Necmi Eren

Is Nebivolol Really Effective in Preventing Contrast Induced Nephropathy

Background/Aims: Contrast induced nephropathy (CIN) has multifactorial etiopatogenesis including oxidative stress and vasoconstriction. Nebivolol is an antioxidant and has vasodilatatory effect via NO release and may prevent CIN development. We have noticed that a few number of studies that have evaluated the effectiveness of nebivolol for the prevention of CIN used serum creatinine (sCr) levels for CIN detection. However, sCr is an insensitive marker for renal damage. Therefore in this study we used serum neutrophil-gelatinase associated lipocalin (NGAL), a more sensitive marker of renal damage, to evaluate preventive role of nebivolol in CIN. Methods: 159 patients undergoing coronary angiography (CAG) who had at least one risk factor for CIN were divided into nebivolol (+) and (-) groups. CIN was defined as a rise in sCr of 0.5mg/dl or a 25% increase from the baseline value. Serum Cr, glomerular filtration rate (eGFR) and NGAL levels were assessed before and 48 h after CAG. Mehran risk scores were calculated for both groups. Results: Both groups were similar in terms of baseline characteristics, Mehran risk scores, and current medications. Clinically, CIN developed at similar rates in both groups. Serum Cr, eGFR and NGAL values were similar in both groups before and after CAG. Serum Cr and NGAL levels increased and eGFR decreased significantly compared to the levels before CAG. Patients who developed CIN were significantly older (p=0.003), and were more likely to have DM (p=0.012), a higher mean contrast agent volume (p<0.001), and a higher Mehran score (p <0.001). We did not observe any favorable effect of Nebivolol in the prevention of CIN in patients undergoing CAG. Conclusion: According to the results of our study Nebivolol does not seem to prevent CIN in patients undergoing CAG. However, further randomised controlled trials with more sensitive renal damage markers are obviously needed to understand the actual effect of nebivolol on CIN especially through oxidative pathways and in high risk patients.

Dasatinib-induced immune mediated-thrombotic thrombocytopenic purpura

Most commonly seen side effects with Tyrosine kinase inhibitors (TKIs) are hematologic toxicities. Besides, with dasatinib autoimmune side effects can be seen. Thrombotic thrombocytopenic purpura (TTP) is a life- threatening disease that can be related to various causes mainly autoimmune disorders or antineoplastic drugs. Few cases of TKI associated secondary thrombotic microangiopathies (TMA) have been reported in literature. Most of cases were diagnosed as hemolytic uremic syndrome (HUS) rather than TTP. Herein, we describe a 37-year-old CML patient who was diagnosed as immune-mediated TTP related to dasatinib.

Neutrophil gelatinase-associated lipocalin is a better biomarker than cystatin C for the prediction of imminent acute kidney injury in critically ill patients

Aims The prevention of acute kidney injury can be lifesaving for the intensive care unit patients. However, conventional methods are not sufficient for the prediction of the risk of future acute kidney injury. In this study, the promising biomarker, neutrophil gelatinase-associated lipocalin, was compared with cystatin C as an indicator for the risk of future acute kidney injury. Methods One hundred and eighty-three adult patients without chronic kidney disease or renal replacement therapy were included in this study. The plasma and urine concentrations of neutrophil gelatinase-associated lipocalin and cystatin C were assessed on the second day after intensive care unit admission and were followed for seven days to monitor the development of acute kidney injury. Acute kidney injury diagnosis was based on the risk, injury, failure, loss, end-stage renal failure criteria. Results Thirty-four per cent of the patients had acute kidney injury; 17 patients who did not fulfil criteria at the beginning, developed acute kidney injury from days 3 to 7 after admission. The mean serum creatinine on admission did not significantly differ between this and control groups (0.72 ± 0.20 and 0.83 ± 0.21; P = 0.060); however, the serum and urinary neutrophil gelatinase-associated lipocalin concentrations on the second day were significantly different (median: 75.69 [54.18–91.18] and 123.68 [90.89–166.31], P = 0.001; and median: 17.60 [8.56–34.04] and 61.37 [24.59–96.63], P = 0.001). Notably, the 48-h serum cystatin C concentration did not differ. Conclusion Neutrophil gelatinase-associated lipocalin concentrations in the urine and serum on the second day of intensive care unit admission could be used to predict the development of acute kidney injury in the following three to seven days in the intensive care unit; however, the cystatin C concentration did not have predictive value.

The Efficacy of Cinacalcet in the Treatment of Hyperparathyroidism in Turkish Hemodialysis Patient Population

OBJECTIVE: Cinacalcet reduces parathyroid hormone levels by increasing the sensitivity of the parathyroid gland to calcium. In this study, we firstly aimed to evaluate the efficacy of cinacalcet in Turkish hemodialysis patients. MATERIAL and METHODS: 4483 hemodialysis patients were screened and 469 patients who had used cinacalcet were included in the study. The patients were divided into 4 groups according to drug usage durations (Group 1: 3 months, Group 2: 6 months, Group 3: 9 months and Group 4: 12 months). The patients’ Parathormone, Ca, P and CaxP levels at the 3rd, 6th, 9th and 12th months were compared to the start of treatment and previous months. RESULTS: The levels of Parathormone, Ca, P and CaxP significantly decreased compared to their initial levels in all groups (from 1412 pg/ml to 1222 pg/mL for Parathormone, p<0,001) in the 3rd month. However, this reduction was not continued in the subsequent months (Parathormone: 1381 pg/ ml for the 12th month).

The effects of serum leptin levels on thrombocyte aggregation in peritoneal dialysis patients.

Objective: Serum leptin levels of chronic kidney disease patients have been detected higher than normal population. The aim of this study was to investigate the effects of serum leptin levels on thrombocyte aggregation in peritoneal dialysis patients. Methods: Fourty three peritoneal dialysis patients were included in the study. Thrombocyte aggregation was calculated from the whole blood subsequently the effects of different concentrations of human recombinant leptin on thrombocyte aggregations were investigated. Four test cells were used for this process. While leptin was not added into the first test cell, increasing amounts of leptin was added into the second, third and fourth test cells to attain the concentrations of 25, 50 and 100 ng/ml respectively. Results: Thrombocyte aggregation was inhibited by recombinant leptin in peritoneal dialysis patients. Thrombocyte aggregation mean values were found statistically significantly higher in first test cell when compared to leptin groups in peritoneal dialysis patients. For leptin groups we could not find any statistically significant differences for thrombocyte aggregation mean values between any of the groups. Conclusion: Further studies with larger number of peritoneal dialysis patients are required to prove the action of leptin on thrombocyte aggregation.

O-23 PREGNANT WOMAN WITH RH(D) ALLOIMMUNIZATION TREATED BY DOUBLE FILTRATE PLASMAPHERESIS AND INTRAVENOUS IMMUNOGLOBULIN

function was deranged in 3 of the five patients with one patient having a complete renal shut down. All patients had some degree of coagulopathy as per laboratory parameters but none had clinical signs/symptoms of coagulopathy. In view of the coagulopathy fresh frozen plasma (FFP) was used as replacement fluid. The blood volume status of 3 patients was normal but 2 patients had some degree of volume overload as per central venous pressure and X-ray findings. In these patients we restricted the replacement plasma to 80% in consultation with a nephrologist. Maintaining plasma ionized Calcium (Ca++) was a challenge and after a few very low Ca++ reading we resorted to initial Ca++ estimation and a loading dose of Ca chloride followed by hourly estimations and repeat doses as required. Discussion/Conclusion: In view of our institute being a tertiary care referral institute, we have a number of critically ill patients coming for treatment. We have developed protocols in the Transfusion Medicine Department to ensure optimum support for these patients during therapeutic apheresis. The important issues in the protocol are as followsAll procedures are done in the Intensive Care Unit with continuous monitoring and support of critical care staff. Nephrology consultation regarding fluid replacement is done in all cases with renal dysfunction. We have a stringent Ca++ estimation protocol which includes initial estimation followed by hourly repeat estimation.