A case of primary aldosteronism with excessive secretion of renin that was unmasked by kidney transplantation.

A 42-year-old man showed marked hypokalemia after kidney transplantation. He was diagnosed with hypertension and suffered from acute myocardial infarction at 33 and 38 years of age. At 40 years of age, hemodialysis was introduced. A left adrenal tumor was noted and suspected as a non-functional adrenal adenoma at that time. Therefore, he received a living-donor kidney transplant at 42 years of age. After kidney transplantation, the serum creatinine level dropped. His blood pressure remained high, and the serum potassium level decreased. The PRA and PAC were elevated, and ARR was not elevated. Based on the results of various confirmatory tests and vein sampling, he was diagnosed with excessive secretion of renin from the native kidneys that was complicated by primary aldosteronism (PA), and left nephrectomy and adrenalectomy were performed. The overproduction of aldosterone in the resected adrenal adenoma and over secretion of renin in the kidney with arteriolosclerosis were immunohistologically confirmed. After surgery, the PAC decreased, but the PRA did not decrease. The postoperative serum potassium level improved, and the blood pressure was well controlled with a small dose of medication. This is the first reported case of PA with hyperreninemia after kidney transplantation. It should be noted that PA in dialysis patients and kidney transplant recipients may not fulfill the usual diagnostic criteria of an elevated ARR. In such patients, PA should be suspected based on the absolute value of the PAC and responsiveness to ACTH stimulation, and adrenal and renal vein sampling is required for a definitive diagnosis.

Verification of the effect of acquisition time for SwiftScan on quantitative bone single-photon emission computed tomography using an anthropomorphic phantom.

BACKGROUND: SwiftScan single-photon emission computed tomography (SPECT) is a recently released scanning technique with data acquired when the detector is stationary and when it moves from one view to the next. The influence of scan time for using SwiftScan on quantitative bone SPECT remains unclear. This study aimed to clarify the effect of the scan time for SwiftScan SPECT on the image quality and quantification of bone SPECT compared to step and shoot mode (SSM) using 99mTc-filled anthropomorphic phantom (SIM2 bone phantom). MATERIALS AND METHODS: Phantom SPECT/computed tomography (CT) images were acquired using Discovery NM/CT 860 (GE Healthcare) with a low-energy high-resolution sensitivity collimator. We used the fixed parameters (subsets 10 and iterations 5) for reconstruction. The coefficient of variation (CV), contrast-to-noise ratio (CNR), full width at half maximum (FWHM), and quantitative value of SwiftScan SPECT and SSM were compared at various acquisition times (5, 7, 17, and 32 min). RESULTS: In the short-time scan (< 7 min), the CV and CNR of SwiftScan SPECT were better than those of SSM, whereas in the longtime scan (> 17 min), the CV and CNR of SwiftScan SPECT were similar to those of SSM. The FWHMs for SwiftScan SPECT (13.6-14.8 mm) and SSM (13.5-14.4 mm) were similar. The mean absolute errors of quantitative values at 5, 7, 17, and 32 min were 38.8, 38.4, 48.8, and 48.1, respectively, for SwiftScan SPECT and 41.8, 40.8%, 47.2, and 49.8, respectively, for SSM. CONCLUSIONS: SwiftScan on quantitative bone SPECT provides improved image quality in the short-time scan with quantification similar to or better than SSM. Therefore, in clinical settings, using SwiftScan SPECT instead of the SSM scan protocol in the short-time scan might provide higher-quality diagnostic images than SSM. Our results could provide vital information on the use of SwiftScan SPECT.

MRI diffusion-weighted imaging detects a fresh portal vein thrombus as a high intensity lesion in a patient with a liver transplant: A case report.

Portal vein thrombosis is one of the most serious complications after liver transplantation. It is important to determine the age of the thrombus for management of portal vein thrombosis. We present a case report of histologically confirmed heterogenous fresh portal vein thrombus which was depicted heterogenous high signal intensity on magnetic resonance diffusion weighted imaging. The sequence may be a useful imaging tool for detecting fresh thrombus components in the portal vein thrombosis.

High Signal Intensity on Diffusion-Weighted Images Reflects Acute Phase of Deep Vein Thrombus.

The effects of antithrombotic therapy on deep vein thrombosis (DVT) can be affected by thrombus age, which cannot be reliably determined by noninvasive imaging modalities. We investigated whether magnetic resonance (MR) diffusion-weighted imaging (DWI) can localize and determine the age of venous thrombus in patients with DVT, animal models, and human blood in vitro. Signal intensity (SI) on DWI and the apparent diffusion coefficient (ADC) of thrombi were assessed in eight patients with DVT using a 1.5-T MR imaging (MRI) system. We assessed the organizing processes as venous thrombus developed in the rabbit jugular vein using a 3.0-T MRI system over time. We also assessed MRI signals of human blood in vitro using the 1.5-T MRI system. Venous thrombi were detected by DWI as areas of high or mixed high and iso SI in all patients. The ADCs were lower in the proximal, than in the distal portion of the thrombi. The thrombi of rabbit jugular veins histologically organized in a time-dependent manner, with high SI on DWI at 4 hours, mixed high and iso SI at 1 and 2 weeks, and iso SI at 3 weeks. The ADC correlated negatively with erythrocyte content, and positively with smooth muscle cells, macrophages, hemosiderin, and collagen content. MRI signals of human blood in vitro showed that ADCs were affected by erythrocyte content, but not by blood clotting. MR-DWI can detect venous thrombus, and high SI on DWI accompanied by a low ADC might reflect erythrocyte-rich, acute-phase thrombi.

Therapeutic response of immunoglobulin 4-related aortitis and pancreatitis demonstrated by diffusion-weighted MRI.

Immunoglobulin (IgG) 4-related disease is a systemic inflammatory disease, and it affects vascular system as aortitis, periaortitis, or aneurysm. However, due to a lack of serum biomarker on aortic damage and the multiorgan involvement, it is difficult to assess aortic inflammatory activity of IgG4-related disease. We described a case of IgG4-related pancreatitis and aortitis, which was visualized with magnetic resonance merged image of diffusion weighted and T1 weighted images. The aortic signal intensity or apparent diffusion coefficient value reduced or increased after oral prednisone administration, respectively. Magnetic resonance diffusion weighted image and apparent diffusion coefficient may be a useful imaging tool for assessment of vascular inflammation in IgG4-related aortitis.

Coronary high-signal-intensity plaques on T1-weighted magnetic resonance imaging reflect intraplaque hemorrhage.

Coronary high-signal-intensity plaques (HIPs) detected by T1-weighted magnetic resonance imaging are associated with future cardiovascular events. This study aimed to identify pathological findings reflecting HIPs in coronary arteries obtained from autopsy cases. Formalin-fixed hearts were imaged with noncontrast T1-weighted imaging with a 1.5-T magnetic resonance system. We defined HIPs or non-HIPs as a coronary plaque to myocardial signal intensity ratio (PMR) of ≥1.4 or <1.4, respectively. We found HIPs in 4 of 37 (10.8%) hearts and analyzed 7 hearts in detail. The corresponding sections to HIPs (n=11) or non-HIPs (n=25) were histologically and immunohistochemically analyzed. We calculated the T1 relaxation time of human venous blood in vitro. Plaque and necrotic core areas, and the frequency of intraplaque hemorrhage in HIPs were significantly larger/higher than those in non-HIPs. HIPs were immunopositive for CD68 (11/11), glycophorin A (10/11), and fibrin (11/11). Glycophorin-A-, matrix metalloprotease 9 (MMP9)-, and tissue factor-immunopositive areas were larger in HIPs than in non-HIPs. The PMR was positively correlated with glycophorin-A-, fibrin-, MMP9-, and tissue factor-immunopositive areas. Blood coagulation shortened the T1 relaxation time of the blood and plasma, and the T1 relaxation times in coagulated whole blood and erythrocyte-rich blood were significantly shorter than those in plasma. Coronary HIPs may reflect intraplaque hemorrhage and may be a novel marker for plaque instability and thrombogenic potential.

Multiple Liver Abscesses with a Skin Pustule due to Chromobacterium violaceum.

A 69-year-old woman was admitted to our hospital with the chief complaints of fever and fatigue. We initially treated the patient for a tick-borne disease after noticing a pustule on her leg; however, abdominal computed tomography (CT) showed multiple low-density areas in the liver and Chromobacterium violaceum was isolated from a blood culture. We diagnosed her with multiple liver abscesses secondary to Chromobacterium violaceum bacteremia. The patient was successfully treated with ciprofloxacin.

Impact of age-dependent adventitia inflammation on structural alteration of abdominal aorta in hyperlipidemic mice.

BACKGROUND: The adventitia is suggested to contribute to vascular remodeling; however, the site-selective inflammatory responses in association with the development of atherosclerosis remain to be elucidated. METHODS AND RESULTS: Wild-type or apolipoprotein E knockout male C57BL/6J background mice were fed standard chow for 16, 32, and 52 weeks, and the morphology of the aortic arch, descending aorta, and abdominal aorta was compared. Atheromatous plaque formation progressed with age, particularly in the aortic arch and abdominal aorta but not in the descending aorta. In addition, we found that the numbers of macrophages, T-lymphocytes, and microvessels, assessed by anti-F4/80, CD3, and CD31 antibodies, were higher in the adventitia of the abdominal aorta at 52 weeks. These numbers were positively correlated with plaque formation, but negatively correlated with elastin content, resulting in the enlargement of the total vessel area. In aortic tissues, interleukin-6 levels increased in the atheromatous plaque with age, whereas the level of regulated on activation, normal T cell expressed and secreted (RANTES) increased with age, and compared with other sites, it was particularly distributed in inflammatory cells in the adventitia of the abdominal aorta. CONCLUSION: This study suggests that adventitial inflammation contributes to the age-dependent structural alterations, and that the activation/inactivation of cytokines/chemokines is involved in the process.

Association between adiponectin production in coronary circulation and future cardiovascular events in patients with coronary artery disease.

Adiponectin has antiatherosclerotic properties and is also produced in the local coronary circulation. We previously reported that significantly less adiponectin was produced in the coronary circulation of patients with than without coronary artery disease (CAD). The goal of this study was to determine whether adiponectin production in the coronary circulation could predict future cardiovascular events in patients with CAD.Forty-eight CAD patients whose left anterior descending coronary arteries required percutaneous coronary intervention (PCI) were enrolled. The amount of adiponectin production in the coronary circulation was defined as the plasma adiponectin level at the great cardiac vein minus that at the orifice of the left coronary artery. All patients were divided by adiponectin production level in the coronary circulation into the adiponectin-positive production group (> 0 µg/ mL) and adiponectin-negative production group (≤ 0 µg/mL). Median follow-up period was 66 months (maximum, 108 months). The primary endpoint was the combined occurrence of major adverse cardiovascular events (MACE), including rehospitalization due to unstable angina, heart failure, nonfatal myocardial infarction, revascularization with PCI or coronary artery bypass grafting, ischemic stroke, and cardiovascular death.Sixteen MACE occurred. The incidence of MACE was significantly higher in the adiponectin-negative production group than in the adiponectin-positive production group (P = 0.02). In multivariate analysis, adiponectin-negative production was a predictor of MACE (P = 0.03). Kaplan-Meier analysis revealed that the MACE-free rate was significantly lower in the adiponectin-negative production group than in the adiponectin-positive production group.Adiponectin production in the coronary circulation with CAD may be associated with MACE.

Different distribution of pentraxin 3 and C-reactive protein in coronary atherosclerotic plaques.

AIM: To understand the differences between histopathological characteristics related to PTX3 (pentraxin 3) and CRP (C-reactive protein) in coronary atherosclerotic plaques. METHODS AND RESULTS: To assess the localization of PTX3 and CRP in coronary plaque, immunohistochemistry was performed using 157 coronary artery specimens from 45 autopsied cases. Overall, immunoreactivity to CRP was more intense than that to PTX3 in lipid rich plaque; however, PTX3 was notably abundant in areas of intraplaque hemorrhage, in which CRP was quite sparse. On quantitative analysis, complicated plaques showed more immunopositive area of PTX3 than fibroatheroma, but with CRP, this trend disappeared. In addition, we examined the phenotype of macrophages in PTX3- and CRP-rich areas using CD163 staining (M2 macrophages). Consequently, these areas were differently characterized by the accumulation of macrophages with high and low magnitude of CD163 positivity, respectively. Next, we immunohistochemically investigated relationships among PTX3, CRP, histological components and clinical presentation in 73 coronary atherectomy specimens obtained from 35 and 38 patients with unstable (UAP) and stable angina pectoris (SAP), respectively. Both PTX3 and CRP were more intense in culprit plaques from patients with UAP than with SAP, and they significantly correlated with CD68 (pan macrophage)-positive areas; however, there was no correlation between PTX3 and CRP. CONCLUSION: Although PTX3 and CRP were more enhanced in unstable than in stable coronary plaques, their distribution distinctly differed, suggesting that they play distinct biological roles in unstable plaques.

Inhibition of development of abdominal aortic aneurysm by glycolysis restriction.

OBJECTIVE: The mechanisms underlying abdominal aortic aneurysm development remain unknown. We hypothesized that acceleration of glucose metabolism with the upregulation of glucose transporters is associated with abdominal aortic aneurysm development. METHODS AND RESULTS: Enhanced accumulation of the modified glucose analogue 18 fluoro-deoxyglucose by positron emission tomography imaging in the human abdominal aortic aneurysm was associated with protein expressions of glucose transporters-1 and -3, assessed by Western blot. The magnitude of glucose transporter-3 expression was correlated with zymographic matrix metalloproteinase-9 activity. Intraperitoneal administration of glycolysis inhibitor with 2-deoxyglucose significantly attenuated the dilatation of abdominal aorta induced by periaortic application of CaCl(2) in C57BL/6J male mice or reduced the aneurysmal formation in angiotensin II-infused apolipoprotein E knockout male mice. In monocytic cell line induced by phorbol 12-myristate 13-acetate or ex vivo culture obtained from human aneurysmal tissues, 2-deoxyglucose abrogated the matrix metalloproteinase-9 activity and interleukin-6 expression in these cells/tissues. Moreover, 2-deoxyglucose attenuated the survival/proliferation of monocytes and the adherence of them to vascular endothelial cells. CONCLUSIONS: This study suggests that the enhanced glycolytic activity in aortic wall contributes to the pathogenesis of aneurysm development. In addition, pharmacological intervention in glycolytic activity might be a potential therapeutic target for the disorder.

Sarcoidosis manifesting as cardiac sarcoidosis and massive splenomegaly.

Sarcoidosis is a multisystemic granulomatous disease of unknown etiology. We report an unusual case of sarcoidosis in a woman presenting with cardiac sarcoidosis and massive splenomegaly with a familial history of cardiac sarcoidosis. Cardiac sarcoidosis was diagnosed based on electrocardiogram, echocardiogram, 18F-fluoro-2-deoxyglucose positron emission tomography (18F-FDG-PET) and skin histological findings. We performed splenectomy to rule out malignant lymphoma, and histological findings confirmed sarcoidosis. After splenectomy, we initiated prednisolone therapy. After 20 months of diagnosis, she was symptom free. Echocardiography and 18F-FDG-PET may be a key diagnostic tool and prednisolone therapy may be safe, effective, and feasible for cardiac sarcoidosis.

Associations of plasma pentraxin 3 and monocyte chemoattractant protein-1 concentrations with cardiovascular disease in patients with chronic kidney disease.

Both pentraxin 3 (PTX3) and monocyte chemoattractant protein-1 (MCP-1) are mediators of inflammation. They also appear to play critical roles in vascular endothelial dysfunction but their associations with cardiorenal syndrome remain largely unknown. The objective of this study was to examine their associations with cardiorenal syndrome. Circulating levels of PTX3, MCP-1, and some other biomarkers were evaluated in 134 patients with chronic kidney disease (CKD) and/or cardiovascular disease (CVD) and 55 age- and gender-matched subjects without CKD or CVD. Levels of PTX3, high-sensitivity C-reactive protein (hsCRP), and tumor necrosis factor α (TNFα) were significantly higher in CKD patients with CVD than in those without CVD. In advanced CKD patients (estimated glomerular filtration rate < 30 mL/min/1.73 m²), the values of area under the curve of PTX3, TNFα, and hsCRP for the detection of the association of CVD were 0.664, 0.507, and 0.318, respectively. In contrast, serum levels of MCP-1 were significantly higher in CKD patients than in control subjects independently of association with CVD. PTX3, hsCRP, and TNFα, but not MCP-1 could predict the presence of CVD as a complication associated with CKD. Additionally, PTX3 might be a more sensitive marker for the association of CVD than hsCRP and TNFα in patients with advanced CKD.