Volume 78 (2012), No. 1/2012(July)
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Original
Dissociation between progression of coronary artery calcification and endothelial function in hemodialysis patients: a prospective pilot study
Roberto S. Kalil, Michael Flanigan, William Stanford and William G. Haynes
Page No. 1
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (1-9)
Dissociation between progression of coronary artery calcification and endothelial function in hemodialysis patients: a prospective pilot study
Roberto S. Kalil1, Michael Flanigan2, William Stanford3 and William G. Haynes1
Departments of 1Internal Medicine and 2Radiology, Roy J. and Lucille Carver College of Medicine, University of Iowa, Iowa City, IA, and 3Marshfield Clinic, Minocqua, WI, USA
Chronic kidney disease profoundly disturbs calcium-phosphate metabolism and predisposes to premature atherosclerosis. Both coronary artery calcification (CAC) and endothelial dysfunction are common in hemodialysis (HD) patients. We hypothesized that a calcium-free phosphate binder would improve endothelial function and delay progression of vascular calcification in HD patients. Methods: This was a randomized parallel-group trial in HD patients comparing lanthanum carbonate (LC) with a non-LC phosphorus binders control group (non-LC) at a 1 : 1 randomization. CAC was obtained at baseline, 6, and 12 months, and endothelial function (brachial artery flow-mediated dilation – FMD) at baseline and 6 months. Results: 13 patients were randomized (LC n = 7 and non-LC n = 6). CAC scores (Log ± SE) at baseline were 7.21 ± 0.62 (LC) and 6.07 ± 0.73 (control). CAC increased in the non-LC group (33 ± 17% and 77 ± 22% at 6 and 12 months), but tended to decrease in the LC group (–10 ± 11% and –2 ± 11% at 6 and 12 months). There was statistically less progression in CAC in the LC group compared to control at 6 (p = 0.002) and 12 months (p = 0.003). There was no difference between groups in FMD (p = 0.7). Markers of inflammation did not change significantly. Conclusion: A slower rate of progression of CAC occurred in the LC group, independent of changes in FMD. This is the first study showing dissociation between progression of CAC and FMD in HD patients. Larger studies are warranted to elucidate the impact of different phosphate sequestration therapies on atherosclerosis in HD patients.Correspondence to:
R.S. Kalil, MD
Department of Internal Medicine
University of Iowa
200 Hawkins Drive, T311-GH
Iowa City, IA, 52240, USA
Email: Roberto-kalil@ uiowa.edu
Original
Kidney transplantation restored uncoupled bone turnover in end-stage renal disease
Hiroo Kawarazaki, Yugo Shibagaki, Ryo Kido, Ichiro Nakajima, Shohei Fuchinoue, Katsuyuki Ando, Toshiro Fujita, Masafumi Fukagawa, Satoshi Teraoka and Seiji Fukumoto
Page No. 10
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (10-16)
Kidney transplantation restored uncoupled bone turnover in end-stage renal disease
Hiroo Kawarazaki1, Yugo Shibagaki1, Ryo Kido2, Ichiro Nakajima3, Shohei Fuchinoue3, Katsuyuki Ando2, Toshiro Fujita1, Masafumi Fukagawa4, Satoshi Teraoka3 and Seiji Fukumoto2
1Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki City, 2Department of Nephrology and Endocrinology, University of Tokyo, 3Department of Surgery, Kidney Center, Tokyo Women’s Medical University, Tokyo, and 4Division of Nephrology and Metabolism, Tokai University School of Medicine, Isehara City, Japan
Background: While kidney transplantation (KTx) reverses many disorders associated with end-stage renal disease (ESRD), patients who have received KTx often have chronic kidney disease and bone and mineral disorder (CKD-MBD). However, it is unknown how bone metabolism changes by KTx. Patients and methods: Living donor-KTx recipients (n = 34) at Tokyo Women’s Medical University were prospectively recruited and the levels of bone-specific alkaline phosphatase (BAP) and serum cross-linked N-telopeptides of Type 1 collagen (NTX) were measured before, 6 and 12 months after transplantation. Results: Before KTx, serum BAP was within the reference range in more than half of patients while NTX was high in most patients. Serum NTX was higher in patients with longer dialysis durations compared to that with shorter durations before KTx. However, there was no difference in serum BAP between these patients. After KTx, BAP increased while NTX decreased along with the decline of PTH. In addition, the numbers of patients who showed high BAP and NTX were comparable after KTx. Conclusion: These results suggest that bone formation is suppressed and uncoupled with bone resorption in patients with ESRD and this uncoupling is restored by KTx. Further studies are necessary to clarify the mechanism of bone uncoupling in patients with ESRD.Correspondence to:
Hiroo Kawarazaki, MD
Division of Nephrology and Hypertension
Department of Internal Medicine
St. Marianna University School of Medicine
2-16-1 Sugao, Miyamaeku
Kawasaki City, Kanagawa, 216-8511, Japan
Email: [email protected]
Original
Acute and long-term effects of corticosteroid therapy on bone metabolism in patients with kidney diseases
Ágnes Haris, András Szabó, Éva Lányi, István Mucsi and Kálmán Polner
Page No. 17
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (17-23)
Acute and long-term effects of corticosteroid therapy on bone metabolism in patients with kidney diseases
Ágnes Haris1, András Szabó2, Éva Lányi3, István Mucsi4,5,6 and Kálmán Polner1
1Szent Margit Hospital Nephrology Department, 2Semmelweis University 2nd Department of Pediatrics, 3Budai Irgalmasrendi Hospital 1st Rheumatology Department, 4Institute of Behavioral Sciences, Semmelweis University, 5Institute of Pathophysiology, Semmelweis University, Budapest, Hungary, and 6Division of Nephrology, Department of Medicine, McGill University Health Center, Montreal, Quebec, Canada
Aim: The aim of our study was to examine parameters of bone metabolism during pulse and long-term methylprednisolone (MP) treatment in patients with kidney diseases. Methods: In 13 patients with RPGN, treated with intravenous MP pulses, followed by tapering oral doses, osteocalcin (OC) and β-CrossLaps (β-CL) were measured before treatment, after the 3rd pulse, then 1 and 3 months later (“acute study”). In a separate set of analyses serum markers of bone metabolism and bone mineral density (BMD) were studied in 40 patients on maintenance MP therapy (“chronic study”). Results: Immediately after the 3rd MP pulse serum OC decreased to 38 ± 23%, β-CL increased to 200 ± 121% of the baseline (p = 0.002 for OC and p = 0.003 for β-CL, respectively), and the OC/β-CL ratio decreased from 55 ± 35 to 9 ± 7 (p = 0.002). OC remained below and β-CL above baseline even at 3 months post pulse steroid treatment. Patients in the “chronic study” who were on maintenance oral steroid therapy received 13,844 ± 7,454 mg MP over 53 ± 47 months. BMD at the end of follow-up revealed reduced bone mineral density in 72.5% of the participants. Zscores both at the hip and at the lumbar spine were significantly correlated with duration of steroid treatment and also with the cumulative steroid dose. Conclusion: MP pulse causes immediate, profound suppression of osteoblast function, and significant increase of osteoclast activity, suggesting uncoupling of bone formation and resorption. Prolonged high dose steroid treatment causes significant bone loss in patients with chronic kidney disease. Appropriate systematic follow up of bone metabolism, preventive measures and therapy when needed would be important for the bone health of this patient population.Correspondence to:
Ágnes Haris, MD, PhD
Szent Margit Hospital
Nephrology Department
132 Bécsi Street
1032 Budapest, Hungary
Email: [email protected]
Original
Prospective multicenter study of HX575 (biosimilar epoetin-alpha) in patients with chronic kidney disease applying a target hemoglobin of 10 – 12 g/dl
Walter H. Hörl, Francesco Locatelli, Marianne Haag- Weber, Marité Ode and Karsten Roth for the Epo-PASS study group
Page No. 24
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (24-32)
Prospective multicenter study of HX575 (biosimilar epoetin-alpha) in patients with chronic kidney disease applying a target hemoglobin of 10 – 12 g/dl
Walter H. Hörl1, Francesco Locatelli2, Marianne Haag-Weber3, Marité Ode4 and Karsten Roth4 for the Epo-PASS study group
1Division of Nephrology and Dialysis, Medical University of Vienna, Vienna, Austria, 2Department of Nephrology, Dialysis and Renal Transplant, Alessandro Manzoni Hospital, Lecco, Italy, 3KfH Kidney Center, St. Elisabeth Hospital, Straubing, Germany, 4Sandoz Biopharmaceuticals, Hexal AG, Holzkirchen, Germany and the Epo-PASS study group
HX575 was approved in the European Union in August 2007 as the firstever biosimilar epoetin-alpha product. The present study extended the safety database on HX575 by monitoring adverse events (AEs) in clinical practice. Hemoglobin (Hb) levels and HX575 doses were recorded for the assessment of efficacy. This open, 6-month single-arm study was conducted in 10 European countries with a target enrollment of 1,500 patients with anemia due to chronic kidney disease (CKD). HX575 was intravenously (i.v.) administered aiming at an Hb target of 10 – 12 g/dl. Most patients (92.3%) had already received erythropoiesis stimulating agents (ESAs) treatment before enrolment into this study; the recorded treatments mainly comprised i.v. or subcutaneous (s.c.) administration of epoetin-alpha, epoetin-beta or darbepoetin. The study period covered 770 patient years. The observed AE profile was in line with expectations for this patient population. Thrombotic vascular events (TVEs) were reported in 11.9% of patients (0.2612 per patient year). Tumor incidence was 1.4% (0.0299 per patient year). No subject developed anti-epoetin antibodies. Mean Hb levels were effectively maintained between 11.2 and 11.3 g/dl following the conversion from a broad spectrum of pre-study ESA treatments with stable overall mean i.v. HX575 doses. The proportion of patients within the Hb target range increased from 57.5% at baseline to 66.8% at study end.Correspondence to:
Marité Ode
Sandoz Biopharmaceutical Development
Hexal AG
Industriestrasse 25
83607 Holzkirchen, Germany
Email: [email protected]
Original
Serum prolactin and macroprolactin levels in diabetic nephropathy
Funda Sari, Ramazan Sari, Sebahat Ozdem, Metin Sarikaya and Ramazan Cetinkaya
Page No. 33
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (33-39)
Serum prolactin and macroprolactin levels in diabetic nephropathy
Funda Sari1, Ramazan Sari2, Sebahat Ozdem3, Metin Sarikaya1 and Ramazan Cetinkaya1
1Division of Nephrology, Antalya Education and Research Hospital, Ministry of Health, 2Division of Endocrinology and Metabolism, Akdeniz University, School of Medicine and 3Central Laboratory, Department of Clinical Biochemistry, Akdeniz University, School of Medicine, Antalya, Turkey
Objective: Three molecular forms of prolactin with molecular weights of 23 (monomeric), 50 – 60 and > 100 kDA (macroprolactin) have been defined. Prolactin levels have been shown to be reduced in especially poorly controlled diabetes mellitus and the prevalence of macroprolactinemia in diabetic patients has been higher than the non-diabetic population. Patients and methods: A total 234 Type 2 diabetic patients with different nephropathy stage was included in the study. Serum prolactin levels were analyzed by the Electrochemiluminescense method. Following polyethylene glycol (PEG) precipitation, recovery less than or equal to 40% was taken as evidence that a significant level of macroprolactin was present in the serum. Results: Hyperprolactinemia and macroprolactinemia were detected in 40 (17%) and 13 (5.5%) patients, respectively. Macroprolactinemia was detected 13 of 40 patients with hyperprolactinemia (32.5%). Increased prolactin and macroprolactin levels in patients with moderate and severe renal failure (Stage 3, 4, and 5) according to the U.S. NKF-DOQI classification (p < 0.001). Prolactin and macroprolactin levels were not increased in patients with normoalbuminuria, microalbuminuria and macroalbuminuria (p > 0.05). Serum creatinine levels correleted positively with both prolactin (r = 0.51, p < 0.001) and macroprolactin levels (r = 0.43, p < 0.001). On the other hand, glomerular filtration rate correlated negatively with both prolactin (r = –0.54, p < 0.001) and macroprolactin levels (r = –0.44, p < 0.001). Albuminuria significantly related with neither prolactin nor macroprolactin levels (p > 0.05). Conclusion: In the present study, we found that not only serum prolactin but also serum macroprolactin levels increased especially in moderate to severe renal failure which was due to decreased glomerular filtration and renal parenchymal function resulting in an increased amount of monomeric prolactin and macroprolactin in the circulation in patients with Type 2 diabetes mellitus.Correspondence to:
Funda Sari, MD
Antalya Education and Research Hospital
Ministry of Health, Division of Nephrology
Antalya, Turkey
Email: [email protected]
Original
Effect of single-dose oral mizoribine pulse therapy twice per week for frequently relapsing steroid-dependent nephrotic syndrome
Mikiya Fujieda, Masayuki Ishihara, Taku Morita, Atsushi Hayashi , Shinichi Okada, Toshiyuki Ohta, Takashi Sakano and Hiroshi Wakiguchi
Page No. 40
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (40-46)
Effect of single-dose oral mizoribine pulse therapy twice per week for frequently relapsing steroid-dependent nephrotic syndrome
Mikiya Fujieda1, Masayuki Ishihara1, Taku Morita1, Atsushi Hayashi2, 3, Shinichi Okada2, Toshiyuki Ohta4, Takashi Sakano4 and Hiroshi Wakiguchi1
1Department of Pediatrics, Kochi Medical School, Kochi University, Kochi, 2Department of Pediatrics, Tottori University, 3Department of Pediatrics, National Hospital Organization, Tottori Medical Center, Tottori, and 4Department of Pediatrics, Hiroshima Prefectural Hospital, Hiroshima, Japan
Aim: To evaluate the efficacy of single-dose oral mizoribine (MZB) pulse therapy given twice weekly for frequently relapsing steroid-dependent nephrotic syndrome (FR-SDNS). Methods: The subjects were 8 patients with FR-SDNS with a median age of 6.9 years old (range 3.1 – 18.0 y). The study was performed as a Phase II trial. The MZB dose was adjusted to achieve a peak blood level of 3 – 5 μg/ml (3.9 – 15.9 mg/kg/d, maximum dose: 750 mg) using a single dose given twice weekly before a meal. The therapeutic benefits of MZB pulse therapy were assessed based on a comparison of the incidence of relapse and the required daily dosage of prednisolone (PSL) in the 12 months prior to and following therapy. Results: The incidence of relapse after therapy was significantly lower than that before therapy (2.5 ± 1.4 vs. 4.3 ± 0.5, p < 0.01) and the required daily dosage of prednisolone (PSL) after therapy was lower than that before therapy (0.48 ± 0.23 vs. 0.52 ± 0.32 mg/kg/d, not significant). However, this therapy was not effective for 3 out of 4 patients treated with cyclosporine. During follow-up, discontinuation of PSL was possible in 4 of 5 patients who showed a decreased rate of relapse after therapy. The peak blood concentration of MZB in these patients was significantly higher than that in 3 patients who did not show a decreased rate of relapse (3.95 ± 0.11 vs. 3.05 ± 0.21 μg/ml, p < 0.01). No adverse effects were observed in any patients. Conclusion: Our results show that singledose oral MZB pulse therapy is effective in decreasing the frequency of relapse in some pediatric patients with FR-SDNS. A peak concentration of MZB of about 3.8 – 4.0 μg/ ml may be required for FR-SDNS therapy.Correspondence to:
M. Fujieda, MD
Department of Pediatrics
Kochi Medical School, Kochi University
Kohasu, Oko-cho, Nankoku, Kochi, 783-8505, Japan
Email: [email protected]
Original
Mutations in podocyte genes are a rare cause of primary FSGS associated with ESRD in adult patients
Anja K. Büscher, Martin Konrad, Mato Nagel, Oliver Witzke, Andreas Kribben, Peter F. Hoyer and Stefanie Weber
Page No. 47
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (47-53)
Mutations in podocyte genes are a rare cause of primary FSGS associated with ESRD in adult patients
Anja K. Büscher1, Martin Konrad2, Mato Nagel3, Oliver Witzke4, Andreas Kribben4, Peter F. Hoyer1 and Stefanie Weber1
1Pediatric Nephrology, Pediatrics II, University-Children’s Hospital Essen, 2Pediatric Nephrology, University-Children’s Hospital Münster, 3Center for Nephrology and Metabolic Disorders, Weißwasser, and 4Department of Nephrology, University of Duisburg-Essen, Germany
Background and aims: Several genes have been identified to be causative for the disease in a subset of patients with focal segmental glomerulosclerosis (FSGS) and nephrotic syndrome (NS). Mutations in genes with autosomal dominant inheritance mostly affect adolescent or adult patients. In rare cases recessive mutations in NPHS2 are associated with late-onset FSGS. Hereditary FSGS is associated with poor renal survival and low rates of disease recurrence after renal transplantation. Aim of the study was to evaluate the incidence of gene mutations within a cohort of adult patients with primary FSGS and/or NS and progression to end-stage renal disease (ESRD). Methods: Genotyping for TRPC6, ACTN4, CD2AP, WT1, INF2, NPHS2 and NPHS1 was performed in all patients with primary FSGS and ESRD registered on the waiting list for kidney transplantation of a large German transplant center (n = 26 out of 478 registered patients). Mean age at onset was 31.7 years; a positive family history for renal disease was documented in 11 (42%) patients, of these one with familiar history of FSGS. Results: A missense mutation (p.R360H) was identified in TRPC6, 2 missense mutations in compound heterozygous state in NPHS1 (p.P368L; p.G412C), a sequence variation of unknown significance (p.R310Q) in ACTN4 and the non-neutral NPHS2 polymorphism p.R229Q in two additional patients. No mutations were detected in INF2, CD2AP and WT1. Conclusions: The observed mutation rate was 8% in this single-center cohort of adult patients with primary FSGS. Mutations in podocyte genes seem to be a rare cause of FSGS and renal failure in adult patients. However, they should be considered as the underlying cause in a subset of patient as the impact on family counseling and patients’ life perspectives are significant.Correspondence to:
Anja K. Büscher, MD
University-Children’s Hospital Essen
Hufelandstraße 55, 45122 Essen, Germany
Email: [email protected]
Original
Clinical and pathological spectrums of aristolochic acid nephropathy
Dongmei Chen, Zheng Tang, Chunlei Luo, Huiping Chen and Zhihong Liu
Page No. 54
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (54-60)
Clinical and pathological spectrums of aristolochic acid nephropathy
Dongmei Chen, Zheng Tang, Chunlei Luo, Huiping Chen and Zhihong Liu
Research Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, P.R. China
Aim: To study the clinical and pathological characteristics of aristolochic acid nephropathy (AAN). Methods: 86 patients with AAN during 2001 and 2009 in our department were recruited in this retrospective study. The clinical and pathological features were analyzed. Results: There were 47 males and 39 females, aging from 12 to 69 years old. Abnormal urine analysis and gastro-intestinal diseases were two main underlying causes for patients taking aristolochic acid (AA) containing drugs. All patients suffered from renal function impairment. 19 patients (22.0%) presented with acute kidney injury (AKI), while 67 patients (78%) presented as chronic cases. Among them, 31 patients (36.0%) lacked symptoms, 30 patients (34.8%) were accompanied with hypertension, and 26 patients (30.2%) presented with gastrointestinal symptoms. Laboratory examination revealed elevated urine retinol-binding protein (RBP) (90.7%) and urine N-acetyl-β-glucosaminidase (NAG) (80.2%). Anemia and glucosuria accounted for 64.0% and 58.1%, respectively. Renal biopsy showed prominent tubular brush border ablation (84.2%) in acute cases, while obvious tubular basement membrane (TBM) thickening (81.4%) and interstitial fibrosis were present in chronic cases. During the follow- up, 11 (57.9%) acute cases gained renal function recovery. They had lower urine RBP level and lower incidence of hypokalemia than the non-recovery acute cases. In the chronic group, 27 patients (40.2%) progressed to endstage renal disease (ESRD), with 11 dialysis and 5 renal transplantation cases. Conclusion: AAN patients usually suffered from renal impairment with an associated history of taking AA containing drugs. Proximal renal tubular dysfunction and structure destroying would be the main positive findings in laboratory tests and renal biopsy. Urine RBP and hypokalemia might determine the outcome of acute AAN patients.Correspondence to:
Zheng Tang, MD
Research Institute of Nephrology
Jinling Hospital
Nanjing University School of Medicine
Nanjing 210002, P.R. China
Email: [email protected]
Nephrology Education
Maximal conservative therapy of calcific uremic ateriolopathy
Charlotte Van Noten, Karin Janssen van Doorn, Evert Vermander, Sonja Vlayen, Gert A. Verpooten and Marie- Madeleine Couttenye
Page No. 61
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (61-63)
Maximal conservative therapy of calcific uremic ateriolopathy
Charlotte Van Noten1, Karin Janssen van Doorn1, Evert Vermander2, Sonja Vlayen3, Gert A. Verpooten1,4 and Marie-Madeleine Couttenye1,4
Departments of 1Nephrology-Hypertension, 2Dermatology, 3Nursing, Antwerp University Hospital, and 4University of Antwerp, Belgium
We present the case of a 61-year- old female patient in long-term hemodialysis who developed calcific uremic arteriolopathy (CUA) upon administration of the oral calcimimetic agent cinacalcet for treatment of secondary hyperparathyroidism. In May 2009, the baseline serum values were parathormone (PTH) 310 pg/ml, calcium 9.1 mg/dl and phosphorous 6.9 mg/dl. Necrotic wounds in the suprapubic fat tissue were successfully treated first, by correcting the calcium phosphorous product; second, through treatment with sodium thiosulfate and third, through intensive wound care with hyperbaric oxygen therapy and vacuum-assisted closure therapy, with no need for parathyroidectomy. Multiple factors have been described to play a role in the development of CUA. Based on the findings of this case, the treatment of CUA should be aimed at correcting different causes simultaneously.Correspondence to:
M.-M. Couttenye, MD, PhD
Antwerp University Hospital
Department of Nephrology-Hypertension
Wilrijkstraat 10, 2650 Edegem (Antwerp), Belgium
Email: [email protected]
Nephrology Education
Cystatin C and acute changes in glomerular filtration rate
Ayodele Odutayo and David Cherney
Page No. 64
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (64-75)
Cystatin C and acute changes in glomerular filtration rate
Ayodele Odutayo1 and David Cherney2
1Division of Nephrology, Sunnybrook Research Institute, Faculty of Medicine, and 2Division of Nephrology, University Health Network, University of Toronto, Toronto, ON, Canada
The identification of an effective marker of acutely changing kidney function is a priority in clinical nephrology. While serum creatinine is the most widely used surrogate for glomerular filtration rate (GFR), its vulnerability to non-glomerular clearance results in biased estimates of GFR and may delay the identification of acute changes. Alternatively, cystatin C (CysC) has been recognized as a promising marker of GFR. Controlled physiological studies in diabetes, protein-induced glomerular hyperfiltration and extreme exercise demonstrated that acute changes in CysC provide a better approximation of GFR than serum creatinine. Clinical studies examining contrast induced nephropathy, acute kidney injury, and kidney transplantation have also demonstrated several possible advantages of CysC with respect to accurately measuring GFR and early diagnosis of renal dysfunction. CysC measurements also provide ancillary benefits such as improved prediction of patient outcomes and prognosis. Our aim was to review the literature on short-term changes in CysC over days, weeks and months to explore the clinical utility of CysC in the acute setting. Based on existing evidence, CysC may improve clinicians’ ability to detect acute changes in kidney function.Correspondence to:
David Cherney, MD, PhD, FRCP(C)
Toronto General Hospital
585 University Ave, 8N-845
Toronto, Ontario, M5G 2N2, Canada
Email: [email protected]
Nephrology Education
Staghorn cystine stone in a 72-year-old recurrent calcium stone former
Adamasco Cupisti, Ilaria Farnesi, Nicola Armillotta and Francesco Francesca
Page No. 76
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (76-80)
Staghorn cystine stone in a 72-year-old recurrent calcium stone former
Adamasco Cupisti1, Ilaria Farnesi1, Nicola Armillotta2 and Francesco Francesca3
1Nephrology Division, Internal Medicine Department, 2Diagnostic and Interventional Radiology, University of Pisa, and 3Division of Urology, AOUPisana, Pisa, Italy
This case deals with the first diagnosis of Type B cystinuria with cystine nephrolithiasis in a 72-year-old male. Cystinuria is an inherited disease that consists of congenital abnormalities of renal and intestinal transport of dibasic amino acids. It often leads to frequent recurrent stone formation. Cystine stones most frequently occur in the 1st through 3rd decades of life with a decreased incidence in old age. This case shows that the first diagnosis of cystinuria may be made even in the 8th decade, without any family history, and in a patient with a history of recurrent calcium stone disease. Therefore, the chance of cystinuria must be always considered, even in older calcium stone formers. Correspondence to:
A. Cupisti, MD, PhD
Nephrology Division, Department of Internal Medicine
University of Pisa
Via Roma 67, 56126 Pisa, Italy
Email: [email protected]
Nephrology Education
Pericardial effusion as a crucial presentation of Erdheim-Chester disease in a hemodialysis patient: an overlooked diagnosis
Meng-Tsai Chen, Shu-Ming Wang, Shih-Yi Lin, I-Wen Ting, Jiung-Hsiun Liu, Huey-Liang Kuo and Chiu-Ching Huang
Page No. 81
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 (81-84)
Pericardial effusion as a crucial presentation of Erdheim-Chester disease in a hemodialysis patient: an overlooked diagnosis
Meng-Tsai Chen1,2, Shu-Ming Wang1,2, Shih-Yi Lin1,2, I-Wen Ting1,2, Jiung-Hsiun Liu1,2, Huey-Liang Kuo1,2 and Chiu-Ching Huang1,2
1Division of Nephrology and Kidney Institute, Department of Internal Medicine, and 2China Medical University, Taichung, Taiwan
Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis whose hallmark is tissue infiltration by CD68-positive, CD1a-negative and usually S-100 protein-positive foamy non-Langerhans histiocytes and mononuclear cells. Here, we report a hemodialysis (HD) patient who presented with fever and pericardial effusion. We performed pericardiocentesis with pericardial biopsy and the histological findings indicated ECD. We administered intravenous methylprednisolone pulse therapy (250 mg/d) followed by oral prednisolone (50 mg/d). The patient’s fever gradually subsided and there was no recurrence of pericardial effusion. This is the first report of an HD patient with ECD. We suggest that ECD be considered in the differential diagnosis of new HD patients who present with pericardial effusion, especially when this did not improve following increased dose of HD.Correspondence to:
Chiu-Ching Huang
Division of Nephrology and Kidney Institute
Department of Internal Medicine
China Medical University Hospital
No 2. Yuh-Der Road, Taichung 404, Taiwan
Email: [email protected]
Letter to the Editor
Decrease of serum sphingosine-1-phosphate levels in hemodialysis patients with secondary hyperparathyroidism treated with cinacalcet
Keitaro Yokoyama, Ichiro Ohkido, Takeo Iwamoto, Mari Ishida, Mitsuyoshi Urashima and Tatsuo Hosoya
Page No. 85
Abstract
Clinical Nephrology, Vol. 78 – No. 1/2012 – Letter to the editor
Decrease of serum sphingosine-1-phosphate levels in hemodialysis patients with secondary hyperparathyroidism treated with cinacalcet
Keitaro Yokoyama1, Ichiro Ohkido1, Takeo Iwamoto2, Mari Ishida3, Mitsuyoshi Urashima4 and Tatsuo Hosoya1
1Division of Kidney and Hypertension, Department of Internal Medicine, 2Core Research Facilities, Division of Biochemistry, The Jikei University School of Medicine, Tokyo, 3Jinyukai Kitasaito Hospital, Asahikawa, and 4Division of Molecular Epidemiology, The Jikei University School of Medicine, Tokyo, Japan
Correspondence to:
Keitaro Yokoyama, MD, PhD
Division of Kidney and Hypertension
Department of Internal Medicine
The Jikei University School of Medicine
3-25-8 Nishi-Shinbashi, Minato-ku
Tokyo 105-8471, Japan
Email: [email protected]
