Correspondence transfusion: systematic review and meta-analysis of randomised clinical trials. BMJ. 2013;347:f4822. 5. Rozen-Zvi B, Gafter-Gvili A, Paul M, Leibovici L, Shpilberg O, Gafter U. Intravenous versus oral iron supplementation for the treatment of anemia in CKD: systematic review and meta-analysis. Am J Kidney Dis. 2008;52(5):897-906. Kliger et al declined to respond. Ó 2014 by the National Kidney Foundation, Inc. http://dx.doi.org/10.1053/j.ajkd.2013.11.026
Nucleic Acid Testing to Screen Potential Kidney Donors for Hepatitis C Virus: Is a Universal Statement Possible Soon? To the Editor: During a pretransplantation evaluation of a potential living kidney donor, we noted mild elevations in transaminase levels (alanine aminotransferase, 44 U/L; aspartate aminotransferase, 48 U/L). Further testing included a liver ultrasound and viral hepatitis workup that tested for hepatitis C virus (HCV) antibody, hepatitis B surface antigen, and hepatitis B core antibody. The ultrasonography results were normal, and testing for hepatitis produced negative results. Due to persistently elevated transaminase levels, we decided to check the donor’s HCV RNA although test results for HCV antibody were negative. HCV RNA was detectable, which led to a diagnosis of window-period acute HCV infection. The individual was advised against donation. Three months later, an HCV antibody test returned positive results, confirming the diagnosis of acute HCV infection.1 This case illustrates the importance of using nucleic acid testing to screen donors for HCV. It is well recognized that no single test can detect all infections reliably due to factors such as false-negative results during a window period or assayrelated issues.1 Thus, a combination of serologic and nucleic acid tests increases the sensitivity of screening donors for HCV. Recently, the US Public Health Service updated its guidelines to include recommending the use of nucleic acid testing for HCV screening of potential donors2; however, the US Organ Procurement Organization policies still recommend serologic testing only.3 Furthermore, there are no clear universal society guidelines worldwide or for many emerging countries, including India and China, where half the world’s population resides and which are experiencing an exponential increase in the number of kidney transplantations.4 We propose that nephrology, hepatology, and public health societies develop a consensus statement on this issue so that standardized transplantation care can be provided worldwide and the risk of HCV transmission can be minimized.5 Anish Chopra, MD Pratish George, MD, DM Kim Mammen, MD, MCh Christian Medical College and Hospital Ludhiana, India Corresponding author: [email protected]
Acknowledgements Financial Support: The authors declare that they have no relevant financial interests.
References 1. Maheshwari A, Ray S, Thuluvath PJ. Acute hepatitis C. Lancet. 2008;372(9635):321-332. Am J Kidney Dis. 2014;63(3):540-542
2. PHS guideline for reducing transmission of human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis C virus (HCV) through solid organ transplantation. Public Health Rep. 2013;128:1-97. http://www.regulations.gov. Accessed December 9, 2013. 3. Health Resources and Services Administration. Minimum procurement standards for an organ procurement organization (OPO). Rockville, MD: Health Resources and Services Administration. http://optn.transplant.hrsa.gov/policiesandbylaws2/policies/ pdfs/policy_2.pdf. Accessed December 9, 2013. 4. Chugh KS. Five decades of Indian nephrology: a personal journey. Am J Kidney Dis. 2009;54(4):753-763. 5. Centers for Disease Control (CDC) and Prevention. Transmission of hepatitis C virus through transplanted organs and tissue–Kentucky and Massachusetts, 2011. MMWR Morbid Mortal Wkly Rep. 2011;60(50):1697-1700. Originally published online December 27, 2013. Ó 2014 by the National Kidney Foundation, Inc. http://dx.doi.org/10.1053/j.ajkd.2013.11.020
Retinal Detachment in Autosomal Dominant Polycystic Kidney Disease To the Editor: Autosomal dominant polycystic kidney disease (ADPKD) is a systemic disorder resulting from mutations of polycystin genes on chromosomes 16 and 4.1 It is considered a ciliopathy—a genetic disorder that causes ciliary dysfunction and involves multiple organs, including retinal degeneration and kidney and cerebral anomalies.2,3 In this letter, we describe 3 patients with ADPKD and retinal detachment. The first, a 35-year-old normotensive woman with normal kidney function, experienced diminished vision in her right eye for 2 months. She had right inferior retinal detachment and refused surgery. The second, a 51-year-old man on maintenance hemodialysis therapy with controlled hypertension, had progressive painless visual loss in the left eye over 15 days. He had left total rhegmatogenous retinal detachment. After undergoing peritomy, scleral buckling, encirclage, and pneumoretinopexy, he experienced marginal improvement in vision. The third patient, a 47-year-old man with stage 1 hypertension and normal kidney function, had right eye visual loss for 20 days. He had right rhegmatogenous retinal detachment and lattice degeneration in both eyes. He underwent scleral buckling, cryopexy, and sulfur hexa fluoride injection into his right eye and laser photocoagulation to his left eye. None of these patients had risk factors for retinal detachment. Previous reports of polycystic kidney disease with retinal involvement have occurred in transgenic rats4 or in the settings of nephronophthisis,5 Senior-Löken syndrome,6 and Bardet-Biedl syndrome and have consisted of retinal degeneration.7 To our knowledge, this is the first report of an association between retinal detachment and ADPKD. We conjecture that this finding may be the result of extracellular matrix defects in the retina due to ciliary dysfunction. Ravindra A. Prabhu, DM Shankar Prasad Nagaraju, DM Krishna Rao Addoor, MD Kasturba Medical College Manipal Manipal University Manipal, India Corresponding author: [email protected]
541
Correspondence
Acknowledgements We acknowledge Manohar Bairy, CCT, and Sarita R.J. Gonsalves, MD, for valuable contributions for reviewing this manuscript. Financial Disclosure: The authors declare that they have no relevant financial interests.
References 1. Torres VE, Harris PC, Pirson Y. Autosomal dominant polycystic kidney disease. Lancet. 2007;369:1287-1301. 2. Waters AM, Beales PL. Ciliopathies: an expanding disease spectrum. Pediatr Nephrol. 2011;26:1039-1056. 3. D’Angelo A, Franco B. The primary cilium in different tissues—lessons from patients and animal models. Pediatr Nephrol. 2011;26:655-662. 4. Gallagher AR, Hoffmann S, Brown N, et al. A truncated polycystin-2 protein causes polycystic kidney disease and retinal
542
degeneration in transgenic rats. J Am Soc Nephrol. 2006;17: 2719-2730. 5. Katsanis N, Beales PL, Woods MO, et al. Mutations in MKKS cause obesity, retinal dystrophy and renal malformations associated with Bardet-Biedl syndrome. Nat Genet. 2000;26: 67-70. 6. Olbrich H, Fliegauf M, Hoefele J, et al. Mutations in a novel gene, NPHP3, cause adolescent nephronophthisis, tapeto-retinal degeneration and hepatic fibrosis. Nat Genet. 2003;34:455-459. 7. Otto EA, Loeys B, Khanna H, et al. Nephrocystin-5, a ciliary IQ domain protein, is mutated in Senior-Löken syndrome and interacts with RPGR and calmodulin. Nat Genet. 2005;37: 282-288. Originally published online January 6, 2014. Ó 2014 by the National Kidney Foundation, Inc. http://dx.doi.org/10.1053/j.ajkd.2013.11.024
Am J Kidney Dis. 2014;63(3):540-542
Nucleic Acid Testing to Screen Potential Kidney Donors for Hepatitis C Virus: Is a Universal Statement Possible Soon? To the Editor: During a pretransplantation evaluation of a potential living kidney donor, we noted mild elevations in transaminase levels (alanine aminotransferase, 44 U/L; aspartate aminotransferase, 48 U/L). Further testing included a liver ultrasound and viral hepatitis workup that tested for hepatitis C virus (HCV) antibody, hepatitis B surface antigen, and hepatitis B core antibody. The ultrasonography results were normal, and testing for hepatitis produced negative results. Due to persistently elevated transaminase levels, we decided to check the donor’s HCV RNA although test results for HCV antibody were negative. HCV RNA was detectable, which led to a diagnosis of window-period acute HCV infection. The individual was advised against donation. Three months later, an HCV antibody test returned positive results, confirming the diagnosis of acute HCV infection.1 This case illustrates the importance of using nucleic acid testing to screen donors for HCV. It is well recognized that no single test can detect all infections reliably due to factors such as false-negative results during a window period or assayrelated issues.1 Thus, a combination of serologic and nucleic acid tests increases the sensitivity of screening donors for HCV. Recently, the US Public Health Service updated its guidelines to include recommending the use of nucleic acid testing for HCV screening of potential donors2; however, the US Organ Procurement Organization policies still recommend serologic testing only.3 Furthermore, there are no clear universal society guidelines worldwide or for many emerging countries, including India and China, where half the world’s population resides and which are experiencing an exponential increase in the number of kidney transplantations.4 We propose that nephrology, hepatology, and public health societies develop a consensus statement on this issue so that standardized transplantation care can be provided worldwide and the risk of HCV transmission can be minimized.5 Anish Chopra, MD Pratish George, MD, DM Kim Mammen, MD, MCh Christian Medical College and Hospital Ludhiana, India Corresponding author: [email protected]
Acknowledgements Financial Support: The authors declare that they have no relevant financial interests.
References 1. Maheshwari A, Ray S, Thuluvath PJ. Acute hepatitis C. Lancet. 2008;372(9635):321-332. Am J Kidney Dis. 2014;63(3):540-542
2. PHS guideline for reducing transmission of human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis C virus (HCV) through solid organ transplantation. Public Health Rep. 2013;128:1-97. http://www.regulations.gov. Accessed December 9, 2013. 3. Health Resources and Services Administration. Minimum procurement standards for an organ procurement organization (OPO). Rockville, MD: Health Resources and Services Administration. http://optn.transplant.hrsa.gov/policiesandbylaws2/policies/ pdfs/policy_2.pdf. Accessed December 9, 2013. 4. Chugh KS. Five decades of Indian nephrology: a personal journey. Am J Kidney Dis. 2009;54(4):753-763. 5. Centers for Disease Control (CDC) and Prevention. Transmission of hepatitis C virus through transplanted organs and tissue–Kentucky and Massachusetts, 2011. MMWR Morbid Mortal Wkly Rep. 2011;60(50):1697-1700. Originally published online December 27, 2013. Ó 2014 by the National Kidney Foundation, Inc. http://dx.doi.org/10.1053/j.ajkd.2013.11.020
Retinal Detachment in Autosomal Dominant Polycystic Kidney Disease To the Editor: Autosomal dominant polycystic kidney disease (ADPKD) is a systemic disorder resulting from mutations of polycystin genes on chromosomes 16 and 4.1 It is considered a ciliopathy—a genetic disorder that causes ciliary dysfunction and involves multiple organs, including retinal degeneration and kidney and cerebral anomalies.2,3 In this letter, we describe 3 patients with ADPKD and retinal detachment. The first, a 35-year-old normotensive woman with normal kidney function, experienced diminished vision in her right eye for 2 months. She had right inferior retinal detachment and refused surgery. The second, a 51-year-old man on maintenance hemodialysis therapy with controlled hypertension, had progressive painless visual loss in the left eye over 15 days. He had left total rhegmatogenous retinal detachment. After undergoing peritomy, scleral buckling, encirclage, and pneumoretinopexy, he experienced marginal improvement in vision. The third patient, a 47-year-old man with stage 1 hypertension and normal kidney function, had right eye visual loss for 20 days. He had right rhegmatogenous retinal detachment and lattice degeneration in both eyes. He underwent scleral buckling, cryopexy, and sulfur hexa fluoride injection into his right eye and laser photocoagulation to his left eye. None of these patients had risk factors for retinal detachment. Previous reports of polycystic kidney disease with retinal involvement have occurred in transgenic rats4 or in the settings of nephronophthisis,5 Senior-Löken syndrome,6 and Bardet-Biedl syndrome and have consisted of retinal degeneration.7 To our knowledge, this is the first report of an association between retinal detachment and ADPKD. We conjecture that this finding may be the result of extracellular matrix defects in the retina due to ciliary dysfunction. Ravindra A. Prabhu, DM Shankar Prasad Nagaraju, DM Krishna Rao Addoor, MD Kasturba Medical College Manipal Manipal University Manipal, India Corresponding author: [email protected]
541
Correspondence
Acknowledgements We acknowledge Manohar Bairy, CCT, and Sarita R.J. Gonsalves, MD, for valuable contributions for reviewing this manuscript. Financial Disclosure: The authors declare that they have no relevant financial interests.
References 1. Torres VE, Harris PC, Pirson Y. Autosomal dominant polycystic kidney disease. Lancet. 2007;369:1287-1301. 2. Waters AM, Beales PL. Ciliopathies: an expanding disease spectrum. Pediatr Nephrol. 2011;26:1039-1056. 3. D’Angelo A, Franco B. The primary cilium in different tissues—lessons from patients and animal models. Pediatr Nephrol. 2011;26:655-662. 4. Gallagher AR, Hoffmann S, Brown N, et al. A truncated polycystin-2 protein causes polycystic kidney disease and retinal
542
degeneration in transgenic rats. J Am Soc Nephrol. 2006;17: 2719-2730. 5. Katsanis N, Beales PL, Woods MO, et al. Mutations in MKKS cause obesity, retinal dystrophy and renal malformations associated with Bardet-Biedl syndrome. Nat Genet. 2000;26: 67-70. 6. Olbrich H, Fliegauf M, Hoefele J, et al. Mutations in a novel gene, NPHP3, cause adolescent nephronophthisis, tapeto-retinal degeneration and hepatic fibrosis. Nat Genet. 2003;34:455-459. 7. Otto EA, Loeys B, Khanna H, et al. Nephrocystin-5, a ciliary IQ domain protein, is mutated in Senior-Löken syndrome and interacts with RPGR and calmodulin. Nat Genet. 2005;37: 282-288. Originally published online January 6, 2014. Ó 2014 by the National Kidney Foundation, Inc. http://dx.doi.org/10.1053/j.ajkd.2013.11.024
Am J Kidney Dis. 2014;63(3):540-542
![[Autosomal-dominant polycystic kidney disease].](/assets/img/hold.png)
