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Abstract

Dietary modifications alone do not improve bone mineral density in children with idiopathic hypercalciuria

A.L. Schwaderer¹, T. Srivastava², L. Schueller³, R. Cronin⁴, J.D. Mahan¹ and D. Hains¹

¹The Ohio State University College of Medicine/Nationwide Children’s Hospital, Department of Pediatrics, Division of Pediatric Nephrology, Columbus, OH, ²Bone and Mineral Disorder Clinic, The Children’s Mercy Hospital and Clinics, University of Missouri, Kansas City, MO, ³The Research Institute at Nationwide Children’s Hospital, and ⁴The Ohio State University College of Medicine, Columbus, OH, USA
Prior cross-sectional studies have demonstrated an association between hypercalciuria and low bone mineral density (BMD) in children and adults. However, the natural history of BMD in children with hypercalciuria and its response to therapy has not been evaluated. The objective of this retrospective study was to determine the change over time in lumbar (L1 – L4) BMD Z-score measured on sequential DXA scans in 19 children with hypercalciuria treated with dietary recommendations without (n = 12, Group A) and with citrate (n = 7, Group B). The mean lumbar bone density Z-score/year decreased in Group A (–0.11 ±/0.41) indicating that children with hypercalciuria lose L1 – L4 BMD over time. In contrast, the L1 – L4 BMD Zscore/ year increased in Group B (0.19 ± 0.38) suggesting that pharmacologic therapy may reverse this trend. Similarly 75% of patients in Group A, but only 29% patients in Group B had a decrease in L1 – L4 BMD. There was a definite, although not significant, trend towards improved mean bone mineral density Z-score per year and a lower percentage of patients with a decreased Z-score in hypercalciuric children treated with potassium citrate. Our findings suggest the possibility that dietary recommendations alone is not adequate as the bone mineral density of children with hypercalciuria will decrease over time, potentially increasing the risk for osteoporosis as an adult.Correspondence to:
Dr. A.L. Schwaderer
700 Children’s Drive
Columbus, OH 43205, USA
Email: schwaderer.5@osu.edu

Abstract

Clinical Nephrology, Vol. 76 – No. 5/2011 (348-353)

Optimal frequency of parathyroid hormone monitoring in chronic hemodialysis patients

S. Greenberg, S. Gadde, M. Pagala, M. Greenberg, I. Shneyderman and K. Janga

Department of Nephrology, Maimonides Medical Center, Brooklyn, NY, USA
Background: Secondary hyperparathyroidism is a common manifestation of chronic kidney disease (CKD). Serum parathyroid hormone (PTH) level is widely used as a marker for hyperparathyroidism. Currently, there is limited data to guide the frequency of PTH monitoring in CKD patients. The present study was undertaken to determine the optimal frequency of monitoring PTH in patients on maintenance hemodialysis. Methods: A cohort of 154 patients on maintenance dialysis at a single outpatient hemodialysis center was included in this retrospective study. In Phase I of the study, PTH was measured every 3 months as per Kidney Disease Outcomes Quality Initiative (KDOQI) recommendations. In Phase II, PTH was measured monthly. In both phases, dietary education and optimization of medications including phosphate binders, vitamin D analogues and calcimimetics were implemented using standard protocols Data from the two phases was compared with each other and with their respective national norms. Results: The percentage of patients with PTH in target range of 150 – 300 pg/ml increased significantly from Phase I to Phase II of the study (25.4 – 40.3%, p < 0.01). There was a significant reduction in the percentage of patients with PTH levels > 300 pg/ml in Phase II compared with national averages (37% vs. 47%, p < 0.02). There was no significant difference in calcium and phosphorus levels or their product. There was a significant increase in the usage of calcimimetics and vitamin D analogues. Conclusion: We observed that increasing the frequency of monitoring PTH from quarterly to monthly was associated with a significant increase in the percentage of patients reaching KDOQI target PTH values.Correspondence to:
Dr. S. Gadde
Department of Nephrology
Maimonides Medical Center
4802 Tenth Avenue
Brooklyn, NY 11219, USA
Email: dr_suneeta@yahoo.co.in

Abstract

Clinical Nephrology, Vol. 76 – No. 5/2011 (354-357)

Evaluating the definition of “stone free status” in contemporary urologic literature

L.A. Deters, C.M. Jumper, P.L. Steinberg and V.M. Pais jr.

Dartmouth Hitchcock Medical Center, Lebanon, NH, USA
Objective: There is no standardized definition of stone free after renal stone surgery. The lack of standardization prompted a review of the current urologic literature, to assess the definitions of stone free status, and how imaging is used to determine stone free status. Methods: A literature search on PubMed for the MeSH terms for percutaneous nephrolithotomy (PCNL), ureteroscopy with lithotripsy, shock wave lithotripsy (SWL), and laser lithotripsy, published in English between January 2007 and January 2010 was performed. Case reports, articles not evaluating stone free outcomes, and review articles were excluded. Articles were evaluated for the treatment modality, definition of stone free status, and the imaging modality employed to determine stone free status. Results: This search yielded 417 articles of which 249 met inclusion criteria. Stone free was defined in 169 articles (68%). The most common definition of stone free was “no stones” (47%), but a total of seven different definitions were encountered. The most common treatment modality was PCNL (47%), followed by SWL (33%), and URS (13%). The most common detection modality was KUB alone (28%), the second most common being KUB and US combined (22%). Conclusions: Nearly one-third of articles evaluating surgical management of urinary calculi do not define stone free status; when stone free is defined, there is wide variation as to that definition. Furthermore, vast differences exist in the type of imaging used to define stone free status. The urologic community should standardize the reporting of stone free outcomes in the urologic literature. Correspondence to:
V.M. Pais, Jr., MD
Section of Urology, DHMC
Lebanon, NH 03766, USA
Email: Vernon.M.Pais.Jr@ hitchcock.org

Abstract

Clinical Nephrology, Vol. 76 – No. 5/2011 (358-364)

Factors related to fatigue and subgroups of fatigue in patients with end-stage renal disease

S. Karakan, S. Sezer and F.N. Ozdemir

Baskent University, Department of Nephrology, Ankara, Turkey
Introduction and aims: Fatigue is a major determinant for quality of life for patients undergoing chronic hemodialysis (HD) treatment. The aim of this study was to determine the severity and contributing factors of fatigue in patients under chronic HD treatment. Methods: 154 end-stage renal disease (ESRD) patients under HD treatment (92 M, 62 F, mean age 53 ± 15 y, mean duration of HD treatment 92 ± 65 months) were enrolled. Patients were given Piper’s fatigue scale (PFS), Epworth sleepiness scale (ESS) and Beck depression test (BDT). Study participants were evaluated at the end of the HD session. Results: ESS score was above 10 (indicating daytime sleepiness) in only 6 (3.9%) patients. The overall PFS scores were normal-to-mild in 25 (16.2%), moderate in 63 (40.9%) and severe in 66 (42.9%) patients. Total PFS score was correlated with presence of depression (OR: 2.48), employment status (OR: 2.25), calcium (OR: 2.64) and phosphate (OR: 3.70) concentration. PFS behavior score was correlated with employment status (OR: 2.29) and phosphate (OR: 1.96). PFS affective score was correlated with presence of depression (OR: 2.56), employment status (OR: 2.72) and creatinine (OR: 2.25) concentration. PFS sensory score was correlated with advanced age (OR: 1.95), presence of depression (OR: 2.90), albumin (nutritional status) (OR: 0.17), postdialysis serum urea level (OR: 2.37), hemoglobin (anemia) (OR: 0.21). Conclusion: Daytime sleepiness is not prevalent; however, fatigue is closely related to presence of depression, employment status, and calcium and phosphate levels.Correspondence to:
S. Karakan
Baskent University
Department of Nephrology
Ankara, Turkey
Email: sebnemkarakan@gmail.com

Abstract

Clinical Nephrology, Vol. 76 – No. 5/2011 (365-372)

Intravenous gammaglobulin-associated renal impairment reported to the FDA: 2004 – 2009

R.Y. Lin¹,², G. Rodriguez-Baez², G.A. Bhargave² and H. Lin⁴

¹New York Downtown Hospital, ²St. Vincent’s Hospital, and ³New York Medical College, ⁴Stuyvesant High School, New York, NY, USA
Since the 1999 US Food and Drug Administration (FDA) warning of renal failure/dysfunction associated with intravenous gammaglobulin (IVIg), there has been a movement towards developing safer, more convenient formulations. Until now, the scope of renal failure associated with IVIg, has not been well described. The FDA Adverse Event Reporting System (AERS) from 2004 through 2009 was examined for renal impairment reactions due to IVIg and associated demographic features, comorbidities and indications. Anaphylaxis cases associated with IVIg administration were used as a comparison group. There were 90 renal impairment cases associated with IVIg administration. Neuromuscular disorders (33/37%) and hematologic disorders (32/36%) were the predominant treatment indications. When reported anaphylaxis versus renal impairment due to IVIg was examined as a binary outcome in logistic regression modeling, renal impairment was predicted by sucrose presence, increasing age and non-hypogammaglobulinemic indications. Of the 34 hemodialysis cases, the excipient was known in 28 and all but 1 consisted of sucrose. IVIg containing sucrose was used in 33 of 48 nonhemodialysis cases. More hemodialysis cases also had diabetes mellitus. When the interval between renal impairment and the first IVIg infusion was determined, the renal impairment was reported by the second day in 43.3% of cases, and between 3 and 5 days in 41.7% of cases. Despite an evolution in clinical usage and formulations, renal impairment after IVIg administration continues to be reported. Sucrose as the excipient in IVIg plays a major role, but other factors are also important. These findings have implications in the management of patients treated with IVIg.Correspondence to:
R.Y. Lin, MD
New York Downtown
Hospital, 83 Gold Street
New York, NY 10038, USA
Email: robert.lin@downtownhospital.org

Abstract

Clinical Nephrology, Vol. 76 – No. 5/2011 (373-379)

B-type natriuretic peptide and interdialytic fluid retention are independent and incremental predictors of mortality in hemodialysis patients

B.D. Westenbrink¹, T.K. Kremer Hovinga¹, W.D. Kloppenburg¹, N.J. Veeger² and W.M.T. Janssen¹

¹Department of Internal Medicine, Martini Hospital Groningen, Groningen, The Netherlands, and ²Department of Internal Medicine, The Trial Coordination Center Groningen, University Medical Center Groningen, Groningen, The Netherlands
Aim: Management of fluid homeostasis remains a major challenge in hemodialysis patients. We aimed to establish whether the cardiac strain marker B-type natriuretic peptide (BNP) could help to identify hypervolemic patients at increased risk of death. Methods: BNP levels were determined before dialysis in the entire HD population at our institution (n = 57). IDWG and BNP were stratified above or below 1.5 kg or the median value, respectively. All patients were prospectively followed for 35 months. The influence of IDWG and BNP on mortality was assessed with a Cox proportional hazards model, adjusted for each other, as well as for demographics, comorbidities, cardiac function, residual diuresis, dialysis duration and efficiency and complications of renal failure. Results: Median BNP was 303 (135 – 692) and 21 (36%) patients displayed an average IDWG below 1.5 kg. During follow up a total of 25 (44%) patients died, 5 (26%) in the low IDWG group and 20 (53%) in the high IDWG group (adjusted hazard ratio (adjusted HR) 5.31 95% CI (1.47 – 19.1), p = 0.011). In the low BNP group 7 (25%) patients died and in the high BNP Group 18 (62%) patients died (adjusted HR 3.53 95 CI (1.37 – 9.09), p = 0.009). When both factors were considered simultaneously, patients with low BNP and low IDWG had an 11 times lower risk of death compared to patients with high BNP and high IDWG (HR. 0.08 95% CI (0.01 – 0.6129, p = 0.015). Conclusions: BNP and IDWG are independent and incremental predictors of mortality in HD patients. These findings suggest that BNP guided fluid management could improve survival in these patients.Correspondence to:
Dr. W.M.T. Janssen
Department of Internal Medicine
Martini Hospital Groningen
Van Swietenplein 1
9728 NT Groningen, The Netherlands
Email: w.m.t.janssen@mzh.nl

Abstract

Clinical Nephrology, Vol. 76 – No. 5/2011 (380-387)

Spondylodiscitis in hemodialysis patients: a case series

B. Faria¹, N. Canto Moreira², T. Couto Sousa¹, C. Pêgo¹, J. Vidinha¹, J. Garrido¹, S. Lemos¹, C. Soares¹, C. Lima¹, G. Sorbo¹ and E. Lorga Gomes¹

¹Unidade de Nefrologia e Diálise and ²Unidade de Neurorradiologia, Hospital São Teotónio, Viseu, Portugal
Background: Although bacterial spondylodiscitis is one of the most serious complications in hemodialysis patients, it is often underdiagnosed, and few reports describe its course and clinical management. Patients and methods: We retrospectively reviewed 11 hemodialysis patients diagnosed with spondylodiscitis, during a 5-year period, and compared them with the general population followed at our center. Nine patients presented with fever on admission. Blood cultures were positive in all patients and Staphylococcus aureus was identified in 8. Ten patients had a central venous catheter as access for hemodialysis and the number of vascular accesses in the patients´ medical history was superior to the rest of our HD population. Results: Four patients (36%) died during follow-up. None of the patients that underwent vancomycin and gentamicin antibiotic therapy died. Conclusion: Bacterial spondylodiscitis must be suspected whenever a patient on hemodialysis is admitted with fever and/or back pain. The presence of a central venous catheter and a history of multiple vascular accesses may be important risk factors. Prolonged antibiotic therapy with initial broad-spectrum coverage seems to be the best therapeutic approach.Correspondence to:
B. Faria, MD
Av. Rei Dom Duarte
3504 509 Viseu, Portugal
Email: faria_bernardo@yahoo.com

Abstract

Clinical Nephrology, Vol. 76 – No. 5/2011 (388-395)

Effect of eplerenone on blood pressure and the renin-angiotensin-aldosterone system in oligo-anuric chronic hemodialysis patients – a pilot study

L. Shavit¹,², D. Neykin², M. Lifschitz¹ and I. Slotki¹

Adult Nephrology Unit, and Department of Internal Medicine, Shaare Zedek Medical Center, Jerusalem, Israel
Introduction and aims: Recent studies have suggested that aldosterone has many effects in addition to its ability to cause the kidney to retain sodium. To test the hypothesis that aldosterone can cause hypertension in a manner that does not involve renal sodium retention, we administered eplerenone, a specific aldosterone antagonist, to oligo-anuric chronic hemodialysis patients who had HTN. Methods: 220 chronic hemodialysis patients underwent initial screening. Of these, 8 patients were followed for 8 weeks and their blood pressure, weight, plasma potassium, aldosterone levels and plasma renin activity were recorded. After a 4 week run in period, each patient received eplerenone 25 mg twice daily for another 4 weeks. Results: Administration of eplerenone for 4 weeks decreased predialysis systolic blood pressure from 166 ± 14 to 153 ± 10 mmHg (p < 0.05). Eplerenone had no effect on diastolic blood pressure, potassium, predialysis weight, intradialytic weight gain, plasma aldosterone or PRA. Conclusion: Eplerenone significantly reduces systolic blood pressure in oligo-anuric hypertensive hemodialysis patients without effect on plasma aldosterone concentrations or plasma renin activity. Plasma potassium increases minimally after 4 weeks of therapy, a finding that raises some concern for long-term eplerenone use in chronic hemodialysis.Correspondence to:
L. Shavit, MD
Adult Nephrology Unit
Shaare Zedek Medical Center
PO Box 3235
Jerusalem 91031, Israel
Email: lshavit@szmc.org.il

Abstract

Clinical Nephrology, Vol. 76 – No. 5/2011 (396-400)

Thrombotic microangiopathy induced by long-term interferon-β therapy for multiple sclerosis: a case report

A. Broughton¹, J.-P. Cosyns² and M. Jadoul¹

Departments of ¹Nephrology and ²Pathology, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium
We report the case of a 53-year-old woman treated for 8 years with Betaferon^® (interferon-β-1b), who developed mild renal failure with hypertension, proteinuria and glomerular hematuria. Kidney biopsy was consistent with thrombotic microangiopathy (TMA). Considering the strong evidence of interferon-α causing TMA and the numerous immunomodulatory activities shared by INF-α and -β, we incriminated Betaferon as the etiological agent of TMA in our patient. To our knowledge, it is the first time such an association has been published.Correspondence to:
Prof. M. Jadoul, MD
Cliniques Universitaires St. Luc
Université Catholique de Louvain
Service de Néphrologie
Avenue Hippocrate 10
1200 Brussels, Belgium
Email: michel.jadoul@uclouvain.be

Abstract

Clin i cal Nephrology, Vol. 76 – No. 5/2011 (401-406)

Disopyramide-induced hypoglycemia in a non-diabetic hemodialysis patient: a case report and review of the literature

M. Abe¹, T. Maruyama¹, Y. Fujii¹, M. Kitai¹, K. Okada¹, K. Matsumoto¹ and M. Soma¹,²

¹Division of Nephrology, Hypertension and Endocrinology, and ²Division of General Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan
Disopyramide, an antiarrhythmic drug, has been reported to cause hypoglycemia; however, its mechanism of action remains unclear. Pre-existing factors that increase the concentration of the drug in the blood increase the risk of hypoglycemia. Furthermore, other factors can also increase the risk of hypoglycemia even when disopyramide levels are in the therapeutic range. It has been proposed that disopyramide-induced hypoglycemia is caused by stimulation of insulin secretion due to the inhibition of the pancreatic β-cell ATP-sensitive K⁺ channels. We report a case of severe disopyramide-induced hypoglycemia in a nondiabetic 72-year-old woman on hemodialysis. Concentrations of counter-regulatory hormones, serum insulin, and C-peptide were measured. From these data, it appears that disopyramide-induced hypoglycemia results from sustained endogenous insulin secretion, with a concomitant inadequate counter-regulatory response. Although hypoglycemia occurs infrequently in patients treated with disopyramide, this adverse effect is clinically important and potentially life-threatening. Evidence suggests that disopyramide-induced hypoglycemia results from endogenous insulin secretion and can occur in patients with therapeutic blood concentrations of the drug. Patients at risk include those with renal impairment, advanced age, and malnutrition, and blood glucose levels should be monitored carefully in such patients.Correspondence to:
M. Abe, MD
Division of Nephrology, Hypertension and Endocrinology
Department of Internal Medicine
Nihon University School of Medicine
30-1, Oyaguchi-Kami-chou
Itabashi-ku, Tokyo 173-8610, Japan
Email: mabe@med.nihon-u.ac.jp

Abstract

Clin i cal Nephrology, Vol. 76 – No. 5/2011 (407-411)

Severe hyperosmolarity and hypernatremia in an adipsic young woman

S. Latcha¹, M. Lubetzky² and A.M. Weinstein³

¹Memorial Sloan Kettering Cancer Center, ²Cornell University Medical Center, and ³Weill Medical College of Cornell University, Cornell University, New York, NY USA
Background: Combined deficits in arginine vasopressin secretion (AVP) and thirst sensation can result in life threatening hyperosmolality and hypernatremia. Complications include seizures, profound volume contraction and renal failure. Fortunately, this is an uncommon clinical condition, with approximately 70 cases reported in the literature over the past 47 years [1]. Defects in AVP secretion and/or synthesis produce central diabetes insipidus (DI), polyuria with polydipsia, hypernatremia and hyperosmolality. Most awake and alert patients with an intact thirst stimulus will “drink” themselves back to a normal serum sodium and osmolality. However, if there is concomitant destruction of the osmoreceptors that regulate thirst, osmolal and volume homeostasis cannot be maintained. The relationships between urine osmolarity and serum osmolarity and plasma vasopressin levels are vital for distinguishing a reset osmostat from central DI. Methods: After obtaining approval from our institutional review board, we retrospectively reviewed the medical record of a 37-year-old patient who presented to our institution with a serum sodium of 176 mEq/l. Results: Admission laboratory examination revealed: hemoglobin 12.8 g/dl; white blood cell count 4.7 × 10³/µl, with a normal differential; random serum glucose 91 mg/dl ; sodium 176 mEq/l; plasma osmolality 366 mOsm/kg; BUN 33 mg/dl; serum creatinine 1 mg/dl; calcium 9.5 mg/dl; urine specific gravity 1.032; and urine osmolality 1,172 mOsm/kg. An MRI with contrast of the sella/ pituitary revealed an enhancing mass centered within the suprasellar cistern and anterior third ventricle, measuring 3.0 × 3.9 × 3.4 cm. The lesion appeared to involve the hypothalamus and displaced the optic chiasm inferiorly. Evaluation of pituitary function revealed normal serum levels of thyroid stimulating hormone, AM cortisol, luteinizing hormone, follicle stimulating hormone and prolactin. Figure 1 illustrates the relationship between measured serum AVP levels and serum osmolality. Figure 2 shows the relationship between measured urine and serum osmolality. If the serum AVP levels were not available, it would appear as though the patient had a reset osmostat. The kidneys appear to appropriately generate maximally concentrated urine at a serum osmolality above 348 but are unable to below this value. Conclusions: When compared with the normal curve, our patient’s AVP levels were lower than expected for the corresponding osmolality. This pattern is consistent with a partial central DI. She does not have a reset osmostat. In the presence of significant volume contraction and a reduced GFR, her kidneys produced more concentrated urine despite markedly decreased central vasopressin production. As the volume contraction abated and the GFR improved, polyuria recurred, despite persistent hyperosmolarity and hypernatremia.Correspondence to:
S. Latcha, MD
Memorial Sloan Kettering Cancer Center
1275 York Avenue, Suite 1204B
New York, NY 10067, USA
Email: latchas@mskcc.org

Abstract

Clinical Nephrology, Vol. 76 – No. 5/2011 (412-416)

A simple renal cyst invaded by infiltrating urothelial carcinoma mimicking a Bosniak Class IV renal cyst

J.-M. Liu¹,⁴, C.-K. Chuang¹,⁴, Y.-H. Chang¹,⁴, K.-F. Ng³,⁴, L.-J. Wang²,⁴, K.-L. Chuang¹,⁴, H.-C. Chuang¹,⁴ and S.-T. Pang¹,⁴

¹Division of Uro-oncology, Department of Surgery, ²Department of Medical Imaging and Intervention, ³Department of Pathology, Chang Gung Memorial Hospital and Graduate Institute of Clinical Medical Sciences, and ⁴College of Medicine, Chang Gung University, Taoyuan, Taiwan
We report a 79-year-old woman with a left side simple renal cyst invaded by infiltrating urothelial carcinoma mimicking a Bosniak Class IV renal cyst. Computerized tomography has high accuracy for the diagnosis of renal cysts and urothelail carcinoma. But, in this case it was still difficult to distinguish a simple renal cyst with infiltrating urothelial carcinoma invasion from a Bosniak Class IV renal cyst on CT scan. The management of a Bosniak Class IV renal cyst and urothelail carcinoma is totally different. Therefore, we performed a left side nephroureterectomy. This patient will have regular follow-up with cystoscopy every 3 months for the first 2 y, every 6 months for the next 2 y, and then annually thereafter.Correspondence to:
Dr. C.-K. Chuang
Division of Urology
Department of Surgery
Chang Gung Memorial Hospital
5 Fu-Shing St
Kweishan, Linkou 333, Taiwan
Email: m7616@cgmh.org.tw

Abstract

Clin i cal Nephrology, Vol. 76 – No. 5/2011 (417-420)

Reversible acute kidney injury (AKI) by active removal of serum light chains in an HIV positive patient with myeloma kidney

L. Sowole¹, A. Burns¹, B. Kaur² and A. Davenport¹

¹Center for Nephrology and ²Histopathology Royal Free Hospital, Royal Free Campus, University College London Medical School, London, UK
Background: The association of HIV and myeloma has rarely been reported in the literature. This following case discusses the presentation of acute kidney injury (AKI) in a 53-year-old lady with HIV, subsequently diagnosed with myeloma. Furthermore, we describe recovery of renal function and dialysis independence using a combination of light chain removal by dialysis with a high cut-off dialyzer and chemotherapy. Investigations: Physical examination, urine, blood tests, renal biopsy, bone marrow aspirate and trephine, US scan. Diagnosis: Myeloma. Management: Dialysis and chemotherapy.Correspondence to:
A. Davenport, FRCP
Center for Nephrology
Royal Free Campus
University College
London Medical School, London, UK
Email: andrewdavenport@nhs.net

Abstract

10.5414/CN107008

Impact of renal transplantation on corneal-conjunctival calcifi cation

Y.-C. Lo¹, T.-W. Lai² and K.-H. Shu¹

¹Division of Nephrology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, and ²Lukang Wen’s Hospital, Changhua,
Taiwan

Abstract

Infectious complications following conversion to buttonhole cannulation / In response

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Volume 76, No. 5/2011(November)