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Daochun Wang - One of the best experts on this subject based on the ideXlab platform.
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Rhein attenuates renal inflammatory injury of Uric Acid Nephropathy via lincRNA-Cox2/miR-150-5p/STAT1 axis.
International immunopharmacology, 2020Co-Authors: Zhijie Yang, Daochun WangAbstract:Rhein has protective effect on Uric Acid Nephropathy (UAN). This article aims to demystify the mechanism of function of rhein in UAN. Mouse kidney epithelial cell line (TCMK-1) was incubated with Uric Acid (UA) to induce inflammatory injury. Then, the TCMK-1 cells were treated with rhein. The relationships among lincRNA-Cox2, miR-150-5p and STAT1 were evaluated by luciferase reporter assay. CCK8 and flow cytometry were performed to detect cell proliferation and apoptosis. The levels of IL-6, IL-1β and TNF-α were investigated by enzyme linked immunosorbent assay. Western blot and quantitative real-time PCR were performed to examine the expression of genes and proteins. We found that UA suppressed proliferation and enhanced apoptosis and the levels of IL-6, IL-1β and TNF-α of TCMK-1 cells, which was effectively improved by rhein treatment. Furthermore, lincRNA-Cox2 overexpression caused an increase of apoptosis and inflammatory factors in the rhein-treated TCMK-1 cells. LincRNA-Cox2 regulated STAT1 expression by sponging miR-150-5p. And lincRNA-Cox2 promoted apoptosis and inflammatory injury of TCMK-1 cells by regulating miR-150-5p/STAT1 axis. In summary, our studies demonstrate that rhein has a protective effect against UAN by inhibiting renal inflammatory injury via lincRNA-Cox2/miR-150-5p/STAT1 axis.
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rhein attenuates renal inflammatory injury of Uric Acid Nephropathy via lincrna cox2 mir 150 5p stat1 axis
International Immunopharmacology, 2020Co-Authors: Zhijie Yang, Daochun WangAbstract:Rhein has protective effect on Uric Acid Nephropathy (UAN). This article aims to demystify the mechanism of function of rhein in UAN. Mouse kidney epithelial cell line (TCMK-1) was incubated with Uric Acid (UA) to induce inflammatory injury. Then, the TCMK-1 cells were treated with rhein. The relationships among lincRNA-Cox2, miR-150-5p and STAT1 were evaluated by luciferase reporter assay. CCK8 and flow cytometry were performed to detect cell proliferation and apoptosis. The levels of IL-6, IL-1β and TNF-α were investigated by enzyme linked immunosorbent assay. Western blot and quantitative real-time PCR were performed to examine the expression of genes and proteins. We found that UA suppressed proliferation and enhanced apoptosis and the levels of IL-6, IL-1β and TNF-α of TCMK-1 cells, which was effectively improved by rhein treatment. Furthermore, lincRNA-Cox2 overexpression caused an increase of apoptosis and inflammatory factors in the rhein-treated TCMK-1 cells. LincRNA-Cox2 regulated STAT1 expression by sponging miR-150-5p. And lincRNA-Cox2 promoted apoptosis and inflammatory injury of TCMK-1 cells by regulating miR-150-5p/STAT1 axis. In summary, our studies demonstrate that rhein has a protective effect against UAN by inhibiting renal inflammatory injury via lincRNA-Cox2/miR-150-5p/STAT1 axis.
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Long non-coding RNA ANRIL-mediated inflammation response is involved in protective effect of rhein in Uric Acid Nephropathy rats.
Cell & bioscience, 2019Co-Authors: Daochun Wang, Zhijie Yang, Na Yang, Junjun DongAbstract:The aim of this study was to investigate the role of long non-coding RNAs (LncRNAs) antisense non-coding RNA in the INK4 locus (ANRIL) in anti-inflammation of rhein in Uric Acid Nephropathy (UAN) rats. Rat models of UAN were induced by adenine and potassium oxonate. Enzyme-linked immunosorbent assay (ELISA) was performed to assess inflammation factor in serum and supernatant. ANRIL mRNA level was detected using real-time reverse transcription PCR (qRT-PCR). Immunostaining was used to observe pathological changes of renal tissues in rats. ANRIL and inflammatory factor levels were highly expressed in patient with UAN. Furthermore, rhein showed an observable effect on anti-inflammatory and renal protection in UAN rats, rhein inhibited expressions of ANRIL in vivo or in vitro. Besides, ANRIL-mediated inflammatory response attenuated protective effect of rhein. ANRIL-mediated inflammatory response attenuated the protective effect of rhein in UAN rats. This study showed an understanding of the role and mechanism of ANRIL in UAN, which provides a new target and therapy for the prevention and treatment of UAN.
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Long non-coding RNA ANRIL-mediated inflammation response is involved in protective effect of rhein in Uric Acid Nephropathy rats
BMC, 2019Co-Authors: Daochun Wang, Zhijie Yang, Na Yang, Junjun DongAbstract:Abstract Background The aim of this study was to investigate the role of long non-coding RNAs (LncRNAs) antisense non-coding RNA in the INK4 locus (ANRIL) in anti-inflammation of rhein in Uric Acid Nephropathy (UAN) rats. Methods Rat models of UAN were induced by adenine and potassium oxonate. Enzyme-linked immunosorbent assay (ELISA) was performed to assess inflammation factor in serum and supernatant. ANRIL mRNA level was detected using real-time reverse transcription PCR (qRT-PCR). Immunostaining was used to observe pathological changes of renal tissues in rats. Results ANRIL and inflammatory factor levels were highly expressed in patient with UAN. Furthermore, rhein showed an observable effect on anti-inflammatory and renal protection in UAN rats, rhein inhibited expressions of ANRIL in vivo or in vitro. Besides, ANRIL-mediated inflammatory response attenuated protective effect of rhein. Conclusions ANRIL-mediated inflammatory response attenuated the protective effect of rhein in UAN rats. This study showed an understanding of the role and mechanism of ANRIL in UAN, which provides a new target and therapy for the prevention and treatment of UAN
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LncRNA ANRIL promotes NLRP3 inflammasome activation in Uric Acid Nephropathy through miR-122-5p/BRCC3 axis.
Biochimie, 2018Co-Authors: Daochun Wang, Zhijie Yang, Junjun DongAbstract:Abstract This study is designed to explore the mechanism by which long non-coding RNA (lncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) plays a pathogenic role in Uric Acid Nephropathy (UAN). The expressions of ANRIL, miR-122-5p, BRCA1-BRCA2-containing complex subunit 3 (BRCC3) and NOD-like receptor protein 3 (NLRP3) were determined in UAN patients and Uric Acid-treated HK-2 cells by qRT-PCR. Protein levels of BRCC3 and NLRP3 were examined by western blot. The levels of inflammatory cytokines were quantified by ELISA. CCK-8 assay was used to assess cell viability. Apoptosis was detected by Annexin V-FITC/PI double-labeled flow cytometry and TUNEL assay. The interaction between ANRIL, miR-122-5p and BRCC3 were studied using luciferase reporter assay. The role of ANRIL in renal injury was evaluated in experimental rats. ANRIL and BRCC3 were highly expressed while miR-122-5p was down-regulated in serum of UAN patients and Uric Acid-treated tubular epithelial cells. Luciferase reporter assay and in vitro rescue experiment confirmed that ANRIL promoted NLRP3 inflammasome activation by up-regulating BRCC3 expression via sponging miR-122-5p. Furthermore, in vivo experiment validated that knockdown of ANRIL alleviated renal injury of UAN rats. ANRIL exerted pathogenic effect in UAN to promote NLRP3 inflammasome activation via miR-122-5p/BRCC3 axis.
Junjun Dong - One of the best experts on this subject based on the ideXlab platform.
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Long non-coding RNA ANRIL-mediated inflammation response is involved in protective effect of rhein in Uric Acid Nephropathy rats.
Cell & bioscience, 2019Co-Authors: Daochun Wang, Zhijie Yang, Na Yang, Junjun DongAbstract:The aim of this study was to investigate the role of long non-coding RNAs (LncRNAs) antisense non-coding RNA in the INK4 locus (ANRIL) in anti-inflammation of rhein in Uric Acid Nephropathy (UAN) rats. Rat models of UAN were induced by adenine and potassium oxonate. Enzyme-linked immunosorbent assay (ELISA) was performed to assess inflammation factor in serum and supernatant. ANRIL mRNA level was detected using real-time reverse transcription PCR (qRT-PCR). Immunostaining was used to observe pathological changes of renal tissues in rats. ANRIL and inflammatory factor levels were highly expressed in patient with UAN. Furthermore, rhein showed an observable effect on anti-inflammatory and renal protection in UAN rats, rhein inhibited expressions of ANRIL in vivo or in vitro. Besides, ANRIL-mediated inflammatory response attenuated protective effect of rhein. ANRIL-mediated inflammatory response attenuated the protective effect of rhein in UAN rats. This study showed an understanding of the role and mechanism of ANRIL in UAN, which provides a new target and therapy for the prevention and treatment of UAN.
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Long non-coding RNA ANRIL-mediated inflammation response is involved in protective effect of rhein in Uric Acid Nephropathy rats
BMC, 2019Co-Authors: Daochun Wang, Zhijie Yang, Na Yang, Junjun DongAbstract:Abstract Background The aim of this study was to investigate the role of long non-coding RNAs (LncRNAs) antisense non-coding RNA in the INK4 locus (ANRIL) in anti-inflammation of rhein in Uric Acid Nephropathy (UAN) rats. Methods Rat models of UAN were induced by adenine and potassium oxonate. Enzyme-linked immunosorbent assay (ELISA) was performed to assess inflammation factor in serum and supernatant. ANRIL mRNA level was detected using real-time reverse transcription PCR (qRT-PCR). Immunostaining was used to observe pathological changes of renal tissues in rats. Results ANRIL and inflammatory factor levels were highly expressed in patient with UAN. Furthermore, rhein showed an observable effect on anti-inflammatory and renal protection in UAN rats, rhein inhibited expressions of ANRIL in vivo or in vitro. Besides, ANRIL-mediated inflammatory response attenuated protective effect of rhein. Conclusions ANRIL-mediated inflammatory response attenuated the protective effect of rhein in UAN rats. This study showed an understanding of the role and mechanism of ANRIL in UAN, which provides a new target and therapy for the prevention and treatment of UAN
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LncRNA ANRIL promotes NLRP3 inflammasome activation in Uric Acid Nephropathy through miR-122-5p/BRCC3 axis.
Biochimie, 2018Co-Authors: Daochun Wang, Zhijie Yang, Junjun DongAbstract:Abstract This study is designed to explore the mechanism by which long non-coding RNA (lncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) plays a pathogenic role in Uric Acid Nephropathy (UAN). The expressions of ANRIL, miR-122-5p, BRCA1-BRCA2-containing complex subunit 3 (BRCC3) and NOD-like receptor protein 3 (NLRP3) were determined in UAN patients and Uric Acid-treated HK-2 cells by qRT-PCR. Protein levels of BRCC3 and NLRP3 were examined by western blot. The levels of inflammatory cytokines were quantified by ELISA. CCK-8 assay was used to assess cell viability. Apoptosis was detected by Annexin V-FITC/PI double-labeled flow cytometry and TUNEL assay. The interaction between ANRIL, miR-122-5p and BRCC3 were studied using luciferase reporter assay. The role of ANRIL in renal injury was evaluated in experimental rats. ANRIL and BRCC3 were highly expressed while miR-122-5p was down-regulated in serum of UAN patients and Uric Acid-treated tubular epithelial cells. Luciferase reporter assay and in vitro rescue experiment confirmed that ANRIL promoted NLRP3 inflammasome activation by up-regulating BRCC3 expression via sponging miR-122-5p. Furthermore, in vivo experiment validated that knockdown of ANRIL alleviated renal injury of UAN rats. ANRIL exerted pathogenic effect in UAN to promote NLRP3 inflammasome activation via miR-122-5p/BRCC3 axis.
Zhijie Yang - One of the best experts on this subject based on the ideXlab platform.
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Rhein attenuates renal inflammatory injury of Uric Acid Nephropathy via lincRNA-Cox2/miR-150-5p/STAT1 axis.
International immunopharmacology, 2020Co-Authors: Zhijie Yang, Daochun WangAbstract:Rhein has protective effect on Uric Acid Nephropathy (UAN). This article aims to demystify the mechanism of function of rhein in UAN. Mouse kidney epithelial cell line (TCMK-1) was incubated with Uric Acid (UA) to induce inflammatory injury. Then, the TCMK-1 cells were treated with rhein. The relationships among lincRNA-Cox2, miR-150-5p and STAT1 were evaluated by luciferase reporter assay. CCK8 and flow cytometry were performed to detect cell proliferation and apoptosis. The levels of IL-6, IL-1β and TNF-α were investigated by enzyme linked immunosorbent assay. Western blot and quantitative real-time PCR were performed to examine the expression of genes and proteins. We found that UA suppressed proliferation and enhanced apoptosis and the levels of IL-6, IL-1β and TNF-α of TCMK-1 cells, which was effectively improved by rhein treatment. Furthermore, lincRNA-Cox2 overexpression caused an increase of apoptosis and inflammatory factors in the rhein-treated TCMK-1 cells. LincRNA-Cox2 regulated STAT1 expression by sponging miR-150-5p. And lincRNA-Cox2 promoted apoptosis and inflammatory injury of TCMK-1 cells by regulating miR-150-5p/STAT1 axis. In summary, our studies demonstrate that rhein has a protective effect against UAN by inhibiting renal inflammatory injury via lincRNA-Cox2/miR-150-5p/STAT1 axis.
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rhein attenuates renal inflammatory injury of Uric Acid Nephropathy via lincrna cox2 mir 150 5p stat1 axis
International Immunopharmacology, 2020Co-Authors: Zhijie Yang, Daochun WangAbstract:Rhein has protective effect on Uric Acid Nephropathy (UAN). This article aims to demystify the mechanism of function of rhein in UAN. Mouse kidney epithelial cell line (TCMK-1) was incubated with Uric Acid (UA) to induce inflammatory injury. Then, the TCMK-1 cells were treated with rhein. The relationships among lincRNA-Cox2, miR-150-5p and STAT1 were evaluated by luciferase reporter assay. CCK8 and flow cytometry were performed to detect cell proliferation and apoptosis. The levels of IL-6, IL-1β and TNF-α were investigated by enzyme linked immunosorbent assay. Western blot and quantitative real-time PCR were performed to examine the expression of genes and proteins. We found that UA suppressed proliferation and enhanced apoptosis and the levels of IL-6, IL-1β and TNF-α of TCMK-1 cells, which was effectively improved by rhein treatment. Furthermore, lincRNA-Cox2 overexpression caused an increase of apoptosis and inflammatory factors in the rhein-treated TCMK-1 cells. LincRNA-Cox2 regulated STAT1 expression by sponging miR-150-5p. And lincRNA-Cox2 promoted apoptosis and inflammatory injury of TCMK-1 cells by regulating miR-150-5p/STAT1 axis. In summary, our studies demonstrate that rhein has a protective effect against UAN by inhibiting renal inflammatory injury via lincRNA-Cox2/miR-150-5p/STAT1 axis.
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Long non-coding RNA ANRIL-mediated inflammation response is involved in protective effect of rhein in Uric Acid Nephropathy rats.
Cell & bioscience, 2019Co-Authors: Daochun Wang, Zhijie Yang, Na Yang, Junjun DongAbstract:The aim of this study was to investigate the role of long non-coding RNAs (LncRNAs) antisense non-coding RNA in the INK4 locus (ANRIL) in anti-inflammation of rhein in Uric Acid Nephropathy (UAN) rats. Rat models of UAN were induced by adenine and potassium oxonate. Enzyme-linked immunosorbent assay (ELISA) was performed to assess inflammation factor in serum and supernatant. ANRIL mRNA level was detected using real-time reverse transcription PCR (qRT-PCR). Immunostaining was used to observe pathological changes of renal tissues in rats. ANRIL and inflammatory factor levels were highly expressed in patient with UAN. Furthermore, rhein showed an observable effect on anti-inflammatory and renal protection in UAN rats, rhein inhibited expressions of ANRIL in vivo or in vitro. Besides, ANRIL-mediated inflammatory response attenuated protective effect of rhein. ANRIL-mediated inflammatory response attenuated the protective effect of rhein in UAN rats. This study showed an understanding of the role and mechanism of ANRIL in UAN, which provides a new target and therapy for the prevention and treatment of UAN.
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Long non-coding RNA ANRIL-mediated inflammation response is involved in protective effect of rhein in Uric Acid Nephropathy rats
BMC, 2019Co-Authors: Daochun Wang, Zhijie Yang, Na Yang, Junjun DongAbstract:Abstract Background The aim of this study was to investigate the role of long non-coding RNAs (LncRNAs) antisense non-coding RNA in the INK4 locus (ANRIL) in anti-inflammation of rhein in Uric Acid Nephropathy (UAN) rats. Methods Rat models of UAN were induced by adenine and potassium oxonate. Enzyme-linked immunosorbent assay (ELISA) was performed to assess inflammation factor in serum and supernatant. ANRIL mRNA level was detected using real-time reverse transcription PCR (qRT-PCR). Immunostaining was used to observe pathological changes of renal tissues in rats. Results ANRIL and inflammatory factor levels were highly expressed in patient with UAN. Furthermore, rhein showed an observable effect on anti-inflammatory and renal protection in UAN rats, rhein inhibited expressions of ANRIL in vivo or in vitro. Besides, ANRIL-mediated inflammatory response attenuated protective effect of rhein. Conclusions ANRIL-mediated inflammatory response attenuated the protective effect of rhein in UAN rats. This study showed an understanding of the role and mechanism of ANRIL in UAN, which provides a new target and therapy for the prevention and treatment of UAN
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LncRNA ANRIL promotes NLRP3 inflammasome activation in Uric Acid Nephropathy through miR-122-5p/BRCC3 axis.
Biochimie, 2018Co-Authors: Daochun Wang, Zhijie Yang, Junjun DongAbstract:Abstract This study is designed to explore the mechanism by which long non-coding RNA (lncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) plays a pathogenic role in Uric Acid Nephropathy (UAN). The expressions of ANRIL, miR-122-5p, BRCA1-BRCA2-containing complex subunit 3 (BRCC3) and NOD-like receptor protein 3 (NLRP3) were determined in UAN patients and Uric Acid-treated HK-2 cells by qRT-PCR. Protein levels of BRCC3 and NLRP3 were examined by western blot. The levels of inflammatory cytokines were quantified by ELISA. CCK-8 assay was used to assess cell viability. Apoptosis was detected by Annexin V-FITC/PI double-labeled flow cytometry and TUNEL assay. The interaction between ANRIL, miR-122-5p and BRCC3 were studied using luciferase reporter assay. The role of ANRIL in renal injury was evaluated in experimental rats. ANRIL and BRCC3 were highly expressed while miR-122-5p was down-regulated in serum of UAN patients and Uric Acid-treated tubular epithelial cells. Luciferase reporter assay and in vitro rescue experiment confirmed that ANRIL promoted NLRP3 inflammasome activation by up-regulating BRCC3 expression via sponging miR-122-5p. Furthermore, in vivo experiment validated that knockdown of ANRIL alleviated renal injury of UAN rats. ANRIL exerted pathogenic effect in UAN to promote NLRP3 inflammasome activation via miR-122-5p/BRCC3 axis.
Chiu-ching Huang - One of the best experts on this subject based on the ideXlab platform.
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Neglected cause of renal failure in cancer patients: Spontaneous tumor lysis syndrome inducing acute Uric Acid Nephropathy
Dialysis & Transplantation, 2004Co-Authors: Hsiang-hao Hsu, Jin-yu Lin, Shu-chen Hsu, Yi-ling Chan, Chiu-ching HuangAbstract:Background. Acute spontaneous tumor lysis syndrome (STLS) presenting with hyperUricemic acute renal failure (ARF) is a rare disease that is probably overlooked in patients with neoplastic disorders. This study attempted to define the incidence, clinical characteristics, therapeutic approaches, and prognosis of this entity. Methods. A retrospective study was conducted, reviewing the records of all patients who developed ARF at Chang Gung Memorial Hospital between July 1, 1999, and June 30, 2003. Results. STLS-induced acute Uric Acid Nephropathy was identified in 12 of 1,072 ARF patients (1.1%) during the study period. Most presentations were non-specific or related to the symptoms of malignancy. All patients had advanced-stage tumors with large tumor burden, and abdominal organs were involved in 66. 7% of cases. All 12 hyperUricemic patients became oligUric despite conservative therapy, and were still hyperUricemic (21.6 ± 5.2 mg/dl) before dialysis therapy. Diuresis developed in 8 patients (66. 7%), with associated resolution of hyperUricemia, azotemia, and metabolic derangements after dialysis initiation. The patients who developed diuresis had mean serum Uric Acid levels of 9.8 ± 3.3 mg/dl, and median levels of 10.3 mg/dl. Four patients (33.3%) survived, with 2 suffering residual renal function impairment. Conclusion. Acute STLS presenting with hyperUricemic ARF is rare and is easily overlooked as a cause of acute Uric Acid Nephropathy in patients with bulky or occult neoplastic disorders. In contrast to hyperUricemia and oliguria, which are constant findings, azotemia or impaired renal function is not always present on initial presentation. Despite poor outcomes in patients with STLS developing acute Uric Acid Nephropathy, early recognition, aggressive management, and prompt dialysis are mandatory.
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Acute spontaneous tumor lysis presenting with hyperUricemic acute renal failure: clinical features and therapeutic approach.
Journal of nephrology, 2004Co-Authors: Hsiang-hao Hsu, Yi-ling Chan, Chiu-ching HuangAbstract:BACKGROUND: Acute spontaneous tumor lysis syndrome (STLS) presenting with hyperUricemic acute renal failure (ARF) is a rare disease which can be overlooked in patients with neoplasic disorders, requiring prompt recognition and aggressive management. This study examined the incidence, clinical characteristics and prognosis of this condition. METHODS: A retrospective study was performed, reviewing the records of all patients who developed ARF at Chang Gung Memorial Hospital between 1st July 1999 and 30th October 2002. Acute STLS was diagnosed based on pretreatment hyperUricemic ARF, ratio of urinary Uric Acid to creatinine (Cr) >1.0, and significantly elevated lactate dehydrogenase (LDH) (>500 units/L), together with a pathologically proven malignancy. Clinical course, metabolic parameters, response to therapeutics and outcome were assessed in all patients. RESULTS: STLS-induced acute Uric Acid Nephropathy was identified in 10 out of 926 ARF patients (1.08%) studied. Most presentations were non-specific or related to malignancy symptoms. All patients had advanced tumors with large tumor burden, and abdominal organ involvement in 80% of patients. The 10 hyperUricemic patients became oligUric despite conservative therapy, and remained hyperUricemic (mean +/- SD: 20.7 +/- 5.0 mg/dL) until dialysis initiation. Seven patients (70%) developed diuresis, with an associated resolution of hyperUricemia, azotemia and metabolic derangements following dialysis initiation. The patients who developed diuresis had mean serum Uric Acid levels 9.3 +/- 3.1 mg/dL and median levels 9.8 mg/dL. Three patients (30%) survived, with two patients suffering residual renal function impairment. CONCLUSIONS: Acute STLS presenting with hyperUricemic ARF is a rare cause of acute Uric Acid Nephropathy in patients with bulky or occult neoplastic disorders. The tumors that developed STLS had advanced stage or large tumor burden. Frequent abdominal organ involvement and non-specific initial presentations can obscure the nature of the disease and delay diagnosis. Unlike hyperUricemia and oliguria, which are constant findings, azotemia or impaired renal function is not always manifest on initial presentation. Poor outcomes in patients with STLS developing acute Uric Acid Nephropathy make early recognition, aggressive management and prompt dialysis mandatory.
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Acute Spontaneous Tumor Lysis in Anaplastic Large T-Cell Lymphoma Presenting with HyperUricemic Acute Renal Failure
International Journal of Hematology, 2004Co-Authors: Hsiang-hao Hsu, Chiu-ching HuangAbstract:Acute spontaneous tumor lysis (ASTL) syndrome, an extremely rare disease, requires prompt recognition and aggressive management because it is fulminant at its outset, associated with severe metabolic derangement, and potentially reversible. We describe an unusual case in which spontaneous tumor lysis occurred in anaplastic large T-cell lymphoma associated with acute Uric Acid Nephropathy, persistent oliguria, and shock. This case contrasts markedly with previously reported cases of ASTL syndrome, which developed mainly in the pathologic type of Burkitt lymphoma. To our knowledge, this is the first reported occurrence of ASTL syndrome associated with anaplastic large T-cell type lymphoma. This report also chronicles our successful experience with continuous renal replacement therapy in the presence of compromised hemodynamic status.
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An enormous abdominal mass associated with acute renal failure.
Renal failure, 2001Co-Authors: Hsiang-hao Hsu, Yung-chang Chen, Ji-tseng Fang, Chun-liang Lin, Chiu-ching HuangAbstract:We report a 67-year-old man with acute Uric Acid Nephropathy, secondary to spontaneous tumor lysis syndrome, that presented itself as a huge intra-abdominal tumor that led to acute renal failure, hyperUricemia, and azotemia. Initial finding of hydronephrosis detected by ultrasonography led us to believe that the azotemia and decreasing amount of urine resulted from obstructive uropathy, a common complication of malignancy, caused by either a direct renal invasion or a urinary outflow tract compression because of a tumor mass effect. However, clinical observations and the response to therapeutic intervention confirmed the diagnosis of spontaneous tumor lysis syndrome, which is a rare cause of acute Uric Acid Nephropathy.
Lan-lan Zhou - One of the best experts on this subject based on the ideXlab platform.
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Protective effect of iridoid glycosides from Paederia scandens (LOUR.) MERRILL (Rubiaceae) on Uric Acid Nephropathy rats induced by yeast and potassium oxonate.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2013Co-Authors: Shi-xiang Hou, Wen-jing Zhu, Ming-qun Pang, Joseph Jeffry, Lan-lan ZhouAbstract:Iridoid glycosides of Paederia scandens (IGPS) are an active component isolated from Chinese herb P. scandens (LOUR.) MERRILL (Rubiaceae). Uric Acid Nephropathy (UAN) is caused by excessive Uric Acid, which results in damage of kidney tissue via urate crystals deposition in the kidneys. This study aimed to investigate the protective effects of IGPS on UAN in rats induced by yeast and potassium oxonate. Treatment groups received different doses of IGPS and allopurinol (AP) daily for 35 days respectively. The results showed that treatment with IGPS significantly prevented the increases of Uric Acid in serum and the elevation of systolic blood pressure (SBP), attenuated renal tissue injury, improved renal function and reserved the biological activity of NOS-1. IGPS also inhibited the biological activity of TNF-α and TGF-β1, and suppressed the mRNA expressions of TNF-α and TGF-β1 in renal tissue. Taken together, the present and our previous findings suggest that IGPS exerts protective effects against kidney damage in UAN rats through its Uric Acid-lowering, anti-inflammatory and immunomodulatory properties. Furthermore, decreasing SBP by up regulation of NOS-1 expression and down regulation of TNF-α and TGF-β1 expression are involved in the effect of IGPS on high Uric Acid-induced Nephropathy.
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Anti-inflammatory and immunomodulatory effects of iridoid glycosides from Paederia scandens (LOUR.) MERRILL (Rubiaceae) on Uric Acid Nephropathy rats
Life sciences, 2012Co-Authors: Wen-jing Zhu, Ming-qun Pang, Liuyi Dong, Xueying Huang, Shuangmiao Wang, Lan-lan ZhouAbstract:Abstract Aims Uric Acid Nephropathy (UAN) is due to excessive Uric Acid, which leads to hyperUricemia and kidney damage via the deposition of urate microcrystals in the kidneys. Iridoid glycosides of Paederia scandens (IGPS) is a major active component isolated from the traditional Chinese herb P. scandens (LOUR.) MERRILL (Rubiaceae). This study aimed to evaluate the anti-inflammatory and immunomodulatory effects of IGPS and its mechanism on UAN rats. Main methods The experimental model of UAN rats was induced by using Uricopoiesis promoter adenine and Uricase inhibitor potassium oxonate (PO). Treatment groups received three different doses of IGPS, allopurinol (AP) and benzbromarone (BEN) daily for 24 days respectively. The histopathology of renal tissues in UAN rats were assessed for conventional morphological evaluation. The nuclear factor-κBp65 (NF- κ Bp65), monocyte chemoattractant protein-1 (MCP-1) and α-smooth muscle actin (α-SMA) protein expression of renal tissues in UAN rats were investigated by immunohistochemistry. MCP-1 and α-SMA mRNA levels were monitored by method of reverse transcription polymerase chain reaction (RT-PCR). Key findings Treatment with IGPS significantly ameliorated UAN induced renal tissue injury, inhibited the biological activity of NF- κ Bp65, MCP-1 and α-SMA, and suppressed the mRNA expressions of MCP-1 and α-SMA. Significance IGPS exerts a protective effect against renal injury in UAN rats, possesses anti-inflammatory and immunomodulatory effects by inactivating NF- κ Bp65 pathway transmembrane signal transduction, down regulating the expression of MCP-1 and α-SMA to modulate pro-inflammatory mediator production in Nephropathy tissue to improve renal fibrosis in UAN rats.
