記述言語：英語   掲載種別：研究論文（学術雑誌）  

Adult kidney stem cells are known to have important roles in renal regeneration after acute kidney injury. Although trophic factors from tissue stem cells have been reported to promote the regeneration of other organs, there is limited number of evidence of this phenomenon in the kidneys. Here, we explored the effects of secreted factors from kidney stem cells. We intraperitoneally administered culture supernatant obtained from adult rat kidney stem/progenitor cells into rat kidney ischemia/reperfusion injury models, and the treatment significantly ameliorated renal tubulointerstitial injury, suppressed tubular cell apoptosis, diminished inflammation and promoted the proliferation of both residual renal cells and immature cells. In vitro, treatment with culture supernatant from kidney stem cells significantly promoted cell proliferation and suppressed cisplatin-induced cell apoptosis in both normal rat kidney cells and kidney stem cells. In addition, treatment with culture supernatant increased the expression of nestin in normal rat kidney cells, suggesting the dedifferentiation of tubular cells into stem-like cells. Analysis of the culture supernatant revealed that it contained a variety of growth factors. Taken together, the results suggest that these factors together lead to renal regeneration. In conclusion, adult kidney stem cells contribute to renal regeneration indirectly through the secretion of regenerative factors.

DOI： 10.1016/j.scr.2020.101865

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Podocyte injury is an independent risk factor for the progression of renal diseases. Semaphorin3A (SEMA3A), expressed in podocytes and tubular cells in the mammalian adult kidneys, has been reported to regulate diverse biological functions and be associated with renal diseases. Here, we investigated pathological roles of SEMA3A signaling on podocyte injury using a doxorubicin (Dox)-induced mouse model and examined the therapeutic effect of SEMA3A-inhibitor (SEMA3A-I). We demonstrated that Dox caused massive albuminuria and podocyte apoptosis as well as an increase of SEMA3A expression in podocytes, all of which were ameliorated with SEMA3A-I treatment. In addition, c-Jun N-terminal kinase (JNK), known as a downstream of SEMA3A signaling, was activated in Dox-injected mouse podocytes while SEMA3A-I treatment partially blocked the activation. In vitro, SEMA3A-I protected against Dox-induced podocyte apoptosis and recombinant SEMA3A caused podocyte apoptosis with activation of JNK signaling. JNK inhibitor, SP600125, attenuated SEMA3A-induced podocyte apoptosis, indicating that the JNK pathway would be involved in SEMA3A-induced podocyte apoptosis. Furthermore, the analysis of human data revealed a positive correlation between levels of urinary SEMA3A and protein, suggesting that SEMA3A is associated with podocyte injury. In conclusion, SEMA3A has essential roles in podocyte injury and it would be the therapeutic target for protecting from podocyte injury.

DOI： 10.3390/ijms21114099

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Obesity is supposed to cause renal injury via autophagy deficiency. Recently, sodium glucose co-transporter 2 inhibitors (SGLT2i) were reported to protect renal injury. However, the mechanisms of SGLT2i for renal protection are unclear. Here, we investigated the effect of SGLT2i for autophagy in renal proximal tubular cells (PTCs) on obesity mice. We fed C57BL/6J mice with a normal diet (ND) or high-fat and -sugar diet (HFSD) for nine weeks, then administered SGLT2i, empagliflozin, or control compound for one week. Each group contained N = 5. The urinary N-acetyl-beta-d-glucosaminidase level in the HFSD group significantly increased compared to ND group. The tubular damage was suppressed in the SGLT2i-HFSD group. In electron microscopic analysis, multi lamellar bodies that increased in autophagy deficiency were increased in PTCs in the HFSD group but significantly suppressed in the SGLT2i group. The autophagosomes of damaged mitochondria in PTCs in the HFSD group frequently appeared in the SGLT2i group. p62 accumulations in PTCs were significantly increased in HFSD group but significantly suppressed by SGLT2i. In addition, the mammalian target of rapamycin was activated in the HFSD group but significantly suppressed in SGLT2i group. These data suggest that SGLT2i has renal protective effects against obesity via improving autophagy flux impairment in PTCs on a HFSD.

DOI： 10.3390/ijms21114054

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: The advent of immune checkpoint inhibitors (ICIs) has significantly improved the prognosis of patients with advanced malignancies. On the other hand, these drugs might cause immune-related adverse events (irAEs) including endocrinopathies and nephropathies. Thyroid dysfunction is one of the most common irAEs. For ICIs-induced nephropathies, most cases are due to tubulointerstitial nephritis, which might require steroid treatment. Here, we report a patient with non-small cell lung cancer treated with ICI who developed increased serum creatinine (s-Cr) levels due to ICIs-induced hypothyroidism. CASE PRESENTATION: A 57-year-old Asian man with refractory non-small cell lung cancer under ICIs therapy (pembrolizumab, an anti-programmed cell death-1 monoclonal antibody) developed increased s-Cr levels 5 months after the pembrolizumab initiation. His laboratory data, renal biopsy, and Gallium-67 scintigraphy findings denied pembrolizumab-induced tubulointerstitial nephritis. His renal function was correlated with thyroid function. Despite the increase of s-Cr levels, serum cystatin C levels were normal, which could be explained by the hypothyroidism. Levothyroxine treatment improved renal function as well as thyroid function. Then pembrolizumab was resumed, and both his thyroid and renal function remained normal level. Ultimately, we concluded that the increased s-Cr levels were caused by pembrolizumab-induced hypothyroidism. CONCLUSION: All clinicians involved in ICI treatment need to recognize the possible increase in s-Cr levels caused by ICIs-induced hypothyroidism, and we propose monitoring serum cystatin C levels to differentiate ICIs-induced hypothyroidism from tubulointerstitial nephritis before invasive renal biopsies or steroid treatment, which are recommended by the prescribing information for pembrolizumab, are performed.

DOI： 10.1186/s12882-020-01775-z

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Mesenchymal stem cells (MSCs) have immunomodulatory and regenerative effects in many organs, including the kidney. Emerging evidence has shown that the trophic effects from MSCs are mainly mediated by the paracrine mechanism rather than the direct differentiation of MSCs into injured tissues. These secretomes from MSCs include cytokines, growth factors, chemokines and extracellular vesicles (EVs) containing microRNAs, mRNAs, and proteins. Many research studies have revealed that secretomes from MSCs have potential to ameliorate renal injury in renal disease models, including acute kidney injury and chronic kidney disease through a variety of mechanisms. These trophic mechanisms include immunomodulatory and regenerative effects. In addition, accumulating evidence has uncovered the specific factors and therapeutic mechanisms in MSC-derived EVs. In this article, we summarize the recent advances of immunomodulatory and regenerative effects of EVs from MSCs, especially focusing on the microRNAs.

DOI： 10.3390/ijms21030756

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Necroptosis is a newly discovered cell death pathway that plays a critical role in AKI. The involvement of integrin-linked kinase (ILK) in necroptosis has not been studied. METHODS: We performed experiments in mice with an Ilk deletion in collecting duct (CD) principal cells (PCs), and cultured tubular epithelial cells treated with an ILK inhibitor or ILK siRNA knockdown. RESULTS: Ilk deletion in CD PCs resulted in acute tubular injury and early mortality in mice. Progressive interstitial fibrosis and inflammation associated with the activation of the canonical TGF-β signaling cascade were detected in the kidneys of the mice lacking ILK in the CD PCs. In contrast to the minimal apoptosis detected in the animals' injured CDs, widespread necroptosis was present in ILK-deficient PCs, characterized by cell swelling, deformed mitochondria, and rupture of plasma membrane. In addition, ILK deficiency resulted in increased expression and activation of necroptotic proteins MLKL and RIPK3, and membrane translocation of MLKL in CD PCs. ILK inhibition and siRNA knockdown reduced cell survival in cultured tubular cells, concomitant with increased membrane accumulation of MLKL and/or phospho-MLKL. Administration of a necroptosis inhibitor, necrostatin-1, blocked cell death in vitro and significantly attenuated inflammation, interstitial fibrosis, and renal failure in ILK-deficient mice. CONCLUSIONS: The study demonstrates the critical involvement of ILK in necroptosis through modulation of the RIPK3 and MLKL pathway and highlights the contribution of CD PC injury to the development of inflammation and interstitial fibrosis of the kidney.

DOI： 10.1681/ASN.2018111162

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Cardiovascular disease constitutes the leading cause of mortality in patients with chronic kidney disease (CKD) and end-stage renal disease. Despite increasing recognition of a close interplay between kidney dysfunction and cardiovascular disease, termed cardiorenal syndrome (CRS), the underlying mechanisms of CRS remain poorly understood. Here we report the development of pathological cardiac hypertrophy and fibrosis in early stage non-uremic CKD. Moderate kidney failure was induced three weeks after unilateral urinary obstruction (UUO) in mice. We observed pathological cardiac hypertrophy and increased fibrosis in UUO-induced CKD (UUO/CKD) animals. Further analysis indicated that this cardiac fibrosis was associated with increased expression of transforming growth factor β (TGF-β) along with significant upregulation of Smad 2/3 signaling in the heart. Moreover early treatment of UUO/CKD animals with an angiotensin-converting-enzyme inhibitor (ACE I), Enalapril, significantly attenuated cardiac fibrosis. Enalapril antagonized activation of the TGF-β signaling pathway in the UUO/CKD heart. In summary our study demonstrates the presence of pathological cardiac hypertrophy and fibrosis in mice early in UUO-induced CKD, in association with early activation of the TGF-β/Smad signaling pathway. We also demonstrate the beneficial effect of ACE I in alleviating this early fibrogenic process in the heart in UUO/CKD animals.

DOI： 10.1038/s41598-018-34216-x

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Aquaporin-2 (AQP2) is a water channel protein expressed in principal cells (PCs) of the kidney collecting ducts (CDs) and plays a critical role in mediating water reabsorption and urine concentration. AQP2 undergoes both regulated trafficking mediated by vasopressin (VP) and constitutive recycling, which is independent of VP. For both pathways, actin cytoskeletal dynamics is a key determinant of AQP2 trafficking. We report here that manganese chloride (MnCl2) is a novel and potent regulator of AQP2 trafficking in cultured cells and in the kidney. MnCl2 treatment promoted internalization and intracellular accumulation of AQP2. The effect of MnCl2 on the intracellular accumulation of AQP2 was associated with activation of RhoA and actin polymerization without modification of AQP2 phosphorylation. Although the level of total and phosphorylated AQP2 did not change, MnCl2 treatment impeded VP-induced phosphorylation of AQP2 at its serine-256, -264, and -269 residues and dephosphorylation at serine 261. In addition, MnCl2 significantly promoted F-actin polymerization along with downregulation of RhoA activity and prevented VP-induced membrane accumulation of AQP2. Finally, MnCl2 treatment in mice resulted in significant polyuria and reduced urinary concentration, likely due to intracellular relocation of AQP2 in the PCs of kidney CDs. More importantly, the reduced urinary concentration caused by MnCl2 treatment in animals was not corrected by VP. In summary, our study identified a novel effect of MnCl2 on AQP2 trafficking through modifying RhoA activity and actin polymerization and uncovered its potent impact on water diuresis in vivo.

DOI： 10.1152/ajprenal.00391.2017

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

A kidney has the ability to regenerate itself after a variety of renal injuries. Mesenchymal stem cells (MSCs) have been shown to ameliorate tissue damages during renal injuries and diseases. The regenerations induced by MSCs are primarily mediated by the paracrine release of soluble factors and extracellular vesicles, including exosomes and microvesicles. Extracellular vesicles contain proteins, microRNAs, and mRNAs that are transferred into recipient cells to induce several repair signaling pathways. Over the past few decades, many studies identified trophic factors from MSCs, which attenuate renal injury in a variety of animal acute kidney injury models, including renal ischemia-reperfusion injury and drug-induced renal injury, using microarray and proteomic analysis. Nevertheless, these studies have revealed the heterogeneity of trophic factors from MSCs that depend on the cell origins and different stimuli including hypoxia, inflammatory stimuli, and aging. In this review article, we summarize the secretomes and regenerative mechanisms induced by MSCs and highlight the possible heterogeneity of trophic factors from different types of MSC and different circumstances for renal regeneration.

DOI： 10.1155/2018/8693137

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1152/ajprenal.00038.2017

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：NATURE PUBLISHING GROUP  

The glomerulus exercises its filtration barrier function by establishing a complex filtration apparatus consisting of podocyte foot processes, glomerular basement membrane and endothelial cells. Disruption of any component of the glomerular filtration barrier leads to glomerular dysfunction, frequently manifested as proteinuria. Ultrastructural studies of the glomerulus by transmission electron microscopy (TEM) and conventional scanning electron microscopy (SEM) have been routinely used to identify and classify various glomerular diseases. Here we report the application of newly developed helium ion scanning microscopy (HIM) to examine the glomerulopathy in a Col4a3 mutant/Alport syndrome mouse model. Our study revealed unprecedented details of glomerular abnormalities in Col4a3 mutants including distorted podocyte cell bodies and disorganized primary processes. Strikingly, we observed abundant filamentous microprojections arising from podocyte cell bodies and processes, and presence of unique bridging processes that connect the primary processes and foot processes in Alport mice. Furthermore, we detected an altered glomerular endothelium with disrupted sub-endothelial integrity. More importantly, we were able to clearly visualize the complex, three-dimensional podocyte and endothelial interface by HIM. Our study demonstrates that HIM provides nanometer resolution to uncover and rediscover critical ultrastructural characteristics of the glomerulopathy in Col4a3 mutant mice.

DOI： 10.1038/s41598-017-12064-5

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：COMPANY OF BIOLOGISTS LTD  

The water channel aquaporin-2 (AQP2) is a major regulator of water homeostasis in response to vasopressin (VP). Dynamic trafficking of AQP2 relies on its close interaction with trafficking machinery proteins and the actin cytoskeleton. Here, we report the identification of ezrin, an actin-binding protein from the ezrin/radixin/moesin (ERM) family as an AQP2-interacting protein. Ezrin was first detected in a co-immunoprecipitation (co-IP) complex using an anti-AQP2 antibody in a proteomic analysis. Immunofluorescence staining revealed the co-expression of ezrin and AQP2 in collecting duct principal cells, and VP treatment caused redistribution of both proteins to the apical membrane. The ezrin-AQP2 interaction was confirmed by co-IP experiments with an anti-ezrin antibody, and by pulldown assays using purified full-length and FERM domain-containing recombinant ezrin. By using purified recombinant proteins, we showed that ezrin directly interacts with AQP2 C-terminus through its N-terminal FERM domain. Knocking down ezrin expression with shRNA resulted in increased membrane accumulation of AQP2 and reduced AQP2 endocytosis. Therefore, through direct interaction with AQP2, ezrin facilitates AQP2 endocytosis, thus linking the dynamic actin cytoskeleton network with AQP2 trafficking.

DOI： 10.1242/jcs.204842

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：NATURE PUBLISHING GROUP  

Helium ion scanning microscopy (HIM) is a novel technology that directly visualizes the cell surface ultrastructure without surface coating. Despite its very high resolution, it has not been applied extensively to study biological or pathology samples. Here we report the application of this powerful technology to examine the three-dimensional ultrastructural characteristics of proteinuric glomerulopathy in mice with CD2-associated protein (CD2AP) deficiency. HIM revealed the serial alteration of glomerular features including effacement and disorganization of the slit diaphragm, followed by foot process disappearance, flattening and fusion of major processes, and eventual transformation into a podocyte sheet as the disease progressed. The number and size of the filtration slit pores decreased. Strikingly, numerous "bleb" shaped microprojections were observed extending from podocyte processes and cell body, indicating significant membrane dynamics accompanying CD2AP deficiency. Visualizing the glomerular endothelium and podocyte-endothelium interface revealed the presence of endothelial damage, and disrupted podocyte and endothelial integrity in 6 week-old Cd2ap-KO mice. We used the HIM technology to investigate at nanometer scale resolution the ultrastructural alterations of the glomerular filtration apparatus in mice lacking the critical slit diaphragm-associated protein CD2AP, highlighting the great potential of HIM to provide new insights into the biology and (patho)physiology of glomerular diseases.

DOI： 10.1038/s41598-017-08304-3

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Semaphorin3A is a secreted protein known to be involved in organogenesis, immune responses and cancer. In the kidney, semaphorin3A is expressed in the glomerular podocytes, distal tubules and collecting tubules, and believed to play a role in the regulation of the kidney development and function. We examined the serum and urinary semaphorin3A levels in 72 patients with renal disease and 5 healthy volunteers. The patients had been diagnosed with thin basement membrane disease (n=4), minimal change nephrotic syndrome (MCNS; n=22), IgA nephritis (n=21), membranous nephropathy (n=16) and focal segmental glomerular sclerosis (n=9). The level of urinary semaphorin3A in MCNS patients tended to be relatively high among all disease groups. We also investigated the urinary semaphorin3A level in 7 patients with MCNS from disease onset to remission during the drug therapy. MCNS patients in pre-remission states had higher urinary semaphorin3A levels than those in post-remission states receiving immunosuppressive therapies. These results suggested that the urinary semaphorin3A level correlates with the MCNS activity. Semaphorin3A has the potential as a biomarker for MCNS to clarify the reactivity for therapy and may be useful in examining other glomerular diseases with proteinuria as well.

DOI： 10.2147/IJNRD.S132980

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Stem cell therapies against renal injury have been advancing. The many trials for renal regeneration are reported to be effective in many kinds of renal injury models. Regarding the therapeutic mechanism, it is believed that stem cells contribute to make regeneration via not only direct stem cell differentiation in the injured space but also indirect effect via secreted factors from stem cells. Direct differentiation from stem cells to renal composed cells has been reported. They differentiate to renal composed cells and make functions. However, regarding renal regeneration, stem cells are discussed to secrete many kinds of growth factors, cytokines, and chemokines in paracrine or autocrine manner, which protect against renal injury, too. In addition, it is reported that stem cells have the ability to communicate with nearby cells via microvesicle-related RNA and proteins. Taken together from many reports, many secreted factors from stem cells were needed for renal regeneration orchestrally with harmony. In this review, we focused on the effects and insights of stem cells and regenerative factors from stem cells.

DOI： 10.1155/2015/537204

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.bbrc.2014.03.111

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：MARY ANN LIEBERT, INC  

Long-term peritoneal dialysis (PD) causes chronic peritoneal damage. Peritoneal mesothelial cells (PMCs) play an important role in peritoneal function. We investigated the possibility of cell therapy using the PMCs to prevent peritoneal damage in PD patients. We harvested human PMCs from the PD effluent of PD patients. The PMCs were separated based on morphological characteristics into epithelial-like (Epi) cells and fibroblast-like (Fib) cells by the limiting dilution method. We transplanted these cells into nude mice whose parietal and visceral peritoneum were scratched by mechanical scraping. The transplanted cells were detected at the parietal and visceral peritoneum. Compared with the positive control, the Epi cell therapy group showed very few adhesions and exhibited no thickening of the parietal and visceral peritoneum. However, the group with Fib cell therapy could not inhibit peritoneal adhesion and thickening. In addition, hepatocyte growth factor was expressed by the grafted Epi cells but not Fib cells. Fib cells expressed vascular endothelial growth factor stronger than Epi cells. These two types of cells from the same patient showed different characteristics and effects for cell therapy. These findings suggest that the PMCs from the PD patient showed different characteristics, such as Epi cells and Fib cells, and the selection of PMCs is important for cell therapy on the point of not only the direct cellular interactions but also cytokine secretion from the grafted cells. Furthermore, the differences in the morphological cell characteristics may influence their role in peritoneal regeneration.

DOI： 10.1089/ten.TEA.2013.0130

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：OKAYAMA UNIV MED SCHOOL  

Immunosuppressive agents are generally administered to treat kidney diseases. However, it is unclear whether renal stem/progenitor cells are directly affected by the immunosuppressive agents. We used normal rat kidney cells, ureteric bud cells and rat kidney stem/progenitor cells in this study. Mizoribine (MZR), cyclophosphamide (CPA) and cyclosporine (CyA) were added to the culture media of these cells. We evaluated the effects of these immunosuppressive agents on cell proliferation using an electrical cell-substrate impedance sensing system (ECIS) and their effects on the process of renal regeneration using the ischemia-reperfusion (I/R) injury rat model. The ECIS data showed that proliferation of each of the 3 types of cells was significantly suppressed by MZR. MZR treatment enhanced renal tubular injury in ischemia-reperfusion (I/R) injured rats, and significantly decreased levels of M-phase cells and Nestin-positive cells. These results suggested that MZR inhibits the cell cycle of renal stem/progenitor cells;thus, physicians should take note that MZR might affect not only inflammation but also renal regeneration.

DOI： 10.18926/AMO/52138

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記述言語：英語  

BACKGROUND: Membranous nephropathy is one of the most common causes of nephrotic syndrome in adults. In contrast, acquired factor V inhibitor is a rare bleeding disorder. CASE PRESENTATION: A 62-year-old Asian man with a history of cerebral hemorrhage, purpura, eosinophilia and hyper immunoglobulin E syndrome developed proteinuria. The bleeding disorder was diagnosed with acquired factor V inhibitors. A renal biopsy revealed that he suffered from membranous nephropathy with glomerular endothelial damage which is reported to be involved in another factor disorder. After the steroid administration, the coagulation test and proteinuria were improved. CONCLUSIONS: The presence of factor V inhibitors may have been involved in the development of membranous nephropathy.

DOI： 10.1186/1756-0500-6-553

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記述言語：英語  

BACKGROUND: Common variable immunodeficiency (CVID) is a disorder characterized by hypogammaglobulinemia without a known predisposing cause. CASE PRESENTATION: We report a 36-year-old man who had suffered membranoproliferative glomerulonephritis (MPGN) in his childhood, later diagnosed with CVID at 35 years of age. He presented at our hospital with signs of proteinuria. A renal biopsy revealed he suffered from focal segmental glomerulosclerosis (FSGS), possibly due to obesity and hypertension, not CVID - associated MPGN. CONCLUSION: This is the first case report of FSGS in a CVID patient. In this case, we have to pay attention not only to the treatment of obesity and hypertension for FSGS but also to the recurrence of immune-complex glomerulonephritis such as MPGN, in case of the restoration of hypogammaglobulinemia.

DOI： 10.1186/1471-2369-13-46

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(社医財)大樹会総合病院回生病院  

静脈性血管瘤(VA)は無症状で経過することが多く、炎症や血栓を形成して血栓性静脈炎や致命的な肺塞栓症(PE)をきたす事があり、注目されている。2011年1月〜2019年3月に当院で経験した静脈性血管瘤(VA)症例を対象に、臨床的検討を行った。当院で経験したVA症例は8例で、男性は3例、女性は5例であった。年齢は39〜84歳で、平均59歳であった。発生部位は、上肢3例、腹壁1例、下肢4例であった。病型分類は2種類あり、嚢胞状タイプ(Sacciform)がI型、紡錘状タイプ(Fusiform)がII型である。I型が4例、II型が4例であった。全例手術治療を行い、全摘出術を行った。術後経過も全例順調で特別問題となった症例はなかった。本稿では、84歳女性、49歳男性、47歳女性の症例について詳述した。

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記述言語：日本語   出版者・発行元：(一社)日本内科学会  

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記述言語：日本語   出版者・発行元：(一社)日本内科学会  

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記述言語：日本語   出版者・発行元：(一社)日本内科学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(株)医学書院  

＜文献概要＞慢性腎臓病(chronic kidney disease:以下、CKD)の進行に伴って、腎予備能が低下するとともに、高血圧、浮腫、高カリウム血症、貧血など、さまざまな異常所見が顕在化しやすく、それぞれが腎障害の加速因子となりうる。腎予後の改善や心血管合併症予防の観点から、臨床所見や検査データを基に、それぞれの病態に対して食事療法や薬剤療法を行い、厳格に管理する。

J-GLOBAL

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その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2020&ichushi_jid=J06514&link_issn=&doc_id=20200612230027&doc_link_id=10.11477%2Fmf.1429202651&url=https%3A%2F%2Fdoi.org%2F10.11477%2Fmf.1429202651&type=%88%E3%8F%91.jp_%83I%81%5B%83%8B%83A%83N%83Z%83X&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

記述言語：日本語   出版者・発行元：(株)医学書院  

J-GLOBAL

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その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2020&ichushi_jid=J06514&link_issn=&doc_id=20200612230029&doc_link_id=10.11477%2Fmf.1429202653&url=https%3A%2F%2Fdoi.org%2F10.11477%2Fmf.1429202653&type=%88%E3%8F%91.jp_%83I%81%5B%83%8B%83A%83N%83Z%83X&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

記述言語：日本語   出版者・発行元：(一社)日本内科学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

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記述言語：日本語   出版者・発行元：(一社)日本内分泌学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：WILEY-BLACKWELL  

Web of Science

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記述言語：日本語  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：一般社団法人 日本透析医学会  

DOI： 10.4009/jsdt.46.163

CiNii Article

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記述言語：日本語   出版者・発行元：(一社)日本透析医学会  

DOI： 10.4009/jsdt.46.163

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語  

DOI： 10.4009/jsdt.46.163

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：中国腎不全研究会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：愛媛県公営企業管理局県立病院課  

59歳男。糖尿病性腎症のため腹膜透析で維持透析を受けていた。今回、発熱、感冒症状の後に意識レベル低下、痙攣発作が出現し、頭部CTで異常なく、髄液検査よりヘルペス脳炎を疑い治療を開始した。しかし、発熱、痙攣発作、四肢不随意運動が持続して当院救急入院となった。脳波、髄液、血液検査所見より無菌性脊髄炎、単純ヘルペス脳炎と診断し、アシクロビル、メロペン、献血ベニロン、グリセオールおよび免疫グロブリンの治療を開始した。また、腹膜透析は継続しながら、溢水管理のため週1回の血液透析を併用した。治療後、単核球優位の細胞数増多を認めた髄液所見は改善し、痙攣発作も消失したが、意識障害、四肢不随意運動は持続し、急性散在性脳脊髄炎を疑いMRIを施行したところ、大脳白質、右優位に線条体に散在性の高信号域を認め診断を確定した。ステロイドパルス療法(ソル・メドロール1000mg/日×3)を開始したところ、急速に意識レベルは改善して四肢不随意運動も消失し、その後のMRIでは高信号域の軽減を認めた。全身状態が安定した後、近医転院となった。

J-GLOBAL

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記述言語：日本語   出版者・発行元：愛媛県公営企業管理局県立病院課  

著者らは腎生検を施行した70歳以上の高齢者ネフローゼ症候群33症例(平均年齢74歳)を対象に病理学的検討を行った。1)続発性ネフローゼ症候群34%と他施設の報告とには差はなかったが、一方で原発性ネフローゼ症候群は膜性腎症の割合が多いとされているものの、微小変化群が多く認められた。また、腎機能低下症例も多く認められた。2)20例でステロイド治療が開始され、4例でネフローゼ症候群から溢水によって心不全を呈し一時的に透析を必要とした。3)治療開始から3ヵ月後に52%、1年後に73%の症例に治療効果が確認され、高齢者であっても積極的な治療によって腎予後、生命予後の改善が期待できる症例の存在が示唆された。4)死亡は経過中8例にみられ、最終的に透析導入となった腎死症例が4例に認められた。5)腎生検による重大な合併症は認められなかったが、ネフローゼ症候群による合併症は感染症を7例、深部静脈血栓症を1例、出血性潰瘍を2例に確認された。尚、悪性腫瘍の合併は10例に認められた。

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本老年医学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：愛媛県公営企業管理局県立病院課  

83歳男。患者は咳嗽があり近医を受診、間質性肺炎と診断され、ブレドニゾロンの内服が開始されたものの、発熱および倦怠感が出現し、あわせて尿異常、炎症反応高値、MPO(myeloperoxidase)-ANCA(anti-neutrophil cytoplasmic autoantibody)陽性が認められた。今回、腎生検目的にて、著者らの施設へ紹介となったが、所見では糸球体に半月体形成はみられなかったものの、小葉間動脈に血管炎像が認められ、MPA(microscopic polyangitis)と診断された。治療はステロイドパルス療法施行後にプレドニゾロンの投与が開始されたが、血管炎腎外病変である間質性肺炎の増悪と感染のコントロールに難渋し、最終的に呼吸状態の悪化により患者は死亡となった。尚、剖検所見では腎臓は小葉間動脈領域の内膜の断裂、線維性肥厚狭小化がみられたが、血管周囲のリンパ節浸潤は軽度であり、血管炎瘢痕期と考えられた。また、死因としては間質性肺炎の増悪が推察された。

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(株)東京医学社  

60歳女。1年4ヵ月前にCAPD導入し、APDにて維持していた。今回、微熱と汎血球減少症が出現し、結核性骨髄炎と診断して治療中、副腎結核による副腎不全を合併した。抗結核薬4剤による治療とヒドロコルチゾンの内服により結核、副腎不全とも改善したが、抗結核薬の副作用が強く治療に難渋した。また副腎結核の診断では組織検査で結核菌が検出されず、悪性腫瘍との鑑別のために副腎摘出を要した。

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本透析医学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：東京医学社  

CiNii Article

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記述言語：日本語   出版者・発行元：(一社)日本透析医学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本腎臓学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本内分泌学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本糖尿病学会  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(一社)日本透析医学会  

J-GLOBAL

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