• Translational and Clinical Pharmacology
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• v.26 no.3
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• pp.111-114
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• 2018

Adding to the complexity of caring for critically ill patients is the fact that many of them have a creatinine clearance that exceeds $130mL/min/1.73m^2$. This phenomenon, termed augmented renal clearance (ARC), has only recently been widely recognized and its pathogenesis remains incompletely understood. However, ARC has been shown to result in increased dose requirements for drugs that are primarily eliminated by renal excretion, including many antimicrobial agents and enoxaparin. Recognition of ARC is hampered by the fact that the standard creatinine-based equations used to estimate renal function are not accurate in this clinical setting and the diagnosis is best established using both serum and urine creatinine measurements to calculate clearance. So a high index of clinical suspicion and awareness is usually required before this step is taken to confirm the diagnosis of ARC.

• The Journal of Korean Medicine
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• v.21 no.3
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• pp.119-128
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• 2000

This study was carried out to determine if Salviae Radix extract (SRE) exerts protective effect against alterations in membrane transport function in rabbits with rhabdomyo lysis-induced acute renal failure. Acute renal failure was induced by intramuscular administration of glycerol (50%, 10 ml/kg). GFR in the glycerol-injected animals was reduced to 11% of the basal value and the fractional $Na^{+}$ excretion was increased to 7.8-fold, indicating generation of acute renal failure. When animals received SRE pretreatment for 7 days prior to glycerol injection, such changes were significantly attenuated. The fractional excretion of glucose and phosphate was increased more than 43-fold and 27-fold, respectively, in rabbits treated with glycerol alone. However, they were increased to 17-and 4.3-fold, respectively, in SRE-pretreated rabbits, and these values were significantly lower than those in rabbits treated with glycerol alone. Uptakes of glucose and phosphate in purified isolated brush-border membrane, the $Na^{+}-K^{+}-ATPase$ activity in microsomal fraction, and cellular ATP levels all were reduced in rabbits treated with glycerol alone. Such changes were prevented by SRE pretreatment. Uptakes of organic ions, PAH and TEA, in renal cortical slices were inhibited by the administration of glycerol, which was prevented by SRE pretreatment. Pretreatment of an antioxidant DPPD significantly attenuated the increase in the fractional excretion of glucose and phosphate induced by rhabdomyolysis. These results indicate that rhabdomyolysis causesimpairment inreabsorption of solutes in the proximal tubule via the generation of reactive oxygen species, and SRE pretreatment may provide the protection against the rhabdomyolysis-induced impairment by its antioxidant action.

• Korean Journal of Acupuncture
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• v.22 no.4
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• pp.117-127
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• 2005

Objective : This study was undertaken to determine if Plantaginis Semen herbal acupuncture(PSA) has a protective effect on glycerol-induced acute renal failure in rats. Methods : Rats were dehydrated for 24hr and then injected with 4 ml/kg of 50% glycerol in each hindlimb muscle. In experiments for PSA effect, rats were received 0.1 ml of PSA extraction in both sides of corresponding $Sh\grave{e}nsh\bar{u}(BL_{23})$ of human body for 3 days after injection of glycerol. The experimental group were divided into the normal group, the control group, the sample 1,2,3 group. Results : Glycerol injection decreased glomerular filtration rate and increased urine volume, serum creatinine, BUN level and fractional excretion of $Na^+,\;K^+\;and\;Cl^-$. These results show that glycerol injection bring about acute renal failure. PSA significantly increased glomerular filtration rate and significantly decreased serum creatinine, BUN level and fractional excretion of $Na^+,\;and\;Cl^-$ as compared with control group. Conclusion : These results suggest that PSA can be used in prevention and treatment for acute renal failure. However, the precise mechanisms of PSA protection remain to be determined.

• Biomolecules & Therapeutics
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• v.1 no.1
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• pp.50-57
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• 1993

This study characterized the effect of liver injury produced by hepatotoxicants on the biliary and urinary excretion of acetaminophen(AA) metabolites. Liver damage was produced in male S.-D. rats, 24 hr after dosing with carbon tetrachloride(4CCl_4,$ 0.75 mι/kg, ip) or thioacetamide(TA, 200 mg/kg, ip), or 16 hr after administration of cadmium chloride(4CdCl_2,$ 3.9 mg/kg, iv). Liver damage without renal injury was confirmed by measuring serum enzymes, creatinine and BUN levels as well as by histopathological examination. AA and its metabolites were measured for 3 hr by HPLC in rats injected iv with 1 mmo1/kg of AA. The excreted amounts of AA-glucuronide into bile were reduced to 60~70% of control rats by hepatotoxicants, but did not change urinary excretion of AA-glucuronide and AA-sulfate. Treatments with $CCl_4,\; CdCl_2$ and TA decreased the total (biliary plus urinary) excretion of thioethers of AA(30~50% of control), suggesting that these toxicants decrease cytochrome P-450-mediated toxification of AA. However, treatments of $CdCl_2$and TA markedly enhanced the excretion of AA-mercapturate into urine. Thus, 4CdCl_2$ and TA not only influence the formation of AA-glutathione, but may also alter the excretory routes (i.e. bile and urine) for the elimination of AA-metabolite.

• The Korean Journal of Pharmacology
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• v.16 no.2 s.27
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• pp.1-7
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• 1980

As it has been reported that morphine induce antidiuresis, and antinatriuresis along with decrease in renal hemodynamics when given intracerebroventricularly[ivt], the renal action of nalorphine, a partial antagonist of morphine action, and its influence upon the morphine action were investigated in this study. $10{\mu}g/kg$ of nalorphine given into the lateral ventricle of the rabbit brain tended to decrease renal plasma flow and glomerular filtration rate and increase the reabsorption of free water in the tubules. $100{\mu}g/kg$ ivt significantly decreased urine flow rate and increased free water reabsorption, and tended to increase electrolyte excretion in spite of decrease in renal plasma flow and glomerular filtration, suggesting that ADH also involved in the antidiuresis. Morphine hydrochloride, $10{\mu}g/kg$, ivt, produced marked decrement in renal hemodynamics along with decreased excretions of sodium, potassium and water, and these morphine actions were alleviated by nalorphine given 20 min later. The natriuretic action of ivt nalorphine manifested itself uninfluenced by the morphine. These observations indicate that nalorphine ivt produces renal actions similar to those of morphine, though less potent, and that it can antagonize the latter action. It is suggested that morphine influences renal hemodynamics through nerve by stimulating the 'morphine receptor' in the brain, whereas nalorphine liberates ADH by the agonistic action on the 'nalorphine receptor'.

• Childhood Kidney Diseases
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• v.1 no.2
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• pp.183-188
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• 1997

Familial juvenile hyperuricemic nephropathy is an autosomal dominant disease characterized by progressive renal disease and hyperuricemia or gout, affecting young people of either sex equally. There are two biochemical markers of this disorder. The first is hyperuricemia disproportionate to the degree of renal dysfunction; the second is a grossly reduced clearance of uric acid relative to creatinine, dispropotionate to age, sex and degree of renal failure. We experienced 2 family members with hyperuricemia. One family member, a 13-year-old girl who had suffered from tophaceous gout and chronic renal failure. Her younger brother also had hyperuricemia and moderately reduced renal function. Their urinary excretion fractions of uric acid($FE_{uric\;acid}$) were reduced and renal biopsy specimens showed interstitial fibrosis with tubular atrophy and interstitial urate crystal deposition. We have treated these two patients with allopurinol but we have done renal transplantation because she progressed to end stage renal disease at 16 year old age.

• YAKHAK HOEJI
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• v.45 no.2
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• pp.205-213
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• 2001

The dopaminergic receptors were consisted of two distinct subtypes, $D_1$and $D_2$, each having different function. The present study was attempted to investigate the effects of R(-)-2,10,11-trihydroxy-N-n-propylnoraporphine (TNPA), a dopamine $D_2$receptor agonist, on renal function in dog. TNPA (5.0~15.0 $\mu$g/kg), when given into the vein, produced a dose-dependently antidiuresis along with the decrease in osmolar clearance ( $C_{osm}$) and urinary excretion of sodium and potassium ( $E_{Na}$ , and $E_{K}$). It also increased reabsorption rates of sodium and potassium in renal tubules ( $R_{Na}$ , $R_{K}$) without any changes in glomerular filtration rate (GFR), renal plasma flow (RPF) and free water clearance ( $C_{H2o}$). TNPA (0.5~1.5 $\mu$g/kg/min) infused into a renal artery decreased urine flow both in the experimental and the control kidneys. TNPA (1.5~5.0 $\mu$g/kg) administered via the carotid artery also greatly exhibited antidiuresis even at intravenously ineffective doses. Changes of renal function by TNPA given into both the renal artery and the carotid artery were almost the same aspect to those induced by intravenous TNPA. These results obtained from the present study suggest that TNPA produces antidiuresis by increasing the reabsorption rates of electrolytes in renal tubules, mainly distal tubule, through changing of central function.unction.

• YAKHAK HOEJI
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• v.26 no.4
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• pp.197-208
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• 1982

In this study attemps were made to obtain evidence as to the action of Mori Radicis Cortex on the renal' function of anesthetized mongrel dogs. 1. A light brown powder isolated from Mori Radicis Cortex (MRC) by a slight modification of Tanemura's method, when given intravenously in doses ranging 0.5 to 5.0mg/kg, elicited diuresis with the increase of positive water clearance and amounts of $Na^{+}$ and $K^{+}$ excreted in the urine. At this time the glomerular filtration rate, renal plasma flow and osmolar clearance were not observed to have any significant changes. This diuresis was augmented in process of time and its maximum effect was exhibited about 30 minutes after administration of MRC. 2. The MRC, when administered into a intra carotid artery, responded promptly with diuresis and natriuresis at a level too small to effect renal functions when administered intravenously. In this experiment the patterns of changes of renal function were the patterns of changes of renal function were the same as those of the above intravenously administered experiment. 3. When infused directly into a renal artery, the MRC exhibited little effect on either kidney. 4. During water diuresis, the MRC did not elicit diuretic action or significant changes in renal functions. The above observations suggest that the diuresis of MRC is brought about by the inhibition of the release of antidiuretic hormone with the mechanism facilitating the excretion of $Na^{+/}$ and $K^{+}$ in urine.

• Childhood Kidney Diseases
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• v.25 no.1
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• pp.44-48
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• 2021

Idiopathic renal hypouricemia (iRHUC) is a rare hereditary disease caused by a defect in urate handling of renal tubules. Type 1 renal hypouricemia (RHUC1) is diagnosed with confirmation of a mutation in SLC22A12 gene which encodes a renal urate-anion exchanger (URAT1). The majority of iRHUC patients are asymptomatic, especially during childhood, and thus many cases go undiagnosed or they are diagnosed late in older age with complications of hematuria, renal stones, or acute kidney injury (AKI). We report a case of a 7-year-old boy with subtle symptoms such as general weakness and dizziness and revealed hypouricemia and incidental nephrolithiasis. Homozygous mutations were detected in the SLC22A12 (c.774G>A) by molecular analysis. The present case suggests that fractional excretion of uric acid (FEUA) screening could be better followed by the coincidental discovery of hypouricemia, to prevent conflicting complications of iRHUC, even with normal urine uric acid to creatinine ratio (U_UA/U_Cr), and sequential genetic analysis if needed.

• Asian-Australasian Journal of Animal Sciences
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• v.20 no.8
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• pp.1201-1207
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• 2007

This study compared the recovery rate of intrajugular-administered allantoin in the urine and saliva between swamp buffaloes and zebu cattle to examine whether it could explain the lower excretion rate of urinary purine derivatives (PD) in the buffaloes. Three male swamp buffalo yearlings, with an average body weight of $349{\pm}40.35$ kg, and three Thai native cattle ($154{\pm}3.26$ kg) of similar age and sex were used in the study. Animals were kept in individual pens and fed at a maintenance energy level with a diet containing 65% monk bean husk (Vigna radiata) as roughage and 35% concentrates. Allantoin solution was infused into the jugular vein in four incremental rates equivalent to 0, 5, 10 and 15 mmol/d and urine was collected daily in acidified form. Daily PD excretion was linearly correlated with intrajugular allantoin infusion in both species. The relationship between daily urinary PD excretion (Y, mmol/d) and intrajugular allantoin infused (X, mmol/d) was $Y=0.75{\pm}0.318X+22.45{\pm}2.98$ ($r^2$ = 0.36, n = 12, MSE = 38.02, CV = 21.9, p<0.01) for swamp buffaloes and $Y=0.96{\pm}0.10X+15.93{\pm}0.92$ ($r^2$ = 0.91, n = 12, MSE = 3.60, CV = 8.27, p<0.01) for zebu cattle. The salivary PD concentration was not correlated with intrajugular allantoin infusion in both species, with values for buffaloes numerically lower than those for cattle. The present study reconfirmed previous studies that buffaloes have a lower plasma PD excretion rate via the renal route and a significant proportion (22%) of the plasma PD loss is via the saliva. However, results of our present and previous studies suggest that differences in purine base (PB) metabolism between buffaloes and zebu cattle occur before the purine compounds reach the plasma pool.