• Journal of Trauma and Injury
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• v.30 no.4
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• pp.192-196
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• 2017

Purpose: Blunt injury accounts for 80-95% of renal injury trauma in the United States. The majority of blunt renal injuries are low grade and 80-85% of these injuries can be managed conservatively. However, there is a debate on the management of patients with high-grade renal injury. We reviewed our experience of renal trauma at our trauma center to assess management strategy for high-grade blunt renal injury. Methods: We reviewed blunt renal injury cases admitted at a single trauma center between August 2007 and December 2015. Computed tomography (CT) scan was used to diagnose renal injuries and high-grade (according to the American Association for the Surgery of Trauma [AAST] organ injury scale III-V) renal injury patients were included in the analysis. Results: During the eight-year study period, there were 62 AAST grade III-V patients. 5 cases underwent nephrectomy and 57 underwent non-operative management (NOM). There was no difference in outcome between the operative group and the NOM group. In the NOM group, 24 cases underwent angioembolization with a 91% success rate. The Incidence of urological complications correlated with increasing grade. Conclusions: Conservative management of high-grade blunt renal injury was considered preferable to operative management, with an increased renal salvage rate. However, high-grade injuries have higher complication rates, and therefore, close observation is recommended after conservative management.

• Clinical and Experimental Pediatrics
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• v.48 no.2
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• pp.212-215
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• 2005

Renal artery stenosis is a major cause of renovascular hypertension and the most common cause of treatable secondary hypertension. There are several methods to treat renal artery stenosis, including surgery, percutaneous transluminal renal angioplasty(PTRA), and renal artery stenting(RAS). But, renal artery embolization can be tried in atherosclerotic stenosis, multiple stenosis, microaneurysm, and stenosis difficult to try PTRA or RAS. We report a case of renovascular hypertension in a 14-year-old female who had multiple segmental renal artery stenosis. Hypertension was controlled by renal ablation therapy with renal artery embolization.

• YAKHAK HOEJI
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• v.31 no.6
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• pp.376-393
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• 1987

This study was performed in order to investigate the effect of nifedipine, a vasodilating drug which acts through calcium antagonism, on renal function using mongrel dog. Nifedipine, when given interavenously in doses ranging from 1.5 to 5.0$\mu\textrm{g}$/kg, elicited diuresis along with less changes of glomerular filtration rate and significant increases of renal plasma flow, so that the filtration fraction(FF) decreased significantly, at the same time both osmolar and free water clearances increased, and amount of sodium, potassium and calcium excreted in urine increased significantly. Nifedipine, when infused into a renal artery in doses from 0.05 to 0.15$\mu\textrm{g}$/kg/min, exhibited identical responses to the actions of intraveneous nifedipine except significant increase of glomerular filtration rate and no change of FF, which was confined only to the infused kidney. The renal action of nifedipine into a renal artery were not influenced by renal denervation, decreased significantly by ouabain, Na$^+$-K$^+$-ATPase inhibitor, which was given into a renal artery. Nifedipine infused into a renal artery in dog pretreated with propranolol i.v. produced diuresis associated with the increase of electrolytes excretion by reduction of electrolyte reabsorption and with no changes of glomerular filtration rate and renal plasma flow. Thus, it is concluded that nifedipine infused into a renal aretery produces diuretic action along with both improvement of hemodynamics and inhibition of electrolytes reabsorption, which may be related to sympathetic $\beta$-receptor or Na$^+$-K$^+$-ATPase activity because the action of nifedipine in kidney is blocked by propranolol or ouabain.

• 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.

• The Korean Journal of Nuclear Medicine
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• v.37 no.3
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• pp.202-205
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• 2003

A 10 days old male infant with congenital megacalyces and megaureter, diagnosed by prenatal ultrasonographic screening, underwent Tc-99m DTPA renal scan for evaluation of urinary tract patency, Tc-99m DMSA scan for evaluation of renal cortical damage. He also underwent intravenous urography(IVU) and renal ultrasonography. Tc-99m DTPA renal scan demonstrates intense tracer accumulation in enlarged both renal pelvocalyses and ureters, which rapidly washout without diuretics administration. Tc-99m DMSA renal cortical scan shows no remarkable photon defect in both renal cortices and visible tracer uptake in both megaureter areas. Ultasonographic and IVU studios show enlarged both renal calyses and bullously dilated ureters, but no dilatation in renal pelvis. Follow up Tc-99m DTPA renal scan, peformed at one year later, also reveals intense tracer accumulation in enlarged both urinary tracts which rapidly washout without diuretics, and shows no significant change compare to the previous Tc-99m DTPA renal scan. Urinary tract obstruction and renal cortical damage can be easily evaluated with Tc-99m DTPA and Tc-99m DMSA scans in patiens with megacalyces and megaureter.

• Childhood Kidney Diseases
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• v.24 no.2
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• pp.98-106
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• 2020

Purpose: The aim of this study is to evaluate the clinical utility of late 6-month dimercapto-succinic acid (DMSA) renal scan in predicting vesicoureteral reflux (VUR) and long-lasting renal scars in children with first acute pyelonephritis (APN). Methods: A retrospective case study of children admitted with APN from January 2010 to July 2017 was performed. The study included patients with voiding cystourethrography (VCUG) and acute and late 6-month DMSA scan. We analyzed the clinical, laboratory and imaging findings of patients with and without late cortical defects at 6 months and those with or without VUR. Results: Among 145 children with APN, 50 (34.5%) had cortical defects on the late DMSA renal scan and 60 (41.4%) showed VUR. Thirteen of 38 (34.2%) children undergoing 18-month DMSA renal scan showed a long-lasting renal scars. Compared with children without late cortical defects, patients with late 6-month cortical defects had a higher incidence of VUR and long-lasting renal scars, and relapse of UTI (all P<0.05). In a multivariable analysis, both high-grade VUR and relapse of UTI were independently correlated with the presence of late 6-month cortical defects (P<0.05). Late cortical defects and relapse of UTI were also associated with the presence of VUR (P<0.05). Only the late 6-mo cortical defects was an independent predictor of long-lasting renal scars in children with APN (P<0.05). Conclusion: An abnormal late 6-month DMSA renal scan may be useful in identifying VUR and long-lasting renal scars in children diagnosed with APN.

• Korean Journal of Radiology
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• v.1 no.3
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• pp.121-126
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• 2000

Objective: To evaluate the therapeutic efficacy of a new liquid embolic material, Embol, in embolization of the renal artery. Materials and Methods: Embol is a new embolic material obtained by partial hydrolysis of polyvinyl acetate mixed in absolute ethanol and Iopromide 370 and manufactured by Schering Korea, Kyonggido, Korea. Six patients who underwent embolization of the renal artery using Embol were evaluated. Four were male and two were female and their ages ranged from 11 to 70 (mean, 53) years. Clinical and radiologic diagnoses referred for renal artery embolization were renal cell carcinoma (n = 3), renal angiomyolipoma (n = 2) and pseudoaneurysm of the renal artery (n = 1). After selective renal angiography, Embol was injected through various catheters, either with or without a balloon occlusion catheter. Changes in symptoms and blood chemistry which may have been related to renal artery embolization with Embol were analyzed. Results: The six patients showed immediate total occlusion of their renal vascular lesions. One of the three in whom renal cell carcinoma was embolized with Embol underwent radical nephrectomy, and the specimen thus obtained revealed 40% tumor necrosis. In the two patients with angiomyolipomas, the tumors decreased in size and abdominal pain subsided. Bleeding from pseudoaneurysm of the renal artery was successfully controlled. Four patients showed symptoms of post-embolization syndrome, and one of these also showed increased levels of blood urea nitrogen and creatinine. One patient experienced transient hypertension. Conclusion: Embol is easy to use, its radiopacity is adequate and it is a safe and effective embolic material which provides immediate and total occlusion of renal vascular lesions.

• Toxicological Research
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• v.17
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• pp.117-125
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• 2001

Envenoming by Russells viper causes a broad spectrum of renal impairment. Renal failure is an important complication in patients bitten by Russells viper. Experimental work in animals and in vitro has elucidated pathophysiological mechanisms that contribute to life threatening complications and have suggested possibilities for therapeutic intervention. The evidence in experimental animals regarding mechanisms of venom action in relation to changes in either extrarenal or intrarenal factors is presented. The cardiovascular system and renal hemodynamics are affected by venom. Reductions of renal function including renal hemodynamics are associated directly with changes in general circulation during envenomation. Possible endogenous mechanisms for releasing the hormone inducing renal vasoconstriction after envenomation are evident. Hormonal factor such as the catecholamine, prostaglandin and renin angiotensin systems induce these changes. Direct nephrotoxicity of venom action is studied in the isolated per-fused kidney. Characteristic polarization of the cell membrane, changes of mitochondrial activity and Na-K ATPase in renal tubular cells are observed. Changes in renal function and the cardiovascular system are observed of ter envenomation and are reversed by the administration of Russells viper antivenom (purified equine immunoglobulin, $Fab_2$ fragment). The neutralizing effects are more efficient when the intravenous injection of antivenom is given within 30 min after the envenomation.

• YAKHAK HOEJI
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• v.34 no.2
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• pp.88-101
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• 1990

Captopril, angiotensin converting enzyme (ACE) inhibitor, when given intravenously in dog, elicited the diuretic action along with the increases of glomerular filtration rates (GFR), renal plasma flow (RPF) and osmolar clearances (Cosm) with no changes of free water clearnces ($C_{H_2O}$), and then captopril produced the enlargement of excretion rates of electrolytes in urine and the reduction of reabsorption rates of electrolytes in renal tubles. Captopril, when given into a renal artery, exhibited no changes of renal function in the experinental kidney, whereas diuretic action with the same mechanism as shown in intravenous captopril in control kidney. Captopril, when injected into a carotid artery, showed increases in rates of urine flow in a small does which did not affect on renal action when it was administered intravenusly. Diuretic action induced by captopril was not influenced by renal artery denervation, propranolol and angiotensin II inhibiters. Above results suggest that captopril produced diuretic action along with renal hemodynamic changes by slight contraction of vas efferense and reduction of reabsorption rate of electrolytes in renal tubules, especilly distal tubules, that may be mediatedby endogenous substances.

• Biomolecules & Therapeutics
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• v.4 no.1
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• pp.7-18
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• 1996

5-Hydroxytryptamine(5-HT, serotonin), when given into the vein, produced antidiuretic action accompanied with reduction of glomerular filtration(GFR), renal plasma flow(RPF), osmolar clearance(Cosm) and amounts of sodium or potassium excreted in urine( $E_{Na}$ , $E_{K}$), with the augmented reabsorption rates of sodium and potassium in renal tubules. 5-HT, when infused into a renal artery, exhibited diuretic action accompanied with the augmented RPF and increased $E_{Na}$ and $E_{K}$ in only infused kidney. Antidiuretic action of 5-HT infused into the vein was not influenced by ketanserin, 5-H $T_2$receptor blockade, given into a renal artery, vein or carotid artery, by methysergide, 5-H $T_1$receptor blockade, given into a renal artery, whereas above antidiuretic action was inhibited by methysergide given into vein or carotid artery. Diuretic action of 5-HT infused into a renal artery in only experimental kidney was blocked by ketanserin injected into a renal artery, was not influenced by methysergide administered into a renal artery. Above results suggest that 5-hydroxytryptamine(5-HT) produced the antidiuretic action through central 5-H $T_1$receptor and the diuretic action through 5-H $T_2$receptor located in renal tubules of kidney.ney.