Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：日本内科学会-関東地方会  

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Language：English   Publishing type：Research paper (scientific journal)  

Leriche syndrome is an aortoiliac occlusive disease with three chief symptoms: claudication, impotence, and weak femoral pulse. It can also cause occlusion of the aorta up to the level of the renal arteries. We report a case in which aortoiliac bypass and renal artery thrombectomy were effective in ameliorating acute kidney injury caused by bilateral renal artery thrombosis.

DOI： 10.1272/jnms.JNMS.2021_88-610

PubMed

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media {LLC}  

BACKGROUND: Clinically applied as anti-gout drugs, xanthine oxidoreductase (XOR) inhibitors, especially the potent, selective, non-purine-analog XOR inhibitors febuxostat and topiroxostat, exert organ-protective effects. We tested the hypothesis that preservation of tissue concentrations of high-energy phosphates, such as ATP and ADP, contributes to organ-protective effects through CE-TOFMS metabolomics. METHODS: Rats were subjected to 30 min of renal ischemia-reperfusion (I/R) injury 60 min after oral administration of 10 mg/kg febuxostat, 10 mg/kg topiroxostat, 50 mg/kg allopurinol, or vehicle. RESULTS: In non-purine-analog XOR inhibitor-treated groups, renal concentrations of high-energy phosphates were greater before and after I/R injury, and renal adenine compounds were less depleted by I/R injury than in the vehicle and allopurinol groups. These findings were well in accordance with the proposed hypothesis that the recomposition of high-energy phosphates is promoted by non-purine-analog XOR inhibitors via the salvage pathway through blockade of hypoxanthine catabolism, whereas non-specific inhibitory effects of allopurinol on purine/pyrimidine enzymes impede this re-synthesis process. CONCLUSIONS: This metabolic approach shed light on the physiology of the organ-protective effects of XOR inhibitors.

DOI： 10.1186/s10020-019-0109-y

PubMed

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Language：English   Publishing type：Research paper (scientific journal)  

Medial arterial calcification (MAC) is a major complication of chronic kidney disease (CKD) and an indicator of poor prognosis. Aortic overexpression of tissue-nonspecific alkaline phosphatase (TNAP) accelerates MAC formation. The present study aimed to assess whether a TNAP inhibitor, SBI-425, protects against MAC and improves survival probability in a CKD-mineral and bone disorder (MBD) mouse model. CKD-MBD mice were divided in three groups: vehicle, SBI-10, and SBI-30. They were fed a 0.2% adenine and 0.8% phosphorus diet from 14 to 20 weeks of age to induce CKD, followed by a high-phosphorus (0.2% adenine and 1.8% phosphorus) diet for another 6 weeks. At 14-20 weeks of age, mice in the SBI-10 and SBI-30 groups were given 10 and 30 mg/kg SBI-425 by gavage once a day, respectively, while vehicle-group mice were given distilled water as vehicle. Control mice were fed a standard chow (0.8% phosphorus) between the ages of 8 and 20 weeks. Computed tomography imaging, histology, and aortic tissue calcium content revealed that, compared to vehicle animals, SBI-425 nearly halted the formation of MAC. Mice in the control, SBI-10 and SBI-30 groups exhibited 100% survival, which was significantly better than vehicle-treated mice (57.1%). Aortic mRNA expression of Alpl, encoding TNAP, as well as plasma and aortic tissue TNAP activity, were suppressed by SBI-425 administration, whereas plasma pyrophosphate increased. We conclude that a TNAP inhibitor successfully protected the vasculature from MAC and improved survival rate in a mouse CKD-MBD model, without causing any adverse effects on normal skeletal formation and residual renal function. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

DOI： 10.1002/path.5346

PubMed

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：NATURE PUBLISHING GROUP  

Medial arterial calcification (MAC) and renal osteodystrophy are complications of mineral bone disease (MBD) associated with chronic kidney disease (CKD). Our aim was to develop a novel mouse model to investigate the clinical course of CKD-MBD. Eight-week-old C57BL/6 J male mice were assigned to the following groups: the control group, fed a standard chow for 6 or 12 weeks; the CKD-normal phosphorus (NP) group, fed a chow containing 0.2% adenine, with normal (0.8%) phosphorus, for 6 or 12 weeks; and the CKD-high phosphorus (HP) group, fed 6 weeks with the 0.2% adenine/0.8% phosphorus diet, followed by a chow with 1.8% phosphorus for 2 weeks, 4 weeks or 6 weeks. Serum phosphorus was significantly increased in the CKD-HP group, and associated with MAC formation; the volume of calcification increased with longer exposure to the high phosphorus feed. MAC was associated with upregulated expression of runt-related transcription factor 2, alkaline phosphatase, and osteopontin, indicative of osteoblastic trans-differentiation of vascular smooth muscle cells. A significant mineral density depletion of cortical bone was observed. We describe the feasibility of developing a model of CKD-MBD and provide findings of a direct association between elevated serum phosphorus and the formation of MAC and renal osteodystrophy.

DOI： 10.1038/s41598-017-02351-6

Web of Science

PubMed

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

We present a case of idiopathic retroperitoneal fibrosis (IRF) complicated by severe renal failure and multiple intracranial lesions, which are probable results of cerebral vasculitis. IRF is an idiopathic hyperplasia of the retroperitoneal tissue that often entraps the ureters and causes post-renal failure. While the etiology of IRF is unclear, researchers consider IRF a systemic autoimmune disease complicated by immune-mediated vasculitides. The chief complaints of the patient were cognitive disorders, and brain MRI findings revealed multiple intracranial lesions with accompanying central degeneration. Given that vasogenic cerebral edemas derive from uremia, we speculated that the lesions in our case were related to more destructive changes such as aortic and periaortic inflammation. Details on this case manifesting rare cerebrovascular complications may help elucidate the pathogenesis of IRF.

DOI： 10.3109/14397595.2013.843754

Web of Science

PubMed

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Publishing type：Research paper (scientific journal)  

We describe a case of IgA nephropathy (IgAN) followed by pulmonary hemorrhage associated with Henoch-Schöenlein purpura (HSP) in an adult female. The patient had a history of renal insufficiency and persistent hematuria and proteinuria, without any extra-renal involvement. She was diagnosed with IgAN 7 years before the onset of HSP and had received immunosuppressive therapy for 6 years. One year after discontinuing oral prednisolone and mizoribine, she suffered a pulmonary hemorrhage. She presented with exacerbated urinary findings, and palpable purpura, resulting in the diagnosis of HSP. Intravenous pulse methylprednisolone followed by oral prednisolone (1 mg/kg/day) and a monthly intravenous cyclophosphamide pulse resolved the pulmonary hemorrhage. In a review of 36 HSP patients complicated with pulmonary hemorrhage, 27.8 % of the patients perished [Rajagopala et al., Semin Arthritis Rheum 42:391-400, 1]. While the most efficient therapeutic strategies for these patients have yet to be determined, we speculate that an aggressive therapy of pulse methylprednisolone combined with immunosuppression agents is likely to bring about the best outcome in cases with pathological conditions similar to our patient's. On the other hand, discontinuance of immunosuppressive therapy might have resulted in the aggravation of the disease, hence we should examine patients carefully not to miss the cue.

DOI： 10.1007/s13730-014-0138-x

PubMed

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Publishing type：Research paper (scientific journal)  

Background: Epoetin beta pegol (MIRCERA®) is a chemically synthesized erythropoiesis stimulating agent with the integration of epoetin beta and linear methoxy polyethylene glycol (mPEG). Serum MIRCERA concentration is determined by sandwich enzyme-linked immunosorbent assay using both anti human epoetin antibody and anti mPEG antibody (MIRCERA determination method). However, this method is not available commercially in Japan. We sought to establish whether RIA2 antibody assay, which is usually used for determining serum epoetin concentration by anti epoetin rabbit antibody, could determine serum MIRCERA concentration appropriately. Methods: Circled digit one10 kinds of standard solution with various MIRCERA concentrations from 10000 to 0 ng/mL were prepared. Each solution was determined by RIA2 antibody assay as epoetin concentration and the correlation between MIRCERA concentration and epoetin concentration was tested. Then, its conversion formula was estimated. Circled digit two100 or 150 μg MIRCERA were administrated intravenously to 8 hemodialysis patients. Serum epoetin concentration was determined by RIA2 antibody assay, then, it was converted to MIRCERA concentration. Area under the serum MIRCERA concentration-time curve (AUClast) and half-lives (t1/2) were estimated. Circled digit threeThese AUClastand t1/2were compared to those obtained previously by MIRCERA determination method. Results: AUClastby RIA2 antibody assay after administration of 100 and 150 μg were respectively equivalent to 42.6 and 40.6% of those obtained by MIRCERA determination method. However, t1/2were 169 and 129 hours by RIA2 method, these values were similar to those obtained by MIRCERA determination method Conclusions: As the concentration determined by RIA2 antibody assay reflected the long t1/2which is the pharmacokinetic feature of MIRCERA successfully, our novel method is substitutable clinically.

Scopus

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Language：Japanese   Publisher：生命科学系学会合同年次大会運営事務局  

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Language：Japanese   Publisher：(一社)日本痛風・尿酸核酸学会  

DOI： 10.6032/gnam.41.22

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Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：(一社)日本腎臓学会  

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Language：Japanese   Publisher：(一社)日本痛風・尿酸核酸学会  

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Language：Japanese   Publisher：(一社)日本腎臓学会  

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Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：(株)東京医学社  

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Language：Japanese   Publisher：(株)東京医学社  

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Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：(公社)日本皮膚科学会  

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Language：Japanese   Publisher：(株)メディカルレビュー社  

電解質異常をきたす疾患は、慢性腎臓病(CKD)、心不全、脳血管障害、内分泌代謝疾患など多岐にわたる。尿中への排泄、再吸収などにより水・電解質を調整して恒常性維持を司るのが腎臓の役割であり、いずれの病態でも内分泌ホルモン、体液調整因子などの変化によって腎臓での恒常性維持が破綻する結果、水・電解質異常をきたす。そのなかでも、腎臓そのものが機能不全に陥るCKDでは、CKDステージの進行に伴い水・電解質異常、酸塩基平衡異常が必発である。本稿では、CKDに関連して起こりうる水・Na代謝異常、K代謝異常、Ca・P・Mg代謝異常、酸塩基平衡異常に注目し、代表的な病態・治療に関して概説する。(著者抄録)

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Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2014&ichushi_jid=J05845&link_issn=&doc_id=20140128280004&doc_link_id=%2Fai1fruid%2F2014%2F000401%2F005%2F0027-0032%26dl%3D0&url=http%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fai1fruid%2F2014%2F000401%2F005%2F0027-0032%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(一社)日本腎臓学会  

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Language：Japanese   Publisher：(一社)日本腎臓学会  

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Language：Japanese   Publisher：(株)東京医学社  

71歳男。CAPD関連腹膜炎の治療開始後9日目に全身痛と肩・肘・手・膝関節の屈曲制限および右指PIP関節の腫脹が出現した。14日目には頸部〜両肩部筋肉の掌握痛や手指のこわばり、筋力低下、発熱なども出現した。諸検査の結果からリウマチ性多発筋痛症(PMR)などのリウマチ性疾患を強く疑い、プレドニゾロンの投与を行ったところ症状は劇的に改善した。腹膜炎がPMR発症の契機となった可能性が考えられた。

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Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：(株)東京医学社  

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Language：Japanese   Publisher：日本内科学会-関東地方会  

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Language：Japanese   Publisher：(一社)日本透析医学会  

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Language：Japanese   Publisher：(一社)日本透析医学会  

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