The University of Osaka · Medicine
Professor Jun-Ya Kaimori's research lab focuses on the molecular mechanisms underlying chronic kidney disease (CKD) progression, with particular emphasis on proteinuric kidney injury, renal fibrosis, and the role of signaling pathways such as STAT and TGF-β in tubular and interstitial pathology. The lab investigates the pathophysiological roles of novel mediators like glia maturation factor-beta (GMF-β) in tubular cell death and oxidative stress, and explores advanced imaging techniques such as diffusion tensor imaging (DTI) MRI for non-invasive assessment of renal fibrosis in diabetic nephropathy. Additionally, the lab examines the renoprotective and circadian-regulating effects of novel renin-angiotensin system inhibitors, such as azilsartan, in experimental models of CKD and salt-sensitive hypertension.
Figures are computed from collected data and may differ slightly.
Renal proximal tubular cells activated by reabsorption of protein are thought to play significant roles in the progression of kidney diseases. It was hypothesized that the signal transducer and activator of transcription (STAT) proteins may be activated by proteinuria in proximal tubular cells. To test this hypothesis, murine proximal tubular cells were treated with albumin (30 mg/ml medium) for various lengths of time. The results showed that albumin could activate Stat1 and Stat5 within 15 min
Proteinuria is an independent risk factor for progression of renal diseases. Glia maturation factor-beta (GMF-beta), a 17-kDa brain-specific protein originally purified as a neurotrophic factor from brain, was induced in renal proximal tubular (PT) cells by proteinuria. To examine the role of GMF-beta in PT cells, we constructed PT cell lines continuously expressing GMF-beta. The PT cells overexpressing GMF-beta acquired susceptibility to cell death upon stimulation with tumor necrosis factor-al
Autosomal recessive polycystic kidney disease (ARPKD) is an important childhood nephropathy, occurring 1 in 20,000 live births. The major clinical phenotypes are expressed in the kidney with dilatation of the collecting ducts, systemic hypertension, and progressive renal insufficiency, and in the liver with biliary dysgenesis, portal tract fibrosis, and portal hypertension. The systemic hypertension has been attributed to enhanced distal sodium reabsorption in the kidney, the structural defects
Renal fibrosis (RF) is an indicator for progression of chronic kidney disease (CKD). Although diabetic nephropathy (DN) is the leading cause of CKD and end-stage renal disease in Western populations, the ability of MRI to evaluate RF in DN patients has not been determined. As a first step to identify possible MRI methods for RF evaluation, we examined the use of diffusion tensor imaging (DTI) MRI to evaluate RF in a rat model of DN (SHR/NDmcr-cp(cp/cp): SHR/ND). The signal-to-noise ratio in DTI
A potent angiotensin II type-1 receptor blocker, azilsartan, has been reported to reduce blood pressure more effectively than candesartan. Interestingly, azilsartan can also restore the circadian rhythm of blood pressure. We hypothesized that azilsartan could also improve salt sensitivity; thus, we examined the effect of azilsartan on sodium handling in renal tubules. Subtotal nephrectomized C57BL/6 mice received azilsartan (1.0 mg/kg/day), candesartan (0.3 mg/kg/day), or vehicle via the oral ro
Among patients with advanced CKD, high anion gap was associated with an increased risk of cardiovascular events.
Effect of Whole Body Vibration on Walking Performance in Elderly Hemodialysis Patients NCT04774731.
The MAFB gene encodes an important basic leucine zipper transcription factor that functions in glomerular podocytes, macrophages, and osteoclasts. Recently, MAFB was identified as the gene that was responsible for causing nephropathy with focal segmental glomerulosclerosis (FSGS) with multicentric carpotarsal osteolysis (MCTO) or Duane retraction syndrome (DRS). Here, we describe a patient with nephropathy associated with FSGS who exhibited a novel stop-gain variant in the MAFB gene (NM_005461:c
The kidney consists of many functional modules called nephrons. Each nephron has a tubular structure made up of several structurally and functionally distinct segments. The analysis of individual segments requires the use of microdissection techniques. We describe protocols that have been used to successfully isolate messenger RNA from proximal tubules of both freshly prepared and archival samples using laser capture microdissection and laser-manipulated microdissection.
2010年10月に，バソプレシンV2受容体拮抗薬であるトルバプタン（サムスカⓇ）が，「ループ利尿剤等の他の利尿薬で効果不十分な心不全における体液貯留」に対し保険適用となって以降，わが国に利尿薬において新たな選択肢が一つ加わることになった．これと共に，今までのナトリウム利尿という考え方に，水利尿という新しい概念を付与することとなった．トルバプタンは，低ナトリウム血症をきたした心不全患者で利尿薬の選択に難渋していた場合に選択的に使われだした．その際，トルバプタンが効果のある患者に関して研究が行われ，効果の期待できる患者の見分け方が明らかにされてきた．また，腎臓内科領域では，特に今まで全く治療法の無かった常染色体優性多発性囊胞腎（ADPKD）に対する治療薬として，高容量のトルバプタンを使用する機会も増えてきた．本総説では，バソプレシンV2受容体拮抗薬（トルバプタン）の作用機序や使用の注意点を腎臓内科の立場から述べてみたい．
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