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Abstract

R. Eriguchi, J. Umakoshi, S. Miura and Y. Sato

Sato Junkanki Hospital, Ehime, Japan
Background: Postmenopausal women undergoing chronic hemodialysis are at risk of uremic bone disease and postmenopausal osteoporosis. There are few reports discussing the effects of raloxifene hydrochloride on chronic hemodialysis patients. We investigated whether differences in the effects of raloxifene on bone mineral density (BMD) are dependent on the level of intact parathyroid hormone (iPTH). Methods: 47 postmenopausal hemodialysis patients with osteoporosis were divided into two groups, i.e. Group A, with treatment, and Group B, without treatment by raloxifene hydrochloride (60 mg/day, three times per week) for 1 year. We evaluated the changes in BMD at the distal one-third of the radial bone and aortic calcification index (ACI) by plain abdominal computerized tomography. Furthermore, we compared the BMD and ACI results for patients with similar iPTH levels within each group. Results: After 1 year of raloxifene treatment, patients with iPTH levels of < 250 pg/ml in Group A showed significantly less BMD deterioration than similar patients in Group B (A: –0.31 ± 1.7% vs. B: –3.71 ± 0.7%, p = 0.04). However, raloxifene showed no difference in patients with iPTH levels of >= 250 pg/ml in the two groups (A: –3.49 ± 0.7% vs. B: –6.10 ± 1.9%, p = 0.09). Among the patients with iPTH levels of < 250 pg/ml, changes in the ACI values were 1.30 ± 0.3% for Group A and 1.67 ± 1.0% for Group B. Among the patients with iPTH levels of ³ 250 pg/ml, the ACI values were 2.58 ± 0.7% for Group A and 3.01 ± 1.2% for Group B. Conclusions: Raloxifene treatment was useful for the prevention of BMD deterioration in postmenopausal dialysis patients with controlled iPTH levels.Correspondence to:
R. Eriguchi, MD
Sato Junkanki Hospital
4-10-25 Asouda-cho
Matsuyama City, Ehime Prefecture, 790-0952, Japan
Email: rieko-eriguchi@satohp.co.jp

Abstract

H. Tanaka, E. Oki, K. Tsuruga, T. Yashiro, I. Hanada and E. Ito

Department of Pediatrics, Hirosaki University School of Medicine, Hirosaki, Japan
Aims: Studies on immunosuppressive treatment with tacrolimus (Tac) in subjects with lupus nephritis (LN) are limited. Here, we report our experience with Tac administered daily as a single-dose for maintenance therapy in young patients with pediatric-onset, long-standing LN. Methods: Eleven consecutive patients with long-standing biopsy-proven LN were recruited for at least 6 months or longer (6 – 24 months) as part of an open-label trial for the single-daily-dose administration of Tac (3 mg/day, 0.04 – 0.075 mg/kg) without dose increases of concomitantly administered prednisolone (PDN). Tac treatment was started at the time of the most recent flare. Data on clinical parameters and serologic lupus activity were collected prospectively. Results: The baseline characteristics of the patients were as follows: mean age, 18 years; urinary protein/creatinine ratio (Up/cr), 0.74 ± 1.49; serum C3 level, 69.5 ± 26.5 mg/dl (normal 79 – 152 mg/dl); serum complement hemolytic activity (CH50), 23.0 ± 8.9 U/ml (normal 23 – 46 U/ml); serum anti-dsDNA antibody titer, 58.9 ± 54.2 IU/ml (normal < 12.0 IU/ml); serum creatinine, 0.54 ± 0.13 mg/dl; and European Consensus Lupus Activity Measurement (ECLAM) index, 4.4 ± 2.2. Despite the gradual tapering of the PDN dose, a marked improvement, compared with the baseline values was observed in the ECLAM index even at 1 month and in the serological parameters at 3 months after the start of treatment. These favorable results persisted until the end of the study. The Up/cre ratio gradually decreased and had dropped significantly at 24 months after the start of treatment. After a mean of 18 months of treatment, complete responses were achieved in 8 patients (73%) and a partial response was achieved in 2 patients. The remaining one patient showed no response. No serious adverse effects were observed. Conclusion: These data suggest that low-dose Tac treatment, administered once daily, is an effective and safe method for managing selected young patients with pediatric-onset, long-standing LN. However, further studies involving a larger number of patients are needed to confirm these results.Correspondence to:
H. Tanaka, MD, PhD
Department of Pediatrics
Hirosaki University School of Medicine
5 Zaifu-cho, Hirosaki, 036-8562, Japan
Email: hirotana@cc.hirosaki-u.ac.jp

Abstract

R. Bologa¹, D. Levine², T. Parker², B. Gordon¹, A. Lanto³, J. Cheigh¹, K. Stenzel¹ and A. Rubin¹

¹The Rogosin Institute and Department of Medicine, ²The Rogosin Institute and Department of Biochemistry, Weill Medical College of Cornell University, and ³The Rogosin Institute, New York, NY, USA
Patients undergoing dialysis treatment have a high incidence of dyslipidemia. Rosuvastatin is a potent statin drug that improves overall lipid profiles in dyslipidemic patients. However, the pharmacokinetics of rosuvastatin has not been studied in patients with end-stage kidney disease undergoing chronic peritoneal dialysis (PD). The goals of this study are to determine the pharmacokinetics and tolerability of a single oral dose of rosuvastatin in patients undergoing continuous ambulatory PD (CAPD). This was a nonrandomized, open-label, 1-week trial. Ten stable PD patients were given a single oral dose of rosuvastatin (10 mg). Serial blood samples were obtained over the next 48 hours, and the patients were followed for 1 week while they underwent CAPD. Rosuvastatin plasma concentration peaked (C_max) at 3.68 ± 2.3 ng/ml (geometric mean), 4.5 hours (median; range 2 – 6 hours) after oral dosing. The plasma concentration of rosuvastatin was 0.44 ± 0.23 ng/ml at 24 hours (C₂₄) and 0.14 ± 0.07 ng/ml, with levels below the detectable range in 5 of 10 subjects, at 48 hours (C₄₈). The area under the plasma concentration-time from 0 to 48 hours (AUC_0–48) was 32.6 ± 1.6 ng/ml/h. These pharmacokinetic profiles of rosuvastatin in CAPD patients are very similar to those observed in healthy volunteers, but different from patients with Stages 4 – 5 chronic kidney disease. A single oral dose of rosuvastatin was well tolerated in this small number of patients. We conclude that pharmacokinetic profiles of rosuvastatin in patients undergoing CAPD are similar to those observed in healthy volunteers. These findings suggest that a lower dose of rosuvastatin (<= 10 mg) may be administered in CAPD patients without dose adjustment.Correspondence to:
R. Bologa, MD
The Rogosin Institute
505 East 70th St.
New York, NY 10021, USA
Email: rmbologa@nyp.org

Abstract

S. Kim¹, K.H. Oh²,³, H.J. Chin²,⁴, K.Y. Na², Y.S. Kim²,⁴, D.-W. Chae²,⁴, C. Ahn²,³, J.S. Han², S. Kim²,⁴ and K.W. Joo²,⁴

¹Department of Internal Medicine, Gachon University of Medicine and Science, Incheon, ²Department of Internal Medicine, Seoul National University College of Medicine, Seoul, ³Transplantation Research Institute, and ⁴Kidney Research Institute, Medical Research Center Seoul National University, Seoul, Korea
Aims: Leptin is a middle-molecular weight uremic toxin. Hemodiafiltration with on-line endogenous reinfusion (HFR) is a novel dialytic method combining the processes of diffusion, convection and adsorption. We performed a prospective crossover study of patients with end-stage renal disease to investigate the effect of HFR therapy on the level of leptin as compared to conventional low flux hemodialysis (LHD). Methods: Eleven stable hemodialysis patients were treated with LHD for 12 weeks and then treated with HFR (SG30 Plus; Sorin Group Italia S.r.1, Mirandola, Italy) for 12 weeks. Results: After 12 weeks of HFR treatment, serum leptin levels significantly decreased (17.1 (2.66 – 39.5) at Week 12 vs. 12.3 (1.80 – 24.3) ng/ml at Week 24, p = 0.014). Although serum adiponectin levels also decreased (1.66 (1.44 – 1.86) at Week 12 vs. 1.12 (0.79 – 1.34) g/ml at Week 24, p = 0.001), the ratio of leptin to adiponectin did not increase after HFR treatment. Serum beta₂-microglobulin (beta₂M) levels significantly decreased (37.7 (29.8 – 42.6) at Week 12 vs. 28.3 (26.5 – 32.2) mg/dl at Week 24, p = 0.002). Dry weight, Kt/V(urea), normalized protein equivalent of nitrogen appearance, subjective global assessment, and serum albumin levels of the patients were not changed after HFR treatment. There was no difference in the serum levels of C-reactive protein or interleukin-6 between Week 12 and Week 24. Conclusions: The results of our study indicate that HFR may be a better therapy than LHD for removal of middle-molecular-weight uremic toxins such as leptin and b2M.Correspondence to:
K.W. Joo, MD, PhD
Department of Internal Medicine
Seoul National University
College of Medicine
28 Yongon-dong
Chongno-gu, 110-744, Seoul, Korea
Email: junephro@paran.com

Abstract

A.S. Bomback¹, P. Muskala², E. Bald³, G. Chwatko³ and M. Nowicki²

¹Department of Medicine, Division of Nephrology, Columbia University College of Physicians and Surgeons, New York, NY, USA, ²Department of Nephrology, Hypertension, and Kidney Transplantation, Medical University of Lodz, and ³Department of Environmental Chemistry, University of Lodz, Poland
Background: For some hypertensive patients, conventional blockade of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers does not adequately protect against target organ damage. This may be particularly true for hypertensive patients with obesity, a condition often associated with elevated aldosterone levels. Methods: We conducted a pre-post study of fixed, low-dose spironolactone (12.5 mg/d), added to chronic ACE inhibitor-based antihypertension regimens, in obese subjects with essential hypertension and preexistent target organ damage. Outcomes of interest were changes in blood pressure (office, 24-h, and nocturnal), urinary albumin excretion, and potassium. Results: 21 subjects with mean age 57.3 ± 7.1 years, BMI 32.4 ± 3.4 kg/m² and 12.0 ± 7.0 years of antihypertensive therapy were enrolled. The mean aldosterone level before spironolactone treatment was 10.1 ± 7.3 ng/dl, and over 40% of subjects had baseline levels greater than mean population levels. During 4 weeks of low-dose spironolactone, mean office (110.6 ± 7.8 to 105.0 ± 8.1 mmHg, p = 0.004), 24-hour ambulatory (100.6 ± 9.4 to 95.5 ± 7.1 mmHg, p = 0.03) and nocturnal (95.3 ± 11.5 to 87.5 ± 8.2, p = 0.004) blood pressures all declined significantly. Log urine albumin : creatinine ratios also significantly dropped during spironolactone treatment (p = 0.002); in multivariate analysis, this decline did not appear to be due to changes in blood pressure but was influenced by concomitant changes in estimated glomerular filtration rate. Both the reductions in blood pressure and albumin excretion reversed after withdrawal of spironolactone. Serum potassium levels were essentially unchanged by low-dose spironolactone (p = 0.9). Conclusions: A fixed, low-dose of spironolactone, added to chronic ACE inhibitor therapy, reduced blood pressure and urinary albumin excretion in obese subjects with hypertension and preexistent target organ damage. A relative hyperaldosteronism due to aldosterone escape and/or obesity may explain the beneficial effects of spironolactone therapy in this study.Correspondence to:
A.S. Bomback, MD
Columbia University Medical Center
622 West 168th Street, PH 4-124
New York, NY 10032, USA
Email: asb68@columbia.edu

Abstract

Y.-T. Lee¹, H.-C. Chiu², C.-T. Huang¹, H.-M. Su³,⁴, C.-L. Wang⁵, T.-H. Lin³,⁴, W.-C. Voon³,⁴, H.-C. Chen⁴,⁶, W.-T. Lai³,⁴ and S.-H. Sheu³,⁴

Division of ¹Nephrology, Department of Pediatric; Division of ³Cardiology and ⁶Nephrology, Department of Internal Medicine,Kaohsiung Medical University Hospital and Department of Internal Medicine, Faculty of Medicine, ⁴College of Medicine and ⁵Graduate Institute of Medicine, and ²Healthcare Administration, Kaohsiung Medical University, Kaohsiung, Taiwan
Aim: The angiotensin II Type 1 receptor (AT1R) A1166C (rs5186) genez polymorphism is equivocally associated with the patients’ susceptibility to chronic kidney disease or end-stage renal disease. We conducted a prospective study to investigate the influence of AT1R A1166C gene polymorphism on the quantitative changes of renal function. Method: Of 1500 people screened, 112 non-diabetic normotensive elderly Chinese were recruited and received biochemistry examination at the baseline, at the second and fourth year follow-up. Serum creatinine and calculated renal parameters, using Cockroft-Gault (CG) formula, Modification of Diet in Renal Disease (MDRD) Study and abbreviated MDRD (abMDRD) equation, were used to evaluate renal function and their progression. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism. Result: Age was 71.9 ± 3.7 years (range 60 – 81). Serum creatinine, CG creatinine clearance (CrCl), MDRD and abMDRD glomerular filtration rate (GFR) were significantly decreased at the 2 and 4-year follow-up (all p < 0.001). The magnitude of 4-year decline of above four renal parameters was significantly higher in subjects carrying the AT1R AA genotype than C-allele carriers (p = 0.014, 0.033, 0.008 and 0.014 for creatinine, CG CrCl, MDRD and abMDRD GFR, respectively). This association was still significant in multivariate analyses (p = 0.019, 0.045, 0.035 and 0.018, respectively). Conclusion: This longitudinal study showed that the aging process was associated with decline of renal function in the healthy elderly. The AT1R A1166C gene polymorphism might modulate these changes in the Chinese. This provides further knowledge essential in the assessment of renal disease and determination of renal function in the older subjects.Correspondence to:
T.-H. Lin, MD, MSc, PHD
Division of Cardiology
Department of Internal Medicine
Kaohsiung Medical University
Hospital
100 Shi-Chuan 1st Road
Kaohsiung. 80708, Taiwan, ROC
Email: lth@kmu.edu.tw

Abstract

J.-S. Chen¹, D.-C. Chan², M.-J. Chung³, L.-C. Chang³ and V.C. Yang⁴

¹Divisions of Nephrology, ²General Surgery, Tri-Service General Hospital, ³School of Pharmacy, National Defense Medical Center, Taipei, Taiwan, and ⁴College of Pharmacy, The University of Michigan, Ann Arbor, MI, USA
Introduction: Although thromboembolism is the most recognized cause of death in cancer and uremic patients following tumorectomy or hemodialysis, respectively, little data exist concerning its etiologies and treatments in post-intervention settings. In this study, we determined the post-intervention fibrinolytic activities to exploit their implications in gastric cancer and uremic patients. Materials and methods: A small-scale case-control study with totally 56 cases aimed to compare the difference of the post-intervention fibrinolytic activities of two hypercoagulable groups of gastric cancer and uremic patients versus healthy controls was conducted. In-house functional assays for plasma plasminogen (Pg) and plasminogen activators (PA) activities were employed. Results: As compared to the control, both variable-stratified patient groups disclosed reduced Pg activities, synonyms at the “hypofibrinolytic” state, suggesting that the alleged post-intervention hypercoagulability of the two patient groups could be rationalized by the hypofibrinolysis mechanism. On the other hand, cancer patients showed elevated PA activity, concomitantly implicating that there was associated fibrinolytic consumption. Moreover, the altered PA activity could be ascribed to tumor metastasis according to literature review. Conclusions: Our data suggested that the PA/Pg fibrinolytic activities were altered in gastric cancer and uremic patients post-interventionally. Measurement of the post-intervention fibrinolytic activities could be useful in projection of some potential risks.Correspondence to:
L.-C. Chang, PhD
School of Pharmacy
National Defense Medical Center
161 MinChuan East Road, Sec#6, Taipei, Taiwan
Email: lichien@ndmctsgh.edu.tw

Abstract

E.A. Romão¹, T.M. Coimbra¹, R.S. Costa¹, O.M. Vieira Neto¹, M.A. Reis², A.L. Rodrigues Júnior¹, R.A. Ribeiro¹, R.C. Ravinal¹ and M. Dantas¹

¹Faculty of Medicine of Ribeirão Preto, University of São Paulo, and ²Federal University of Triangulo Mineiro, Uberaba, Brazil
Aims: The protein alpha1-microglobulin (alpha1-µg) is filtered by the glomeruli and fully reabsorbed by the proximal tubules, and tubulointerstitial injury compromises its reabsorption. The aim of this study was to determine which functional, morphological and inflammatory renal disorders associated with tubulointerstitial damage interfere with urinary excretion of alpha1-µg in patients with glomerulopathies. Patients and methods: 38 patients (33.6 ± 11.3 years) with primary or secondary glomerulopathies diagnosed by renal biopsies were studied. The urinary fractional excretion of alpha1-µg (FEalpha1-µg), the urinary monocyte chemoattractant protein-1/urinary creatinine (U_MCP-1) index and 24-h proteinuria were determined. In the cortex of renal biopsies, the number of macrophages/10⁴ µm² of glomerular tuft (GT) and tubulointerstitial (TI) areas, the relative interstitial area (RCIA), and the relative interstitial fibrosis area (CIF) were measured. Results are reported as median and range and the Spearman non-parametric test was used to determine the correlations. Results: FEalpha1-µg was 0.165% (0.008% – 14,790.0%) in patients with glomerulopathies and 0.065% (0.010% – 0.150%) in the control group (p < 0.05; Mann-Whitney U-Test). FEalpha1-µg was correlated with creatinine clearance (r = –0.4396; p = 0.0358), U_MCP-1 index (r = 0.5978; p < 0.0001), number of macrophages/TI area (r = 0.5634; p = 0.0034) and RCIA (r = 0.7436; p < 0.0001). However, FEa1-µg was not correlated with proteinuria (r = 0.1465; p = 0.5153) or with CIF (r = 0.0039; p = 0.98). Conclusions: renal MCP-1 and the expansion and number of macrophages of the tubulointerstitial area participate in the increase of urinary excretion of alpha1-µg in patients with glomerulopathies. Although proteinuria and interstitial fibrosis have not been associated with this effect, the present study does not exclude some of these disorders in the pathophysiology of urinary excretion of alpha1-µg.Correspondence to:
M. Dantas, MD
Division of Nephrology
Faculty of Medicine of Ribeirão Preto, USP
Av. Bandeirantes, 3900
14048-900, Ribeirão Preto, SP, Brazil
Email: mdantas@fmrp.usp.br

Abstract

B. Rogachev, M. Vorobiov, A. Shnaider, M. Hausmann, M. Zlotnik and A. Basok

Department of Nephrology, Soroka Medical Center, Ben Gurion University of the Negev Center for Health Sciences, Beer-Sheva, Israel
Two patients were contaminated by hepatitis during kidney transplantation from unrelated living donors, performed abroad in 2006. One patient died from fulminant hepatitis C (the first case of virus genotype 6a diagnosed in Israel) 2 months after transplantation and the other developed acute hepatitis B with YMDD to YVDD mutation necessitating life-long antiviral therapy. The dilemma of antiviral therapy in transplant recipients is discussed in this paper. Patients awaiting kidney transplantation by far outnumber the kidneys available for cadaver transplantation. International trade with living non-related kidneys has therefore become common. Comorbid conditions, although significant, are often ignored. After transplantation, the first patient presented with a picture of fulminant hepatitis C; immunosuppressive medication was tapered rapidly. This patient subsequently died from hepatic failure. The patient with active hepatitis B with YVDD mutation is receiving ongoing treatment by lamivudine and adefovir.Correspondence to:
A. Basok, MD
Department of Nephrology
Soroka Medical Center
Ben Gurion University of the Negev
Center for Health Sciences
PO Box 151, Beer-Sheva 84101, Israel
Email: basok@bgu.ac.il

Abstract

Y.K. Lee, J.K. Kim, S.E. Oh, J. Lee and J.W. Noh

Department of Internal Medicine, Hallym Kidney Research Institute, College of Medicine, Hallym University, Seoul, Korea
We describe two patients receiving peritoneal dialysis who experienced refractory peritonitis caused each by Gram-negative bacteria: Acinetobacter baumannii and Stenotrophomonas maltophilia. These patients did not respond to appropriate intraperitoneal antibiotic therapy. We assumed bacterial colonization in the intra-abdominal portion of the catheter with biofilm. Therefore, patients were treated with additional instillation of a ceftazidime-heparin lock into the catheter lumen after each exchange, as an adjunct to systemic antibiotic treatment which was successful. This study suggests that antibiotic lock therapy in the treatment of refractory peritonitis can be an effective method without catheter removal.Correspondence to:
J.W. Noh, MD
Department of Internal Medicine
Hallym University
Kangnam Sacred Heart Hospital
Seoul, Korea
Email: jwn8671@unitel.co.kr

Abstract

K.D. Jhaveri¹, A. Aelion² and R. Wanchoo¹,³

¹Department of Nephrology and Hypertension, ²Department of Obstetrics and Gynecology, New York Presbyterian Hospital at Weill Cornell Medical Center, New York, NY, and ³Rogosin Institute, New York, NY, USA
Pre-eclampsia affects 5 – 8% of pregnancies in the USA and 3 – 14% of pregnancies worldwide. Classically, the syndrome includes hypertension and proteinuria that may be associated with edema, headache and worsening epigastric pain. This is postulated from vasospasm and endothelial cell damage. Hyponatremia in pre-eclamptic pregnancies has been described in few cases, most of which were twin pregnancies, and four of them had nephrotic syndrome. The management of hyponatremia requires a multidisciplinary approach and significant attention, as this condition can predispose to convulsions along with pre-eclampsia, thus, endangering the life of the mother and the child. We describe a case of a patient who developed pre-eclampsia and hyponatremia in the absence of proteinuria, at 34 weeks of a twin pregnancy; there was progression to oliguria with complete remission following delivery by cesarean section.Correspondence to:
K.D. Jhaveri, MD
Dept. of Nephrology and Hypertension
Weill Cornell Medical Center New York
Presbyterian Hospital
525 East 68th Street
New York NY 10021, USA
Email: Kej9015@nyp.org

Abstract

T. Miyazawa, M. Nakano, Y. Takemura, K. Miyazaki, H. Yanagida, S. Fujita, K. Sugimoto, M. Okada and T. Takemura

Department of Pediatrics, Kinki University School of Medicine, Osaka, Japan
A case of an adolescent male with renal-coloboma syndrome (RCS) showing developmental delay is described. Birth and perinatal histories were typical. Proteinuria was initially observed at the age of 7 years during an annual mass screening program for school children. His urine was checked periodically at a local hospital. Because of an increase in proteinuria, he was referred to our hospital for further clinical evaluation. Proteinuria was moderate, ranging from 1.0 to 1.5 g/day, and was coupled with mild renal dysfunction. At that time, he was found to have myopia associated with astigmatism. He exhibited mild developmental delay, assessed by a WISC-III test. A renal biopsy sample showed marked glomerular enlargement, collapse of glomerular capillaries, mesangial matrix expansion, and tubulointerstitial change, demonstrating typical histologic features of RCS. Approximately five years after starting follow-up, the patient had severe renal dysfunction. Furthermore, optic nerve coloboma was also evident. Genetic analysis of the patient revealed a novel heterozygous mutation in exon 3 of the PAX2 gene (P130H).Correspondence to:
T. Takemura, MD, PhD
Department of Pediatrics
Kinki University School of Medicine
377-2 Ohno Higasi, Osaka-Sayama-shi
Osaka 589-8511, Japan
Email: tsukasa@med.kindai.ac.jp

Abstract

S.C. Chen, J.-M. Chang, S.-J. Hwang, C.-S. Wang, W.-C. Liu, J.-H. Chen, H.-M. Su and H.-C. Chen

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Volume 72, No. 6/2009(December)