• Toxicological Research
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• v.34 no.2
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• pp.143-150
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• 2018

It has been demonstrated that vanadate causes nephrotoxicity. Vanadate inhibits renal sodium potassium adenosine triphosphatase (Na, K-ATPase) activity and this is more pronounced in injured renal tissues. Cardiac cyclic adenosine monophosphate (cAMP) is enhanced by vanadate, while increased cAMP suppresses Na, K-ATPase action in renal tubular cells. There are no in vivo data collectively demonstrating the effect of vanadate on renal cAMP levels; on the abundance of the alpha 1 isoform (${\alpha}_1$) of the Na, K-ATPase protein or its cellular localization; or on renal tissue injury. In this study, rats received a normal saline solution or vanadate (5 mg/kg BW) by intraperitoneal injection for 10 days. Levels of vanadium, cAMP, and malondialdehyde (MDA), a marker of lipid peroxidation were measured in renal tissues. Protein abundance and the localization of renal ${\alpha}_1-Na$, K-ATPase was determined by Western blot and immunohistochemistry, respectively. Renal tissue injury was examined by histological evaluation and renal function was assessed by blood biochemical parameters. Rats treated with vanadate had markedly increased vanadium levels in their plasma, urine, and renal tissues. Vanadate significantly induced renal cAMP and MDA accumulation, whereas the protein level of ${\alpha}_1-Na$, K-ATPase was suppressed. Vanadate caused renal damage, azotemia, hypokalemia, and hypophosphatemia. Fractional excretions of all studied electrolytes were increased with vanadate administration. These in vivo findings demonstrate that vanadate might suppress renal ${\alpha}_1-Na$, K-ATPase protein functionally by enhancing cAMP and structurally by augmenting lipid peroxidation.

• 한국생물공학회:학술대회논문집
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• 2003.04a
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• pp.307-309
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• 2003

To develop a new treatment for end stage renal disease, we examined the possibility of regenerating renal tissues by implanting renal cells on biodegradable polymer scaffolds. Histological examination of the implanted tissues revealed formation of renal-like structures including glomerulus and renal tubule.

• Journal of Microbiology and Biotechnology
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• v.15 no.1
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• pp.105-111
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• 2005

End-stage renal disease is a fatal and devastating disease that is caused by progressive and irreversible loss of functioning nephrons in the kidney. Dialysis and renal transplantation are the common treatments at present, but these treatments have severe limitations. The present study investigated the possibility of reconstructing renal tissues by transplantation of renal precursor cells to replace the current treatments for end-stage renal disease. Embryonic renal precursor cells, freshly isolated from metanephroi of rat fetus at day 15 post-gestation, were seeded on biodegradable polymer scaffolds and transplanted into peritoneal cavities of athymic mice for three weeks. Histologic sections stained with hematoxylin & eosin and periodic acid-Schiff revealed the formation of primitive glomeruli, tubules, and blood vessels, suggesting the potential of embryonic renal precursor cells to reconstitute renal tissues. Immunohistochemical staining for proliferating cell nuclear antigen, a marker of proliferating cells, showed intensive nuclear expression in the regenerated renal structures, suggesting renal tissue reconstitution by transplanted embryonic renal precursor cells. This study demonstrates the reconstitution of renal tissue in vivo by transplanting renal precursor cells with biodegradable polymer scaffolds, which could be utilized as a new method for partial or full restoration of renal structure and function in the treatment of end-stage renal disease.

• The Journal of Internal Korean Medicine
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• v.31 no.1
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• pp.66-78
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• 2010

Objective : This study was designed to investigate the possibility of AR for chronic renal injury. Methods : The author first investigated the expression levels of DNA by inducing of chronic renal injury. Then, the author investigated the effects of AR on chronic renal injury induced by combination treatment with Adriamycin and cisplatin in terms of changes in body weights and renal tissues, urine volume, BUN and creatinine levels, creatinine clearance and histopathological changes in renal tissues. Total expression levels of 546 genes were elevated or lowered by induction of chronic renal injury. Genes of which whose expression levels were elevated by induction of chronic renal injury were related to the PPAR signaling pathway and fatty acid mechanism, etc. Genes of which expression levels were lowered by induction of chronic renal injury were related to the neuroactive ligand-receptor signaling pathway. Results : Oral administration of AR restored renal mass which was reduced by induction of chronic renal injury. AR also restored creatinine clearance and lowered serum BUN level. In histopathological observation, the AR group has a tendency to prevent tissue damages as shown in the chronic renal injury group. Conclusions : AR can be used to treat patients with chronic renal injury although further study will be needed to elucidate the exact mechanisms in the efficacy of AR on chronic renal injury.

• The Journal of Internal Korean Medicine
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• v.19 no.1
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• pp.442-451
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• 1998

This study was carried out to examine mechanisms by which Holotrichia (HTC) produces protective effect against renal cell injury. HTC extraction (5%) prevented $H_2O_2(50mM)$-induced LDH release and lipid peroxidation in renal cortical slices. When slices were treated with 5% HTC extraction, cellular glutathione content and the superoxide dismutase activity were not altered in control and $H_2O_2$-treated tissues. When slices were treated with 50 mM $H_2O_2$, the catalase activity was significantly inhibited, which was completely restored by addition of 5% HTC. Treatment of slices with 5% HTC extraction increased the glutation peroxidase activity in $H_2O_2$-treated tissues. These results suggest that HTC prevents oxidant-induced cell injury and lipid peroxidation by increasing the activities of catalase and glutathione peroxidase in renal cortical slices.

• The Korean Journal of Physiology
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• v.16 no.2
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• pp.159-163
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• 1982

Vasoactive intestinal peptide (VIP) found in duodenal mucosa originally has been suggested as a neurotransmitter. Its localization, however, now known, is not limited to the gastrointestinal tract, but scattered at many different kinds of tissues, smooth muscles, endocrine gland and exocrine gland as well as central and peripheral neural tissues. To investigate the effect of VIP on renal function, an experiment has been done in anesthetized male rats. The results obtained were: 1) Urinary output and creatinine clearance decreased significantly during the period of infusion of VIP, 2.0ug/rat/7minutes. 2) Urinary excretion of sodium, potassium and chloride decreased but without significance by infusion of VIP. 3) Blood pressure, systolic and diastolic, decreased by VIP administered intravenously in the period of infusion. 4) Changes of urinary output, sodium and chloride excretion was correlated with changes of creatinine clearance. The above data suggest that VIP administered intravenously can suppress the renal hemodynamics indirectly, and also decrease electrolyte excretion through its renal hemodynamic change.

• Childhood Kidney Diseases
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• v.23 no.2
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• pp.67-76
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• 2019

Kidney disease is a major global health issue. Hemodialysis and kidney transplantation have been used in the clinic to treat renal failure. However, the dialysis is not an effective long-term option, as it is unable to replace complete renal functions. Kidney transplantation is the only permanent treatment for end-stage renal disease (ESRD), but a shortage of implantable kidney tissues limits the therapeutic availability. As such, there is a dire need to come up with a solution that provides renal functions as an alternative to the current standards. Recent advances in cell-based therapy have offered new therapeutic options for the treatment of damaged kidney tissues. Particularly, cell secretome therapy utilizing bioactive compounds released from therapeutic cells holds significant beneficial effects on the kidneys. This review will describe the reno-therapeutic effects of secretome components derived from various types of cells and discuss the development of efficient delivery methods to improve the therapeutic outcomes.

• Journal of Veterinary Clinics
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• v.18 no.1
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• pp.35-43
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• 2001

Present study was undertaken in order to document early renal ultrasonographic changes of gentamicin nephrotoxicosis and to show the value of renal ultrasonography as a contributory means of early diagnosis of acute renal failure in dogs. The experimental design was a randomized complete block design with six treatments in two blocks (gentamicin-treated & saline-treated). Acute renal failure was induced by toxic dosage of gentamicin (30 mg/kg) and saline solution sham equivalent in volume to that of the toxic dosage of gentamicin (1.5-3ml). Subjective visualization of increased renal cortex was visible as homogenous echoes that were hypoechoic relative to the surrounding tissues, whereas the renal medulla was anechoic to slightly hypoechoic. After treatment, the renal cortex was hyperechoic relative to the surrounding tissue. Increased renal cortex echogenicity was associated with significant nephrotoxicosis and was superior to serum creatinine elevation in nephrotoxicosis detection. Urine GGT was superior to other clinicopathological data utilized in the diagnosis of nephrotoxicosis. Based on the above results, increased renal cortex echogenicity seemed to be of use in detecting of acute renal failure.

• Journal of Veterinary Clinics
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• v.17 no.1
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• pp.270-274
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• 2000

A seven-year-old female Jindo-dog was presented with a history of progressive abdominal distension. Except for severe bilateral abdominal swelling, other abnormal signs were not detected. The patient showed normal appetite and defecation. In the radiographic examination, the abdomen was filled with large masses. Suspected a certain neoplastic disease, laparotomy was taken through the cranial abdominal midline. Large pale-yellow masses were proliferated to fill the abdomen. In the masses, grey-brown or black portion presumed hemorrhagic or necrotic spots were found. Even though neoplastic tissues were not detected in the right kidney, they were infiltrated in the left kidney except for a part of the cortex. Obtaining the owner's consent, the patient was euthanized and samples were collecte for further study. In microscopic examination, the parenchyma of the medulla was substituted with tumor cells and the cortex was impressed by the expansive proliferation of the neoplastic tissues. This neoplasm was estimated as renal carcinoma originated from tubular epithelium, being based upon that tumor cells were largely cuboidal cells and they had obscure tubular forms.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.5651-5655
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• 2013

Objective: Major histocompatibility complex class I chain-related A (MICA) is a stress-inducible glycoprotein that can be shed as a soluble protein. This study was conducted to determine the expression of MICA in renal cell carcinoma (RCC) and examine the clinical relevance of soluble MICA (sMICA) in this disease. Methods: Immunohistochemistry and real-time PCR analyses were performed to assess the expression of MICA in 48 pairs of RCC and adjacent normal renal tissues. Serum levels of sMICA were measured in 48 RCC patients, 12 patients with benign renal tumors, and 20 healthy individuals. The correlations between sMICA levels and clinicopathological parameters were analyzed and the diagnostic performance of sMICA in RCC was evaluated. Results: RCCs exhibited elevated expression of MICA compared to adjacent normal tissues. Serum concentrations of sMICA were significantly greater in RCC patients ($348.5{\pm}32.5pg/ml$) than those with benign disease ($289.3{\pm}30.4pg/ml$) and healthy controls ($168.4{\pm}43.2pg/ml$) and significantly correlated with advanced tumor stage, lymph node metastasis, distant metastasis, vascular invasion, and higher histological grade. Using a cut-off point of 250 pg/ml, sMICA demonstrated a specificity and sensitivity of 63.2% and 75.6%, respectively, in distinguishing between RCC and benign renal tumors. Conclusion: MICA expression is upregulated in RCC and increased serum sMICA levels predict aggressive tumor behavior. However, the applicability of sMICA alone is limited in distinguishing RCC from benign renal tumors.