• Title/Summary/Keyword: Polycystic kidneys

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Mitogen-activated Protein Kinases in the Development of Normal and Diseased Kidneys

  • Awazu, Midori
    • Childhood Kidney Diseases
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    • v.21 no.1
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    • pp.1-7
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    • 2017
  • Mitogen-activated protein kinases (MAPKs) play important roles in various cellular functions including proliferation, differentiation, and apoptosis. We showed that MAPKs are developmentally regulated in the rat kidney. p38 MAPK (p38) and extracellular signal-regulated kinase (ERK) were strongly expressed in the fetal kidney, whereas c-Jun N-terminal kinase (JNK) was detected predominantly in the adult kidney. The inhibition of p38 or ERK in organ culture resulted in reduced nephron formation with or without reduced kidney size. On the other hand, persistent fetal expression pattern of MAPKs, i.e., upregulation of p38 and ERK and downregulation of JNK, was observed in the cyst epithelium of human renal dysplasia, ovine fetal obstructive uropathy, and pcy mice, a model of polycystic kidney disease. Furthermore, activated p38 and ERK induced by cyclic stretch mediated proliferation and $TGF-{\beta}1$ expression in ureteric bud cells, probably leading to cyst formation and dysplastic changes. Inhibition of ERK slowed the disease progression in pcy mice. Finally, ERK and p38 were inactivated in the early embryonic kidney subjected to maternal nutrient restriction, characterized by reduced ureteric branching and nephron number. Thus, MAPKs mediate the development of normal and diseased kidney. Their modulation may result in novel therapeutic strategies against developmental abnormalities of the kidney.

NCAM as a cystogenesis marker gene of PKD2 overexpression

  • Yoo, Kyung-Hyun;Lee, Tae-Young;Yang, Moon-Hee;Park, Eun-Young;Yook, Yeon-Joo;Lee, Hyo-Soo;Park, Jong-Hoon
    • BMB Reports
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    • v.41 no.8
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    • pp.593-596
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    • 2008
  • ADPKD (Autosomal Dominant Polycystic Kidney Disease) is characterized by the progressive expansion of multiple cystic lesions in the kidneys. ADPKD is caused by mutations in Ed-pl. consider PKD1 and PKD2. Recently a relation between c-myc and the pathogenesis of ADPKD was reported. In addition, c-Myc is a downstream effector of PKD1. To identify the gene regulated by PKD2 and c-Myc, we performed gene expression profiling in PKD2 and c-Myc overexpressing cells using a human 8K cDNA microarray. NCAM (neuronal cell adhesion molecule) levels were significantly reduced in PKD2 overexpressing systems in vitro and in vivo. These results suggest that NCAM is an important molecule in the cystogenesis induced by PKD2 overexpession.

How to delay the progression of chronic kidney disease: focusing on medications

  • Jeesu Min
    • Childhood Kidney Diseases
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    • v.28 no.2
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    • pp.51-58
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    • 2024
  • Patients with chronic kidney disease (CKD) bear a significant financial burden and face numerous complications and higher mortality rates. The progression of CKD is associated with glomerular injury caused by glomerular hyperfiltration and oxidative stress. Factors such as uncontrolled hypertension, elevated urine protein levels, anemia, and underlying glomerular disease, contribute to CKD progression. In addition to conservative treatment, several medications are available to combat the progression of CKD to end-stage kidney disease. Renin-angiotensin-aldosterone system blockers could slow the progression of CKD by reducing glomerular hyperfiltration, lowering blood pressure, and decreasing inflammation. Mineralocorticoid receptor antagonists inhibit the mineralocorticoid receptor signaling pathway, thereby attenuating inflammation and fibrosis. Sodium-glucose cotransporter 2 inhibitors exhibit protective effects on the kidneys and against cardiovascular events. Tolvaptan, a selective vasopressin V2-receptor antagonist, decelerates the rate of increase in total kidney volume and deterioration of kidney function in patients with rapidly progressive autosomal dominant polycystic kidney disease. The protective effects of AST-120 remain controversial. Due to a lack of evidence regarding the efficacy and safety of these medications in children, it is imperative to weigh the benefits and adverse effects carefully. Further research is essential to establish the efficacy and safety profiles in pediatric populations.

Effects of Long-Term Intake of Korean Medicine on Gynecology Patients' Livers and Kidneys; Panel Study - Focus on Before Intake, After 3, 6 Months - (장기간 한약복용이 부인과 환자의 간 및 신장기능에 미치는 영향: panel연구 - 복용 전과 후 3, 6개월 비교를 중심으로 -)

  • Yang, Junmo;Sung, Dongmin;Kim, Eu Gene;Lee, Sundong
    • The Journal of Korean Medicine
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    • v.41 no.1
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    • pp.84-92
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    • 2020
  • Objectives: To observe the effects on liver and kidney of gynecology patients' during long term Korean Medicine. Methods: This research was conducted as a panel study on 29 female gynecology patients at Korean medicine clinic and compares their conditions before, 3 months after, and 6 months after Intake of Korean medicine. This analysis was conducted to frequency(%), repeated measure ANOVA and significantly statistics was p<0.05, confidence interval. Results: The most common conditions among the subjects were polycystic ovary syndrome, endometriosis, adenomyosis, and uterine myoma. Except in a few instances, liver functions (AST, ALT, γ-GTP) were within the normal range before and after the intake of Korean medicine. Further, while there was a slight change in liver functions when three months and six months after the intake, but there was no statistical significance (p>0.05). As for the kidney functions (BUN, Creatinine, BUN/Creatinine), they were within the normal range before and after the intake of Korean medicine. Further, while there was a slight change in kidney functions three months and six months after the intake, there was no statistical significance(p>0.05) either. Conclusions: Based on these results, it can be concluded that Korean medicine does not have a negative impact on the gynecology patients' liver and kidney.