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Article: Melinjo seed extract stimulates intestinal ABCG2 expression to reduce serum uric acid levels in hyperuricemic rats

Tamura, Yoshifuru / Morimoto, Chikayuki / Kuribayashi-Okuma, Emiko / Uchida, Shunya / Hosoyamada, Makoto / Nakagawa, Takahiko / Shibata, Shigeru

Journal of functional foods. 2021 Dec., v. 87

2021

Abstract: Melinjo resveratrol (MjR) is a resveratrol derivative from the seed extract of melinjo (Gnetum gnemon L.). Although it may reduce serum uric acid concentration in humans, the underlying mechanism remains unclear. Thus, we investigated the effect of MjR ... ...

Abstract	Melinjo resveratrol (MjR) is a resveratrol derivative from the seed extract of melinjo (Gnetum gnemon L.). Although it may reduce serum uric acid concentration in humans, the underlying mechanism remains unclear. Thus, we investigated the effect of MjR on the uric acid metabolism in the setting of hyperuricemia model rats induced by orally administered oxonic acid. MjR administered for three weeks significantly lowered serum uric acid levels in hyperuricemia rats. While urinary excretion of uric acid did not change, fecal excretion of uric acid significantly increased by MjR. The expression of ATP-binding cassette sub-family G member (ABCG2) was upregulated with MjR treatment in the ileum but not in the kidney. In a human epithelial colorectal cell line, Caco-2, uric acid and MjR additively stimulated ABCG2 expression. These data suggest that MjR could reduce serum uric acid by enhancing fecal excretion of uric acid in the ileum by upregulating ABCG2 protein expression.
Keywords	ABC transporters ; Gnetum gnemon ; blood serum ; epithelium ; excretion ; humans ; hyperuricemia ; ileum ; kidneys ; protein synthesis ; resveratrol ; seed extracts ; uric acid
Language	English
Dates of publication	2021-12
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2511964-3
ISSN	1756-4646
ISSN	1756-4646
DOI	10.1016/j.jff.2021.104849
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Cardio-renal protective effect of the xanthine oxidase inhibitor febuxostat in the 5/6 nephrectomy model with hyperuricemia

Hiroki Omizo / Yoshifuru Tamura / Chikayuki Morimoto / Masaki Ueno / Yuto Hayama / Emiko Kuribayashi-Okuma / Shunya Uchida / Shigeru Shibata

Scientific Reports, Vol 10, Iss 1, Pp 1-

2020 Volume 10

Abstract: Abstract Although hyperuricemia has been shown to be associated with the progression of cardiovascular disorder and chronic kidney disease (CKD), there is conflicting evidence as to whether xanthine oxidase (XO) inhibitors confer organ protection besides ...

Abstract	Abstract Although hyperuricemia has been shown to be associated with the progression of cardiovascular disorder and chronic kidney disease (CKD), there is conflicting evidence as to whether xanthine oxidase (XO) inhibitors confer organ protection besides lowering serum urate levels. In this study, we addressed the cardio-renal effects of XO inhibition in rodent CKD model with hyperuricemia. Sprague-Dawley rats underwent 5/6 nephrectomy and received a uricase inhibitor oxonic acid for 8 weeks (RK + HUA rats). In some rats, a XO inhibitor febuxostat was administered orally. Compared with control group, RK + HUA group showed a significant increase in albuminuria and renal injury. Febuxostat reduced serum uric acid as well as urinary albumin levels. Histological and immunohistochemical analysis of the kidney revealed that febuxostat alleviated glomerular, tubulointerstitial, and arteriolar injury in RK + HUA rats. Moreover, in the heart, RK + HUA showed individual myofiber hypertrophy and cardiac fibrosis, which was significantly attenuated by febuxostat. We found that renal injury and the indices of cardiac changes were well correlated, confirming the cardio-renal interaction in this model. Finally, NF-E2-related factor 2 (Nrf2) and the downstream target heme oxygenase-1 (HO-1) protein levels were increased both in the heart and in the kidney in RK + HUA rats, and these changes were alleviated by febuxostat, suggesting that tissue oxidative stress burden was attenuated by the treatment. These data demonstrate that febuxostat protects against cardiac and renal injury in RK + HUA rats, and underscore the pathological importance of XO in the cardio-renal interaction.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2020-06-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cardio-renal protective effect of the xanthine oxidase inhibitor febuxostat in the 5/6 nephrectomy model with hyperuricemia.

Omizo, Hiroki / Tamura, Yoshifuru / Morimoto, Chikayuki / Ueno, Masaki / Hayama, Yuto / Kuribayashi-Okuma, Emiko / Uchida, Shunya / Shibata, Shigeru

Scientific reports

2020 Volume 10, Issue 1, Page(s) 9326

Abstract: Although hyperuricemia has been shown to be associated with the progression of cardiovascular disorder and chronic kidney disease (CKD), there is conflicting evidence as to whether xanthine oxidase (XO) inhibitors confer organ protection besides lowering ...

Abstract	Although hyperuricemia has been shown to be associated with the progression of cardiovascular disorder and chronic kidney disease (CKD), there is conflicting evidence as to whether xanthine oxidase (XO) inhibitors confer organ protection besides lowering serum urate levels. In this study, we addressed the cardio-renal effects of XO inhibition in rodent CKD model with hyperuricemia. Sprague-Dawley rats underwent 5/6 nephrectomy and received a uricase inhibitor oxonic acid for 8 weeks (RK + HUA rats). In some rats, a XO inhibitor febuxostat was administered orally. Compared with control group, RK + HUA group showed a significant increase in albuminuria and renal injury. Febuxostat reduced serum uric acid as well as urinary albumin levels. Histological and immunohistochemical analysis of the kidney revealed that febuxostat alleviated glomerular, tubulointerstitial, and arteriolar injury in RK + HUA rats. Moreover, in the heart, RK + HUA showed individual myofiber hypertrophy and cardiac fibrosis, which was significantly attenuated by febuxostat. We found that renal injury and the indices of cardiac changes were well correlated, confirming the cardio-renal interaction in this model. Finally, NF-E2-related factor 2 (Nrf2) and the downstream target heme oxygenase-1 (HO-1) protein levels were increased both in the heart and in the kidney in RK + HUA rats, and these changes were alleviated by febuxostat, suggesting that tissue oxidative stress burden was attenuated by the treatment. These data demonstrate that febuxostat protects against cardiac and renal injury in RK + HUA rats, and underscore the pathological importance of XO in the cardio-renal interaction.
MeSH term(s)	Animals ; Cardiotonic Agents/pharmacology ; Disease Models, Animal ; Febuxostat/pharmacology ; Heart/drug effects ; Hyperuricemia/drug therapy ; Hyperuricemia/etiology ; Hyperuricemia/physiopathology ; Kidney Diseases/drug therapy ; Kidney Diseases/etiology ; Kidney Function Tests ; Male ; Myocardium/pathology ; Nephrectomy/adverse effects ; Oxidative Stress/drug effects ; Oxonic Acid/pharmacology ; Protective Agents/pharmacology ; Rats, Sprague-Dawley ; Xanthine Oxidase/antagonists & inhibitors
Chemical Substances	Cardiotonic Agents ; Protective Agents ; Febuxostat (101V0R1N2E) ; Oxonic Acid (5VT6420TIG) ; Xanthine Oxidase (EC 1.17.3.2)
Language	English
Publishing date	2020-06-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-65706-6
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Article ; Online: ABCG2 expression and uric acid metabolism of the intestine in hyperuricemia model rat.

Morimoto, Chikayuki / Tamura, Yoshifuru / Asakawa, Shinichiro / Kuribayashi-Okuma, Emiko / Nemoto, Yoshikazu / Li, Jinping / Murase, Takayo / Nakamura, Takashi / Hosoyamada, Makoto / Uchida, Shunya / Shibata, Shigeru

Nucleosides, nucleotides & nucleic acids

2020 Volume 39, Issue 5, Page(s) 744–759

Abstract: To elucidate roles of the intestine in uric acid (UA) metabolism, we examined ABCG2 expression, tissue UA content and xanthine oxidoreductase (XOR) activity in different intestinal segments. Male SD rats were assigned to control group or oxonic acid- ... ...

Abstract	To elucidate roles of the intestine in uric acid (UA) metabolism, we examined ABCG2 expression, tissue UA content and xanthine oxidoreductase (XOR) activity in different intestinal segments. Male SD rats were assigned to control group or oxonic acid-induced hyperuricemia (HUA) group. In control rats, ABCG2 was present both in villi and crypts in each segment. Tissue UA content and XOR activity were relatively high in duodenum and jejunum. However, in HUA rats, tissue UA content was significantly elevated in the ileum, whereas it remained unaltered in other segments. Moreover, ABCG2 expression in the HUA group was upregulated both in the villi and crypts of the ileum. These data indicate that the ileum may play an important role in the extra-renal UA excretion.
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily G, Member 2/genetics ; ATP Binding Cassette Transporter, Subfamily G, Member 2/metabolism ; Animals ; Hyperuricemia/chemically induced ; Hyperuricemia/metabolism ; Intestines ; Male ; Oxonic Acid ; Rats ; Rats, Sprague-Dawley ; Uric Acid/metabolism ; Xanthine Dehydrogenase/metabolism
Chemical Substances	ATP Binding Cassette Transporter, Subfamily G, Member 2 ; Abcg2 protein, rat ; Uric Acid (268B43MJ25) ; Oxonic Acid (5VT6420TIG) ; Xanthine Dehydrogenase (EC 1.17.1.4)
Language	English
Publishing date	2020-01-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2008956-9
ISSN	1532-2335 ; 1525-7770
ISSN (online)	1532-2335
ISSN	1525-7770
DOI	10.1080/15257770.2019.1694684
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model

Yoshikazu Nemoto / Takanori Kumagai / Kenichi Ishizawa / Yutaka Miura / Takeshi Shiraishi / Chikayuki Morimoto / Kazuhiro Sakai / Hiroki Omizo / Osamu Yamazaki / Yoshifuru Tamura / Yoshihide Fujigaki / Hiroshi Kawachi / Makoto Kuro-o / Shunya Uchida / Shigeru Shibata

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Volume 11

Abstract: Abstract Recent clinical studies indicate that the disturbed phosphate metabolism in chronic kidney disease (CKD) may facilitate kidney injury; nonetheless, the causal role of phosphate in CKD progression remains to be elucidated. Here, we show that ... ...

Abstract	Abstract Recent clinical studies indicate that the disturbed phosphate metabolism in chronic kidney disease (CKD) may facilitate kidney injury; nonetheless, the causal role of phosphate in CKD progression remains to be elucidated. Here, we show that intestinal phosphate binding by sucroferric oxyhydroxide (SF) ameliorates renal injury in the rat remnant kidney model. Sprague-Dawley rats received 5/6 nephrectomy (RK) and had a normal chow or the same diet containing SF (RK + SF). RK rats showed increased plasma FGF23 and phosphate levels, which were suppressed by SF administration. Of note, albuminuria in RK rats was significantly ameliorated by SF at both 4 and 8 weeks. SF also attenuated glomerulosclerosis and tubulointerstitial injury. Moreover, several different approaches confirmed the protective effects on podocytes, explaining the attenuation of glomerulosclerosis and albuminuria observed in this study. As a possible mechanism, we found that SF attenuated renal inflammation and fibrosis in RK rats. Interestingly, von Kossa staining of the kidney revealed calcium phosphate deposition in neither RK nor RK + SF rats; however, plasma levels of calciprotein particles were significantly reduced by SF. These data indicate that latent positive phosphate balance accelerates CKD progression from early stages, even when overt ectopic calcification is absent.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2019-02-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model.

Nemoto, Yoshikazu / Kumagai, Takanori / Ishizawa, Kenichi / Miura, Yutaka / Shiraishi, Takeshi / Morimoto, Chikayuki / Sakai, Kazuhiro / Omizo, Hiroki / Yamazaki, Osamu / Tamura, Yoshifuru / Fujigaki, Yoshihide / Kawachi, Hiroshi / Kuro-O, Makoto / Uchida, Shunya / Shibata, Shigeru

Scientific reports

2019 Volume 9, Issue 1, Page(s) 1732

Abstract: Recent clinical studies indicate that the disturbed phosphate metabolism in chronic kidney disease (CKD) may facilitate kidney injury; nonetheless, the causal role of phosphate in CKD progression remains to be elucidated. Here, we show that intestinal ... ...

Abstract	Recent clinical studies indicate that the disturbed phosphate metabolism in chronic kidney disease (CKD) may facilitate kidney injury; nonetheless, the causal role of phosphate in CKD progression remains to be elucidated. Here, we show that intestinal phosphate binding by sucroferric oxyhydroxide (SF) ameliorates renal injury in the rat remnant kidney model. Sprague-Dawley rats received 5/6 nephrectomy (RK) and had a normal chow or the same diet containing SF (RK + SF). RK rats showed increased plasma FGF23 and phosphate levels, which were suppressed by SF administration. Of note, albuminuria in RK rats was significantly ameliorated by SF at both 4 and 8 weeks. SF also attenuated glomerulosclerosis and tubulointerstitial injury. Moreover, several different approaches confirmed the protective effects on podocytes, explaining the attenuation of glomerulosclerosis and albuminuria observed in this study. As a possible mechanism, we found that SF attenuated renal inflammation and fibrosis in RK rats. Interestingly, von Kossa staining of the kidney revealed calcium phosphate deposition in neither RK nor RK + SF rats; however, plasma levels of calciprotein particles were significantly reduced by SF. These data indicate that latent positive phosphate balance accelerates CKD progression from early stages, even when overt ectopic calcification is absent.
MeSH term(s)	Animals ; Biomarkers ; Biopsy ; Disease Models, Animal ; Disease Susceptibility ; Drug Combinations ; Ferric Compounds/metabolism ; Glomerulosclerosis, Focal Segmental/etiology ; Glomerulosclerosis, Focal Segmental/metabolism ; Glomerulosclerosis, Focal Segmental/pathology ; Immunohistochemistry ; Male ; Phosphates/metabolism ; Podocytes/metabolism ; Podocytes/pathology ; Podocytes/ultrastructure ; Rats ; Renal Insufficiency, Chronic/etiology ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology ; Sucrose/metabolism
Chemical Substances	Biomarkers ; Drug Combinations ; Ferric Compounds ; Phosphates ; sucroferric oxyhydroxide ; Sucrose (57-50-1)
Language	English
Publishing date	2019-02-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-38389-3
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Article ; Online: Inhibition of Sodium Glucose Cotransporter 2 Attenuates the Dysregulation of Kelch-Like 3 and NaCl Cotransporter in Obese Diabetic Mice.

Ishizawa, Kenichi / Wang, Qin / Li, Jinping / Xu, Ning / Nemoto, Yoshikazu / Morimoto, Chikayuki / Fujii, Wataru / Tamura, Yoshifuru / Fujigaki, Yoshihide / Tsukamoto, Kazuhisa / Fujita, Toshiro / Uchida, Shunya / Shibata, Shigeru

Journal of the American Society of Nephrology : JASN

2019 Volume 30, Issue 5, Page(s) 782–794

Abstract: Background: Mechanisms underlying the frequent association between salt-sensitive hypertension and type 2 diabetes remain obscure. We previously found that protein kinase C (PKC) activation phosphorylates Kelch-like 3 (KLHL3), an E3 ubiquitin ligase ... ...

Abstract	Background: Mechanisms underlying the frequent association between salt-sensitive hypertension and type 2 diabetes remain obscure. We previously found that protein kinase C (PKC) activation phosphorylates Kelch-like 3 (KLHL3), an E3 ubiquitin ligase component, at serine 433. We investigated whether impaired KLHL3 activity results in increased renal salt reabsorption Methods: We used the db/db diabetes mouse model to explore KLHL3's role in renal salt handling in type 2 diabetes and evaluated mechanisms of KLHL3 dysregulation in cultured cells. Results: We observed PKC activity in the db/db mouse kidney and phosphorylation of serine 433 in KLHL3 (KLHL3 Conclusions: Dysregulation of KLHL3 is involved in the pathophysiology of type 2 diabetes. These data offer a rationale for use of thiazide in individuals with diabetes and provide insights into the mechanism for cardiorenal protective effects of SGLT2 inhibitors.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Animals ; Carrier Proteins/metabolism ; Cells, Cultured ; Diabetes Mellitus, Experimental/metabolism ; Glucosides/pharmacology ; Humans ; Hypertension/etiology ; Hypertension/physiopathology ; Kidney Tubules, Distal/cytology ; Mice ; Mice, Obese ; Microfilament Proteins/genetics ; Microfilament Proteins/metabolism ; Phosphorylation ; Protein Kinase C/metabolism ; Sensitivity and Specificity ; Signal Transduction ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Solute Carrier Family 12, Member 3/metabolism ; Thiophenes/pharmacology ; WNK Lysine-Deficient Protein Kinase 1/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Carrier Proteins ; Glucosides ; KLHL3 protein, mouse ; Microfilament Proteins ; Sodium-Glucose Transporter 2 Inhibitors ; Solute Carrier Family 12, Member 3 ; Thiophenes ; ipragliflozin (3N2N8OOR7X) ; WNK Lysine-Deficient Protein Kinase 1 (EC 2.7.11.1) ; Protein Kinase C (EC 2.7.11.13)
Language	English
Publishing date	2019-03-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2018070703
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Podocyte Injury and Albuminuria in Experimental Hyperuricemic Model Rats.

Asakawa, Shinichiro / Shibata, Shigeru / Morimoto, Chikayuki / Shiraishi, Takeshi / Nakamura, Takashi / Tamura, Yoshifuru / Kumagai, Takanori / Hosoyamada, Makoto / Uchida, Shunya

Oxidative medicine and cellular longevity

2017 Volume 2017, Page(s) 3759153

Abstract: Although hyperuricemia is shown to accelerate chronic kidney disease, the mechanisms remain unclear. Accumulating studies also indicate that uric acid has both pro- and antioxidant properties. We postulated that hyperuricemia impairs the function of ... ...

Abstract	Although hyperuricemia is shown to accelerate chronic kidney disease, the mechanisms remain unclear. Accumulating studies also indicate that uric acid has both pro- and antioxidant properties. We postulated that hyperuricemia impairs the function of glomerular podocytes, resulting in albuminuria. Hyperuricemic model was induced by oral administration of 2% oxonic acid, a uricase inhibitor. Oxonic acid caused a twofold increase in serum uric acid levels at 8 weeks when compared to control animals. Hyperuricemia in this model was associated with the increase in blood pressure and the wall-thickening of afferent arterioles as well as arcuate arteries. Notably, hyperuricemic rats showed significant albuminuria, and the podocyte injury marker, desmin, was upregulated in the glomeruli. Conversely, podocin, the key component of podocyte slit diaphragm, was downregulated. Structural analysis using transmission electron microscopy confirmed podocyte injury in this model. We found that urinary 8-hydroxy-2'-deoxyguanosine levels were significantly increased and correlated with albuminuria and podocytopathy. Interestingly, although the superoxide dismutase mimetic, tempol, ameliorated the vascular changes and the hypertension, it failed to reduce albuminuria, suggesting that vascular remodeling and podocyte injury in this model are mediated through different mechanisms. In conclusion, vasculopathy and podocytopathy may distinctly contribute to the kidney injury in a hyperuricemic state.
MeSH term(s)	Actins/metabolism ; Albuminuria/complications ; Animals ; Blood Pressure/drug effects ; Cyclic N-Oxides/pharmacology ; Deoxyguanosine/analogs & derivatives ; Deoxyguanosine/urine ; Desmin/metabolism ; Disease Models, Animal ; Hyperuricemia/chemically induced ; Hyperuricemia/complications ; Hyperuricemia/pathology ; Immunohistochemistry ; Kidney Glomerulus/drug effects ; Kidney Glomerulus/metabolism ; Male ; Microscopy, Electron, Transmission ; Oxidative Stress/drug effects ; Oxonic Acid/pharmacology ; Rats ; Rats, Sprague-Dawley ; Spin Labels ; Urate Oxidase/antagonists & inhibitors ; Urate Oxidase/metabolism ; Uric Acid/blood ; Xanthine Dehydrogenase/metabolism
Chemical Substances	Actins ; Cyclic N-Oxides ; Desmin ; Spin Labels ; smooth muscle actin, rat ; Uric Acid (268B43MJ25) ; Oxonic Acid (5VT6420TIG) ; 8-oxo-7-hydrodeoxyguanosine (88847-89-6) ; Xanthine Dehydrogenase (EC 1.17.1.4) ; Urate Oxidase (EC 1.7.3.3) ; Deoxyguanosine (G9481N71RO) ; tempol (U78ZX2F65X)
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2017/3759153
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Article: Discontinuation of Hemodialysis in a Patient with Anti-GBM Disease by the Treatment with Corticosteroids and Plasmapheresis despite Several Predictors for Dialysis-Dependence.

Fujigaki, Yoshihide / Morimoto, Chikayuki / Iino, Risa / Taniguchi, Kei / Kawamorita, Yosuke / Asakawa, Shinichiro / Toyoki, Daigo / Miyano, Shinako / Fujii, Wataru / Ota, Tatsuru / Shibata, Shigeru / Uchida, Shunya

Case reports in nephrology

2017 Volume 2017, Page(s) 7143649

Abstract: A 26-year-old man highly suspected of having antiglomerular basement membrane (GBM) disease was treated with corticosteroid pulse therapy 9 days after initial infection-like symptoms with high procalcitonin value. The patient required hemodialysis the ... ...

Abstract	A 26-year-old man highly suspected of having antiglomerular basement membrane (GBM) disease was treated with corticosteroid pulse therapy 9 days after initial infection-like symptoms with high procalcitonin value. The patient required hemodialysis the next day of the treatment due to oliguria. In addition to corticosteroid therapy, plasmapheresis was introduced and the patient could discontinue hemodialysis 43 days after the treatment. Kidney biopsy after initiation of hemodialysis confirmed anti-GBM disease with 86.3% crescent formation. Physician should keep in mind that active anti-GBM disease shows even high procalcitonin value in the absence of infection. To pursue recovery of renal function, the challenge of the immediate and persistent treatment with high-dose corticosteroids plus plasmapheresis for highly suspected anti-GBM disease is vitally important despite the presence of reported predictors for dialysis-dependence including oliguria and requiring hemodialysis at presentation.
Language	English
Publishing date	2017-10-11
Publishing country	United States
Document type	Case Reports
ZDB-ID	2627652-5
ISSN	2090-665X ; 2090-6641
ISSN (online)	2090-665X
ISSN	2090-6641
DOI	10.1155/2017/7143649
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Article ; Online: Emergence of Smoldering ANCA-associated Glomerulonephritis during the Clinical Course of Mixed Connective Tissue Disease and Sjögren's Syndrome.

Morimoto, Chikayuki / Fujigaki, Yoshihide / Tamura, Yoshifuru / Ota, Tatsuru / Shibata, Shigeru / Asako, Kurumi / Kikuchi, Hirotoshi / Kono, Hajime / Kondo, Fukuo / Yamaguchi, Yutaka / Uchida, Shunya

Internal medicine (Tokyo, Japan)

2017 Volume 57, Issue 12, Page(s) 1757–1762

Abstract: A 67-year-old woman presented with hematuria and proteinuria 16 and 11 months ago, respectively. She had been followed up as mixed connective tissue disease and Sjögren's syndrome for over 19 years. Blood chemistry showed no elevated serum creatinine or ... ...

Abstract	A 67-year-old woman presented with hematuria and proteinuria 16 and 11 months ago, respectively. She had been followed up as mixed connective tissue disease and Sjögren's syndrome for over 19 years. Blood chemistry showed no elevated serum creatinine or C-reactive protein but did reveal myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA) of 300 U/dL. A kidney biopsy showed pauci-immune focal necrotizing glomerulonephritis. She was treated with prednisolone and rituximab, resulting in normal urinalysis and decreased MPO-ANCA. The complication of ANCA-associated glomerulonephritis should not be overlooked when abnormal urinalysis findings appear in the course of connective tissue disease, irrespective of the presence of rapidly progressive glomerulonephritis.
MeSH term(s)	Aged ; Antibodies, Antineutrophil Cytoplasmic/metabolism ; Female ; Glomerulonephritis/complications ; Glomerulonephritis/drug therapy ; Glomerulonephritis/immunology ; Humans ; Mixed Connective Tissue Disease/complications ; Mixed Connective Tissue Disease/drug therapy ; Peroxidase/immunology ; Prednisolone/therapeutic use ; Proteinuria/complications ; Rituximab/therapeutic use ; Sjogren's Syndrome/complications ; Sjogren's Syndrome/drug therapy
Chemical Substances	Antibodies, Antineutrophil Cytoplasmic ; Rituximab (4F4X42SYQ6) ; Prednisolone (9PHQ9Y1OLM) ; Peroxidase (EC 1.11.1.7)
Language	English
Publishing date	2017-12-21
Publishing country	Japan
Document type	Case Reports ; Journal Article
ZDB-ID	32371-8
ISSN	1349-7235 ; 0021-5120 ; 0918-2918
ISSN (online)	1349-7235
ISSN	0021-5120 ; 0918-2918
DOI	10.2169/internalmedicine.9844-17
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