Volume 80 (2013), No. 6/2013(December)
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Review
Diagnosis and treatment of C3 glomerulopathy
Carla M. Nester and Richard J. Smith
Page No. 395
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (395-404)
Diagnosis and treatment of C3 glomerulopathy
Carla M. Nester1,2,3 and Richard J. Smith1,2,3
1Molecular Otolaryngology and Renal Research Laboratories, 2Department of Internal Medicine and Pediatrics, Divisions of Nephrology, and 3Rare Renal Disease Clinic, Carver College of Medicine, University of Iowa, Iowa City, IA, USA
Purpose of review: The purpose of this review is to summarize our current understanding of the principal characteristics of C3 glomerulopathy as a framework for patient evaluation with the goal of setting the stage for a mechanistic approach to treatment. We also review published treatment experience and comment on future initiatives to devise treatment protocols for this rare renal disease patient population. Diagnosis and treatment: Both animal and human data support the role of the alternative pathway of complement in the C3 glomerulopathies. The finding of dominant C3 deposition on renal biopsy, a marker of aberrant complement activity and the primary diagnostic criterion, defines C3 glomerulopathy as a group of diseases that despite variable light and electron microscopy appearance, shares important phenotypic characteristics; namely the presence of genetic mutations in complement genes, the presence of C3 nephritic factors with or without other complement protein abnormalities, and finally a substantial risk for both end-stage renal disease (ESRD) and recurrence after renal transplant. Traditional immune suppressive treatment strategies are often ineffective in this group of patients. Case reports and a single small trial support the efficacy of anti-complement therapy in this setting. Summary: The diagnosis of C3 glomerulopathy is established by renal biopsy and requires a C3 dominant pattern on immunofluorescence in a patient with active glomerulonephritis. Laboratory studies characterizing an individual patient’s complement profile form the basis of an expanded phenotype that has the potential to inform not only the relative activity of disease, but also the risk for adverse outcome or treatment nonresponse. Understanding an individual patient’s complement pathology will facilitate an optimal therapeutic approach to their disease.Correspondence to:
Carla Nester, MD, MSA, Assistant Professor
Director Pediatric Glomerular Disease Clinic
University of Iowa Hospitals and Clinics
200 Hawkins Drive, BT 4036
Iowa City, IA 52242-1081, USA
and
Richard Smith, MD, Director Iowa Institute of Human Genetics
200 Hawkins Dr, 21151
Iowa City, IA 52242-1078, USA
Email: [email protected] and [email protected]
Original
Urinary neutrophil gelatinase-associated lipocalin for early detection of acute kidney injury in geriatric patients with urinary tract infection treated by colistin
Linda Shavit, Rackhel Manilov, Yonit Wiener-Well, Nurit Algur and Itzchak Slotki
Page No. 405
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (405-416)
Urinary neutrophil gelatinase-associated lipocalin for early detection of acute kidney injury in geriatric patients with urinary tract infection treated by colistin
Linda Shavit1, Rackhel Manilov2, Yonit Wiener-Well3, Nurit Algur4 and Itzchak Slotki1
1Division of Adult Nephrology, 2Department of Geriatrics, 3Infectious Diseases Unit, and 4Endocrinology laboratory, Shaare Zedek Medical Center, Jerusalem, Israel
Introduction: Colistin (polymyxin E) was developed ~ 60 years ago but was rarely used in clinical practice during the last 20 years because of concerns related to high rates of nephrotoxicity. However, it was recently reintroduced to clinical practice in many parts of the world for the treatment of multi-drug resistant gram-negative bacilli. In the current study, we evaluated the predictive capacity of urine neutrophil gelatinase-associated lipocalin (NGAL) for early diagnosis of acute kidney injury (AKI) in geriatric patients with urinary tract infection (UTI) receiving colistin therapy. Methods: We studied 116 patients aged 80.7 ± 12 treated with colistin who suffered from UTI. Urinary NGAL was measured at baseline and 1 – 2 hours after the second dose of colistin. The primary outcome was AKI. Secondary outcome was in-hospital morbidity and mortality. Results: 52 patients (44.8%) developed acute tubular necrosis (ATN) (14% of these had underlying CKD), 8 (7%) had prerenal azotemia, 8 (7%) had stable CKD without changes in renal function during hospitalization and the remaining 48 patients (41%) had normal kidney function. The mean duration of colistin therapy was 9.1 ± 4.8 days. At baseline, urine NGAL was 405 ± 452 g/l in ATN, 285 ± 256 g/l in prerenal azotemia, 390 ± 468 g/l in CKD and 347 ± 877 g/l in normal kidney function patients (difference non-significant). We were unable to demonstrate statistically significant increments of urine NGAL following colistin administration in either ATN or non-ATN patient groups. Urine NGAL was not correlated with urinary leukocyte or erythrocyte counts or baseline comorbidities such as CKD, heart failure, or diabetes. For primary outcome (ATN), receiver operating characteristics curve revealed AUC 0.59 (95% CI 0.49 – 0.7) sensitivity 0.65, and specificity 0.62 for a cutoff value of urinary NGAL 140 g/l. Similar results were obtained for secondary outcomes. Conclusions: Our data suggest limited predictive capacity of urinary NGAL for early diagnosis of AKI in a large clinical setting of geriatric patients hospitalized for UTI and receiving the potentially nephrotoxic colistin. This finding is likely due to the powerful influence of UTI on NGAL levels in both patients with normal kidney function and those with a wide spectrum of acute or chronic kidney diseases.Correspondence to:
Linda Shavit, MD
Adult Nephrology Unit
Shaare Zedek Medical Center
PO Box 3235, Jerusalem 91031, Israel
Email: [email protected]
Original
The impact of documentation of severe acute kidney injury on mortality
Francis Perry Wilson, Amar D. Bansal, Sravan K. Jasti, Jennie J. Lin, Michael G.S. Shashaty, Jeffrey S. Berns, Harold I. Feldman and Barry D. Fuchs
Page No. 417
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (417-425)
The impact of documentation of severe acute kidney injury on mortality
Francis Perry Wilson1,3, Amar D. Bansal1, Sravan K. Jasti1, Jennie J. Lin1, Michael G.S. Shashaty1,3, Jeffrey S. Berns1, Harold I. Feldman1,2,3 and Barry D. Fuchs1
1Department of Medicine, 2Department of Biostatistics and Epidemiology, and 3Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA
Aims: Modification of the mortality risk associated with acute kidney injury (AKI) necessitates recognition of AKI when it occurs. We sought to determine whether formal documentation of AKI in the medical record, assessed by billing codes for AKI, would be associated with improved clinical outcomes. Methods: Retrospective cohort study conducted at three hospitals within a single university health system. Adults without severe underlying kidney disease who suffered in-hospital AKI as defined by a doubling of baseline creatinine (n = 5,438) were included. Those whose AKI was formally documented according to discharge billing codes were compared to those without such documentation in terms of 30-day mortality. Results: Formal documentation of AKI occurred in 2,325 patients (43%). Higher baseline creatinine, higher peak creatinine, medical admission status, and higher Sequential Organ Failure Assessment (SOFA) score were strongly associated with documentation of AKI. After adjustment for severity of disease, formal AKI documentation was associated with reduced 30-day mortality – OR 0.81 (0.68 – 0.96, p = 0.02). Patients with formal documentation were more likely to receive a nephrology consultation (31% vs. 6%, p < 0.001) and fluid boluses (64% vs. 45%, p < 0.001), and had a more rapid discontinuation of angiotensin-converting enzyme inhibitor and angiotensin-receptor blocker medications (HR 2.04, CI 1.69 – 2.46, p < 0.001). Conclusions: Formal documentation of AKI is associated with improved survival after adjustment for illness severity among patients with creatinine-defined AKI.Correspondence to:
Francis Perry Wilson, MD
Perelman School of Medicine at the University of Pennsylvania
1 Founders, 3400 Spruce St
Philadelphia PA 19104. USA
Email: [email protected]
Original
Role of ultrasound in revealing complications following percutaneous renal biopsy in children
Daishi Hirano, Shuichiro Fujinaga, Naoto Nishizaki, Hiroaki Kanai and Hiroyuki Ida
Page No. 426
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (426-432)
Role of ultrasound in revealing complications following percutaneous renal biopsy in children
Daishi Hirano1,2, Shuichiro Fujinaga1, Naoto Nishizaki1, Hiroaki Kanai1 and Hiroyuki Ida2
1Division of Nephrology, Saitama Children’s Medical Center, Saitama, and 2Department of Pediatrics, The Jikei University School of Medicine, Minato-ku, Tokyo, Japan
Background: This retrospective case series aimed to investigate the role of ultrasound immediately post-percutaneous renal biopsy (PRB) for detecting post-biopsy complications in pediatric patients. Methods: Data from 380 (male/female = 209/171) consecutive biopsies of native kidney tissue of 344 children from January 2001 to October 2009 were analyzed to investigate the role of an ultrasound immediately post-PRB and the predictive value of demographic, clinical, and baseline chemistry factors in predicting the risk of post-PRB complications. Results: Post-PRB ultrasound identified hematoma formation in 33 (8.7%) patients. Of the 19 (5.0%) patients whose hematomas were large (≥ 1 cm), post-biopsy courses of 16 patients were clinically complicated. On the other hand, of the 14 patients whose hematomas were small (< 1 cm), all patients but one showed an uncomplicated clinical course. Of the 17 complications, 79.1% were detected within the first 24 hours and 21.9% (cases of resorption fever) between 24 and 144 hours post-PRB. Age ≥ 10 is an independent risk factor for post-PRB complication. Conclusions: Age ≥ 10 is an independent risk factor for post-PRB complication. After the procedure, the formation of a large hematoma predicted a complicated clinical course.Correspondence to:
Daishi Hirano, MD
Department of Pediatrics
The Jikei University School of Medicine
3-25-8 Nishi-Shimbashi, Minato-ku
Tokyo, 105-0003, Japan
Email: [email protected]
Original
Readmission after hospitalization for heart failure among patients with chronic kidney disease: a prediction model
Robert M. Perkins, Amir Rahman, Ion D. Bucaloiu, Evan Norfolk, William DiFilippo, James E. Hartle and H. Lester Kirchner
Page No. 433
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (433-440)
Readmission after hospitalization for heart failure among patients with chronic kidney disease: a prediction model
Robert M. Perkins1,2, Amir Rahman3, Ion D. Bucaloiu4, Evan Norfolk4, William DiFilippo4, James E. Hartle4 and H. Lester Kirchner5
1Nephrology Department, Bassett Medical Center, 2Bassett Research Institute, Bassett Health Network, Cooperstown, NY, 3Geisinger Medical Group-Lewiston, Lewistown, 4Nephrology Department, and 5Division of Medicine, Geisinger Medical Center, Danville, PA, USA
Aims: 30-day readmission rates after hospitalization for heart failure (HF) approach 25%, and patients with chronic kidney disease (CKD) are disproportionately represented. A retrospective cohort study was conducted to develop a prediction tool for 30-day readmission after hospitalization for HF among those with non-dialysis dependent CKD. Methods: Geisinger primary care patients with Stage 3 – 5 CKD hospitalized with a primary discharge diagnosis of HF during the period July 1, 2004 through February 28, 2010 were eligible. Multivariate logistic regression was employed to build models from predictors of 30-day readmission, drawn from demographic, clinical, laboratory, and pharmaceutical variables in the electronic health record. Variables were manually removed to achieve a model with satisfactory goodness-of-fit and parsimony while maximizing area under the receiver operating characteristic curve (AUC). Internal validation was performed using the bootstrap resampling method (1,000 samples) to provide a bias-corrected AUC. Results: 607 patients with CKD were admitted for HF during the study period; 116 (19.1%) were readmitted within 30 days. A model incorporating 23 variables across domains of medical history, active outpatient pharmaceuticals, vital signs, laboratory tests, and recent inpatient and outpatient resource utilization yielded an AUC (95% CI) of 0.792 (0.746 – 0.838). The bias-corrected AUC was 0.743. At an estimated readmission probability of 20%, the model correctly classified readmission status for 73% of the population, with a sensitivity of 69% and a specificity of 73%. Conclusion: A robust electronic health record may facilitate the identification of CKD patients at risk for readmission after hospitalization for HF.Correspondence to:
Robert M. Perkins, MD
Department of Nephrology
Bassett Medical Center
One Atwell Drive
Cooperstown, NY 13326, USA
Email: [email protected]
Original
Mycophenolate mofetil therapy in children with idiopathic membranous nephropathy
Rajendra Bhimma, Elaene Naicker and Pratistadevi K. Ramdial
Page No. 441
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (441-448)
Mycophenolate mofetil therapy in children with idiopathic membranous nephropathy
Rajendra Bhimma1, Elaene Naicker1 and Pratistadevi K. Ramdial2,3
1Department of Pediatrics, 2Department of Anatomical Pathology, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, KwaZulu-Natal, and 3National Health Laboratory Service, South Africa
Background: Idiopathic membranous nephropathy (IMN) is a rare form of childhood nephropathy. To date there are no standardized protocols of management for this condition in children. The aim of this study is to report on 4 children with IMN who were treated with mycophenolate mofetil (MMF). Methods: MMF was given in combination with low dose steroids and angiotensin converting enzyme antagonists in a dose of 1,200 mg/m2 body surface area in two divided doses for a minimum of 6 months. Results: All children had histopathological findings in keeping with Stage III membranous nephropathy. At the last hospital visit, 3 children had achieved a > 50% reduction of proteinuria with preservation of renal function. One patient who failed to respond progressed to Stage III chronic kidney disease. None of the children who were treated with MMF experienced any major side effects of the drug. Conclusions: MMF, administered over a limited period, served as a safe and effective immunosuppressive agent in the treatment of this condition, in conjunction with low dose steroids and angiotensin converting enzyme inhibitors. Large multicenter randomized studies of children with IMN are necessary to assess the efficacy and long term safety of MMF.Correspondence to:
Rajendra Bhimma
Department of Pediatrics and Child Health
Nelson R Mandela School of Medicine
University of KwaZulu-Natal
Private Bag 7, Congella, 4013, South Africa
Email: [email protected]
Original
C-reactive protein and carotid and femoral intima media thickness: predicting inflammation
Mona Boaz, Gil Chernin, Idit Schwartz, Zeev Katzir, Doron Schwartz, Amir Agbaria, Amir Gal-Oz and Talia Weinstein
Page No. 449
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (449-455)
C-reactive protein and carotid and femoral intima media thickness: predicting inflammation
Mona Boaz1,2, Gil Chernin3,4, Idit Schwartz3,4, Zeev Katzir4,5, Doron Schwartz3,4, Amir Agbaria3, Amir Gal-Oz3 and Talia Weinstein3,4
1Epidemiology and Research Unit, 2Department of Nutrition, School of Health Sciences, Ariel University Center, Ariel, Israel, 3Department of Nephrology, Tel Aviv Medical Center, Tel Aviv, Israel, 4Sackler Faculty of Medicine, Tel Aviv University, Israel, and 5Institute of Nephrology, E. Wolfson Medical Center, Holon, Israel
Background: C-reactive protein (CRP) is a recognized marker of systemic inflammation. Its association with carotid and femoral intima media thickness (surrogate measures of atherosclerosis) may explain excess cardiovascular disease risk in hemodialysis patients. Objectives: To estimate the association between CRP and both carotid and femoral IMT in hemodialysis (HD) patients; to predict CRP in these patients. Methods: The present cross-sectional study is nested in the Sevelamer hydrochloride and ultrasound-measured femoral and carotid intima media thickness progression in end-stage renal disease (SUMMER) clinical trial. Carotid (common, internal, and bifurcation) and femoral arteries were visualized in B-mode ultrasonography. CRP was measured in serum. Results: The study cohort included 144 HD patients (39.5% female, mean age 67.8 ± 11.5 years). All measures of both carotid and femoral IMT were significantly positively associated with CRP. Subjects with a history of smoking or coronary revascularization had significantly higher CRP levels, while subjects treated with sevelamer hydrochloride had significantly lower CRP. CRP was significantly positively associated with serum phosphorus, calcium, alkaline phosphatase, and PTH, and significantly inversely associated with HDL and albumin. Conclusions: CRP is significantly positively associated with both femoral and carotid IMT. Treatment with sevelamer hydrochloride is associated with lower CRP in HD patients.Correspondence to:
Talia Weinstein, MD, PhD
Department of Nephrology
Tel Aviv Medical Center
6 Weizman st, Tel Aviv 64239, Israel
Email: [email protected]
Nephrology Education
Renal involvement in MELAS syndrome – a series of 5 cases and review of the literature
Alexandre Seidowsky, Maxime Hoffmann, François Glowacki, Claire-Marie Dhaenens, Jean-Philippe Devaux, Celia Lessore de Sainte Foy, François Provot, Jean-Dominique Gheerbrant, Aurelie Hummel, Marc Hazzan, Michel Dracon, Anne Dieux-Coeslier, Marie- Christine Copin, Christian Noël and David Buob
Page No. 456
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (456-463)
Renal involvement in MELAS syndrome – a series of 5 cases and review of the literature
Alexandre Seidowsky1, Maxime Hoffmann2, François Glowacki1,9, Claire-Marie Dhaenens3,9, Jean-Philippe Devaux4, Celia Lessore de Sainte Foy1, François Provot1, Jean-Dominique Gheerbrant5, Aurelie Hummel6, Marc Hazzan1,9, Michel Dracon1,9, Anne Dieux-Coeslier7, Marie-Christine Copin8,9, Christian Noël1,9 and David Buob8,9
1Nephrology Department, University Hospital of Lille, 2Nephrology Department, La Louvière Polyclinic, 3Biochemistry and Molecular Biology Department, Pathology and Biology Center, University Hospital of Lille, 4Nephrology Department, Lille Clinique du Bois, Lille, 5Nephrology Department, Hénin Beaumont Polyclinic, Hénin Beaumont, 6Nephrology Department, Necker Hospital, Paris, 7Genetics Department, University Hospital of Lille, 8Pathology Department, Biology and Pathology Center, University Hospital of Lille, and 9University Lille Nord de France, Lille, France
Renal dysfunction is increasingly recognized as a potential clinical feature of mitochondrial cytopathies such as mitochondrial encephalomyopathy, lacticacidosis and stroke-like episodes (MELAS) syndrome. Five cases of MELAS syndrome with renal involvement from 4 unrelated families are presented in this case series. Three of the 5 patients had a history of maternally-inherited diabetes and/or deafness. Focal and segmental glomerulosclerosis and arteriolar hyaline thickening were the most striking findings on renal biopsy. In addition to clinical presentation with the typical symptoms of MELAS syndrome, genetic testing in these patients identified the A3243G point mutation in the tRNALeu gene of the mitochondrial DNA (mtDNA). The diagnosis of MELAS syndrome was thus considered to be unequivocal. The incidence of kidney disease in MELAS syndrome may be underestimated although a study is required to investigate this hypothesis. As the A3243G mtDNA mutation leads to a progressive adult-onset form of focal segmental glomerulosclerosis (FSGS), screening for the MELAS A3243G mtDNA mutation should therefore be performed especially in patients with maternally-inherited diabetes or hearing loss presenting with FSGS.Correspondence to:
Alexandre Seidowsky
University Hospital of Lille
Nephrology Department, CHRU Lille
rue Michel Polonovski, 59037 LILLE CEDEX, France
Email: [email protected]
Nephrology Education
Bradycardia without “classical” EKG changes in hyperkalemic hemodialysis patients
Viresh Mohanlal, Abdolreza Haririan and Edward J. Weinman
Page No. 464
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (464-468)
Bradycardia without “classical” EKG changes in hyperkalemic hemodialysis patients
Viresh Mohanlal1, Abdolreza Haririan1 and Edward J. Weinman1,2,3
Department of 1Medicine and 2Physiology, University of Maryland School of Medicine, and 3Department of Veterans Affairs Medical Center, Baltimore, MD, USA
While the classic electrocardiographic (EKG) findings of hyperkalemia are well known to clinicians, the association between hyperkalemia and bradycardia is not widely appreciated. Three cases of profound bradycardia due to hyperkalemia in patients with End Stage Renal Disease (ESRD) on hemodialysis are described to provide a base for discussion of specific issues in the management of such patients. The patients presented with hyperkalemia and severe bradycardia that did not improve after administration of atropine. Urgent hemodialysis in two cases led to resolution of the bradycardia. In the third case, the failure to recognizethat bradycardia was the consequence of the hyperkalemia led to unnecessary interventions and delays in initiating dialysis. These cases highlight the causal relation between hyperkalemia and bradycardia in ESRD patients and emphasize the need for increased awareness of this association.Correspondence to:
Edward J. Weinman, MD
Division of Nephrology, Department of Medicine
University of Maryland Medical Center
22 South Greene Street, Baltimore, MD 21201, USA
Email: [email protected]
Nephrology Education
Minimal change disease in graft versus host disease: a podocyte response to the graft?
Janna Huskey, Chris Rivard, Han Myint, Scott Lucia, Maxwell Smith, Michiko Shimada, Takuji Ishimoto, Carlos Araya, Eduardo H. Garin and Richard J Johnson
Page No. 469
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (469-473)
Minimal change disease in graft versus host disease: a podocyte response to the graft?
Janna Huskey1, Chris Rivard1, Han Myint2, Scott Lucia3, Maxwell Smith4, Michiko Shimada1, Takuji Ishimoto1, Carlos Araya5, Eduardo H. Garin5 and Richard J. Johnson1
1Division of Renal Disease and Hypertension, 2Division of Hematology and Oncology, and 3Department of Pathology, University of Colorado, Denver, CO, 4Division of Pathology Mayo Clinic Phoenix, Phoenix, AZ, and 5Division of Pediatric Nephrology, University of Florida, Gainesville, FL, USA
Nephrotic syndrome is a rare complication of hematopoietic cell transplantation. It has been suggested that nephrotic syndrome may represent a limited form of graft-versus-host disease although the pathological link between these two entities remains unclear. In this paper, we report a case of a 61-year-old female who underwent nonmyeloablative allogenic stem cell transplantation for T-cell prolymphocytic leukemia and subsequently developed biopsy proven minimal change disease shortly after cessation of her immunosuppression therapy. Urinary CD80 was markedly elevated during active disease and disappeared following corticosteroid-induced remission. We hypothesize that alloreactive donor T cells target the kidney and induce podocyte expression of CD80 that results in proteinuria from limited ‘graft versus host’ disease. Correspondence to:
Dr. Janna Huskey
Division of Nephrology, Mayo Clinic Arizona
Phoenix, AZ, USA
Email: [email protected]
Nephrology Education
Acute prolonged neurotoxicity associated with recommended doses of ertapenem in 2 patients with advanced renal failure
Min-Jie Wen, Chih-Chien Sung, Tom Chau and Shih-Hua Lin
Page No. 474
Abstract
Clinical Nephrology, Vol. 80 – No. 6/2013 (474-478)
Acute prolonged neurotoxicity associated with recommended doses of ertapenem in 2 patients with advanced renal failure
Min-Jie Wen1, Chih-Chien Sung2, Tom Chau3 and Shih-Hua Lin2
1Division of Endocrinology and Metabolism, 2Division of Nephrology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, and 3Department of Medicine, Providence St. Vincent Medical Center, Portland, OR, USA
Ertapenem, a novel carbapenem with long-acting antimicrobial activity, is predominantly eliminated by the kidneys. Acute prolonged neurotoxicity associated with recommended doses of ertapenem in patients with advanced renal failure not yet on dialysis has not been reported. Two patients with Stage 5 chronic kidney disease (CKD) developed progressive hallucinations, asterixis, myoclonic jerks, and cognitive impairment after receiving the recommended dose reduction for CKD of ertapenem (500 mg/d) for 4 days (Case 1: acute cholecystitis) and 5 days (Case 2: arteriovenous fistula infection). Exhaustive diagnostic workups were non-revealing. Plasma ertapenem level measured 24 h after the last dose in Patient 2 was 53.7 mg/l, much higher than the therapeutic MIC90 (2 mg/l). Despite the cessation of ertapenem and initiation of high-flux hemodialysis, their neurologic manifestations lasted for 2 weeks. The structural and pharmacokinetic characteristics of ertapenem such as its high lipophilicity, central nervous penetration, and volume of distribution contributed to sustained neurotoxicity even with significant reduction in plasma ertapenem levels by high-flux hemodialysis. Although ertapenem 500 mg/d has been recommended in patients with glomerular filtration rate less than 30 ml/min/1.73 m2, our 2 cases highlight that this dosage might be excessive for patients with Stage 5 CKD, especially those not yet on dialysis.Correspondence to:
Shih-Hua Lin, MD
Division of Nephrology
Department of Internal Medicine
Tri-Service General Hospital, #325, Section 2
Cheng-Kung Road, Neihu 114, Taipei, Taiwan
Email: [email protected]
