis. In subjects with primary NS, MPV is associated with the prognosis or the disease. This study provides the background for longer trials and the role of platelet activation in NS.

Does arterio-venous fistula creation affects development of pulmonary hypertension in hemodialysis patients?

BACKGROUND: Pulmonary arterial hypertension (PAH) is a common complication in hemodialysis (HD) patients and its pathogenesis is not explained clearly. Arterio-venous fistulas (AVFs) creation may contribute to the development of PAH because of increased pulmonary artery blood flow. However, it was not prospectively evaluated that effect of AVF on the development of PAH. AIM: We aimed to evaluate the effects of AVF on PAH and the relationship between blood flow rate of AVF and pulmonary artery pressure (PAP) in HD patients. PATIENTS AND METHOD: The prospective study included 50 patients with end-stage renal disease. Before an AVF was surgically created for hemodialysis, the patients were evaluated by echocardiography. Then, an AVF was surgically created in the patients. After mean 76.14 ± 11.37 days, the second evaluation was performed by echocardiography. RESULTS: Before AVF creation, 17 (34%) out of 50 patients had PAH. The systolic PAP was significantly higher in the patients with PAH compared with patients without PAH (47.82 ± 9.82 mmHg vs. 30.15 ± 5.70 mmHg, respectively, p = 0.001). In the second evaluation, 19 (38%) out of 50 patients had PAH. The systolic PAP values were significantly higher in the patients with PAH compared with patients without PAH (47.63 ± 8.92 mmHg vs. 25.03 ± 7.69 mmHg, P = 0.001, respectively). There was no relationship between the blood flow rate of AVF and PAP. CONCLUSION: PAH is a common problem in HD patients. AVF has no significant effect on the development of PAH within a short period. Similarly, blood flow rate of AVF also did not affect remarkably the systolic PAP.

Association between depression, nutritional status, and inflammatory markers in peritoneal dialysis patients.

BACKGROUND: To investigate the relationship between depression, nutritional status, and inflammatory markers in patients on peritoneal dialysis (PD). PATIENTS AND METHODS: This prospective study included 40 PD patients and 20 healthy people. The severity of depressive symptoms was assessed using the Beck depression inventory, the Hamilton depression rating scale, and the Hamilton anxiety rating scale. The depressive patients received antidepressant drug for 8 weeks. Blood samples were taken before and after antidepressant treatment for the high-sensitive C-reactive protein (hs-CRP), interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) levels. RESULTS: Ten (25%) of the 40 PD patients had depression. No significant difference was determined between depressive patients and nondepressive patients. The mean erythrocyte sedimentation rate was higher in depressive patients. There was no significant difference for other inflammation parameters, including hs-CRP, TNF-α, IL-1, and IL-6, between depressive patients and nondepressive patients. In the depressive patients, we did not observe any significant change in nutritional parameters after antidepressant treatment. When we evaluated inflammation parameters of the depressive patients before and after antidepressant treatment, only IL-1 and IL-6 levels were significantly increased after antidepressant treatment. CONCLUSION: The depressive disorder in PD patients is a common psychopathology and has no significant effects on nutritional status and inflammation.

The lack of benefit of a combination of an angiotensin receptor blocker and calcium channel blocker on contrast-induced nephropathy in patients with chronic kidney disease.

AIM: Contrast-induced nephropathy (CIN) is a relatively common and serious complication, which occurs after the administration of contrast materials to patients. Although the pathophysiology of CIN is not exactly understood, ischemia of the medulla, oxidative stress, and direct toxicity of the contrast material are some of the factors that are implicated for the pathogenesis of CIN. To date, the only therapy that reduces the risk of CIN is volume expansion. There are conflicting results about the roles of angiotensin receptor blockers (ARB) and calcium channel blockers (CCB) in studies on CIN. For this reason the aim of this study was to compare the efficiency of the prophylactic use of amlodipine/valsartan plus hydration versus hydration only for the prevention of CIN in patients undergoing coronary angiography (CAG). PATIENTS AND METHODS: We prospectively enrolled 90 patients whose baseline serum creatinine levels were under 2.1 mg/dL and who were scheduled for CAG. Patients were divided into two groups. Group I (n = 45), consisted of patients who received amlodipine/valsartan plus hydration, group II (n = 45) consisted of patients who received only hydration. The patients in group I were given amlodipine/valsartan 5/160 mg once a day for a total of 3 days, starting one day before CAG and continuing on the day of and the day after the procedure. A 1 mL/kg/h sodium chloride infusion was administered for a total of 24 h, starting 12 h before the procedure and 12 h after, in all patients. The baseline serum creatinine (Scre) level was obtained before the procedure and repeated 48 h after. CIN was defined as an increase of ≥0.5 mg/dL or an increase of >25% in baseline Scre on the second day after CAG. RESULTS: The baseline clinical characteristics of the treatment groups were similar. Baseline Scre was 1.13 ± 0.33 in group I and 1.07 ± 0.23 mg/dL in group II (p = 0.31). There was a significant difference between the Scre levels 48 h after CAG between the two groups (1.18 ± 0.33-1.05 ± 0.23) (p = 0.03). The reason for this was the increase of Scre in group I. CIN occurred in 17.8% (8/45) of patients in group I and in 6.7% (3/45) of patients in group II (p = 0.197). In the diabetic subgroup, CIN occurred in 10.5% (2/19) of patients taking amlodipine/valsartan and in none of the patients in group II (p = 0.486). The Mehran scores of the patients who developed CIN were significantly higher than those patients who did not develop CIN. CONCLUSION: Amlodipine/valsartan therapy plus hydration did not reduce the risk of CIN in chronic kidney disease (CKD) Stage 2 patients who underwent elective CAG using a low-osmolar nonionic contrast medium. This is because there was a decrease in the glomerular filtration rate (GFR) using the Levey Modification of Diet in Renal Disease (MDRD) formula in the amlodipine/valsartan group and CIN occurred at a higher frequency in this group; ARBs and CCBs may be withheld before CAG in high-risk patients.

Carpal tunnel release surgery and venous hypertension in early hemodialysis patients without amyloid deposits.

AIM: Carpal tunnel syndrome (CTS) is one of the frequent problems of the patients who underwent hemodialysis (HD). The role of venous hypertension due to arteriovenous fistula (AVF) has not been clarified completely; therefore, we aimed to investigate the role of venous hypertension due to AVF in hemodialysis patients who had CTS. PATIENTS AND METHODS: We included 12 patients who had been receiving HD treatment for less than 8 years and the newly diagnosed CTS patients with the same arm of AVF. All patients were diagnosed clinically and the results were confirmed by both nerve conduction studies and electromyography. Open carpal tunnel release surgery was performed on all of them. Venous pressure was measured in all patients before and after two weeks of surgery. RESULTS: There were significant differences before and after the surgery with regard to pressures (P > 0.05). After the surgery, all carpal ligament specimens of the patients were not stained with Congo red for the presence of amyloid deposition. CONCLUSION: Increased venous pressure on the same arm with AVF could be responsible for CTS in hemodialysis patients. Carpal tunnel release surgery is the main treatment of this disease by reducing the compression on the nerve.