Effect of radio contrast media on residual renal function in peritoneal dialysis patients--a prospective study.
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BACKGROUND: Residual renal function is an independent predictor of survival in peritoneal dialysis patients. Systemic administration of radio contrast media (CM) may increase the risk of acute renal failure in patients with impaired renal function not on dialysis. There are few data on the influence of CM administration in dialysis patients. METHODS: We investigated residual renal function in 10 continuous ambulatory peritoneal dialysis (CAPD) patients who underwent elective diagnostic intravenous or intra-arterial administration of CM (study group). Iopromide (a iodinated, non-ionic hypo-osmolar CM) was used for all interventions. The median dose of CM given was 107.5 ml/patient. Residual renal function (calculated as the average of renal creatinine and renal urea clearance) was measured on the day before the intervention (baseline), on days 1-7, day 10 and day 30 after intervention. Eight CAPD patients without exposure to CM acted as the control group. RESULTS: There was no significant difference between the two groups in age, gender, diabetes, duration of dialysis and renal clearance at baseline. In the study group, we observed a temporary decline of residual renal clearance after administration of CM (P<0.05; Friedman test). On day 30, clearances were not significantly different from baseline. In the control group, there was no significant change of residual clearance during the observation period. Repeated measures ANOVA revealed no significant difference in the course of residual renal function between study and control groups. The decline of residual renal clearance between baseline and a routine visit after 4 months was comparable between groups. CONCLUSION: Administration of iopromide did not lead to a persistent decline of residual renal function in CAPD patients. Nevertheless, non-ionic hypo-osmolar CM should be given to these patients with the lowest possible dose and only if there is a real clinical indication. (+info)
Intracellular lipidation of newly synthesized apolipoprotein A-I in primary murine hepatocytes.
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Hepatocytes, which are the main site of apolipoprotein (apo)A-I and ATP-binding cassette transporter A1 (ABCA1) expression, are also the main source of circulating high density lipoprotein. Here we have characterized the intracellular lipidation of newly synthesized apoA-I, in primary hepatocytes cultured with [3H]choline to label choline-phospholipids, low density lipoprotein-[3H]cholesterol to label the cell surface, or [3H]mevalonate to label de novo synthesized cholesterol. Phospholipidation of apoA-I is significant and most evident in endoplasmic reticulum (ER) and medial Golgi, both in the lumen and on the membrane fractions of the ER and medial Golgi. In the presence of cycloheximide, endogenous apoA-I is substantially phospholipidated intracellularly but acquires some additional lipid after export out of the cell. In cells labeled with low density lipoprotein-[3H]cholesterol, intracellular cholesterol lipidation of apoA-I is entirely absent, but the secreted apoA-I rapidly accumulates cholesterol after secretion from the cell in the media. On the other hand, de novo synthesized cholesterol can lipidate apoA-I intracellularly. We also showed the interaction between apoA-I and ABCA1 in ER and Golgi fractions. In hepatocytes lacking ABCA1, lipidation by low density lipoprotein-cholesterol was significantly reduced at the plasma membrane, phospholipidation and lipidation by de novo synthesized sterols were both reduced in Golgi compartments, whereas ER lipidation remained mostly unchanged. Therefore, the early lipidation in ER is ABCA1 independent, but in contrast, the lipidation of apoA-I in Golgi and at the plasma membrane requires ABCA1. Thus, we demonstrated that apoA-I phospholipidation starts early in the ER and is partially dependent on ABCA1, with the bulk of lipidation by phospholipids and cholesterol occurring in the Golgi and at the plasma membrane, respectively. Finally, we showed that the previously reported association of newly synthesized apoA-I and apoB (Zheng, H., Kiss, R. S., Franklin, V., Wang, M. D., Haidar, B., and Marcel, Y. L. (2005) J. Biol. Chem. 280, 21612-21621) occurs after secretion at the cell surface. (+info)
Comparison of renal damage by iodinated contrast or gadolinium in an acute renal failure rat model based on serum creatinine levels and apoptosis degree.
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This study was undertaken to compare renal damage, as determined by serum creatinine and degree of apoptosis, caused by iodinated contrast or gadolinium in an acute renal failure (ARF) rat model. Rats were divided into three groups; controls (n=3), a CT contrast medium group (n=9), and an MR contrast medium group (n=9). The CT and MR groups were further subdivided into three groups, namely, low, standard, and high dose subgroups. Renal function was evaluated by determining serum creatinine levels; before ARF, and 48 hr after ARF and contrast administration. Apoptosis was assayed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). No significant creatinine level differences were observed between the CT and MR groups (p=0.116). Degrees of apoptosis in the renal cortex and medulla were more severe in the CT contrast medium group than in the control or MR contrast medium group (p<0.05). The study shows that CT contrast medium did not aggravate renal function more so than MR contrast medium in this ARF rat model. However, apoptosis examination in the renal cortex and medulla indicated that CT contrast medium induced more severe apoptosis than MR contrast medium (p<0.05). We conclude that CT contrast medium can be used for renal imaging studies when subjects are well hydrated and preventive medication is administered. (+info)
Comparison of the effect of non-ionic and ionic contrast agents on pancreatic histology in a canine model.
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CONTEXT: Pancreatitis is the most frequent complication of endoscopic retrograde cholangiopancreatography. Controversy exists whether low osmolarity non-ionic contrast agents lessen the rate of pancreatitis and pancreatic injury. To evaluate we used a canine model to compare pancreatography performed with ionic and non-ionic contrast. DESIGN: Dogs were anesthetized and underwent open transduodenal cannulation of the main pancreatic duct under fluoroscopic control until complete acinarization was achieved to maximize injury. Three dogs received diatrozate, an ionic contrast agent with osmolarity of 1,415 mosM and three dogs were injected with omnipaque a non-ionic agent with osmolarity of 672 mosM. MAIN OUTCOME MEASURES: Serial amylase and white cell counts were followed for 48 hours at which time dogs were sacrificed. Each pancreas was then examined for evidence of pancreatitis and cellular injury with both light and electron microscopy. RESULTS: All animals developed significant hyperamylasemia and elevated white blood cell counts, without significant difference in the mean peak amylase (10,721 U/L vs. 9,367 U/L, P=0.876) or white cell counts (25.8 k/mL vs. 24.1 k/mL, P=0.586) between the ionic and non-ionic contrast groups. Light microscopy showed no evidence of pancreatitis in either group of dogs. Electron microscopy showed cellular injury of the ductal cells in two dogs injected with non-ionic contrast. CONCLUSION: In a pancreatic canine model, low osmolarity, non-ionic contrast does not appear to lessen cellular injury. (+info)
A1 adenosine receptor knockout mice are protected against acute radiocontrast nephropathy in vivo.
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The role of renal A1 adenosine receptors (A1AR) in the pathogenesis of radiocontrast nephropathy is controversial. We aimed to further elucidate the role of A1AR in the pathogenesis of radiocontrast nephropathy and determine whether renal proximal tubule A1AR contribute to the radiocontrast nephropathy. To induce radiocontrast nephropathy, A1AR wild-type (WT) or knockout (KO) mice were injected with a nonionic radiocontrast (iohexol, 1.5-3 g iodine/kg). Some A1WT mice were pretreated with 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; a selective A1AR antagonist) before iohexol injection. A1AR contribute to the pathogenesis of radiocontrast nephropathy in vivo as the A1WT mice developed significantly worse acute renal failure, more renal cortex vacuolization, and had lower survival 24 h after iohexol treatment compared with the A1KO mice. DPCPX pretreatment also protected the A1WT mice against radiocontrast-induced acute renal failure. No differences in renal cortical apoptosis or inflammation were observed between A1WT and A1KO mice. To determine whether the proximal tubular A1AR mediate the direct renal cytotoxicity of radiocontrast, we treated proximal tubules in culture with iohexol with or without 2-chloro-N6-cyclopentyladenosine (a selective A1AR agonist) or DPCPX pretreatment. We also subjected cultured proximal tubule cells overexpressing A1AR or lacking A1AR to radiocontrast injury. Iohexol caused a direct dose-dependent reduction in proximal tubule cell viability as well as proliferation. Neither the A1AR agonist nor the antagonist treatment affected proximal tubule viability or proliferation. Moreover, overexpression or lack of A1AR failed to impact the iohexol toxicity on proximal tubule cells. Therefore, we conclude that radiocontrast causes acute renal failure via mechanisms dependent on A1AR; however, renal proximal tubule A1AR do not contribute to the direct tubular toxicity of radiocontrast. (+info)
First-pass quantitative CT perfusion identifies thresholds for salvageable penumbra in acute stroke patients treated with intra-arterial therapy.
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BACKGROUND AND PURPOSE: The purpose of this study was to determine whether, in acute stroke patients treated with intra-arterial (IA) recanalization therapy, CT perfusion (CTP) can distinguish ischemic brain tissue destined to infarct from that which will survive. METHODS: Dynamic CTP was obtained in 14 patients within 8 hours of stroke onset, before IA therapy. Initial quantitative cerebral blood volume (CBV) and flow (CBF) values were visually segmented and normalized in the "infarct core" (region 1: reduced CBV and CBF, infarction on follow-up), "penumbra that infarcts" (region 2: normal CBV, reduced CBF, infarction on follow-up), and "penumbra that recovers" (region 3: normal CBV, reduced CBF, normal on follow-up). Normalization was accomplished by dividing the ischemic region of interest value by that of a corresponding, contralateral, uninvolved region, which resulted in CBV and CBF "ratios." Separate CBV and CBF values were obtained in gray matter (GM) and white matter (WM). RESULTS: Mean CBF ratios for regions 1, 2, and 3 were 0.19 +/- 0.06, 0.34 +/- 0.06, and 0.46 +/- 0.09, respectively (all P < .001). Mean CBV ratios for regions 1, 2, and 3 were similarly distinct (all P < .05). Absolute CBV and CBF values for regions 2 and 3 were not significantly different. All regions with CBF ratio <0.32, CBV ratio <0.68, CBF <12.7 mL/100 g/min, or CBV <2.2 mL/100 g infarcted. No region with CBF ratio >0.44 infarcted. GM versus WM CBF and CBV values were significantly different for region 2 compared with region 3 (P < .05). CONCLUSIONS: In acute stroke patients, quantitative CTP can distinguish ischemic tissue likely to infarct from that likely to survive. (+info)
Vasospasm after subarachnoid hemorrhage: utility of perfusion CT and CT angiography on diagnosis and management.
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PURPOSE: To evaluate the utility of perfusion CT (PCT) combined with CT angiography (CTA) for the diagnosis and management of vasospasm, by using conventional digital subtraction angiography (DSA) as the gold standard. METHODS: We retrospectively identified 27 patients with acute subarachnoid hemorrhage who had undergone CTA/PCT, DSA, and transcranial Doppler (TCD) ultrasonography within a time interval of 12 hours of one another. The patients' charts were reviewed for treatment of vasospasm. CTA, PCT, TCD, and DSA examinations were independently reviewed and quantified for vasospasm. PCT thresholds, CTA findings, noncontrast CT (NCT) hypodensities, and TCD thresholds were evaluated for accuracy, sensitivity, and specificity, as well as for negative (NPV) and positive predictive values (PPV) in the prediction of angiographic vasospasm and endovascular treatment, considering DSA as the gold standard. RESULTS: Thirty-five CTA/PCT, TCD, and DSA examinations were performed on these 27 patients. A total of 123 arterial territories in 11 patients demonstrated angiographic vasospasm. Six patients underwent endovascular therapy. CTA qualitative assessment and PCT-derived mean transit time (MTT) with a threshold at 6.4 seconds represented the most accurate (93%) combination for the diagnosis of vasospasm, whereas MTT considered alone represented the most sensitive parameter (NPV, 98.7%). A cortical regional cerebral blood flow value +info)
Influence of partial volume on venous output and arterial input function.
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BACKGROUND: CT perfusion (CTP) is an important diagnostic tool for the imaging of cerebral hemodynamics. To obtain quantitative values of cerebral blood volume (CBV), blood flow (CBF), and mean transit time (MTT), measurement of the arterial input function (AIF) is required. To correct for partial volume effects (PVEs), it is common to normalize the AIF with respect to the venous output function (VOF). This correction assumes that measurement of the VOF is unhampered by PVEs. The purpose of this study was to evaluate the effect of PVE on the measurement of the AIF and VOF and, consequently, on the absolute perfusion parameters. METHODS: In 10 patients the mean area under the curve (AUC) of the AIF and VOF were quantified for 3-, 6-, and 12-mm-thick sections. Differences in the mean (1) AUC of the VOF, (2) AUC of the AIF, and (3) width of the AIF were compared for the 3 section thicknesses, and the influence on the absolute values of CBV, CBF, and MTT were studied. RESULTS: With thinner sections, the AUC of the VOF and the AIF increased significantly and the width of the AIF decreased slightly. Differences in AUC between the 3 section thicknesses were larger for the AIF than for the VOF. CONCLUSION: PVEs affect not only the AIF, but also the VOF. This results in an overestimation of CBV and CBF when a thicker section is used. To avoid PVE, VOF measurements should be performed at lower section thicknesses. (+info)