Publications by authors named "Satoshi Kumakura"

Patients with chronic kidney disease (CKD) commonly exhibit hypercoagulability. Increased levels of uremic toxins cause thrombogenicity by increasing tissue factor (TF) expression and activating the extrinsic coagulation cascade. TF is induced in monocytes and macrophages under pathological conditions, such as inflammatory diseases.

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Nicotinamide adenine dinucleotide (NAD) supplies energy for deoxidation and anti-inflammatory reactions fostering the production of adenosine triphosphate (ATP). The kidney is an essential regulator of body fluids through the excretion of numerous metabolites. Chronic kidney disease (CKD) leads to the accumulation of uremic toxins, which induces chronic inflammation.

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Background: Protease-activated receptor 2 (PAR2) is activated by serine proteases such as coagulation tissue factor/VIIa complex, factor Xa or trypsin and is pro-angiogenic in several disease models. Impaired angiogenesis in placenta causes placental dysfunction and fetal growth restriction. PAR2 is expressed in the placenta trophoblast.

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Protease-activated receptors (PARs) are coagulation protease targets, and they increase expression of inflammatory cytokines and chemokines in various diseases. Of all PARs, previous reports have shown that PAR1 or PAR2 inhibition is protective against diabetic glomerular injury. However, how PAR1 and PAR2 cooperatively contribute to diabetic kidney disease (DKD) pathogenesis and whether dual blockade of PARs is more effective in DKD remain elusive.

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Background: Studies among pregnant Asian women with chronic kidney disease (CKD) have not been widely performed; therefore, clinical criteria for these patients have not been well established.

Methods: We conducted a retrospective study among pregnant women with CKD who received prenatal care at our institution for 8 consecutive years. Primary outcome was the development of severe adverse events (SAEs).

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Nephrotic syndrome (NS) is a renal disease characterized by severe proteinuria and hypoproteinemia. Although several single-gene mutations have been associated with steroid-resistant NS, causative genes for steroid-sensitive NS (SSNS) have not been clarified. While seeking to identify causative genes associated with SSNS by whole-exome sequencing, we found compound heterozygous variants/mutations (c.

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Article Synopsis
  • * The study explores how inhibiting a protein called protease-activated receptor 2 (PAR2) affects kidney inflammation using a mouse model of SLE.
  • * Results show that blocking PAR2 actually worsens kidney inflammation, suggesting that activating PAR2 may have protective, anti-inflammatory effects and could be a new treatment strategy for SLE.
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Article Synopsis
  • A 66-year-old man with severe kidney dysfunction was admitted to the hospital due to numerous stubborn skin ulcers, initially suspected to be calciphylaxis due to systemic arterial calcification.
  • A skin biopsy revealed the actual diagnosis of cholesterol crystal embolization, prompting treatments like hemodialysis and steroids.
  • Unfortunately, the patient died from multiple intestinal perforations, with an autopsy confirming blockage of organ arterioles by cholesterol crystals, highlighting the critical link between skin ulcers and serious underlying conditions in chronic kidney disease patients.
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