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BackgroundProteinuria is an important predictor of cardiovascular disease and mortality. Several studies reported the association between skipping breakfast and the prevalence of proteinuria. Furthermore, skipping breakfast was associated with an increased risk of obesity. Although proteinuria is highly prevalent in obese individuals, the association between the prevalence of proteinuria and low body mass index (BMI) was reported in a previous cross-sectional study in asymptomatic individuals without known kidney diseases. The aim of this cross-sectional study was to assess the clinical impact of BMI on the association between skipping breakfast and the prevalence of proteinuria in normal renal function subjects.MethodsThe present study included 26,888 subjects (15,875 males and 11,013 females) with an estimated glomerular filtration rate ≥60 ml/min/1.73 m2 and no history of kidney disease who underwent a health checkup in Sumitomo Hospital. The association between skipping breakfast and the prevalence of proteinuria (defined as dipstick proteinuria of ≥1+) was assessed using logistic regression models adjusted for clinically relevant factors.ResultsSkipping breakfast was reported in 3,306 males (20.8%) and 1,514 females (13.8%). Multivariable adjusted logistic regression models showed that skipping breakfast was significantly associated with the prevalence of proteinuria above 1+. This association was evident in lower BMI subjects, even after adjusting for clinically relevant factors (adjusted odds ratios of males and females were 1.67 [1.17–2.38] and 1.92 [1.31–2.82], respectively), whereas this association was not evident in higher BMI subjects.ConclusionLower BMI subjects with proteinuria might need to be careful about skipping breakfast.

BackgroundAdipokine dysregulation is a key feature of insulin resistance and a metabolic syndrome associated with obesity. Low adiponectin levels are associated with higher risks of cardiovascular diseases (CVD). However, high adiponectin levels have also been associated with increased all-cause and cardiovascular mortality in the elderly. This adiponectin paradox has yet to be clarified, which has hindered our understanding of the biological role of adiponectin. Adipokine dysregulation and insulin resistance are also associated with energy-deprivation conditions, such as frailty in old age. The objective of this study was to investigate the association between plasma adiponectin and insulin resistance using the homeostasis model assessment for insulin resistance (HOMA-IR) classified by age. In particular, we sought to determine the factors of the subjects associated with both high adiponectin levels and HOMA-IR (H-adiponectin/H-HOMA) and high adiponectin levels and low HOMA-IR (H-adiponectin/L-HOMA).MethodsThe eligible subjects in this cross-sectional study were 33,216 individuals who had undergone health checkups at the Physical Checkup Center of Sumitomo Hospital between April 2008 and December 2018. After excluding 26,371 individuals who were under 60 years old, 529 who had been taking medications for diabetes mellitus, and 690 with missing data, the present study included 5,673 (3,467 males, 2,206 females) subjects with no missing data. The relationship between serum adiponectin levels and HOMA-IR was assessed using logistic regression models adjusted by clinically relevant factors.ResultsIn the multivariable logistic regression analysis, age and low BMI were shown to positively correlate with the characteristics of H-adiponectin/H-HOMA. In females, systolic blood pressure was also shown to be an associated factor.ConclusionIn conclusion, this study showed that aging or a low BMI may contribute to high adiponectin levels and insulin resistance.

As a MYH9 disorder, Fechtner syndrome is characterized by nephritis, giant platelets, granulocyte inclusion bodies (Döhle-like bodies), cataract, and sensorineural deafness. Observation of peripheral blood smear for the presence of thrombocytopenia, giant platelets, and granulocyte inclusion bodies (Döhle-like bodies) is highly important for the early diagnosis of MYH9 disorders. In our two cases, sequencing analysis of the MYH9 gene indicated mutations in exon 24. Both cases were diagnosed as the MYH9 disorders Fechtner syndrome before end-stage renal failure on the basis of the observation of peripheral blood smear.

Takotsubo cardiomyopathy is a disorder characterized by left ventricular apical ballooning and electrocardiographic changes in the absence of coronary artery disease. While reversible in many cases, the mechanism of this disorder remains unclear. The most frequent clinical symptoms of takotsubo cardiomyopathy on admission are chest pain and dyspnea, resembling acute myocardial infarction. Here, we describe two cases of takotsubo cardiomyopathy without chest pain or dyspnea in patients on maintenance hemodialysis. The asymptomatic nature of these two cases may be due to the patients being on hemodialysis. Periodic electrocardiograms (ECG) may be helpful in screening this population for asymptomatic takotsubo cardiomyopathy and in evaluating its incidence.

A 34-year-old Japanese woman was admitted to our hospital complaining of developing bilateral pedal edema. Imaging studies led to a diagnosis of Budd-Chiari syndrome combined with internal jugular vein thrombus. We investigated the cause of thrombosis and found that the anticoagulant activity of protein C was decreased. Genetic analysis showed the presence of a c.125C>A (Arg42Ser) substitution in the protein C gene (PROC) of the proband, which generates an Arg42Ser mutation that replaces the scissile bond Arg42-Ala43 normally cleaved by a furin-like processing protease. Her father and younger brother also carried this mutation, although they had no evidence of thrombosis.

A 42-year-old female who was an asymptomatic carrier of hepatitis B virus (HBV) was diagnosed with antineutrophil cytoplasm antibody- (ANCA-) associated vasculitis and was induced to remission with 30 mg/day prednisolone nine years ago. Four years ago, she suffered recurrence of ANCA-associated vasculitis and with 30 mg/day prednisolone was induced to remission. This time, laboratory data showed 3-fold increase in myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA) levels. Administration of 30 mg/day prednisolone was started. Three days later, she was admitted to our hospital suffering from fatigue. After admission, urinalysis showed glomerular hematuria. Despite administration of 30 mg/day prednisolone, MPO-ANCA titer had been of high level, ranging from 42 to 83 EU for 2.5 months. Furthermore, the adverse effects of steroid were seen. We decided the tapering of prednisolone (25 mg/day) and the start of mizoribine (4-carbamoyl-1-β-D-ribofuranosyl imidazolium-5-olate) administration. After mizoribine treatment, MPO-ANCA titer was decreased without any mizoribine-related adverse effects. Six months later, MPO-ANCA titer was decreased to normal levels and she was induced to clinical remission without reactivation of HBV. We describe the effectiveness of mizoribine for the ANCA-associated vasculitis complicated with HBV-carrier.