Immunological parameters associated with the severity of COVID-19 pneumonia in kidney transplant recipients.

PURPOSE: An outbreak of a novel respiratory disease due to coronavirus species was emerged in 2019 and named as Coronavirus Disease-2019 (COVID-19). Clinical and immunological factors affecting the course of COVID-19 in kidney transplant recipients (KTR) are not well-known. METHODS: In this prospective observational study, we presented 20 KTR with COVID-19 pnemonia and examined the factors predicting the severity of COVID-19. A total of 10 KTR without COVID-19 was used as control group. Lymphocyte subsets were determined by flow cytometry. In 13/20 patients, immunophenotyping was repeated 1 week later. RESULTS: Mean age of the patients was 50 ± 9 years. Patients were classified as mild-moderate (oxygen saturation: SO2 > 90%) and severe disease groups (SO2 ≤ 90%). Serum albumin and hemoglobin were lower and CRP, fibrinogen and peak D-dimer were higher in severe group. Peak CRP was inversely associated with nadir SO2 (r = - 0.68, p = 0.001). Neutrophil/lymphocyte ratio was higher in severe group (p = 0.01). CD3 + and CD4 + cells were lower and NK cell percentage (CD16 + 56 +) was higher in severe group. Percentage of spontaneously activated CD8 cells (CD8 + CD69 +) was higher in severe group. In comparison of KTR with and without COVID-19, CD8 + cells were lower but NK cell percentage was higher in KTR with COVID-19. CONCLUSION: In this pilot study, increased NK cells, activated CD8 + cells and decreased CD3 + and CD4 + cells were associated with severity of COVID-19 in KTR. Peripheral immunophenotyping of lymphocyte subtypes may provide prognostic information about the clinical course of COVID-19 in KTR.

Predicting the outcome of COVID-19 infection in kidney transplant recipients.

BACKGROUND: We aimed to present the demographic characteristics, clinical presentation, and outcomes of our multicenter cohort of adult KTx recipients with COVID-19. METHODS: We conducted a multicenter, retrospective study using data of patients hospitalized for COVID-19 collected from 34 centers in Turkey. Demographic characteristics, clinical findings, laboratory parameters (hemogram, CRP, AST, ALT, LDH, and ferritin) at admission and follow-up, and treatment strategies were reviewed. Predictors of poor clinical outcomes were analyzed. The primary outcomes were in-hospital mortality and the need for ICU admission. The secondary outcome was composite in-hospital mortality and/or ICU admission. RESULTS: One hundred nine patients (male/female: 63/46, mean age: 48.4 ± 12.4 years) were included in the study. Acute kidney injury (AKI) developed in 46 (42.2%) patients, and 4 (3.7%) of the patients required renal replacement therapy (RRT). A total of 22 (20.2%) patients were admitted in the ICU, and 19 (17.4%) patients required invasive mechanical ventilation. 14 (12.8%) of the patients died. Patients who were admitted in the ICU were significantly older (age over 60 years) (38.1% vs 14.9%, p = 0.016). 23 (21.1%) patients reached to composite outcome and these patients were significantly older (age over 60 years) (39.1% vs. 13.9%; p = 0.004), and had lower serum albumin (3.4 g/dl [2.9-3.8] vs. 3.8 g/dl [3.5-4.1], p = 0.002), higher serum ferritin (679 µg/L [184-2260] vs. 331 µg/L [128-839], p = 0.048), and lower lymphocyte counts (700/µl [460-950] vs. 860 /µl [545-1385], p = 0.018). Multivariable analysis identified presence of ischemic heart disease and initial serum creatinine levels as independent risk factors for mortality, whereas age over 60 years and initial serum creatinine levels were independently associated with ICU admission. On analysis for predicting secondary outcome, age above 60 and initial lymphocyte count were found to be independent variables in multivariable analysis. CONCLUSION: Over the age of 60, ischemic heart disease, lymphopenia, poor graft function were independent risk factors for severe COVID-19 in this patient group. Whereas presence of ischemic heart disease and poor graft function were independently associated with mortality.

Cholesterol-embolization syndrome: current perspectives.

Cholesterol-embolization syndrome (CES) is a multisystemic disease with various clinical manifestations. CES is caused by embolization of cholesterol crystals (CCs) from atherosclerotic plaques located in the major arteries, and is induced mostly iatrogenically by interventional and surgical procedures; however, it may also occur spontaneously. Embolized CCs lead to both ischemic and inflammatory damage to the target organ. Therefore, anti-inflammatory agents, such as corticosteroids and cyclophosphamide, have been investigated as treatment for CES in several studies, with conflicting results. Recent research has revealed that CES is actually a kind of autoinflammatory disease in which inflammasome pathways, such as NLRP3 and IL1, are induced by CCs. These recent findings may have clinical implications such that colchicine and IL1 inhibitors, namely canakinumab, may be beneficial in the early stages of CES.

Tympanogram Findings in Hemodialysis Patients.

BACKGROUND: The aim of this study is to investigate whether changes in cerebrospinal fluid (CSF) pressure during the hemodialysis (HD) treatment are reflected on tympanometric measurements. METHODS: The study was performed on 24 HD patients. The static compliance and absorbance values of the patients before and after HD were measured using a wideband tympanometry. The tympanogram tests were performed immediately before and at the end of the HD session. RESULTS: The static compliance values of the patients after HD were significantly lower than those before HD. This decrease significantly correlated with the adequacy of dialysis determined by urea reduction rate and Kt/V. The absorbance values showed a decrease in the band 343 and 727 Hz, but no significant difference was found in other frequencies. The static admittance and absorbance values were influenced by the HD process. DISCUSSION: This influence might be due to the increase in CSF pressure as a result of the removal of urea from blood during HD session.

Acute renal infarction in Turkey: a review of 121 cases.

PURPOSE: Renal infarction is a clinical condition which is caused by renal artery occlusion and leads to permanent renal parenchymal damage. In the literature, there are generally case reports on this subject, and few studies that include a large group of patients. Therefore, we aimed to present the data of a large group of patients who were diagnosed with acute renal infarction in our country in this retrospective study. METHODS: The data of patients who were diagnosed with acute renal infarction according to clinical and radiological findings in Turkey in the last 3 years were examined. For this purpose, we contacted with more than 40 centers in 7 regions and obtained support from clinically responsible persons. Demographic data of patients, laboratory data at the time of diagnosis, tests performed for etiologic evaluation, given medications, and patients' clinical status during follow-up were obtained from databases and statistical analysis was performed. RESULTS: One-hundred and twenty-one patients were included in the study. The mean age was 53 ± 1.4 (19-91) years. Seventy-one (58.7%) patients were male, 18 (14.9%) had diabetes, 53 (43.8%) had hypertension, 36 (30%) had atrial fibrillation (AF), and 6 had a history of lupus + antiphospholipid syndrome (APS). Forty-five patients had right renal infarction, 50 patients had left renal infarction, and 26 (21.5%) patients had bilateral renal infarction. The examinations for the ethiologies revealed that, 36 patients had thromboemboli due to atrial fibrillation, 10 patients had genetic anomalies leading to thrombosis, 9 patients had trauma, 6 patients had lupus + APS, 2 patients had hematologic diseases, and 1 patient had a substance abuse problem. Fifty-seven (57%) patients had unknown. The mean follow-up period was 14 ± 2 months. The mean creatinine and glomerular filtration rate (GFR) values at 3 months were found to be 1.65 ± 0.16 mg/dl and 62 ± 3 ml/min, respectively. The final mean creatinine and GFR values were found to be 1.69 ± 0.16 mg/dl and 62 ± 3 ml/min, respectively. CONCLUSIONS: Our study is the second largest series published on renal infarction in the literature. More detailed studies are needed to determine the etiological causes of acute renal infarction occurring in patients.

Volume status and arterial blood pressures are associated with arterial stiffness in hemodialysis patients.

BACKGROUND: Arterial stiffness is a strong predictor of mortality in hemodialysis patients. In this study, we aimed to investigate possible relations of arterial stiffness with volume status determined by bioimpedance analysis and aortic blood pressure parameters. Also, effects of a single hemodialysis session on these parameters were studied. METHODS: A total of 75 hemodialysis patients (M/F: 43/32; mean age: 53 ± 17) were enrolled. Carotid-femoral pulse wave velocity, augmentation index, and aortic pulse pressure were measured by applanation tonometry before and after hemodialysis. Extracellular fluid and total body fluid volumes were determined by bioimpedance analysis. RESULTS: Carotid-femoral pulse wave velocity (9.30 ± 3.30 vs 7.59 ± 2.66 m/s, p < 0.001), augmentation index (24.52 ± 9.42 vs 20.28 ± 10.19, p < 0.001), and aortic pulse pressure (38 ± 14 vs 29 ± 8 mmHg, p < 0.001) significantly decreased after hemodialysis. Pre-dialysis carotid-femoral pulse wave velocity was associated with age (r2 = 0.15, p = 0.01), total cholesterol (r2 = 0.06, p = 0.02), peripheral mean blood pressure (r2 = 0.10, p = 0.005), aortic-mean blood pressure (r2 = 0.06, p = 0.02), aortic pulse pressure (r2 = 0.14, p = 0.001), and extracellular fluid/total body fluid (r2 = 0.30, p < 0.0001). Pre-dialysis augmentation index was associated with total cholesterol (r2 = 0.06, p = 0,02), aortic-mean blood pressure (r2 = 0.16, p < 0.001), and aortic pulse pressure (r2 = 0.22, p < 0.001). Δcarotid-femoral pulse wave velocity was associated with Δaortic-mean blood pressure (r2 = 0.06, p = 0.02) and inversely correlated with baseline carotid-femoral pulse wave velocity (r2 = 0.29, p < 0.001). Pre-dialysis Δaugmentation index was significantly associated with Δaortic-mean blood pressure (r2 = 0.09, p = 0.009) and Δaortic pulse pressure (r2 = 0.06, p = 0.03) and inversely associated with baseline augmentation index (r2 = 0.14, p = 0.001). In multiple linear regression analysis (adjusted R2 = 0.46, p < 0.001) to determine the factors predicting Log carotid-femoral pulse wave velocity, extracellular fluid/total body fluid and peripheral mean blood pressure significantly predicted Log carotid-femoral pulse wave velocity (p = 0.001 and p = 0.006, respectively). CONCLUSION: Carotid-femoral pulse wave velocity, augmentation index, and aortic pulse pressure significantly decreased after hemodialysis. Arterial stiffness was associated with both peripheral and aortic blood pressure. Furthermore, reduction in arterial stiffness parameters was related to reduction in aortic blood pressure. Pre-dialysis carotid-femoral pulse wave velocity was associated with volume status determined by bioimpedance analysis. Volume control may improve not only the aortic blood pressure measurements but also arterial stiffness in hemodialysis patients.

Endothelial Progenitor Cells and Kidney Diseases.

Endothelial progenitor cells (EPC) are bone marrow derived or tissue-resident cells that play major roles in the maintenance of vascular integrity and repair of endothelial damage. Although EPCs may be capable of directly engrafting and regenerating the endothelium, the most important effects of EPCs seem to be depended on paracrine effects. In recent studies, specific microvesicles and mRNAs have been found to mediate the pro-angiogenic and regenerative effects of EPCs on endothelium. EPC counts have important prognostic implications in cardiovascular diseases (CVD). Uremia and inflammation are associated with lower EPC counts which probably contribute to increased CVD risks in patients with chronic kidney disease. Beneficial effects of the EPC therapies have been shown in studies performed on different models of CVD and kidney diseases such as acute and chronic kidney diseases and glomerulonephritis. However, lack of a clear definition and specific marker of EPCs is the most important problem causing difficulties in interpretation of the results of the studies investigating EPCs.

IL-33 deficiency slows cancer growth but does not protect against cisplatin-induced AKI in mice with cancer.

The effect of IL-33 deficiency on acute kidney injury (AKI) and cancer growth in a 4-wk model of cisplatin-induced AKI in mice with cancer was determined. Mice were injected subcutaneously with murine lung cancer cells. Ten days later, cisplatin (10 mg·kg-¹·wk-¹) was administered weekly for 4 wk. The increase in kidney IL-33 preceded the AKI and tubular injury, suggesting that IL-33 may play a causative role. However, the increase in serum creatinine, blood urea nitrogen, serum neutrophil gelatinase-associated lipoprotein, acute tubular necrosis, and apoptosis scores in the kidney in cisplatin-induced AKI was the same in wild-type and IL-33-deficient mice. There was an increase in kidney expression of pro-inflammatory cytokines CXCL1 and TNF-α, known mediators of cisplatin-induced AKI, in IL-33-deficient mice. Surprisingly, tumor weight, tumor volume, and tumor growth were significantly decreased in IL-33-deficient mice, and the effect of cisplatin on tumors was enhanced in IL-33-deficient mice. As serum IL-33 was increased in cisplatin-induced AKI in mice, it was determined whether serum IL-33 is an early biomarker of AKI in patients undergoing cardiac surgery. Immediate postoperative serum IL-33 concentrations were higher in matched AKI cases compared with non-AKI controls. In conclusion, even though the cancer grows slower in IL-33-deficient mice, the data that IL-33 deficiency does not protect against AKI in a clinically relevant model suggest that IL-33 inhibition may not be useful to attenuate AKI in patients with cancer. However, serum IL-33 may serve as a biomarker of AKI.

Serum heparanase levels are associated with endothelial dysfunction in patients with obstructive sleep apnea.

BACKGROUND AND AIM: Obstructive sleep apnea syndrome (OSAS) is well-known to be associated with high risk for cardiovascular (CV) diseases. Heparanase has been recently shown to be related to increased inflammation and vulnerability of the atherosclerotic plaques. Herein we aimed to investigate the relationships between OSAS, heparanase and endothelial dysfunction. MATERIALS AND METHODS: A total of 120 patients with varying severity of OSAS and 31 controls without OSAS were enrolled. Flow-mediated dilatation (FMD) was measured as an indicator of endothelial dysfunction. Serum heparanase levels were measured with ELISA. RESULTS: Serum heparanase levels increased in a stepwise fashion from controls to patients with more severe OSAS. When FMD was compared with controls and various degrees of severity of OSAS, a stepwise decrease in FMD was observed. Serum heparanase levels were found to be significantly associated with apnea hypopnea index (AHI) (r = .57, P < .001) and FMD (r= -.37, P < .001) in patients with OSAS. Serum heparanase levels were significantly associated with hemoglobin-A1c and body mass index in patients with OSAS. Serum heparanase and uric acid levels were independent predictors of FMD in linear regression analysis (R2 = .506, P < .001; P < .001 and P = .001 respectively). CONCLUSIONS: Serum heparanase levels were significantly increased in patients with OSAS and associated with the severity of OSAS (AHI) and endothelial dysfunction (FMD). Increased heparanase activity in OSAS may be related to increased cardiovascular risk in patients with OSAS.

CD133+ cells are associated with ADIPOCYTOKINES and endothelial dysfunction in hemodialysis patients.

BACKGROUND: Hemodialysis (HD) patients have increased risk of cardiovascular disease (CVD). Impaired stem cell health and adipocytokine metabolism may play important roles in the complex pathophysiological mechanisms of CVD in this patient population. We aimed to investigate the relationships between CD133+ cell counts, adipocytokines and parameters of endothelial dysfunction and atherosclerosis in HD patients. METHODS: In 58 chronic HD patients (male/female:28/30, mean age:58 ± 14 years), serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), leptin, adiponectin and resistin were measured by ELISA. Left ventricular mass index (LVMI), carotid intima-media thickness (CIMT), flow-mediated dilatation (FMD) of the brachial artery were measured. CD133+ cells were counted by flow cytometry (BD FACSCalibur-BD Bioscience,CA). RESULTS: CD133+ cell counts were inversely associated with FMD (r = -0.39, p = 0.007) and positively correlated with serum resistin (r = 0.45, p < 0.001) and serum TNF-α (r = 0.31, p = 0.02). Serum leptin levels were higher in high CD133 group compared to low CD133 group [32.37(12.74-72.29) vs 15.50(5.38-37.12)ng/mL, p = 0.03]. Serum leptin levels were correlated with TNF-α(r = 0.35, p = 0.009). Serum adiponectin levels were negatively correlated with serum leptin (r = -0.28, p = 0.03). Serum resistin levels were associated with TNF-α (r = 0.54, p < 0.001) and leptin (r = 0.29, p = 0.03). Serum IL-6 levels were significantly associated with LVMI (r = 0.31, p = 0.03). Serum IL-6 levels were significantly higher in patients with carotid plaque compared to patients without plaque [12.75(9.91-28.68) vs 8.27(5.97-14.04) pg/mL, p = 0.02]. In multiple linear regression analysis to determine the factors predicting LogFMD; dialysis vintage, LVMI and LogCD133+ cell counts were included as independent variables(R = 0.57, adjusted R-square = 0.27, p = 0.001). CD133+ cell count and LVMI were found to significantly predict FMD (p = 0.03 and p = 0.04 respectively). CONCLUSION: CD133+ cells were associated with inflammation and endothelial dysfunction in HD patients. Serum leptin, resistin and TNF-α levels were positively related to CD133+ cell count. Impaired regulation of undifferentiated stem cells and adipocytokines might contribute to endothelial dysfunction in HD patients.

Contrast-induced acute kidney injury: A review of practical points.

Contrast-induced acute kidney injury (CI-AKI) is one of the most common causes of AKI in clinical practice. CI-AKI has been found to be strongly associated with morbidity and mortality of the patients. Furthermore, CI-AKI may not be always reversible and it may be associated with the development of chronic kidney disease. Pathophysiology of CI-AKI is not exactly understood and there is no consensus on the preventive strategies. CI-AKI is an active research area thus clinicians should be updated periodically about this topic. In this review, we aimed to discuss the indications of contrast-enhanced imaging, types of contrast media and their impact on nephrotoxicity, major pathophysiological mechanisms, risk factors and preventive strategies of CI-AKI and alternative non-contrast-enhanced imaging methods.

Hemodialysis-induced repolarization abnormalities on ECG are influenced by serum calcium levels and ultrafiltration volumes.

PURPOSE: Hemodialysis (HD) patients are known to have high cardiovascular mortality rate. Sudden cardiac death (SCD) due to arrhythmias causes most of the cardiac deaths. HD per se may lead to ECG abnormalities and ventricular arrhythmias. Monitoring ECG parameters such as corrected QT interval, QT dispersion (QTd), Tpe interval may be useful to stratify the patients with high risk of arrhythmia and SCD. Herein we aimed to investigate the effects of changes in serum electrolyte levels and pH on ECG parameters before and after the HD. METHODS: A total of 50 chronic HD patients (mean age 58 ± 19; male 27) were enrolled. Patients with unmeasurable T waves; atrial fibrillation; bundle branch block; use of class I or class III antiarrhythmic drugs were excluded. Serum potassium, magnesium, calcium, urea, creatinine and pH were measured before and after HD treatment. Standard surface 12-lead ECGs were recorded before and after HD. QTc, QTd, Tpe, JT interval, P-wave-duration, P-wave dispersion were determined. RESULTS: Serum potassium and magnesium decreased, and calcium, pH and bicarbonate levels increased; QRS and Tpe interval were increased after HD. Basal Tpe was correlated with urea (r = 0.31, p = 0.02). Tpe interval was higher in hypocalcemic compared to normocalcemic patients (77 ± 11 vs 70 ± 9 ms, p = 0.02). ∆Tpe was correlated with ∆calcium (r = -0.32, p = 0.02). Basal QTc was correlated with calcium (r = -0.62, p < 0.001). ∆QTc was correlated with basal calcium (r = 0.39, p = 0.005) and ∆calcium (r = -0.46, p < 0.001). Basal JT was correlated with calcium (r = -0.55, p < 0.001). ∆JT was correlated with pH (r = 0.35, p = 0.01), ∆calcium (r = -0.53, p < 0.001) and ∆magnesium (r = -0.30, p = 0.03). Before HD, 12 patients (12%) were hypermagnesemic of whom JT intervals were lower (314 ± 20 vs 332 ± 23 ms, p = 0.02). Ultrafiltration per body weight was associated with ∆QTc (r = -0.40, p = 0.007) and ∆JT (r = -0.36, p = 0.01). CONCLUSION: QRS and Tpe intervals were increased after HD. Tpe interval was longer in hypocalcemic patients. Change in Tpe was negatively associated with the change in calcium. Ultrafiltration was associated with ∆QTc and ∆JT. Calcium and ultrafiltration seem to be the most important determinants of ECG parameters of HD-induced repolarization abnormalities.

Cholesterol embolization syndrome: A report of two cases.

Cholesterol embolization syndrome (CES) is a multisystemic disease with immunological features, and a rare but an important cause of acute kidney injury (AKI) following invasive angiography. It frequently occurs in the elderly male population with extensive atherosclerosis. CES should be considered in the differential diagnosis of AKI following angiography, as prognosis and treatment are completely different from contrast-induced nephropathy. Two cases of CES that developed after invasive angiography are described in the present report. In the first case, renal biopsy was performed, and CES was diagnosed by presence of characteristic renal lesions. The second patient had blue toe syndrome and persistent renal dysfunction.

Chronic rhinosinusitis, endothelial dysfunction, and atherosclerosis.

BACKGROUND: Chronic inflammation is associated with accelerated atherosclerosis, endothelial dysfunction (ED), and cardiovascular diseases. Because chronic rhinosinusitis (CRS) is an inflammatory disease, it may be associated with the development of ED and accelerated atherosclerosis. OBJECTIVE: To investigate the relationship between CRS and carotid intima-media thickness (CIMT), flow-mediated dilation (FMD) of the brachial artery, and microalbuminuria. MATERIALS AND METHODS: This cross-sectional study included 38 patients with CRS and 29 healthy controls. In addition to measuring spot urine albumin-creatinine ratios, FMD of the brachial artery and CIMT were assessed noninvasively. RESULTS: Patients with CRS had lower FMD scores (p = 0.031), higher CIMT scores (p = 0.005), and a higher urinary albumin-creatinine ratio (p = 0.036) compared with healthy controls. In a multivariate analysis, CIMT and FMD were independently associated with the presence of CRS. However, the relationship between urinary albumin and creatinine, and the presence of CRS was no longer observed. CONCLUSIONS: CRS is associated with ED and atherosclerosis, as indicated by decreased FMD and increased CIMT in patients with CRS. Further studies are necessary to identify the exact pathophysiologic mechanisms responsible for our findings.

NF-κB transcriptional inhibition ameliorates cisplatin-induced acute kidney injury (AKI).

The nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) cell signaling pathway is important in inflammation and cell survival. Inflammation and cell death in the kidney are features of cisplatin-induced AKI. While it is known that cisplatin induces NF-κB signaling in the kidney, the NF-κB responsive genes and the effect of direct NF-κB transcriptional inhibition in cisplatin-induced AKI is not known. Mice injected with cisplatin, 25mg/kg, developed AKI, acute tubular necrosis (ATN) and apoptosis on day 3. Mice were treated with JSH-23 (20 or 40 mg/kg) which directly affects NF-κB transcriptional activity. Kidney function, tubular injury (ATN, serum neutrophil gelatinase-associated lipocalin [NGAL], but not apoptosis) and myeloperoxidase (MPO) activity were significantly improved by JSH-23 (40 mg/kg). Sixty one NF-κB responsive genes were increased by cisplatin of which 21 genes were decreased by JSH-23. Genes that were decreased by JSH-23 that are known to play a role in cisplatin-induced AKI were IL-10, IFN-γ, chemokine [C-C motif] ligand 2 (CCL2) and caspase-1. Another gene, caspase recruitment domain family, member 11 (CARD11), not previously known to play a role in AKI, was increased more than 20-fold and completely inhibited by JSH-23. CXCL1 and TNF-α, known mediators of cisplatin-induced AKI, were decreased by JSH-23. RIPK1 and 3, receptor-interacting serine/threonine-protein kinases, that play an important role in necroptosis, were decreased by JSH-23. In mouse proximal tubule cells in culture, JSH-23 resulted in an increase in apoptosis suggesting that the mechanism of protection against AKI by JSH-23 is not due to a direct effect on proximal tubules. In conclusion, NF-κB transcriptional inhibition in cisplatin-induced AKI ameliorates kidney function and ATN without a significant effect on apoptosis and is associated with a decrease pro-inflammatory mediators and CARD11.

C-reactive protein but not hepcidin, NGAL and transferrin determines the ESA resistance in hemodialysis patients.

BACKGROUND: Erythropoiesis-stimulating agents (ESA) are commonly used for the treatment of anemia in hemodialysis (HD) patients, however, 5-10% of these patients have resistance to ESA treatment. Hepcidin and neutrophil-gelatinase associated lipocalin (NGAL) are induced by inflammation and these proteins may take role in ESA resistance. Herein, we aimed to investigate the effects of serum hepcidin, NGAL, transferrin and C-reactive protein (CRP) levels on ESA resistance in HD patients. METHODS: A total of 63 chronic HD patients (6.0 ± 17 years, M/F:44/19) and 20 healthy controls (6.0 ± 4 years, M/F:14/6) were enrolled. ESA resistance index (ERI) was calculated as weekly ESA dose (IU)/body weight (kg)/hemoglobin level (g/dL). Patients on ESA treatment were divided into two groups depending on the median ERI value as low and high ERI groups. RESULTS: Serum ferritin, hepcidin and NGAL levels were significantly higher in HD patients compared with controls. Serum transferrin levels were lower in high ESA index group compared with patients without ESA treatment and healthy controls. ERI was significantly correlated with serum CRP levels (r = 0.55, p < 0.001). In HD patients, serum hepcidin levels were associated with ferritin (r = 0.55, p < 0.01) and creatinine (r = 0.27, p = 0.03). Dose of ESA was significantly associated with serum CRP (r = 0.34, p = 0.02), total protein (r = -0.34, p = 0.01), transferrin (r = -0.28, p = 0.04) and ferritin (r = 0.31, p = 0.02). In linear regression analysis to predict ERI, age, gender, serum CRP, hepcidin, NGAL, albumin, ferritin and BMI were included (Model R = 0.62, R(2) =0 .38, p = 0.02). Serum CRP was the only significant factor predicting ERI. CONCLUSION: CRP was the only predictor of ESA resistance index in HD patients. Hepcidin, NGAL and transferrin were not found to be markers of ESA resistance.

Clinical value of ambulatory blood pressure: Is it time to recommend for all patients with hypertension?

Hypertension is a very common disease, and office measurements of blood pressure are frequently inaccurate. Ambulatory Blood Pressure Monitoring (ABPM) offers a more accurate diagnosis, more detailed readings of average blood pressures, better blood pressure measurement during sleep, fewer false positives by detecting more white-coat hypertension, and fewer false negatives by detecting more masked hypertension. ABPM offers better management of clinical outcomes. For example, based on more accurate measurements of blood pressure variability, ABPM demonstrates that taking antihypertensive medication at night leads to better controlled nocturnal blood pressure, which translates into less end organ damage and fewer clinical complications of hypertension. For these reasons, albeit some shortcomings which were discussed, ABPM should be considered as a first-line tool for diagnosing and managing hypertension.