Objectives Not much is known about influenza‐associated neurological complications. We aimed to describe the case series of hospitalized patients who were confirmed with influenza A and presented with neurological symptoms in order to capture the broad spectrum of influenza clinical manifestation and suggest including influenza diagnostic in some neurological conditions. Materials and methods The inclusion criteria were age ≥ 18 and laboratory‐confirmed influenza presenting with neurological symptoms. Influenza‐associated neurological complication was described as a development of neurological symptom with no other origin. The outcomes were classified into 5 categories: 1. recovery with no significant disability; 2. minor disability (able to manage on their own); 3. moderate disability (requiring some help but able to walk without assistance); 4. severe disability (unable to walk without assistance and perform daily activities); 5. death. Results In total, 12 patients (five women and seven men) were enrolled, with age range 18–71 years old. Neurological complications of pandemic A(H 1 N 1 )2009pdm influenza developed in seven out of 69 (10.1%) hospitalized patients. The most common neurological complication was encephalopathy. Neurological complications developed in two out of 24 (8.3%) hospitalized patients during postpandemic (H 1 N 1 ) V period. One patient presented with encephalopathy, another with meningoencephalitis. During the 2018 influenza season, there was one patient who has developed influenza A neurological complications. Overall, two out of 104 (1.9%) influenza A patients developed influenza‐associated neurological complications in 2019. Conclusions Every patient with unexplained neurological symptoms and signs similar to aseptic and septic meningitis/encephalitis has to be tested for influenza virus during epidemics and pandemics.
Objective: Malignant hypertension (MH) is a form of hypertensive emergency defined by a severe increase in blood pressure (BP) with multiple organ injuries. One possible pathophysiology of MH is an acute activation of the renin-angiotensin system (RAS) driven by the intense stimulation of renin secretion in the juxtaglomerulosa cells. Considering this mechanism, aliskiren, a direct renin inhibitor (DRI), can be a treatment option for MH. However, there is little information on the efficacy and safety of DRI in controlling MH. We herein report four cases with MH that have been successfully controlled by DRI for a long term.Case description: All of the four cases (three male and one female; 34 to 57 years of age) developed advanced retinopathy (III or IV grade on Keith-Wagener classification) and severe hypertension (> 200/120 mmHg) at presentation, meeting the criteria for MH according to the 2020 ISH global hypertension practice guideline. Mean systolic/diastolic BP was 215 ± 5/148 ± 8 mmHg. All developed acute kidney injury, with the mean serum creatinine (sCr) of 4.47 ± 1.13 mg/dl on admission. The ranges of plasma renin activity (PRA) and plasma aldosterone concentration (PAC, as measured by RIA) were 11-33 ng/mL/hr and 371-1370 pg/mL, respectively. Followed by initial treatment with an intra-venous calcium channel blocker, these patients were prescribed aliskiren, starting at 150 mg/day once daily, after confirmation of the elevated PRA levels. In general, aliskiren was well tolerated and BP was successfully controlled in all of the four cases (at discharge, mean systolic/diastolic BP was 123/74 mmHg and mean sCr was 3.84 mg/dL). Patients continued to receive aliskiren (at a dose of 150 or 300 mg/day) after the discharge and mean systolic/diastolic BP and sCr were 131 ± 4/84 ± 3 mmHg and 2.02 ± 0.16 mg/dl at two years of follow-up, respectively. The ranges of PRA and PAC of four cases have fallen to 0.2-0.8 ng/mL/hr and 105-203 pg/ mL, respectively.Literature review: The voltage-dependent K(+) channel responsible for activating delayed K(+) current is composed of pore-forming KCNQ1 and regulatory KCNE1/3 subunits which loss of function predispose to sustained torsade de pointes. Animal models demonstrate that KCNQ1 and KCNE1 mRNAs are expressed in the zona glomerulosa of adrenal glands where potassium channels directly participate in the control of aldosterone production. Although KCNE3 is not expressed in mouse adrenals, its deletion is thought to cause activation of lymphocytes targeting adrenal glands, leading to hyperaldosteronism. Furthermore, administration of spironolactone to KCNE3 knockout mice ameliorates their QT
Objective: We aimed to investigate the association of BMI in late adolescence and BMI trajectories in adulthood with chronic kidney disease (CKD), end-stage kidney disease (ESKD) and acute kidney injury (AKI) later in life. Design and method: Two cohort analyses were performed, firstly evaluating the link between adolescent BMI and CKD, ESKD and AKI throughout life, secondly assessing the link between BMI change from adolescence to midlife, and the risk of CKD, ESKD and AKI thereafter. Data from the Swedish Conscription Register, the Northern Sweden Health and Disease Study, the Swedish National Patient Register and the Cause of Death Register were included. Patients were stratified into quintiles of BMI in adolescence and BMI change until midlife. Data were analysed using Cox proportional hazards model. Results: 1 324 831 subjects met the inclusion criteria for BMI evaluation in late adolescence. The mean age at conscription was 18.3±0.8 years and the average BMI was 21.6±2.6 kg/m2. 5593 subjects developed CKD, 2358 developed ESKD and 8029 developed AKI. In the adjusted analyses, an increased risk of developing CKD and ESKD was seen from the fourth BMI quintile (HR 1.25, 95% CI 1.15-1.36 for BMI 21.9-23.6 kg/m2; HR 2.13, 95% CI 1.97-2.31 for BMI >23.6 kg/m2, for CKD), whereas the risk of AKI was increased already from the third BMI quintile (HR 1.15, 95%CI 1.15-1.24 for BMI 20.7-21.9 kg/m2). 32 221 subjects in a regional cohort had an additional BMI evaluation at mean age 42.1±8.6 years. The mean change in BMI between assessments was 4.8±3.2 kg/m2. We found that BMI increase of >7 kg/m2 from late adolescence to mid-life was associated with higher risk of CKD (HR 2.78, 95%CI 1.45-5.30) and AKI (3.49, 2.23-5.47) in non-adjusted analyses; only AKI persisted after adjustment (HR 2.60, 95%CI 1.58-4.28). Conclusions: To conclude, BMI in late adolescence is associated with CKD and ESKD, with increased risk from BMI levels >21.9 kg/m2. BMI increase during adulthood was only associated with an increased risk of AKI after covariate-adjustment, suggesting that adolescence is a critical period for the association between BMI and future kidney disease.
Background and Aims Kidney transplant rejection is diagnosed by the kidney biopsy which is an invasive diagnostic method, however, non-invasive biomarkers, distinguishing normal kidney transplant from transplant rejection would be prefered but are lacking. CXC chemokine ligand 9 (CXCL9) and CXC chemokine ligand 10 (CXCL10) are gamma interferon inducible small cytokines. The aim of this study was to evaluate urinary CXCL9 and CXCL10 as potential biomarkers of allograft rejection. Method 117 kidney transplant recipients undergoing kidney transplant biopsy (surveillance or indication) were included into this study. Spot urine samples were collected before kidney biopsy for urinary creatinine, CXCL9 and CXCL10 measurement. The ratios of CXCL9 over urinary creatinine and CXCL10 over urinary creatinine were calculated. Kidney biopsies were analyzed according to Banff criteria by an experienced pathologist. Results 26 (22.2%) of kidney biopsies were defined as normal histology, 24 (20.5%) – antibody mediated rejection, 9 (7.7%) – T cell mediated rejection, 10 (8.6%) mixed rejection, 5 (4.3%) BK virus nephopathy and 43 (36.8%) were defined as other histological lesions. Average CXCL9/creatinine was 0.39 ng/mmol in normal histology group and 12.1 ng/mmol in allograft rejection groups (p<0.01). Average CXCL10/creatinine was 0.26 ng/mmol in normal histology and 4.55 ng/mmol in allograft rejection group (p<0.01). CXCL9/creatinine and CXCL10 moderately correlated to proteinuria at the time of kidney biopsy (accordingly r = 0.595, p<0.01 and r = 0.408, p<0.01). ROC curve for CXCL9/creatinine detecting antibody mediated rejection was 0.79, CI 0.67 to 0.90, p<0.01. ROC curve for CXCL10/creatinine detecting antibody mediated rejection was 0.79, CI 0.64 to 0.94, p<0.01. Conclusion Urinary biomarkers CXCL9/creatinine and CXCL10/creatinine has a potential to distinguish normal renal histology from allograft rejection and correlates to proteinuria at the time of the biopsy.
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