Sternoclavicular xanthogranulomatous osteomyelitis in a patient after kidney transplantation: a case report.

Xanthogranulomatous osteomyelitis (XO) is a rare chronic inflammatory bone disease characterized by the presence of cholesterol-laden foam macrophages, histiocytes, and plasma cells. We report the case of a 41-year-old man with end-stage renal disease who had undergone deceased donor kidney transplantation 4 years earlier. He presented with a chest wall mass that he had first identified 2 weeks prior to admission. Computed tomography revealed a periosseous heterogeneously enhancing soft tissue mass adjacent to the sternal end of the left clavicle, accompanied by irregular and destructive osteolytic lesions on the left side of the sternal manubrium. A total mass resection, which included partial clavicle and sternum removal, was performed. Pathological examination revealed foamy histiocytes along with numerous lymphoplasmacytic cells, confirming the diagnosis of XO. This case underscores the potential for XO to develop following kidney transplantation.

Association between Neck Circumference and Chronic Kidney Disease in Korean Adults in the 2019-2021 Korea National Health and Nutrition Examination Survey.

Chronic kidney disease (CKD) is a major public health problem and a leading cause of cardiovascular disease and death. Early recognition and management of CKD risk factors are necessary to prevent its onset and progression. Neck circumference (NC) is a non-invasive and easily accessible anthropometric measure associated with central obesity and subcutaneous fat accumulation in the upper body. Our study aimed to explore the relationship between NC and the prevalence of CKD using data from the nationally representative Korea National Health and Nutrition Examination Survey (2019-2021). We analyzed data from 10,219 subjects (age > 19 years, no missing values). CKD was defined as an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2. Logistic regression analysis was performed, which revealed a significant association between NC and CKD prevalence even after adjusting for confounding factors, both when NC was considered a continuous variable (OR [95% CI], 1.11 [1.03-1.19]) and in quartiles (Q1 as reference; Q2 OR [95% CI], 1.23 [0.91-1.67]; Q3 OR [95% CI], 1.59 [1.16-2.18]; Q4 OR [95% CI], 1.70 [1.16-2.50]). Our findings suggest that NC could be a simple and effective anthropometric measurement for identifying individuals at risk for CKD.

Severe Hypophosphatemia-Induced Acute Toxic-Metabolic Encephalopathy in Continuous Renal Replacement Therapy.

Acute toxic-metabolic encephalopathy (TME) is an acute condition of global cerebral dysfunction in the absence of primary structural brain disease. Severe hypophosphatemia leads to muscle weakness and involves the diaphragm but hypophosphatemia-induced TME is very rare. Herein, we report the case of a 43-year-old woman with encephalopathy with severe hypophosphatemia during continuous renal replacement therapy. She presented with features of oliguric acute kidney injury on diabetic kidney disease due to volume depletion. At admission, her mental status was alert but gradually changed to stupor mentation during continuous renal replacement therapy. Her phosphate level was less than 0.41 mEq/L and Glasgow coma scale decreased from 15 to 5. After phosphate intravenous replacement and administration of phosphate-containing replacement solution, the phosphate level increased to 2.97 mEq/L and mental state returned to alert state. This case demonstrates that the level of phosphorus should be observed during continuous renal replacement therapy.

Efficacy and safety of CKD-11101 (darbepoetin-alfa proposed biosimilar) compared with NESP in anaemic chronic kidney disease patients not on dialysis.

OBJECTIVE: To evaluate the efficacy and safety of CKD-11101 (biosimilar darbepoetin-alfa, Chong Kun Dang Pharm.) compared with NESP® in treatment of anaemia in patients with chronic kidney disease not on dialysis. CLINICAL TRIAL REGISTRATION: NCT03431623. METHOD: In this multi-centre, randomized, double-blind study, patients were treated with CKD-11101 and NESP. The efficacy evaluation period (EEP) was 24 weeks, during which patients were treated every 2 weeks. All patients who completed the EEP were treated with CKD-11101 every 2 weeks for the first 4 weeks and every 4 weeks for the safety evaluation period (SEP), which was from 24 weeks to 52 weeks. The primary efficacy endpoint was the change in mean haemoglobin (Hb) level from baseline to end of EEP and mean dose needed to achieve the target Hb. RESULTS: The mean Hb level was increased in both groups during the EEP (both p < 0.001). The difference in mean Hb level change between the two groups was 0.01 g/dL (95% CI = -0.213-0.242), indicating that CKD-11101 was equivalent to NESP. The difference in mean administration dose between groups was -1.40 mcg (95% CI = -6.859-4.059) included in the equivalent range. The incidence of AEs and ADRs was not different between the two groups, and the frequency of ADRs was favourable in both groups (1.2% in CKD-11101 vs 7.7% in the NESP to CKD-11101 conversion group). CONCLUSION: CKD-11101 has an equivalent therapeutic effect as NESP in chronic kidney disease patients with renal anaemia. CKD-11101 can be safely used for long-term treatment and in patients converted from NESP.

Association between indication for therapy by nutrition support team and nutritional status.

The nutrition support team is a multidisciplinary team composed of medical doctors, registered nurses, pharmacists, and nutritionists, who evaluate the nutritional status of patients. The objective of this study was to determine the relationship between indications for nutrition support team therapy and the nutritional status of patients hospitalized in local major hospitals.Patients who were referred to a nutrition support team from January to December 2016 were enrolled. Patients were classified into 4 age groups, and the weight categories were determined using body mass index (BMI). Four of 6 indications were used for referral to a nutrition support team. The required calories were estimated, and the nutritional status was classified into malnutrition or eutrophia, based on the estimation.The proportion of elderly patients (37.0%) was higher than that of younger ones (28.3%). Patients with higher BMI had a relatively lower proportion of malnutrition. Patients receiving enteral nutrition had greater risk of malnutrition (adjusted odds ratio [aOR] = 3.77, 95% confidence interval [CI] = 2.71-5.24). Patients receiving parenteral nutrition (aOR = 0.38, 95% CI = 0.30-0.47) and treated in the intensive care unit (aOR = 0.70, 95% CI = 0.54-0.91) had lower risk of malnutrition. Patients with >3 indications for nutrition support team therapy had a lower risk of malnutrition than those with only 1 indication (aOR = 0.54, 95% CI = 0.37-0.77).Parenteral nutrition was the most common indication for referral to nutrition support team therapy; however, enteral nutrition had the poorest nutritional status. Patients receiving enteral nutrition who are referred to a nutrition support team need an intensive nutrition support strategy.

State of education regarding ultrasound-guided interventions during pain fellowships in Korea: a survey of recent fellows.

BACKGROUND: Recently, the use of ultrasound (US) techniques in regional anesthesia and pain medicine has increased significantly. However, the current extent of training in the use of US-guided pain management procedures in Korea remains unknown. The purpose of the present study was to assess the current state of US training provided during Korean Pain Society (KPS) pain fellowship programs through the comparative analysis between training hospitals. METHODS: We conducted an anonymous survey of 51 pain physicians who had completed KPS fellowships in 2017. Items pertained to current US practices and education, as well as the types of techniques and amount of experience with US-guided pain management procedures. Responses were compared based on the tier of the training hospital. RESULTS: Among the 51 respondents, 14 received training at first- and second-tier hospitals (Group A), while 37 received training at third-tier hospitals (Group B). The mean total duration of pain training during the 1-year fellowship was 7.4 months in Group A and 8.4 months in Group B. Our analysis revealed that 36% and 40% of respondents in Groups A and B received dedicated US training, respectively. Most respondents underwent US training in patient-care settings under the supervision of attending physicians. Cervical root, stellate ganglion, piriformis, and lumbar plexus blocks were more commonly performed by Group B than by Group A (P < 0.05). CONCLUSIONS: Instruction regarding US-guided pain management interventions varied among fellowship training hospitals, highlighting the need for the development of educational standards that mandate a minimum number of US-guided nerve blocks or injections during fellowships in interventional pain management.

Stroke or left atrial thrombus prediction using antithrombin III and mean platelet volume in patients with nonvalvular atrial fibrillation.

BACKGROUND: CHADS2 (congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, stroke) and CHA2 DS2 -VASc (congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, stroke, vascular disease, age 65 to 74 years, sex category) scores showed just moderate discrimination ability in predicting thromboembolic complications in patients with nonvalvular atrial fibrillation (AF). HYPOTHESIS: To determine the association of antithrombin III (AT-III) deficiency and mean platelet volume (MPV) with the development of stroke or left atrial (LA) thrombus in patients with AF. METHODS: AT-III and MPV were analyzed in 352 patients with AF. The primary endpoint was a composite of ischemic stroke event and incidental LA thrombus. RESULTS: There were 50 events (14.2%) during a mean 35.4 months of follow-up. A significantly higher stroke or LA thrombus rate was observed in the low-AT-III group (<70%) than that in the high-AT-III group (≥70%). A significantly higher stroke or LA thrombus rate was observed in the high-MPV group (≥7.0 fL) than that in the low-MPV group (<7.0 fL). AF patients with an MPV ≥7.0 fL and AT-III deficiency had higher stroke or LA thrombus risk than those without an MPV ≥7.0 fL and AT-III deficiency. In the Cox proportional hazard analysis, high MPV was found to be an independent predictor of stroke or LA thrombus risk (hazard ratio: 6.408; 95% confidence interval: 2.874-14.286). Although AT-III deficiency was not an independent predictor of stroke or LA thrombus risk, a trend was observed. CONCLUSIONS: High MPV and AT-III deficiency were predictive markers for stroke or LA thrombus. Their predictive power for stroke was independent of antiplatelet treatment, anticoagulation therapy, and a high CHA2 DS2 -VASc score in patients with AF.

The Impact of Renin-Angiotensin System Blockade on Renal Outcomes and Mortality in Pre-Dialysis Patients with Advanced Chronic Kidney Disease.

Renin-angiotensin-system (RAS) blockade is thought to slow renal progression in patients with chronic kidney disease (CKD). However, it remains uncertain if the habitual use of RAS inhibitors affects renal progression and outcomes in pre-dialysis patients with advanced CKD. In this multicenter retrospective cohort study, we identified 2,076 pre-dialysis patients with advanced CKD (stage 4 or 5) from a total of 33,722 CKD patients. RAS blockade users were paired with non-users for analyses using inverse probability of treatment-weighted (IPTW) and propensity score (PS) matching. The outcomes were renal death, all-cause mortality, hospitalization for hyperkalemia, and interactive factors as composite outcomes. RAS blockade users showed an increased risk of renal death in PS-matched analysis (hazard ratio [HR], 1.381; 95% CI, 1.071-1.781; P = 0.013), which was in agreement with the results of IPTW analysis (HR, 1.298; 95% CI, 1.123-1.500; P < 0.001). The risk of composite outcomes was higher in RAS blockade users in IPTW (HR, 1.154; 95% CI, 1.016-1.310; P = 0.027), but was marginal significance in PS matched analysis (HR, 1.243; 95% CI, 0.996-1.550; P = 0.054). The habitual use of RAS blockades in pre-dialysis patients with advanced CKD may have a detrimental effect on renal outcome without improving all-cause mortality. Further studies are warranted to determine whether withholding RAS blockade may lead to better outcomes in these patients.

Coronary artery calcification in Korean patients with incident dialysis.

INTRODUCTION: Patients with chronic kidney disease have an extremely high risk of developing cardiovascular disease (CVD). In patients with end-stage renal disease (ESRD), coronary artery calcification (CAC) is associated with increased mortality from CVD. METHODS: The present study aimed to investigate the risk factors for CAC in Korean patients with incident dialysis. Data on 423 patients with ESRD who started dialysis therapy between December 2012 and March 2014 were obtained from 10 university-affiliated hospitals. CAC was identified by using noncontrast-enhanced cardiac multidetector computed tomography. The CAC score was calculated according to the Agatston score, with CAC-positive subjects defined by an Agatston score >0. FINDINGS: Patients' mean age was 55.6 ± 14.6 years, and 64.1% were men. The CAC-positive rate was 63.8% (270 of 423). Results of univariate analyses showed significant differences in age, sex, etiology of ESRD and comorbid conditions according to the CAC score. However, results of multiple regression analysis showed that only a higher age was significantly associated with the CAC score. Receiver operating characteristic curves showed that the sensitivity and specificity of L-spine radiography for diagnosing CAC were 56% and 91%, respectively, for diagnosing CAC (area under the curve, 0.735). DISCUSSION: CAC was frequent in patients with incident dialysis, and multiple regression analysis showed that only age was significantly associated with the CAC score. In addition, L-spine radiography could be a helpful modality for diagnosing CAC in patients with incident dialysis.

Direct vascular actions of quercetin in aorta from renal hypertensive rats.

BACKGROUND: Chronic treatment with the dietary flavonoid quercetin is known to lower blood pressure and restore endothelial dysfunction in animal models of hypertension. This study investigated the direct effects of quercetin on vascular response in chronic 2-kidney, 1-clip (2K1C) renal hypertensive rats. The effects of antioxidant vitamin ascorbic acid on the vasoreactivity were also examined. METHODS: 2K1C renal hypertension was induced by clipping the left renal artery; age-matched rats that received sham treatment served as controls. Thoracic aortae were mounted in tissue baths for the measurement of isometric tension. RESULTS: Relaxant responses to acetylcholine were significantly attenuated in 2K1C rats in comparison with sham rats. Quercetin or ascorbic acid augmented acetylcholine-induced relaxation in 2K1C rats, whereas no significant differences were noted in sham rats. The relaxation response to sodium nitroprusside was comparable between 2K1C and sham rats, and sodium nitroprusside-induced relaxation was not altered by quercetin or ascorbic acid in either group. The contractile response to phenylephrine was significantly enhanced in 2K1C rats compared with sham rats. Phenylephrine-induced contraction was inhibited by pretreatment with quercetin or ascorbic acid in 2K1C rats, whereas neither chemical affected responses in sham rats. N(w)-nitro-L-arginine methyl ester markedly augmented the contractile response to phenylephrine in sham rats, whereas no significant differences were observed in 2K1C rats. Quercetin or ascorbic acid did not affect phenylephrine-induced contraction in the presence of N(w)-nitro-L-arginine methyl ester in either 2K1C or sham rats. CONCLUSION: Acute exposure to quercetin appears to improve endothelium-dependent relaxation and inhibit the contractile response, similar to the effect of ascorbic acid in 2K1C hypertension. These results partially explain the vascular beneficial effects of quercetin in renal hypertension.

Value of Low Triiodothyronine and Subclinical Myocardial Injury for Clinical Outcomes in Chest Pain.

BACKGROUND: Low triiodothyronine (T3) levels and subclinical myocardial injury may be associated with adverse cardiac and cerebrovascular (CCV) events in individuals without clinically apparent coronary heart disease (CHD). The aim of this study was to determine the associations of a low T3 level and subclinical myocardial injury with the development of adverse CCV events in individuals without clinically apparent CHD. METHODS: T3 and high-sensitivity cardiac troponin T (hs-cTnT) levels were analyzed in 250 patients with chest pain free of CHD and heart failure. The primary end point was the composite of sudden cardiac death, ischemic stroke, newly developed atrial fibrillation, pericardial effusion and thrombosis. RESULTS: Throughout a mean follow-up of 15.6 months, the primary end point happened in 17 patients (6.8%). Kaplan-Meier analysis disclosed a notably higher overall occurrence rate in patients with hs-cTnT levels ≥0.014 ng/mL and in patients with T3 <60 ng/dL. An exaggerated hazard was observed in patients with combined high hs-cTnT and low T3 levels. After adjustment, the hazard ratio for overall events in patients with high hs-cTnT/low T3 versus normal hs-cTnT/T3 was 11.72 (95% confidence interval, 2.83-48.57; P = 0.001). CONCLUSIONS: In patients with chest pain without clinically obvious CHD, high hs-cTnT combined with low T3 was associated with adverse cardiac/CCV events and was an independent predictor of overall events even after adjustment. These data suggest the importance of systemic factors, such as low T3 syndrome, in the development of adverse cardiac/CCV events beyond advancing clinical atherosclerotic coronary disease in patients with chest pain.

Cutoff value of serum procalcitonin as a diagnostic biomarker of infection in end-stage renal disease patients.

BACKGROUND/AIMS: Serum procalcitonin (PCT) levels are low in healthy individuals but are elevated in patients with a serious bacterial infection or sepsis. In this study, we examined the ability of serum PCT concentration to diagnose infections in end-stage renal disease (ESRD) patients, and sought to determine an appropriate threshold level. METHODS: Serum PCT levels were measured in ESRD patients on antibiotic therapy for a suspected bacterial infection (ESRD infection [iESRD] group, n = 21), and compared with those of ESRD patients on hemodialysis with no sign of infection (ESRD control [cESRD] group, n = 20). RESULTS: The mean serum PCT concentration of the iESRD group was significantly higher than in the cESRD group (2.95 ± 3.67 ng/mL vs. 0.50 ± 0.49 ng/mL, p = 0.006), but serum PCT concentrations did not correlate with severity of infection. The optimized threshold level derived for serum PCT was 0.75 ng/mL, rather than the currently used 0.5 ng/mL; this threshold demonstrated a sensitivity and specificity of 76.2% and 80.0% for infection and 100% and 60.6% for systemic inflammatory response syndrome, respectively, compared with the cutoff of 0.5 ng/mL. CONCLUSIONS: This study suggests that serum PCT at a cutoff value of 0.75 ng/mL is an appropriate indicator of infection in ESRD patients.

Protective effects of epigallocatechin gallate (EGCG) on streptozotocin-induced diabetic nephropathy in mice.

There is increasing evidence suggesting that antioxidants in green tea extracts may protect kidneys on the progression of end-stage renal disease. We investigated the protective impacts of (-)-epigallocatechin 3-O-gallate (EGCG) against streptozotocin (STZ)-induced diabetic nephropathy in mice. The mice were divided into 5 groups (n=10 per group): control (saline, i.p.), STZ (200mg/kg, i.p.), EGCG50 (50mg/kg, S.Q.), EGCG100 (100mg/kg, S.Q.), and EGCG200 (200mg/kg, S.Q.). Animals were sacrificed at scheduled times after EGCG administration and then quantitative and qualitative analysis were performed. Compared with the control group, the STZ group showed an increase in levels of blood glucose, blood urea nitrogen, creatinine and urine protein amounts with a decrease in body weight. All the above parameters were significantly reversed with EGCG treatment, especially in the EGCG100 group. After STZ injection, there was a mesangial proliferation with increased renal osteopontin accumulation and its protein expression in the glomeruli and the proximal tubules. Mice kidneys after EGCG-treatment showed a reduced expression of above parameters and relatively improved histopathological findings. These results indicated that EGCG 100mg/kg might provide an effective protection against STZ-induced diabetic nephropathy in mice by osteopontin suppression.

Mechanisms of phytoestrogen biochanin A-induced vasorelaxation in renovascular hypertensive rats.

BACKGROUND: The plant-derived estrogen biochanin A is known to cause vasodilation, but its mechanism of action in hypertension remains unclear. This study was undertaken to investigate the effects and mechanisms of biochanin A on the thoracic aorta in two-kidney, one clip (2K1C) renovascular hypertensive rats. METHODS: Hypertension was induced by clipping the left renal artery, and control age-matched rats were sham treated. Thoracic aortae were mounted in tissue baths to measure isometric tension. RESULTS: Biochanin A caused concentration-dependent relaxation in aortic rings from 2K1C hypertensive and sham-treated rats, which was greater in 2K1C rats than in sham rats. Biochanin A-induced relaxation was significantly attenuated by removing the endothelium in aortic rings from 2K1C rats, but not in sham rats. N (ω)-Nitro-l-arginine methyl ester, a nitric oxide synthase inhibitor, or indomethacin, a cyclooxygenase inhibitor, did not affect the biochanin A-induced relaxation in aortic rings from 2K1C and sham rats. By contrast, treatment with glibenclamide, a selective inhibitor of adenosine triphosphate-sensitive K(+) channels, or tetraethylammonium, an inhibitor of Ca(2+)-activated K(+) channels, significantly reduced biochanin A-induced relaxation in aortic rings from both groups. However, 4-aminopyridine, a selective inhibitor of voltage-dependent K(+) channels, inhibited the relaxation induced by biochanin A in 2K1C rats, whereas no significant differences were observed in sham rats. CONCLUSION: These results suggest that the enhanced relaxation caused by biochanin A in aortic rings from hypertensive rats is endothelium dependent. Vascular smooth muscle K(+) channels may be involved in biochanin A-induced relaxation in aortae from hypertensive and normotensive rats. In addition, an endothelium-derived activation of voltage-dependent K(+) channels contributes, at least in part, to the relaxant effect of biochanin A in renovascular hypertension.

The effect of intravenous ascorbic acid in hemodialysis patients with normoferritinemic anemia.

BACKGROUND: Hemodialysis (HD) patients with functional iron deficiency often develop resistance to recombinant human erythropoietin (rhEPO). Recent studies have shown that intravenous ascorbic acid (IVAA) administration could override rhEPO resistance in HD patients. This study was undertaken to test the effects of IVAA in HD patients with normoferritinemic functional iron deficiency accompanied by EPO-hyporesponsive anemia. METHODS: Fifty-eight HD patients with normoferritinemic anemia (between 100 and 500 µg/L) were included and divided into the control (N=25) and IVAA (N=33) groups. IVAA patients received 500 mg of IVAA with each dialysis session for 3 months and an additional 4-month follow-up after the end of the therapy. RESULTS: Twenty patients had a response to IVAA with a significant increase in hemoglobin level (Hgb>1.0 g/dL) and reduction of weekly rhEPO dosage compared with the control group after 3 months of treatment (P<0.05). Compared with non-responders, transferrin saturation (TSAT) was significantly decreased in the responders group (26±11 vs. 35±14%, P<0.05) on baseline data. There was a significant increase in serum iron and TSAT (baseline vs. 3 months, serum iron 57±22 vs. 108±22 µg/dL, TSAT 26±11 vs. 52±7%, P<0.05) and a decrease in serum ferritin (377±146 vs. 233±145 ng/mL, P<0.05) in the responders group (N=20), but no significant changes in the control and non-responders groups (N=13) at 3-month treatment. CONCLUSION: IVAA can be a potent and effective adjuvant therapy for HD patients with rhEPO-resistant normoferritinemic anemia. In addition, IVAA can reduce the dosage of rhEPO for anemia correction.

Protective effects of chitosan oligosaccharide on paraquat-induced nephrotoxicity in rats.

We investigated the apoptotic pathway during paraquat (PQ)-induced nephrotoxicity as well as renoprotective effects of chitosan oligosaccharide (COS) in male Sprague-Dawley rats because increasing evidences suggest that antioxidants may prevent PQ-induced apoptosis. Animals were pretreated with normal saline or COS (500 mg/kg, p.o.) 3 days before PQ (60 mg/kg, i.p.) administration, and were sacrificed at scheduled times after PQ administration. Rats administered PQ showed increased serum PQ concentrations, blood urea nitrogen, and creatinine levels in a time-dependent manner and creatinine clearance was decreased compared with control rats. All of these parameters were reversed significantly by COS pretreatment. After the PQ injection, cell deaths occurred in the proximal renal tubules with increased APE, PUMA, and cleaved caspase-3 expression, while APE and cleaved caspase-3 were immunolocalized mainly in the proximal tubules of control kidneys. COS-pretreated rat kidneys showed increased expression of the above parameters before PQ injection. APE and cleaved caspase-3 were immunolocalized ubiquitously in the renal cortex of COS-pretreated rats until 24h after the PQ injection. These results showed that PQ-induced nephrotoxicity may be caused by apoptosis in rat kidneys and that COS could protect kidneys from PQ-induced toxicity in association with the basal higher level of APE.

Renoprotective effects of green tea extract on renin-angiotensin-aldosterone system in chronic cyclosporine-treated rats.

BACKGROUND: Renin-angiotensin-aldosterone system (RAAS) activation plays an important role in cyclosporine (CsA)-induced nephropathy. The main aim of this study was to test whether the administration of green tea extract (GTE) prevents the development of CsA-induced nephrotoxicity. METHODS: The rats were treated for 21 days and divided into four groups (n = 6/group): control group (0.9% saline injection), CsA group (30 mg/kg/day by intraperitoneal injection), CsA-GTE group (CsA plus GTE 100 mg/kg/day subcutaneous injection) and GTE group (GTE alone). RESULTS: There were significant increased levels of serum blood urea nitrogen and creatinine in the CsA group compared with that of the control group and significantly improved in the CsA-GTE group. Biochemical analysis showed that the plasma renin activity (PRA) and serum concentration of aldosterone were significantly increased in the CsA group compared with the control group and significantly decreased in the CsA-GTE group compared with the CsA group. The total level of renin protein expression was significantly higher in the CsA group than in the control group, and it was lower in the CsA-GTE group than in the CsA group. CONCLUSIONS: CsA treatment increases the PRA and intrarenal renin levels and induces nephrotoxicity. The protective effects of GTE on CsA-induced structural and functional alternations of the kidney may be the blockage of RAAS.

The protective effects of green tea extract against L-arginine toxicity to cultured human mesangial cells.

The aim of this study was to investigate whether green tea extract (GTE) has the protective effects on excess L-arginine induced toxicity in human mesangial cell. Human mesangial cells treated with L-arginine were cultured on Dulbecco's modified eagle medium in the presence and absence of inducible nitric oxide synthase (iNOS) inhibitor and GTE. The cell proliferation was determined by 3 (4,5-dimethylthiazol-2-yl)-2, 5-diphengltetrqzolium bromide, a tetrazole assay. The iNOS mRNA and its protein expression were detected by reverse transcription polymerase chain reaction and Western blot, respectively. The concentration of nitric oxide (NO) was measured by NO enzyme-linced immuno sorbent assay kit. L-arginine significantly inhibited the proliferation of human mesangial cells, and induced the secretion of NO to the media. NO production by L-arginine was significantly suppressed by GTE and iNOS inhibitor (p<0.01). The expression level of iNOS mRNA and its protein that was significantly increased by L-arginine was decreased by iNOS inhibitor but not by GTE. GTE protected the mesangial cells from the NO-mediated cytotoxicity by scavenging the NO rather than by iNOS gene expression. Therefore, we conclude that GTE has some protective effect for renal cells against oxidative injury possibly by polyphenols contained in GTE.