Objective Chronic kidney disease (CKD) is present in patients with nonalcoholic fatty liver disease (NAFLD). The aim of this retrospective study was to assess the cumulative development incidence and predictive factors for new onset of CKD in Japanese patients with NAFLD.
Methods A total of 5,561 NAFLD patients without CKD were enrolled. CKD was defined as either an estimated glomerular filtration rate of <60 mL/min/1.73 m² or dipstick proteinuria (≥+1). A blood sample and a urine sample were taken for routine analyses during follow-up. The mean observation period was 5.5 years. The primary goal is the new development of CKD. Independent factors associated with new development of CKD were analyzed by using the Kaplan-Meyer method and the Cox proportional hazards model.
Results Of 5.561 NAFLD patients, 263 patients developed CKD. The cumulative development rate of CKD was 3.1% at the 5th year and 12.2% at the 10th year. Multivariate Cox proportional hazards analysis showed that CKD development in patients with NAFLD occurred when patient had low level of GFR of 60-75 mL/min/1.73 m² [hazard ratio:2.75; 95% confidence interval (CI)=1.93-3.94; p<0.001], age of ≥50 years (hazard ratio: 2.67; 95% CI=2.06-3.46; p<0.001), diabetes (hazard ratio: 1.92; 95% CI=1.45-2.54; p<0.001), hypertension (hazard ratio: 1.69; 95% CI=1.25-2.29; p<0.001), and elevated serum gamma-glutamyltransferase of ≥109 IU/L (hazard ratio: 1.35; 95% CI=1.02-1.78; p=0.038).
Conclusion Our retrospective study indicates that the annual incidence of CKD in Japanese patients with NAFLD is about 1.2%. Five factors of low eGFR level, aging, type 2 diabetes, hypertension, and elevated gamma-glutamyltransferase, increases the risk of the development of CKD.

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Background The transforming growth factor β1 (TGFB1) +869T/C gene polymorphism has been suggested to be linked to susceptibility to essential hypertension (EH).
Objective and Methods To investigate the relationship between TGFB1 +869T/C gene polymorphism and EH, 5 separate studies with 2,708 subjects in the Chinese population on the relation between TGFB1 +869T/C gene polymorphism and EH were analyzed by meta-analysis. The random effect model was selected to calculate the pooled odds ratio (ORs) and its corresponding 95% confidence interval (95%).
Results There was a significant association between TGFB1 +869T/C gene polymorphism and EH. The pooled OR for CC/TC+TT genotype was 2.50 (95% CI: 1.46-4.28, P _{heterogeneity} <0.0001, p=0.0008). The pooled OR for the frequency of C allele was 1.43 (95% CI:1.18-1.73, P _{heterogeneity} =0.02, p=0.0002).
Conclusion The current meta-analysis suggested that C allele and CC genotype of TGFB1 +869T/C gene polymorphism might be related to the increased risk of EH in the Chinese population.

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Objective Patients with metabolic syndrome (MetS) are at a high risk for developing atherosclerosis and cardiovascular disease. Serum levels of chemerin have been found elevated in subjects with MetS and are associated with several cardiovascular factors. This study was undertaken to determine whether serum chemerin levels are associated with coronary artery disease (CAD) in patients with MetS.
Methods A total of 112 patients with MetS (66 patients with CAD and 46 without CAD) and 52 healthy subjects who underwent coronary angiography for the evaluation of CAD were enrolled in this study. Serum levels of chemerin were measured by enzyme-linked immunosorbent assay.
Results Serum chemerin levels were significantly elevated in MetS patients with CAD compared to in those without CAD and healthy subjects. MetS patients without CAD also had higher serum chemerin levels compared with healthy subjects. Multivariate logistic regression analysis revealed that serum chemerin levels were significantly associated with the presence of CAD in patients with MetS. Simple linear regression analysis showed that the serum levels of chemerin were positively correlated with body mass index (BMI), systolic blood pressure (SBP), serum triglycerides and C-reactive protein (CRP) in patients with MetS. Only BMI and CRP remained significantly associated with serum chemerin after multiple stepwise regression analysis.
Conclusion Elevated serum chemerin levels could be considered as an independent predictive marker of the presence of CAD in patients with MetS.

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Small-cell carcinoma (SCC) of the esophagus is rare, and its clinical characteristics remain poorly understood. A 54-year-old man was given a diagnosis of esophageal SCC and underwent esophagectomy. Four months after surgery, he was admitted to our hospital because of rapidly developing hyponatremia. Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH) due to extensive recurrence of SCC was diagnosed. Combined chemotherapy with irinotecan and cisplatin has dramatically reduced metastatic tumors, and it was concomitantly effective for SIADH. This case demonstrates that esophageal SCC could induce SIADH as a paraneoplastic syndrome and that the above combined chemotherapy was feasible and effective.

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Here we report a 79-year-old woman who presented with a 7-day history of headache, nausea, vomiting, and was found to have proptosis and ptosis. Laboratory findings showed hyponatremia, hypocortisolism, secondary hypothyroidism and low follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels. CT angiography (CTA) showed a vascular lesion in sella causing a mass affect on the pituitary gland which proved to be a carotid cavernous fistula (CCF) by conventional angiography. The lesion was subsequently treated with coil placement and patient's hyponatremia was successfully treated with corticosteroid and thyroid hormone replacement. Though rare, CCF should be considered in the differential diagnosis of sellar lesions. Also, in patients with CCF hyponatremia, hypotension or signs of hypothyroidism should warrant a work-up for pituitary function.

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A 58-year-old Japanese woman presented with recurrent abdominal pain, chronic urticaria, and petechiae on her extremities, and hypocomplementemia, findings that were consistent with hypocomplementemic urticarial vasculitis syndrome (HUVS). A laboratory examination revealed that she had markedly elevated IgG levels (4,448 mg/dL; normal range, 870-1,700 mg/dL) with particularly high IgG4 levels (1,050 mg/dL; normal range, 48-105 mg/dL) and a high IgG4/total IgG ratio (0.22; normal range, 0.02-0.05). A skin biopsy demonstrated leukocytoclastic vasculitis with IgG4 deposition in the vascular lumen and vascular walls. A lymph node biopsy revealed reactive lymphoid hyperplasia with numerous IgG4-positive cells in the perifollicular area, but no sclerotic findings. A chromosomal analysis of an enlarged lymph node, without phytohemagglutinin (PHA) stimulation, demonstrated that one in every three analyzed cells had abnormalities, such as 44, XX, -13, add(15)(p11), -17, -17, and mar.

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A 25-year-old woman complained of numbness of the extremities, following muscle rigidity and tenderness. The presence of anti-voltage-gated potassium channel antibody led to the diagnosis of Isaacs' syndrome. Twenty-seven months after the first symptom, she developed a pricking pain sensation in the lateral left foot, and then gradually developed a purple skin lesion resembling frostbite. The lesion completely disappeared 2 days later. An incidental episode occurred at the same site 8 months later. Frostbite-like skin lesions may be a rare autonomic manifestation in Isaacs' syndrome.

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A 23-year-old woman presented with trigeminal neuralgia four months after hematopoietic stem cell transplantation (HSCT) for acute myeloblastic leukemia. No leukemic cells were found in the cerebrospinal fluid. Initial brain magnetic resonance imaging (MRI) did not reveal any abnormality. After symptom exacerbation with diplopia, second MRI showed an irregular mass at the right petrous apex, with uniform enhancement and a clear margin which was interpreted as a meningioma. The pathology and immunohistochemistry finally confirmed the diagnosis of granulocytic sarcoma. This case suggests that granulocytic sarcoma should be remembered as a very rare and a malignant pathology in the differential diagnosis of neurologic complications following HSCT.

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A 64-year-old woman presented with fever and headache. Lumbar puncture revealed cerebrospinal fluid (CSF) that contained 67,386 /mm³ of WBC; CSF culture revealed Actinomyces species. She was diagnosed with purulent meningitis caused by actinomyces, and treated with intravenous ampicillin 12 g/day. The administration of ampicillin was effective, but not sufficient to control the inflammation in CSF. CSF inflammation persisted and a gradual increase in granulation tissue was found in the subdural space on lumbar MRI. After administration of rifampicin 450 mg/day, the CSF was normalized and the enhancement of granulation tissue decreased. The patient completely recovered 5 months after the therapy was initiated. We suggest that rifampicin may be an option for the treatment of meningitis caused by actinomyces.

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