• 제목/요약/키워드: Kidney function

검색결과 877건 처리시간 0.028초

분리 대두단백질 섭취와 염분 제한이 Streptozotocin으로 유도된 당뇨 횐쥐의 혈청 지질 수준 및 신장기능에 미치는 영향 (The Effects of Isolated Soyprotein and Salt Restriction on Serum Lipid and Kidney Function of Streptozotocin-Induced Diabetic Rats)

  • 정수현;박양자
    • 동아시아식생활학회지
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    • 제11권5호
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    • pp.368-378
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    • 2001
  • This study was performed to investigate the effects of isolated soyprotein and salt (NaCl) restriction on the serum lipid and the kidney functions of streptozotocin-induced diabetic rats. Sprague-Dawley males of normal and streptozotocin-induced diabetic rats were raised for 6 weeds divided into 4 groups each according to protein sources and salt levels. The sources of protein were isolated soyprotein and casein. Salt levels tested were 0.1% (normal) and 0.01% (low). The results are summarized as fellows: kidney weight, blood glucose, hemoglobinAlc, GFR and urinary protein of diabetic groups were higher than those of normal groups. Isolated soyprotein lowered total lipids, triglycerides, and total cholesterol in serum and plasma angiotensin II concentration as well as alleviated kidney enlargement and GFR in diabetic rats. Salt restriction didn\\`t affect serum lipid level but decreased GFR and increased angiotensin If concentration. In conclusion, isolated soyprotein decreased serum lipids, plasma angiotensin II concentration, sidney enlargement and GFR, while salt restriction increased plasma angiotensin II concentration. The results suggest that isolated soyprotein and salt restriction seem to cause different effects on plasma angiotensin II concentration and that isolated soyprotein might be of value in the prevention of diabetic artherosclerosis and diabetic hypertension.

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Dopamine $D_1$ Receptor 효능제인 SKF 81297의 신장작용 (Renal Action of SKF 81297, Dopamine $D_1$ Receptor Agonist, in Dogs)

  • 고석태;정경희
    • Biomolecules & Therapeutics
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    • 제9권3호
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    • pp.209-217
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    • 2001
  • This study was attempted to investigate on renal effect of ($\pm$)6-chloro-7,8-dihydroxy-1-phenol 2,3,4,5-tetrahydro-lH-3 benzazepine (SKF 81297), dopamine $D_1$ receptor agonist, in dog. SKF 81297, when gluten intravenously, produced diuretic action along with the increases of renal plasma flow (RPF), glomerular filtration rate (GFR), amounts of N $a^{+}$ and $K^{+}$ excreted into urine ( $E_{Na}$ , $E_{K}$) and osmolar clearance ( $C_{osm}$). It also decreased the reabsorption rates of N $a^{+}$ and $K^{+}$ in renal tubule ( $R_{Na}$ , $R_{K}$) and free water clearance ( $C_{H2O}$), whereas ratios of $K^{+}$ agonist N $a^{+}$ in urine and filtration fraction (FF) was not changed. SKF 81297, when administered into a renal artery, elicited diuresis both in experimental kidney given the SKF 81297 and control kidney not given, while the effect was more remarkable in experimental kidney than those exhibited in control kidney. SKF 81297 given into carotid artery also exhibited diuresis, the potency at this time, compared to those induced by intravenous SKF 81297, was magnusgreat. Above results suggest that SKF 81297 produces diuresis by both indirect action through changes of central function and direct action being induced in kidney. Central diuretic action is mediated by improvement of renal hemodynamics, but direct action by inhibition of electrolytes reabsorption in renal tubule.enal tubule. tubule.

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Carbon monoxide releasing molecule-2 protects mice against acute kidney injury through inhibition of ER stress

  • Uddin, Md Jamal;Pak, Eun Seon;Ha, Hunjoo
    • The Korean Journal of Physiology and Pharmacology
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    • 제22권5호
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    • pp.567-575
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    • 2018
  • Acute kidney injury (AKI), which is defined as a rapid decline of renal function, becomes common and recently recognized to be closely intertwined with chronic kidney diseases. Current treatment for AKI is largely supportive, and endoplasmic reticulum (ER) stress has emerged as a novel mediator of AKI. Since carbon monoxide attenuates ER stress, the objective of the present study aimed to determine the protective effect of carbon monoxide releasing molecule-2 (CORM2) on AKI associated with ER stress. Kidney injury was induced after LPS (15 mg/kg) treatment at 12 to 24 h in C57BL/6J mice. Pretreatment of CORM2 (30 mg/kg) effectively prevented LPS-induced oxidative stress and inflammation during AKI in mice. CORM2 treatment also effectively inhibited LPS-induced ER stress in AKI mice. In order to confirm effect of CO on the pathophysiological role of tubular epithelial cells in AKI, we used mProx24 cells. Pretreatment of CORM2 attenuated LPS-induced ER stress, oxidative stress, and inflammation in mProx24 cells. These data suggest that CO therapy may prevent ER stress-mediated AKI.

Effects of Albizia julibrissin Durazz through Suppression of Mitochondrial Fission and Apoptosis in Cisplatin-induced Acute Kidney Injury

  • Hui-Ju Lee;Kyung-Hyun Kim;Yae-Ji Kim;Sung-Pil Cho;Geum-Lan Hong;Ju-Young Jung
    • Natural Product Sciences
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    • 제28권4호
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    • pp.194-200
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    • 2022
  • Albizia julibrissin Durazz. (AJ; family Minosaceae) is widely distributed worldwide, and its stem bark has been used as a traditional herbal medicine. Acute kidney injury (AKI) is a clinical syndrome that results in sudden loss of renal function. This study aimed to investigate the effects of AJ against cisplatin-induced AKI using a human kidney proximal tubule epithelial cell line (HK-2) and cisplatin-treated mice. In vitro, cisplatin treatment increased apoptosis in HK-2 cells. However, AJ treatment decreased apoptosis of cisplatin-treated HK-2 cells. In vivo, cisplatin treatment accelerated renal injury by increasing the levels of renal injury markers, such as blood urea nitrogen, creatinine, kidney injury molecule 1, and neutrophil gelatinase-associated lipocalin, which were reversed by AJ treatment. Histopathologically, AJ treatment resulted in decreased renal damage with less tubular necrosis and brush border desquamation compared with the AKI group. Additionally, cisplatin treatment upregulated mitochondrial fission, a pathological characteristic of AKI, which was downregulated by AJ treatment. Along with increased mitochondrial fission, AJ treatment also reduced cisplatin-induced apoptosis. These results suggest that AJ may be a potential therapeutic agent for cisplatin-induced AKI.

왕호고(王好古)의 음증학설(陰證學說)에 대한 연구(硏究) (The Research of Wang HaoGu's Eum Syndrom Theory)

  • 조병일;김용진
    • 대한한의학원전학회지
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    • 제20권2호
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    • pp.125-135
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    • 2007
  • Eum Syndrom include symptoms which is because by the cold thingsand by the infection of SamEum of TaeEum, SoEum, GualEum in Treatise On Exogenous Febrile Diseases(傷寒論). After Wang HoGo, many medical people had proceed the research of Eum Syndrom, but recently, we have almost never or no nothing research about that. So, I want to make modern base of Eum syndrom, and researched mainly for the "YinZhengLueLi". That can be summarized like below. Eum Syndrom shows firstly red face, tremor, waist-and-leg heaviness, lastly body heaviness, fatigue, narcolepsy, congestion of the pupils because of from exogenous attack of wind-cold, impairment of spleen due to Cold things, and dew and mist and rain and damp's invation by mouth and nose, greedy of sexual desire, So, in the diagnosis of Eum Syndrom, we have to look over precisely the color and pulse, especially, by pulse. We can know that, he used the prescription which are have heating kidney function, Byuklyuksan, Jungyangsan, Huahamsan, Huiyangdan, Baneumdan etc, and the prescription which are have strengthening spleen and kidney, Bujasan, Yukgyesan, Bakchulsan etc. So, we can know that he was very interested in deficiency and cold of kidney's function. While, he newly made the prescriptions of Sinchultang, Bakchultang, Huanggitang, Jujunghuan, and he used various prescriptions.

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Deficiency of antidiuretic hormone: a rare cause of massive polyuria after kidney transplantation

  • Jang, Kyung Mi;Sohn, Young Soo;Hwang, Young Ju;Choi, Bong Seok;Cho, Min Hyun
    • Clinical and Experimental Pediatrics
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    • 제59권4호
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    • pp.202-204
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    • 2016
  • A 15-year-old boy, who was diagnosed with Alport syndrome and end-stage renal disease, received a renal transplant from a living-related donor. On postoperative day 1, his daily urine output was 10,000 mL despite normal graft function. His laboratory findings including urine, serum osmolality, and antidiuretic hormone levels showed signs similar to central diabetes insipidus, so he was administered desmopressin acetate nasal spray. After administering the desmopressin, urine specific gravity and osmolality increased abruptly, and daily urine output declined to the normal range. The desmopressin acetate was tapered gradually and discontinued 3 months later. Graft function was good, and urine output was maintained within the normal range without desmopressin 20 months after the transplantation. We present a case of a massive polyuria due to transient deficiency of antidiuretic hormone with the necessity of desmopressin therapy immediately after kidney transplantation in a pediatric patient.

Melatonin Protects Chronic Kidney Disease Mesenchymal Stem/Stromal Cells against Accumulation of Methylglyoxal via Modulation of Hexokinase-2 Expression

  • Go, Gyeongyun;Yoon, Yeo Min;Yoon, Sungtae;Lee, Gaeun;Lim, Ji Ho;Han, Su-Yeon;Lee, Sang Hun
    • Biomolecules & Therapeutics
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    • 제30권1호
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    • pp.28-37
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    • 2022
  • Treatment options for patients with chronic kidney disease (CKD) are currently limited; therefore, there has been significant interest in applying mesenchymal stem/stromal cell (MSC)-based therapy to treat CKD. However, MSCs harvested from CKD patients tend to show diminished viability and proliferation due to sustained exposure to uremic toxins in the CKD environment, which limits their utility for cell therapy. The application of melatonin has been demonstrated to improve the therapeutic efficacy of MSCs derived from and engrafted to tissues in patients suffering from CKD, although the underlying biological mechanism has not been elucidated. In this study, we observed overexpression of hexokinase-2 (HK2) in serum samples of CKD patients and MSCs harvested from an adenine-fed CKD mouse model (CKD-mMSCs). HK2 upregulation led to increased production levels of methylglyoxal (MG), a toxic metabolic intermediate of abnormal glycolytic processes. The overabundance of HK2 and MG was associated with impaired mitochondrial function and low cell proliferation in CKD-mMSCs. Melatonin treatment inhibited the increases in HK2 and MG levels, and further improved mitochondrial function, glycolytic metabolism, and cell proliferation. Our findings suggest that identifying and characterizing metabolic regulators such as HK2 in CKD may improve the efficacy of MSCs for treating CKD and other kidney disorders.

염분 섭취에 의한 시스플라틴 유도 급성 신장 손상의 촉진과 염증 반응과의 연관성 (Facilitation of cisplatin-induced acute kidney injury by high salt intake through increased inflammatory response)

  • 지선영;황보현;김민영;김다혜;박범수;박정현;이배진;이혜숙;최영현
    • 한국해양바이오학회지
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    • 제13권2호
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    • pp.86-93
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    • 2021
  • A high salt diet contributes to kidney damage by causing hypoxia and oxidative stress. Recently, an increase in dietary salt has been reported to induce an inflammatory phenotype in immune cells, further contributing to kidney damage. However, studies on the exact mechanism and role of a high salt diet on the inflammatory response in the kidneys are still insufficient. In this study, a cisplatin-induced acute kidney injury model using C57BL/6 mice was used to analyze the effect of salt intake on kidney injury. Results showed that high salt administration aggravated kidney edema in mice induced by treatment with cisplatin. Moreover, the indicators of kidney and liver function impairment were significantly increased in the group cotreated with high salt compared with that treated with cisplatin alone. Furthermore, the exacerbation of kidney damage by high salt administration was also associated with a decrease in the number of cells in the immune regulatory system. Additionally, high salt administration further decreased renal perfusion functions along with increased cisplatin-induced damage to proximal tubules. This was accompanied by increased expression of T cell immunoglobulin, mucin domain 1 (a biomarker of kidney injury), and Bax (a pro-apoptotic factor). Moreover, cisplatin-induced expression of proinflammatory mediators and cytokines, including cyclooxygenase-2 and tumor necrosis factor-α in kidney tissue, was further increased by high salt intake. Therefore, these results indicate that the kidney's inflammatory response by high salt treatment can further promote kidney damage caused by various pathological factors.

신장 조직의 방사선 손상과 천연물질의 방어기전 연구 (Protection Effect of Natual Matter and Radiation Damage on Kidney Tissue)

  • 지태정
    • 한국콘텐츠학회논문지
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    • 제9권12호
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    • pp.376-384
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    • 2009
  • 본 연구는 방사선조사 후 신장 조직의 손상과 방어기전을 알아보고자 생쥐 모델을 이용하여 미세구조를 관찰하였다. 광학현미경(LM)의 관찰 결과; 5Gy 조사 후 10일된 신장 조직에서는 정상조직과 비교하여 사구체가 위축되었으며, 10Gy 관찰에서는 곱슬세관(convoluted tubules)의 막이 파괴되어 세포질이 유출되었다. 투과전자현미경(TEM) 관찰 결과; 5Gy 조사에서는 사립체의 막이 파괴되거나 함몰된 것으로 관찰되었으며, 내부 크리스테의 형태도 소실되었다. 또한 일부에서는 핵막의 파괴도 확인되었다. 10Gy 조사한 조직에서는 기저막의 파괴가 뚜렷하게 관찰되고, 용해소체도 비후 된 것을 관찰하였다. 하지만 프로폴리스 섭식한 실험 군에서는 소기관의 형태가 뚜렷하게 관찰되었고, 핵막과 염색질도 선명하게 관찰되어 방어효과를 확인할 수 있었다.

Cisplatin 유도 급성신부전에서 Klotho 단백질의 발현 (Localization of Klotho in cisplatin induced acute kidney failure)

  • 박소라;김태원;김영중;김현태;류시윤;정주영
    • 대한수의학회지
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    • 제54권4호
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    • pp.225-231
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    • 2014
  • Klotho deficiency is an early event in acute kidney injury (AKI) that exacerbates acute kidney damage. The present study explored the expression of Klotho and inflammation related factors in cisplatin-induced AKI. Rats (n = 18) were treated with cisplatin intraperitoneal injection (5 mg/kg) or left untreated as controls (n = 6), then sacrificed at 5 (n = 6) and 10 days (n = 6) treatment. Five days after cisplatin injection, the serum kidney enzymes and kidney cell apoptosis were significantly increased. Moreover, the expression of Klotho was decreased when compared to the control group, especially in the cortex and outer medulla regions. In contrast, inflammation related signals including nuclear factor kappa B, tumor necrosis factor-${\alpha}$, and tumor necrosis factor-like weak inducer of apoptosis were enhanced. However, 10 days after cisplatin injection, Klotho expression was enhanced upon both IHC and Western blot analysis, with slightly recovered renal function and decreased apoptosis. Furthermore, inflammation related signals expression was decreased relative to the 5 days group. Overall, this study confirmed the opposite expression patterns between Klotho and inflammation related signals and their localization in cisplatin-induced AKI kidney.