Large-Vessel Occlusion Stroke Treated by Endovascular Thrombectomy in Patient with Coronavirus Disease 2019.

We report a case of acute ischemic stroke caused by large-vessel occlusion in a patient infected with coronavirus disease 2019 (COVID-19) who was treated by endovascular thrombectomy. The patient was a 41-year-old man hospitalized with moderately severe COVID-19. Fourteen days after the onset of COVID-19, dysarthria and right hemiplegia were observed, and acute occlusion of the left middle cerebral artery was diagnosed. Mechanical thrombectomy was performed with a stent retriever while the patient was under local anesthesia and sedation. The staff involved in the intervention was as minimal as possible. The interventional surgeon wore a disposable surgical gown, an N95 mask, a face shield, and two pairs of gloves, while the patient was fitted with a surgical mask. The intervention involved the usual procedures, such as sheath insertion, catheter manipulation, and stent deployment, and the thrombus was removed with the stent retriever. The time from puncture to recanalization was within 30 minutes. No infection was observed in our staff or inpatients after the intervention. Thus, we were able to perform neuroendovascular treatment without spreading COVID-19 by taking appropriate measures to prevent infection.

Cerebral Salt-Wasting Syndrome Caused by Minor Head Injury.

A 34-year-old woman was admitted to hospital after sustaining a head injury in a motor vehicle accident (day 1). No signs of neurological deficit, skull fracture, brain contusion, or intracranial bleeding were evident. She was discharged without symptoms on day 4. However, headache and nausea worsened on day 8, at which time serum sodium level was noted to be 121 mEq/L. Treatment with sodium chloride was initiated, but serum sodium decreased to 116 mEq/L on day 9. Body weight decreased in proportion to the decrease in serum sodium. Cerebral salt-wasting syndrome was diagnosed. This case represents the first illustration of severe hyponatremia related to cerebral salt-wasting syndrome caused by a minor head injury.

Delayed rupture of a basilar artery aneurysm treated with coils: case report and review of the literature.

Delayed rupture of a previously unruptured cerebral aneurysm after uneventful saccular coil packing is rare, particularly when the quality of aneurysm occlusion is appropriate (neck remnant or total occlusion). The present report describes the case of a 70-year-old woman with an incidentally detected, asymptomatic, small basilar tip non-thrombosed aneurysm who experienced rupture of the aneurysm 2 years after coiling. Cerebral angiography taken on the day of rupture revealed only small recanalization of the aneurysm neck with no dome-filling. This is the first report of delayed rupture due to minor recurrence of a previously unruptured small asymptomatic cerebral aneurysm after saccular coil packing. A literature review of 26 reports of late bleeding after coil embolization of previously unruptured cerebral aneurysms showed that dome-filling after coil embolization, symptomatic aneurysms and large/giant aneurysms all increase the risk of delayed rupture in previously unruptured aneurysms after saccular coil packing.

Virtual histology analysis of carotid atherosclerotic plaque: plaque composition at the minimum lumen site and of the entire carotid plaque.

BACKGROUND: Virtual Histology intravascular ultrasound (VH IVUS) volumetric analysis (analysis of the entire plaque responsible for stenosis) has been used for carotid plaque diagnosis. Knowing the carotid plaque characteristics by analyzing the plaque composition only at the minimum lumen site will facilitate plaque diagnosis using VH IVUS. PURPOSE: To detect the relationship between the VH IVUS volumetric analysis of the entire plaque responsible for carotid artery stenosis and the VH IVUS cross-section plaque analysis at the minimum lumen site. METHODS: Forty-eight atherosclerotic cervical carotid stenoses in 45 consecutive patients were included in the study. VH IVUS was obtained during the carotid artery stenting procedure. RESULTS: Simple regression analysis revealed that the volumetric proportion of each plaque type correlated significantly with the corresponding plaque-type area at the minimum lumen site. The adjusted coefficients of determination of the simple regression analyses were .782 (P < .001) for fibrous tissue, .741 (P < .001) for fibrofatty tissue, .864 (P < .001) for dense calcium, and .918 (P < .001) for necrotic core. CONCLUSION: The plaque composition at the minimum lumen site represents the volumetric composition of the entire carotid plaque that causes atherosclerotic cervical carotid artery stenosis.

[A case of theophylline induced hypercalcemia].

We report a case of theophylline-induced hypercalcemia. The patient, a 51 year old women, had been administered theophylline for about five years because of bronchial asthma. She was referred to us in March 2003 for the treatment of renal failure and hypercalcemia(15.2 mg/dL), which had been increasing since 2001. Clinical and laboratory findings were not consistent with any endocrinopathy. We suspected drug induced hypercalcemia. Three months after discontinuation of theophylline therapy, the hypercalcemia was completely cured. When admitted to our hospital, the patient was diagnosed as also having Hashimoto's disease. Hyperthyroidism might enhance the effect of theophylline on parathyroid hormone action. Therefore, theophylline induced hypercalcemia even though she was taking the therapeutic level. Moreover, her calcium excretion did not increase despite hypercalcemia. We concluded that her hypercalcemia was induced by theophylline and hyperthyroidism, and that hypocalciuria might have enhanced these conditions.

The role of angiotensin AT1 receptor-associated protein in renin-angiotensin system regulation and function.

We cloned a novel molecule, AT1 receptor-associated protein (ATRAP), which is expressed in many tissues but specifically interacts with the AT1 receptor carboxyl-terminal. In the kidney, ATRAP was broadly distributed along the renal tubules; salt intake modulated its expression. In cardiovascular cells, angiotensin II (Ang II) stimulation made ATRAP co-localized with AT1 receptor in cytoplasm; ATRAP overexpression decreased cell surface AT1 receptor. In downstream signaling pathways, ATRAP suppressed Ang II-induced phosphorylation of mitogen-activated protein kinase, activation of c-fos gene transcription, and enhancement of amino acid or bromodeoxyuridine incorporation in cardiovascular cells. Thus, cardiovascular ATRAP may promote AT1 receptor internalization and attenuate Ang II-mediated cardiovascular remodeling. We would expect ATRAP to become a new therapeutic target molecule to treat and prevent cardiovascular remodeling in hypertension.

Expression of MAK-V/Hunk in renal distal tubules and its possible involvement in proliferative suppression.

MAK-V/Hunk is an SNF1-related serine/threonine kinase which was previously shown to be highly expressed in the mammary gland and central nervous system. In this study, we found MAK-V/Hunk is abundantly and specifically expressed in the thick ascending limbs and distal convoluted tubules (DCT) of the kidney from the embryonic stage to the adult stage. We demonstrated that dietary salt depletion significantly enhances renal MAK-V/Hunk mRNA levels compared with a normal-salt diet. To analyze the possible renal cellular function of this kinase, we employed mouse distal convoluted tubule (mDCT) cells. The results of reverse transcriptase-polymerase chain reaction and Western blot analysis revealed that MAK-V/Hunk is expressed endogenously in mDCT cells. Overexpression of MAK-V/Hunk by adenoviral gene transfer significantly inhibited the ANG II-induced stimulation of c-fos gene transcription and suppressed the ANG II-mediated increases in transforming growth factor-beta production into the medium. This phenomenon was accompanied by inhibition of ANG II-induced activation of BrdU incorporation. On the other hand, the MAK-V/Hunk knockdown by siRNA activated the ANG II-induced c-fos gene expression. In the consecutive sections stained for MAK-V/Hunk and AT(1) receptor, MAK-V/Hunk-immunopositive distal tubules expressed the AT(1) receptor. This is the first report on the intrarenal localization of MAK-V/Hunk and its cellular function in renal tubular cells.

A possible relationship of nocturnal blood pressure variability with coronary artery disease in diabetic nephropathy.

Evidence suggests a relationship between short-term blood pressure (BP) variability and cardiovascular target-organ damage. Although a blunted nocturnal decrease in BP and reduced heart rate variability have been shown to be associated with cardiovascular morbidity in diabetic patients, little information is available on short-term BP variability. In this study, short-term BP variability was assessed in 36 subjects with type 2 diabetes and overt nephropathy who underwent ambulatory BP monitoring, and the factors that correlated with short-term BP variability were examined. The incidence of coronary artery disease (CAD) was significantly greater in the patients with increased 24-h systolic BP variability (67% versus 11%; p < 0.0005), while that of cerebrovascular disease was not significantly affected (61% versus 50%). Multiple stepwise regression analysis revealed that serum cholesterol (cholesterol) and plasma norepinephrine (p-NE) were significant and independent contributors to nighttime systolic BP variability (partial R2 = 0.490, p < 0.001; partial R2 = 0.470, p < 0.001) and demonstrated that body mass index and p-NE were primary determinants of nighttime diastolic BP variability (partial R2 = 0.539, p < 0.0005; partial R2 = 0.304, p < 0.05). Diabetic nephropathy patients with CAD had significantly increased daytime systolic (17.8 mmHg versus 13.1 mmHg, p < 0.0005), nighttime systolic (17.4 mmHg versus 10.5 mmHg, p < 0.0001), and nighttime diastolic (10.4 mmHg versus 7.2 mmHg, p < 0.05) BP variability. Furthermore, logistic regression analysis demonstrated that nighttime systolic BP variability was an independent risk factor for CAD (odds ratio 3.13 [95% CI 1.02-9.61]; p < 0.05). The increase in nighttime BP variability is associated with a proportional sympathetic activation in diabetic nephropathy. Elevated short-term BP variability combined with relative sympathetic prevalence during the night might represent an important risk factor for cardiovascular events in the diabetic population.

Analysis of factors that affect short-term blood pressure variability in patients with chronic renal failure.

Recent reports suggest the relationship of short-term blood pressure (BP) variability to cardiovascular target organ damage. In this study, short-term BP variability was assessed as the standard deviation of daytime and nighttime BP in 36 hospitalized patients with chronic renal failure (CRF) who underwent ambulatory BP monitoring. Positive correlations were observed between body mass index (BMI) and daytime systolic and diastolic BP variability, BMI and nighttime diastolic BP variability, cholesterol and daytime systolic BP variability, cholesterol and nighttime systolic and diastolic BP variability, nocturnal decline in BP and nighttime diastolic BP variability, and plasma concentration of norepinephrine (p-NE) and nighttime systolic BP variability. In multivariate linear regression analyses, BMI showed the strongest association with daytime and nighttime diastolic BP variability (p < .005 and p < .05). On the other hand, cholesterol and p-NE were the primary determinants of daytime and nighttime systolic BP variability, respectively (p < .01 and p < .0005). Interestingly, CRF patients with ischemic heart disease (IHD) had significantly increased daytime systolic and diastolic BP variability and nighttime systolic BP variability (p < .05 or less). Furthermore, logistic regression analysis demonstrated that nighttime systolic BP variability was an independent risk factor of IHD in patients with CRF (odds ratio 1.50 [95% confidence interval 1.01 to 2.25]; p < .05). Taken together, short-term BP variability is suggested to be affected by BMI, cholesterol, and p-NE in CRF patients. Furthermore, sympathetic nerve overactivity may be involved in cardiovascular complications in CRF patients through the increase in nighttime systolic BP variability.

The novel angiotensin II type 1 receptor (AT1R)-associated protein ATRAP downregulates AT1R and ameliorates cardiomyocyte hypertrophy.

Activation of angiotensin II (Ang II) type 1 receptor (AT1R) signaling is reported to play an important role in cardiac hypertrophy. We previously cloned a novel molecule interacting with the AT1R, which we named ATRAP (for Ang II type 1 receptor-associated protein). Here, we report that overexpression of ATRAP significantly decreases the number of AT1R on the surface of cardiomyocytes, and also decreases the degree of p38 mitogen-activated protein kinase phosphorylation, the activity of the c-fos promoter and protein synthesis upon Ang II treatment. These results indicate that ATRAP significantly promotes downregulation of the AT1R and further attenuates certain Ang II-mediated hypertrophic responses in cardiomyocytes.

Nuclear receptor LXRalpha is involved in cAMP-mediated human renin gene expression.

The cAMP-signaling pathway plays a crucial role in the regulation of the renin gene, but the mechanism involved remains poorly understood. We have focused our studies of renin gene regulation on the unique cAMP responsive element (huREN/CNRE, -135 to -107) in the human renin promoter. We have cloned a protein that binds to this unique CNRE and demonstrated that this protein is liver X receptor-alpha (LXRalpha), a transcriptional factor of the nuclear receptor family. Transient expression of LXRalpha in human renin-producing Calu-6 cells increased cAMP inducibility of human renin promoter. Similarly, LXRalpha-stably transfected Calu-6 cells exhibited increased cAMP inducibility of renin promoter as well as the endogenous renin gene. Site-directed mutation of huREN/CNRE, which disrupted LXRalpha binding, decreased cAMP-induced transcriptional activity of human renin promoter. Furthermore, we demonstrated that the binding of LXRalpha derived from human juxtaglomerular cells, the main production site of renin in the kidney, to the huREN/CNRE in vivo. These results suggest that LXRalpha plays an important role in the cAMP-mediated regulation of human renin gene transcription by binding to CNRE.

Acute renal failure due to cholesterol crystal embolism treated with LDL apheresis followed by corticosteroid and candesartan.

Cholesterol crystal embolism (CCE) is caused by the shedding of cholesterol crystals into the bloodstream, and it has been recently recognized as a serious complication after vascular procedures. Our case of CCE, which was diagnosed by skin and renal biopsies, occurred in a patient with hypertension and diabetes mellitus, 3 months after coronary angiography, with the development of renal failure and blue toes. After low-density lipoprotein apheresis (LDL-A), the skin lesions, including livedo reticularis and pain from the acrocyanotic toes, dramatically improved, with partial recovery of renal function. Following the administration of low-dose corticosteroid and candesartan--an angiotensin II type 1 receptor antagonist (ARB)--the eosinophilia disappeared and renal function improved gradually with a decrease in urinary protein excretion. Therefore, a combination therapy of LDL-A, low-dose corticosteroid, and an ARB is a possible treatment for CCE, although the possibility of spontaneous recovery of renal function cannot be eliminated for this patient.