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Case 1, a 53-year-old man with hyperparathyroidism, had been on HD for 22 years, and Case 2, a 54-year-old woman with hypoparathyroidism, for 20 years. Intact parathyroid hormone levels were 1070 and 3 pg\u002FmL, respectively. Case 1 had mixed renal osteodystrophy (fibrous tissue volume to total volume [Fb.V\u002FTV], 5.21%; osteoid volume to bone volume [OV\u002FBV], 19.8%), and Case 2 had adynamic renal osteodystrophy (Fb.V\u002FTV, 0%; OV\u002FBV, 0.54%). Case 1 showed cortical bone thinning (cortical width, 0.2 mm) and porosis (cortical porosity, 14.1%), but case 2 did not (cortical width, 0.84 mm; cortical porosity, 11.6%). Trabecular connectivity of cancellous bone was preserved in both patients, with a bone volume to total volume of 18.2% in case 1 and 35.1% in case 2. Both patients had been doing daily strength training and treadmill walking (2–3 h\u002Fday) for over 10 years. Although case I showed cortical thinning and porosis, we suggest that long-term loaded exercise therapy may help to preserve cancellous trabecular bone in both hyperparathyroidism and hypoparathyroidism.",{"EN":132},"Effect of loaded exercise for renal osteodystrophy",{"VOID":134},"[\"16410913775638600100\"]",{"VOID":136},"Sprague SM, Bellorin-Font E, Jorgetti V, Carvalho AB, Malluche HH, Ferreira A, D’Haese PC, Drüeke TB, Du H, Manley T, Rojas E, Moe SM. Diagnostic accuracy of bone turnover markers and bone histology in patients with CKD treated by dialysis. Am J Kidney Dis. 2016;67(4):559–66.\nPimentel A, Ureña-Torres P, Zillikens MC, Bover J, Cohen-Solal M. Fractures in patients with CKD-diagnosis, treatment, and prevention: a review by members of the European Calcified Tissue Society and the European Renal Association of Nephrology Dialysis and Transplantation. Kidney Int. 2017;92(6):1343–55.\nHiramatsu R, Ubara Y, Suwabe T, Sumida K, Hayami N, Yamanouchi M, Mise K, Hasegawa E, Hoshino J, Sawa N, Takaichi K. Osteomalacia and insufficiency fracture in a hemodialysis patient with autosomal dominant polycystic kidney disease. Intern Med. 2012;51(23):3277–80.\nIwamoto J, Shimamura C, Takeda T, Abe H, Ichimura S, Sato Y, Toyama Y. Effects of treadmill exercise on bone mass, bone metabolism, and calciotropic hormones in young growing rats. J Bone Miner Metab. 2004;22(1):26–31.\nUbara Y, Tagami T, Nakanishi S, Sawa N, Hoshino J, Suwabe T, Katori H, Takemoto F, Hara S, Takaichi K. Significance of minimodeling in dialysis patients with adynamic bone disease. Kidney Int. 2005;68(2):833–9.\nJimbo-Saito R, Ubara Y, Kadoguchi H, Suwabe T, Nakanishi S, Higa Y, Hoshino J, Sawa N, Katori H, Takemoto F, Nishimura H, Nakamura M, Tomikawa S, Ohashi K, Takaichi K. A case of primary hyperparathyroidism with severe bone and renal changes. J Bone Miner Metab. 2009;27(6):727–32.\nSherrard DJ, Hercz G, Pei Y, Maloney NA, Greenwood C, Manuel A, Saiphoo C, Fenton SS, Segre GV. The spectrum of bone disease in end-stage renal failure—an evolving disorder. Kidney Int. 1993;43(2):436–42.\nRecker RR, Kimmel DB, Parfitt MA, Davies KM, Keshawarz N, Hinders S. Static and tetracycline-based bone histomorphometric data from 34 normal postmenopausal females. J Bone Miner Res. 1988;3(2):133–44.\nUbara Y, Fushimi T, Tagami T, Sawa N, Hoshino J, Yokota M, Katori H, Takemoto F, Hara S. Histomorphometric features of bone in patients with primary and secondary hypoparathyroidism. Kidney Int. 2003;63(5):1809–16.\nYajima A, Inaba M, Tominaga Y, Ito A. Minimodeling reduces the rate of cortical bone loss in patients with secondary hyperparathyroidism. Am J Kidney Dis. 2007;49(3):440–51.\nKobayashi S, Takahashi HE, Ito A, Saito N, Nawata M, Horiuchi H, Ohta H, Ito A, Iorio R, Yamamoto N, Takaoka K. Trabecular minimodeling in human iliac bone. Bone. 2003;32(2):163–9.\nHernandez JD, Wesseling K, Pereira R, Gales B, Harrison R, Salusky IB. Technical approach to iliac crest biopsy. 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de Logt AE, Fresquet M, Wetzels JF, Brenchley P. The anti-PLA2R antibody in membranous nephropathy: what we know and what remains a decade after its discovery. Kidney Int. 2019;96(6):1292–302. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.kint.2019.07.014.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0085253819308075",{"doi":537},"10.1016\u002Fj.kint.2019.07.014",{"id":18,"text":539,"url":540,"identifiers":541},"Couser WG. Primary membranous nephropathy. Clin J Am Soc Nephrol. 2017;12(6):983–97. https:\u002F\u002Fdoi.org\u002F10.2215\u002FCJN.11761116.","https:\u002F\u002Fdoi.org\u002F10.2215\u002Fcjn.11761116",{"mag":542,"pmc":543,"openalex":544,"pm":545,"doi":546},"2617482626","5460716","W2617482626","28550082","10.2215\u002Fcjn.11761116",{"id":548,"text":549,"url":550,"identifiers":551},"50c17722-baff-40e7-87fe-378762a8f569","Ruggenenti P, Cravedi P, Chianca A, Perna A, Ruggiero B, Gaspari F, et al. Rituximab in idiopathic membranous nephropathy. J Am Soc Nephrol. 2012;23(8):1416–25. https:\u002F\u002Fdoi.org\u002F10.1681\u002FASN.2012020181.","https:\u002F\u002Fjournals.lww.com\u002F00001751-201208000-00020",{"doi":552},"10.1681\u002Fasn.2012020181",{"id":554,"text":555,"url":556,"identifiers":557},"b877ffde-dc69-4ad6-ba01-c29cfbccaf82","Fervenza FC, Appel GB, Barbour SJ, Rovin BH, Lafayette RA, Aslam N, et al. Rituximab or cyclosporine in the treatment of membranous nephropathy. N Engl J Med. 2019;381(1):36–46. https:\u002F\u002Fdoi.org\u002F10.1056\u002FNEJMoa1814427.","http:\u002F\u002Fwww.nejm.org\u002Fdoi\u002F10.1056\u002FNEJMoa1814427",{"doi":558},"10.1056\u002Fnejmoa1814427",{"id":560,"text":561,"url":562,"identifiers":563},"27b12b60-3c05-4d22-b9b2-bf9a9ff10c45","Ondrussek-Sekac M, Navas-Carrillo D, Orenes-Pinero E. Intestinal microbiota alterations in chronic kidney disease and the influence of dietary components. Crit Rev Food Sci Nutr. 2020. https:\u002F\u002Fdoi.org\u002F10.1080\u002F10408398.2020.1761771.","https:\u002F\u002Fwww.tandfonline.com\u002Fdoi\u002Ffull\u002F10.1080\u002F10408398.2020.1761771",{"doi":564},"10.1080\u002F10408398.2020.1761771",{"id":18,"text":566,"url":567,"identifiers":568},"Sun S, Dong R, Bai M, et al. A Comparative study of the gut microbiota associated with immunoglobulin A nephropathy and membranous nephropathy. 2020. https:\u002F\u002Fdoi.org\u002F10.21203\u002Frs.2.24727\u002Fv1. https:\u002F\u002Fwww.researchgate.net\u002Fpublication\u002F340188456_A_Comparative_Study_of_the_Gut_Microbiota_Associated_with_Immunoglobulin_A_Nephropathy_and_Membranous_Nephropathy.","https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffcimb.2020.557368",{"mag":569,"pmc":570,"openalex":571,"pm":572,"doi":573},"3093578073","7606180","W3093578073","33194798","10.3389\u002Ffcimb.2020.557368",{"id":575,"text":576,"url":577,"identifiers":578},"544f732f-87ab-4383-86fb-1fc5f0af1a23","Quraishi MN, Shaheen W, Oo YH, Iqbal TH. Immunological mechanisms underpinning faecal microbiota transplantation for the treatment of inflammatory bowel disease. Clin Exp Immunol. 2020;199(1):24–38. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fcei.13397.","https:\u002F\u002Facademic.oup.com\u002Fcei\u002Farticle\u002F199\u002F1\u002F24\u002F6402736",{"doi":579},"10.1111\u002Fcei.13397",{"id":581,"text":582,"url":583,"identifiers":584},"3f9929df-8d42-4997-8f13-93814450c92b","Zhao H, Shi Y, Luo X, Peng L, Yang Y, Zou L. The effect of fecal microbiota transplantation on a child with tourette syndrome. Case Rep Med. 2017;2017:6165239. https:\u002F\u002Fdoi.org\u002F10.1155\u002F2017\u002F6165239.","https:\u002F\u002Fwww.hindawi.com\u002Fjournals\u002Fcrim\u002F2017\u002F6165239\u002F",{"doi":585},"10.1155\u002F2017\u002F6165239",{"id":587,"text":588,"url":589,"identifiers":590},"4c68646b-0035-4279-8000-0006b275d4fa","Ren R, Sun G, Yang Y, et al. A pilot study of treating ulcerative colitis with fecal microbiota transplantation. Zhonghua Nei Ke Za Zhi. 2015;54(5):411–5.","https:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs10440-022-00541-7",{"doi":591},"10.1007\u002Fs10440-022-00541-7",{"id":593,"text":594,"url":595,"identifiers":596},"d137f87d-b915-448b-a074-14a70e147e00","Croxen MA, Law RJ, Scholz R, Keeney KM, Wlodarska M, Finlay BB. Recent advances in understanding enteric pathogenic Escherichia coli. Clin Microbiol Rev. 2013;26(4):822–80. https:\u002F\u002Fdoi.org\u002F10.1128\u002FCMR.00022-13.","https:\u002F\u002Fjournals.asm.org\u002Fdoi\u002F10.1128\u002FCMR.00022-13",{"doi":597},"10.1128\u002Fcmr.00022-13",{"id":599,"text":600,"url":601,"identifiers":602},"7749b077-32a6-4e27-9982-f3751df60770","Furusawa Y, Obata Y, Fukuda S, Endo TA, Nakato G, Takahashi D, et al. Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells. Nature. 2013;504(7480):446–50. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnature12721.","https:\u002F\u002Fwww.nature.com\u002Farticles\u002Fnature12721",{"doi":603},"10.1038\u002Fnature12721",{"id":605,"createTime":606,"updateTime":607,"relativeEntities":608,"slug":609,"properties":610,"entityType":139,"verifyStatus":140,"verifyTime":621,"verifyNote":142,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":622,"fullTextUrl":18,"authors":623,"publicationType":304,"publisherRelationship":743,"citationCount":19,"citationInfo":783,"publishDate":785,"publishYear":525,"citationAnalyzeStatus":17,"lastCitationAnalyze":607,"indexDatabases":786,"openAccess":18,"references":18,"isForceReanalyzing":353},"9a1ecf63-3678-4712-80ff-31baed86a267","2023-12-26T13:30:21.064+00:00","2026-07-22T20:46:39.231+00:00",[],"A-case-of-Stappia-indica-induced-relapsing-peritonitis-confirmed-by-16S-ribosomal-RNA-gene-sequencing-analysis-in-a-patient-undergoing-continuous-ambulatory-peritoneal-dialysis",{"abstract":611,"title":613,"gsPaper":615,"references":617,"doi":619},{"EN":612},"A 69-year-old woman with 26-year history of systemic lupus erythematosus and 4-year history of peritoneal dialysis was hospitalized for treatment of bacterial peritonitis. On admission, peritoneal dialysate was collected and subjected to bacterial culture. Cell count in the cloudy peritoneal dialysate was 4194\u002FμL, and Gram-negative bacilli were detected. Vancomycin (1 g\u002Fday) and ceftazidime (1 g\u002Fday) were administered intraperitoneally, which resulted in rapid decrease in cell count in the peritoneal dialysate. However, on the 7th hospital day, peritonitis relapsed with abdominal pain and cloudy dialysate. 16S ribosomal RNA gene sequencing analysis identified Stappia indica sp. as the causative bacteria. Although treatment with 1 g\u002Fday meropenem for an additional 3 weeks was effective, bacterial peritonitis relapsed 7 days after its discontinuation. Because biofilm formation was suspected, the peritoneal catheter was removed, and she was transferred to maintenance hemodialysis. After removal of the peritoneal catheter, bacterial peritonitis never relapsed. Stappia indica was initially discovered in the deep seawater of the Indian Ocean. The bacterium is rod-shaped, Gram-negative, and oxidase- and catalase-positive. There have been no reports on the clinical effects of genus Stappia. Given the frequent relapse in the present case, Stappia indica sp. may easily form biofilms and are likely resistant to antibiotics. Timely peritoneal catheter removal may be required in some cases of bacterial peritonitis as in the present case. Further case reports are required to further elucidate the clinical effects of Stappia indica on humans.",{"EN":614},"A case of Stappia indica-induced relapsing peritonitis confirmed by 16S ribosomal RNA gene sequencing analysis in a patient undergoing continuous ambulatory peritoneal dialysis",{"VOID":616},"[\"9913940549141397308\"]",{"VOID":618},"Pérez Fontan M, Rodríguez-Carmona A, García-Naveiro R, Rosales M, Villaverde P, Valdés F. Peritonitis-related mortality in patients undergoing chronic peritoneal dialysis. Perit Dial Int. 2005;25(3):274–84.\nBoudville N, Kemp A, Clayton P, Lim W, Badve SV, Hawley CM, McDonald SP, Wiggins KJ, Bannister KM, Brown FG, Johnson DW. Recent peritonitis associates with mortality among patients treated with peritoneal dialysis. J Am Soc Nephrol. 2012;23(8):1398–405.\nLi PK, Szeto CC, Piraino B, de Arteaga J, Fan S, Figueiredo AE, Fish DN, Goffin E, Kim YL, Salzer W, Struijk DG, Teitelbaum I, Johnson DW. ISPD peritonitis recommendations: 2016 update on prevention and treatment. Perit Dial Int. 2016;36(5):481–508.\nMatsukuma Y, Sugawara K, Shimano S, Yamada S, Tsuruya K, Kitazono T, Higashi H. A case of bacterial peritonitis caused by roseomonas mucosa in a patient undergoing continuous ambulatory peritoneal dialysis. CEN Case Rep. 2014;3(2):127–31.\nHelvaci O, Hızel K, Guz G, Arinsoy T, Derici U. A very rare pathogen in peritoneal dialysis peritonitis: serratia liquefaciens. Saudi J Kidney Dis Transpl. 2019;30(3):738–40.\nCho Y, Struijk DG. Peritoneal dialysis-related peritonitis: atypical and resistant organisms. Semin Nephrol. 2017;37(1):66–76.\nSong SH, Choi HS, Ma SK, Kim SW, Shin JH, Bae EH. Micrococcus aloeverae – a rare cause of peritoneal dialysis-related peritonitis confirmed by 16S rRNA gene sequencing. J Nippon Med Sch. 2019;86(1):55–7.\nLai Q, Qiao N, Wu C, Sun F, Yuan J, Shao Z. Stappia indica sp. nov., isolated from deep seawater of the Indian Ocean. Int J Syst Evol Microbiol. 2010;60:733–6.\nWeber CF, King GM. Physiological, ecological, and phylogenetic characterization of Stappia, a marine CO-oxidizing bacterial genus. Appl Environ Microbiol. 2007;73(4):1266–76.\nHenao J, Pérez H, Abril D, Ospina K, Piza A, Botero K, Rincón C, Donato J, Hurtado A, García E, Otero V, Del Risco A, Guerra B, Cifuentes Y, Ordoñez A, Rojas D, Suarez K, Osorio D, Pinzón A. Genome sequencing of three bacteria associated to black band disease from a Colombian reef-building coral. Genom Data. 2016;11:73–4.\nChen WM, Sheu FS, Arun AB, Young CC, Sheu SY. Stappia aquimarina sp. nov., isolated from seawater. Int J Syst Evol Microbiol. 2011;18:1763.\nKim BC, Park JR, Bae JW, Rhee SK, Kim KH, Oh JW, Park YH. Stappia marina sp. nov., a marine bacterium isolated from the yellow sea. Int J Syst Evol Microbiol. 2006;56(1):75–9.\nKämpfer P, Arun AB, Frischmann A, Busse HJ, Young CC, Rekha PD, Chen WM. Stappia taiwanensis sp. nov., isolated from a coastal thermal spring. Int J Syst Evol Microbiol. 2013;63(Pt 4):1350–4.\nPujalte MJ, Macián MC, Arahal DR, Garay E. Stappia alba sp. nov., isolated from mediterranean oysters. Syst Appl Microbiol. 2005;28(8):672–8.\nXiao Y, Zheng Y, Wu S, Zhang EH, Chen Z, Liang P, Huang X, Yang ZH, Ng IS, Chen BY, Zhao F. Pyrosequencing reveals a core community of anodic bacterial biofilms in bioelectrochemical systems from China. Front Microbiol. 2015;6:1410.\nBosma JW, Siegert CE, Peerbooms PG, Weijmer MC. Reduction of biofilm formation with trisodium citrate in haemodialysis catheters: a randomized controlled trial. 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report describes a 70-year-old man who developed systemic lupus erythematosus (SLE) during treatment with maintenance hemodialysis. At initiation of maintenance dialysis, the etiology of end-stage renal disease (ESRD) was diabetic nephropathy and no clinical symptom or laboratory data suggested SLE. Fever, pleural effusion that did not respond to ultrafiltration, and immunological findings such as low complement and elevated anti-double-strand DNA antibody level appeared 4 years after maintenance dialysis initiation. Immunosuppressive therapy with corticosteroids improved these abnormalities remarkably. This case underscores the necessity of considering SLE in the differential diagnosis of pleural effusion with male ESRD patients, even if another etiology of ESRD exists.",{"EN":797},"Development of systemic lupus erythematosus in an elderly male hemodialysis patient with 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MP, Santhanam S, Del Greco F. The clinical course of end-stage renal disease in systemic lupus erythematosus. Arch Intern Med. 1983;143:1353–6.",{"doi":591},{"id":587,"text":958,"url":589,"identifiers":959},"Friedman AS, Folkert V, Khan GA. Recurrence of systemic lupus erythematosus in a hemodialysis patient presenting as a unilateral abducens nerve palsy. Clin Nephrol. 1995;44:338–9.",{"doi":591},{"id":587,"text":961,"url":589,"identifiers":962},"Hernandez-Jaras J, Bernis C, Paraiso V, Barril G, Alvarez V, Traver JA. Development of systemic lupus erythematosus in a patient on hemodialysis. Am J Nephrol. 1992;12:105–7.",{"doi":591},{"id":587,"text":964,"url":589,"identifiers":965},"Al-Hawas F, Abdalla AH, Al-Sulaiman MH, Mousa DH, Owda AK, Al-Khader AA. Development of systemic lupus erythematosus in a male patient after 14 years on hemodialysis. Am J Kidney Dis. 1997;29:631–2.",{"doi":591},{"id":587,"text":967,"url":589,"identifiers":968},"Tsokos GC. Systemic lupus erythematosus. N Eng J Med. 2011;365:2110–21.",{"doi":591},{"id":587,"text":970,"url":589,"identifiers":971},"Tan EM, Cohen AS, Fries JF, et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum. 1982;25:1271–7.",{"doi":591},{"id":587,"text":973,"url":589,"identifiers":974},"Tan TC, Fang H, Magder LS, Petri MA. Differences between male and female systemic lupus erythematosus in a multiethnic population. J Rheumatol. 2012;39:759–69.",{"doi":591},{"id":976,"text":977,"url":978,"identifiers":979},"70ab77e4-4d47-4a19-abbc-24856f91fd98","de Carvalho JF, do Nascimento AP, Testagrossa LA, Barros RT, Bonfá E. Male gender results in more severe lupus nephritis. Rheumatol Int. 2010;30:1311–5.","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00296-009-1151-9",{"doi":980},"10.1007\u002Fs00296-009-1151-9",{"id":982,"text":983,"url":984,"identifiers":985},"837f9549-2014-43aa-9323-8eb116708e89","Rovenský J, Tuchynová A. Systemic lupus erythematosus in the elderly. Autoimmun Rev. 2008;7:235–9.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS1568997207001747",{"doi":986},"10.1016\u002Fj.autrev.2007.11.014",{"id":587,"text":988,"url":589,"identifiers":989},"Coplon NS, Diskin CJ, Petersen J, Swenson RS. The long-term clinical course of systemic lupus erythematosus in end-stage renal disease. N Engl J Med. 1983;308:186–90.",{"doi":591},{"id":991,"createTime":992,"updateTime":993,"relativeEntities":994,"slug":995,"properties":996,"entityType":139,"verifyStatus":140,"verifyTime":1007,"verifyNote":142,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1008,"fullTextUrl":18,"authors":1009,"publicationType":304,"publisherRelationship":1116,"citationCount":18,"citationInfo":18,"publishDate":1157,"publishYear":948,"citationAnalyzeStatus":1158,"lastCitationAnalyze":1159,"indexDatabases":1160,"openAccess":18,"references":18,"isForceReanalyzing":353},"9efdf3a3-dd99-46d9-811a-ee273a69eef6","2024-01-05T03:24:15.014+00:00","2026-05-10T00:41:42.719+00:00",[],"Lupus-like-glomerulonephritis-an-autoimmune-complication-of-hepatitis-C-infection",{"abstract":997,"title":999,"gsPaper":1001,"references":1003,"doi":1005},{"EN":998},"Lupus-like glomerulnephritis in patients with negative lupus serologies and no extra-renal manifestations of lupus can create a diagnostic dilemma. We describe a 53-year-old gentleman with chronic hepatitis C virus (HCV) infection who presented with dialysis-requiring renal failure, renal histologic findings of “full-house” immunofluorescence label and tubuloreticular inclusions on electronic microscopy, but no extra-renal or laboratory signs of systemic lupus erythematosis. Attempted treatment with cyclophosphamide and corticosteroids was limited by cyclophosphamide hypersensitivity. The patient remained dialysis-dependent over 18 months of observation and did not develop extra-renal clinical or biological manifestations of lupus. Mimics of seronegative lupus with isolated renal involvement can include HCV-related autoimmunity. Treatment of acute glomerulonephritis may be similar initially, but other concerns in patients with HCV infection include excluding cryoglobulinemia, the potential impact of immunosuppression therapy on liver disease and consideration of subsequent use of antiviral therapy. Given the increasing prevalence of HCV globally, the recognition of extra-hepatic autoimmune manifestations of HCV infection will likely increase.",{"EN":1000},"Lupus-like glomerulonephritis: an autoimmune complication of hepatitis C infection",{"VOID":1002},"[]",{"VOID":1004},"Wen YK, Chen ML. Clinicopathological study of originally non-lupus “full-house” nephropathy. Ren Fail. 2010;32(9):1025–30.\nGianviti A, Barsotti P, Barbera V, Faraggiana T, Rizzoni G. Delayed onset of systemic lupus erythematosus in patients with “full-house” nephropathy. Pediatr Nephrol. 1999;13(8):683–7.\nDaghestani L, Pomeroy C. Renal manifestations of hepatitis C infection. Am J Med. 1999;106(3):347–54.\nBandi L. Renal manifestations of hepatitis C virus infection. Extrahepatic complications often are silent–and thus overlooked. Postgrad Med. 2003;113(2):73–76, 86.\nBaskin E, Agras PI, Menekse N, Ozdemir H, Cengiz N. Full-house nephropathy in a patient with negative serology for lupus. Rheumatol Int. 2007;27(3):281–4.\nLee LC, Lam KK, Lee CT, Chen JB, Tsai TH, Huang SC. “Full house” proliferative glomerulonephritis: an unreported presentation of subacute infective endocarditis. J Nephrol. 2007;20(6):745–9.\nShearn MA, Hopper J, Biava CG. Membranous lupus nephropathy initially seen as idiopathic membranous nephropathy. Possible diagnostic value of tubular reticular structures. Arch Intern Med 1980;140:1521–1523\nNakahara C, Hayashi D, Kinugasa H, Horigome H, Matsui A, Takagi A, et al. Delayed onset of systemic lupus erythematosus in a child with endothelial tubuloreticular inclusion. Clin Nephrol. 2001;56(4):332–5.\nGarancis JC, Komorowski RA, Bernhard GC, Straumfjord JV. Significance of cytoplasmic microtubules in lupus nephritis. Am J Pathol. 1971;64(1):1–12.\nSchaff Z, Heine U, Dalton AJ. Ultramorphological and ultracytochemical studies on tubuloreticular structures in lymphoid cells. Cancer Res. 1972;32(12):2696–706.\nLuu JY, Bockus D, Remington F, Bean MA, Hammar SP. Tubuloreticular structures and cylindrical confronting cisternae: a review. Hum Pathol. 1989;20(7):617–27.\nVenkataseshan VS, Marquet E, Grishman E. Significance of cytoplasmic inclusions in lupus nephritis. Ultrastruct Pathol. 1991;15(1):1–14.\nD’Agati V, Suh JI, Carbone L, Cheng JT, Appel G. Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study. Kidney Int. 1989;35(6):1358–70.\nBourgoignie JJ, Pardo V. The nephropathology in human immunodeficiency virus (HIV-1) infection. Kidney Int Suppl. 1991;35:S19–23.\nKlippel JH, Carette S, Preble OT, Friedman RM, Grimley PM. Serum alpha interferon and lymphocyte inclusions in systemic lupus erythematosus. Ann Rheum Dis. 1985;44(2):104–8.\nGrimley PM, Davis GL, Kang YH, Dooley JS, Strohmaier J, Hoofnagle JH. Tubuloreticular inclusions in peripheral blood mononuclear cells related to systemic therapy with alpha-interferon. Lab Investig. 1985;52(6):638–49.\nLenzi M, Bellentani S, Saccoccio G, Muratori P, Masutti F, Muratori L, et al. Prevalence of non-organ-specific autoantibodies and chronic liver disease in the general population: a nested case-control study of the Dionysos cohort. Gut. 1999;45(3):435–41.\nFerri S, Muratori L, Lenzi M, Granito A, Bianchi FB, Vergani D. HCV and autoimmunity. Curr Pharm Des. 2008;14(17):1678–85.\nSutti S, Vidali M, Mombello C, Sartori M, Ingelman-Sundberg M, Albano E. Breaking self-tolerance toward cytochrome P4502E1 (CYP2E1) in chronic hepatitis C: possible role for molecular mimicry. J Hepatol. 2010;53(3):431–8.\nRamos-Casals M, Font J, Garcia-Carrasco M, Cervera R, Jimenez S, Trejo O, et al. Hepatitis C virus infection mimicking systemic lupus erythematosus: study of hepatitis C virus infection in a series of 134 Spanish patients with systemic lupus erythematosus. Arthritis Rheumat. 2000;43(12):2801–6.\nMiller SE, Howell DN. Glomerular diseases associated with hepatitis C virus infection. Saudi J Kidney Dis Transpl. 2000;11(2):145–60.\nMolino C, Fabbian F, Longhini C. Clinical approach to lupus nephritis: recent advances. Eur J Intern Med. 2009;20(5):447–53.\nCanada R, Chaudry S, Gaber L, Waters B, Martinez A, Wall B. Polyarteritis nodosa and cryoglobulinemic glomerulonephritis related to chronic hepatitis C. Am J Med Sci. 2006;331(6):329–33.\nAdu D, Pall A, Luqmani RA, Richards NT, Howie AJ, Emery P, et al. Controlled trial of pulse versus continuous prednisolone and cyclophosphamide in the treatment of systemic vasculitis. QJM. 1997;90(6):401–9.\nShahin AA, El Desouky SM, Zayed HS. A retrospective analysis of treatment outcomes in patients with hepatitis C related systemic vasculitis receiving intravenous methylprednisolone and cyclophosphamide. Clin Rheumatol. 2011;30(5):607–14.\nQuigg RJ, Brathwaite M, Gardner DF, Gretch DR, Ruddy S. Successful cyclophosphamide treatment of cryoglobulinemic membranoproliferative glomerulonephritis associated with hepatitis C virus infection. Am J Kidney Dis. 1995;25(5):798–800.\nSaleh F, Ko HH, Davis JE, Apiratpracha W, Powell JJ, Erb SR, et al. Fatal hepatitis C associated fibrosing cholestatic hepatitis as a complication of cyclophosphamide and corticosteroid treatment of active glomerulonephritis. Ann Hepatol. 2007;6(3):186–9.\nMagrin S, Craxi A, Fabiano C, Simonetti RG, Fiorentino G, Marino L, et al. Hepatitis C viremia in chronic liver disease: relationship to interferon-alpha or corticosteroid treatment. Hepatology. 1994;19(2):273–9.\nUto H, Stuver SO, Hayashi K, Kumagai K, Sasaki F, Kanmura S, et al. Increased rate of death related to presence of viremia among hepatitis C virus antibody-positive subjects in a community-based cohort study. Hepatology. 2009;50(2):393–9.\nJefferson JA, Johnson RJ. Treatment of hepatitis C-associated glomerular disease. 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Nephrol Dial Transplant. 2008;23(12):3888–94.",{"doi":1410},"10.1093\u002Fndt\u002Fgfn363",{"id":18,"text":1412,"url":18,"identifiers":1413},"Omokawa A, Komatsuda A, Hirokawa M, et al. Membranous nephropathy with monoclonal IgG4 deposits and associated IgG4-related lung disease. Clin Kidney J. 2014;7(5):475–8.",{"doi":1414},"10.1093\u002Fckj\u002Fsfu077",{"id":18,"text":1416,"url":18,"identifiers":1417},"Gerth J, Sachse A, Busch M, et al. Screening and differential diagnosis of renal light chain-associated diseases. Kidney Blood Press Res. 2012;35(2):120–8.",{"doi":1418},"10.1159\u002F000330715",{"id":18,"text":1420,"url":18,"identifiers":1421},"Ranghino A, Tamagnone M, Messina M, et al. A case of recurrent proliferative glomerulonephritis with monoclonal IgG deposits after kidney transplant treated with plasmapheresis. Case Rep Nephrol Urol. 2012;2(1):46–52.",{"doi":1422},"10.1159\u002F000339405",{"id":18,"text":1424,"url":18,"identifiers":1425},"Ohashi R, Sakai Y, Otsuka T, et al. Proliferative glomerulonephritis with monoclonal IgG2kappa deposit successfully treated with steroids: a case report and review of the literature. CEN Case Rep. 2013;2(2):197–203.",{"doi":1426},"10.1007\u002Fs13730-013-0064-3",{"id":18,"text":1428,"url":18,"identifiers":1429},"Komatsuda A, Wakui H, Ohtani H, et al. Steroid-responsive nephrotic syndrome in a patient with proliferative glomerulonephritis with monoclonal IgG deposits with pure mesangial proliferative features. NDT Plus. 2010;3(4):357–9.",{},{"id":18,"text":1431,"url":18,"identifiers":1432},"Katsuno T, Kato M, Fujita T, et al. Chronological change of renal pathological findings in the proliferative glomerulonephritis with monoclonal IgG deposits considered to have recurred early after kidney transplantation. CEN Case Rep. 2019;8(3):151–8.",{"doi":1433},"10.1007\u002Fs13730-019-00384-6",{"id":18,"text":1435,"url":18,"identifiers":1436},"Tamura T, Unagami K, Okumi M, et al. A case of recurrent proliferative glomerulonephritis with monoclonal IgG deposits or de novo C3 glomerulonephritis after kidney transplantation. Nephrology (Carlton). 2018;23(Suppl 2):76–80.",{"doi":1437},"10.1111\u002Fnep.13280",{"id":18,"text":1439,"url":18,"identifiers":1440},"Said SM, Cosio FG, Valeri AM, et al. Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits is associated with high rate of early recurrence in the allograft. Kidney Int. 2018;94(1):159–69.",{"doi":1441},"10.1016\u002Fj.kint.2018.01.028",{"id":18,"text":1443,"url":18,"identifiers":1444},"Merhi B, Patel N, Bayliss G, et al. Proliferative glomerulonephritis with monoclonal IgG deposits in two kidney allografts successfully treated with rituximab. Clin Kidney J. 2017;10(3):405–10.",{"doi":1445},"10.1093\u002Fckj\u002Fsfx001",{"id":18,"text":1447,"url":18,"identifiers":1448},"Torrealba J, Gattineni J, Hendricks AR. Proliferative glomerulonephritis with monoclonal immunoglobulin G lambda deposits: report of the first pediatric case. Case Rep Nephrol Dial. 2018;8(1):70–5.",{"doi":1449},"10.1159\u002F000488641",{"id":1451,"createTime":1452,"updateTime":1453,"relativeEntities":1454,"slug":1455,"properties":1456,"entityType":139,"verifyStatus":140,"verifyTime":1469,"verifyNote":142,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1470,"fullTextUrl":18,"authors":1471,"publicationType":304,"publisherRelationship":1554,"citationCount":78,"citationInfo":1590,"publishDate":1593,"publishYear":1591,"citationAnalyzeStatus":17,"lastCitationAnalyze":1453,"indexDatabases":1594,"openAccess":18,"references":18,"isForceReanalyzing":353},"93458987-2b0a-45a2-808d-0939dfb99247","2024-04-08T15:41:25.560+00:00","2026-04-02T21:47:58.139+00:00",[],"Expression-of-aquaporin-2-in-the-collecting-duct-and-responses-to-tolvaptan",{"abstract":1457,"title":1459,"gsPaper":1461,"keywords":1463,"references":1465,"doi":1467},{"EN":1458},"Tolvaptan, a vasopressin type-2 receptor antagonist, is indicated for fluid retention. It is considered that the response to tolvaptan reduces as renal function deteriorates, whereas we sometimes experience “non-responders” to tolvaptan despite well-preserved renal function. While the expression of aquaporin-2 might be a key to response to tolvaptan, detailed mechanism of refractoriness to tolvaptan remains unknown. We experienced two patients with congestive heart failure and diabetic nephropathy, in whom the responses to tolvaptan were uniquely opposite. In one case, immunohistochemical staining showed expression of aquaporin-2 in the collecting duct despite severely reduced renal function, followed by the good response to tolvaptan with increased urine output. In another case, immunohistochemical staining showed absence of aquaporin-2 with infiltration of inflammatory cells in the kidney medulla despite relatively preserved renal function, followed by refractoriness to tolvaptan without any increase in urine output. Inactivated aquaporin-2 expression in the collecting duct, which was for example caused by pre-clinical urinary infection as our latter case, might have an association with refractoriness to tolvaptan.",{"EN":1460},"Expression of aquaporin-2 in the collecting duct and responses to tolvaptan",{"VOID":1462},"[\"13110350811396428158\"]",{"EN":1464},"",{"VOID":1466},"Imamura T, Kinugawa K. Urine aquaporin-2: a Promising marker of response to the arginine vasopressin type-2 antagonist, tolvaptan in patients with congestive heart failure. Int J Mol Sci. 2016;17:105.\nImamura T, Kinugawa K. Update of acute and long-term tolvaptan therapy. J Cardiol. 2019;73:102–7.\nImamura T, Kinugawa K, Fujino T, Inaba T, Maki H, Hatano M, Yao A, Komuro I. Increased urine aquaporin-2 relative to plasma arginine vasopressin is a novel marker of response to tolvaptan in patients with decompensated heart failure. Circ J. 2014;78:2240–9.\nImamura T, Kinugawa K, Shiga T, Kato N, Muraoka H, Minatsuki S, Inaba T, Maki H, Hatano M, Yao A, Kyo S, Nagai R. Novel criteria of urine osmolality effectively predict response to tolvaptan in decompensated heart failure patients–association between non-responders and chronic kidney disease. Circ J. 2013;77:397–404.\nBricker NS, Dewey RR, Lubowitz H, Stokes J, Kirkensgaard T. Observations on the concentrating and diluting mechanisms of the diseased kidney. J Clin Investig. 1959;38:516–23.\nTanaka A, Nakamura T, Sato E, Node K. Aquaporin-2 is a potential biomarker for tolvaptan efficacy in decompensated heart failure complicated by diabetic nephrotic syndrome. Int J Cardiol. 2016;210:1–3.\nTanaka A, Nakamura T, Sato E, Ueda Y, Node K. Different effects of tolvaptan in patients with idiopathic membranous nephropathy with nephrotic syndrome. Intern Med. 2017;56:191–6.",{"VOID":1468},"10.1007\u002Fs13730-020-00518-1","2024-05-10T13:29:07.482+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs13730-020-00518-1",[1472,1487,1500,1515,1528,1541],{"id":1473,"sortIndex":19,"researcher":18,"roles":1474,"affiliations":1475,"properties":1484,"displayName":1486,"givenName":18,"familyName":18},"a4f3535e-c4e4-4ff6-8ae7-e0e5b5e475c6",[148],[1476],{"id":1477,"sortIndex":19,"affiliation":1478,"properties":18},"46512d6e-e3a5-4d34-8170-2fd86de9425c",{"id":1477,"createTime":18,"updateTime":18,"relativeEntities":1479,"slug":18,"properties":1480,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1483,"statistic":18},[],{"title":1481},{"VI":1482},"The Second Department of Internal Medicine, University of Toyama, Toyama, Japan",[],{"title":1485},{"VI":1486},"Kota 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a large randomized placebo-controlled trial indicated a beneficial effect of tolvaptan on the progression of autosomal dominant polycystic kidney disease (ADPKD) with near-normal kidney function. Meanwhile, the evidence of tolvaptan’s efficacy in ADPKD with severe renal insufficiency was limited and higher frequency of liver enzyme elevations were observed in patients taking tolvaptan. Liver transplantation (LT) is the only curative treatment for patients with severe polycystic liver disease associated with ADPKD, but considering that liver injuries should be avoided particularly in patients who underwent LT, we must be careful to start tolvaptan in post-LT ADPKD patients. We describe the case of a patient who had developed severe renal insufficiency after living donor LT, for whom tolvaptan therapy showed marked reduction of total kidney volume and maintenance of renal function without any serious adverse events. This is the first report to show the beneficial effect and safety of tolvaptan, in a post-LT ADPKD patient with severe renal insufficiency, and hopefully will help broaden the spectrum of patients who will benefit from tolvaptan.",{"EN":1605},"Effect of tolvaptan in a patient with autosomal dominant polycystic kidney disease after living donor liver transplantation",{"VOID":1607},"[\"2927545134762793523\"]",{"VOID":1609},"Patel V, Chowdhury R, Igarashi P. Advances in the pathogenesis and treatment of polycystic kidney disease. Curr Opin Nephrol Hypertens. 2009;18(2):99–106.\nDrenth JP, Chrispijn M, Nagorney DM, Kamath PS, Torres VE. Medical and surgical treatment options for polycystic liver disease. Hepatology. 2010;52(6):2223–30.\nTorres VE, Chapman AB, Devuyst O, Gansevoort RT, Grantham JJ, Higashihara E, Perrone RD, Krasa HB, Ouyang J, Czerwiec FS. Tolvaptan in patients with autosomal dominant polycystic kidney disease. N Engl J Med. 2012;367(25):2407–18.\nShoaf SE, Bricmont P, Mallikaarjun S. Pharmacokinetics and pharmacodynamics of oral tolvaptan in patients with varying degrees of renal function. Kidney Int. 2014;85(4):953–61.\nWatkins PB, Lewis JH, Kaplowitz N, Alpers DH, Blais JD, Smotzer DM, Krasa H, Ouyang J, Torres VE, Czerwiec FS, Zimmer CA. Clinical pattern of tolvaptan-associated liver injury in subjects with autosomal dominant polycystic kidney disease: analysis of clinical trials database. Drug Saf. 2015;38(11):1103–13.\nAbu-Wasel B, Walsh C, Keough V, Molinari M. Pathophysiology, epidemiology, classification and treatment options for polycystic liver diseases. World J Gastroenterol. 2013;19(35):5775–86.\nBhatt PR, McNeely EB, Lin TE, Adams KF, Patterson JH. Review of tolvaptan’s pharmacokinetic and pharmacodynamic properties and drug interactions. J Clin Med. 2014;3:1276–90.\nHebert MF. Contributions of hepatic and intestinal metabolism and P-glycoprotein to cyclosporine and tacrolimus oral drug delivery. Adv Drug Deliv Rev. 1997;27(2–3):201–14.\nShoaf SE, Bricmont P, Mallikaarjun S. Effects of CYP3A4 inhibition and induction on the pharmacokinetics and pharmacodynamics of tolvaptan, a non-peptide AVP antagonist in healthy subjects. Br J Clin Pharmacol. 2012;73(4):579–87.\nShoaf SE, Ohzone Y, Ninomiya S, Furukawa M, Bricmont P, Kashiyama E, Mallikaarjun S. In vitro P-glycoprotein interactions and steady-state pharmacokinetic interactions between tolvaptan and digoxin in healthy subjects. J Clin Pharmacol. 2011;51(5):761–9.\nTakakura A, Contrino L, Zhou X, Bonventre JV, Sun Y, Humphreys BD, Zhou J. Renal injury is a third hit promoting rapid development of adult polycystic kidney disease. Hum Mol Genet. 2009;18(14):2523–31.",{"VOID":1611},"10.1007\u002Fs13730-016-0230-5","2024-05-12T08:21:10.301+00:00","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs13730-016-0230-5",[1615,1630,1643,1656,1669,1682,1695],{"id":1616,"sortIndex":19,"researcher":18,"roles":1617,"affiliations":1618,"properties":1627,"displayName":1629,"givenName":18,"familyName":18},"8a0057dd-3e0d-4a56-8ae2-0387b4685b97",[148],[1619],{"id":1620,"sortIndex":19,"affiliation":1621,"properties":18},"4d9f520a-c4e8-4aea-a663-bf19dea3b7e3",{"id":1620,"createTime":18,"updateTime":18,"relativeEntities":1622,"slug":18,"properties":1623,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1626,"statistic":18},[],{"title":1624},{"VI":1625},"Division of Nephrology, Japanese Red Cross Medical Center, Tokyo, Japan",[],{"title":1628},{"VI":1629},"Kiyotaka 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AKI definition. Kidney Int Suppl. 2012;2:19–36. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fkisup.2011.32.",{"doi":1928},"10.1038\u002Fkisup.2011.32",{"id":18,"text":1930,"url":18,"identifiers":1931},"Luciano RL, Moeckel GW. Update on the native kidney biopsy: core curriculum 2019. Am J Kidney Dis. 2019;73(3):404–15. https:\u002F\u002Fdoi.org\u002F10.1053\u002Fj.ajkd.2018.10.011.",{"doi":1932},"10.1053\u002Fj.ajkd.2018.10.011",{"id":18,"text":1934,"url":18,"identifiers":1935},"Leung N, Gertz M, Kyle RA, et al. Urinary albumin excretion patterns of patients with cast nephropathy and other monoclonal gammopathy-related kidney diseases. Clin J Am Soc Nephrol. 2012;7:1964–8.",{"doi":1936},"10.2215\u002FCJN.11161111",{"id":18,"text":1938,"url":18,"identifiers":1939},"Greipp PR, San Miguel J, Durie BG, et al. International staging system for multiple myeloma. J Clin Oncol. 2005;23(15):3412–20. https:\u002F\u002Fdoi.org\u002F10.1200\u002FJCO.2005.04.242.",{"doi":1940},"10.1200\u002FJCO.2005.04.242",{"id":18,"text":1942,"url":18,"identifiers":1943},"Cohen Tervaert TW, Mooyaart AL, Amann K, Cohen AH, Cook HT, Drachenberg CB, et al. Pathologic classification of diabetic nephropathy. J Am Soc Nephrol. 2010;21:556–63. https:\u002F\u002Fdoi.org\u002F10.1681\u002FASN.2010010010.",{"doi":1944},"10.1681\u002FASN.2010010010",{"id":18,"text":1946,"url":18,"identifiers":1947},"Greenlee RT, Murray T, Bolden S, Wingo PA. Cancer statistics, 2000. CA Cancer J Clin. 2000;50:7–33.",{"doi":1948},"10.3322\u002Fcanjclin.50.1.7",{"id":18,"text":1950,"url":18,"identifiers":1951},"Clyne DH, Pesce AJ, Thompson RE. Nephrotoxicity of Bence Jones proteins in the rat: importance of protein isoelectric point. Kidney Int. 1979;16:345–52.",{"doi":1952},"10.1038\u002Fki.1979.137",{"id":18,"text":1954,"url":18,"identifiers":1955},"Leung N, Bridoux F, Batuman V, et al. The evaluation of monoclonal gammopathy of renal significance: a consensus report of the International Kidney and Monoclonal Gammopathy Research Group. Nat Rev Nephrol. 2019;15(1):45–59. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41581-018-0077-4.",{"doi":1956},"10.1038\u002Fs41581-018-0077-4",{"id":18,"text":1958,"url":18,"identifiers":1959},"Seth S, Rajkumar SV, D’Agati V, et al. Heterogeneity of monoclonal immunoglobulin associated renal diseases. J Am Soc Nephrol. 2018;29:1810–23.",{"doi":1960},"10.1681\u002FASN.2017121319",{"id":1962,"createTime":1963,"updateTime":1964,"relativeEntities":1965,"slug":1966,"properties":1967,"entityType":139,"verifyStatus":140,"verifyTime":1980,"verifyNote":142,"languages":18,"translateLanguages":1981,"viewCount":19,"primaryUrl":1983,"fullTextUrl":18,"authors":1984,"publicationType":304,"publisherRelationship":2206,"citationCount":18,"citationInfo":18,"publishDate":2246,"publishYear":525,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":2247,"openAccess":18,"references":18,"isForceReanalyzing":353},"48d67c26-2aa5-4218-a8c3-ba5da9038de3","2023-12-27T03:58:18.741+00:00","2025-02-26T23:45:45.503+00:00",[],"A-case-of-early-onset-cystinuria-in-a-4-month-old-girl",{"abstract":1968,"title":1971,"keywords":1974,"references":1976,"doi":1978},{"EN":1969,"VI":1970},"Cystinuria is an autosomal recessive disorder characterized by a decrease in the reabsorption of cystine and dibasic amino acids (lysine, ornithine, and arginine) in the renal proximal tubule. It presents with recurrent urolithiasis. Cystinuria accounts for 6–8% of all pediatric urolithiasis. The age of onset is typically 10–30 years. Here, we report a case of early-onset cystinuria. A 4-month-old girl presented with hematuria. We noticed multiple renal calculi in ultrasonography and abdominal computerized tomography scans. The diagnosis was cystinuria with urinary calculus analysis and urinary amino acid analysis. The patient was treated with urine alkalinization and cystine chelating drugs. Gene analysis showed a P482L heterozygous mutation from her mother, and an A70V heterozygous mutation from her father, in the SLC7A9 gene. This gene encodes a putative subunit of the neutral and basic amino acid transport protein, BAT1. Although cystinuria is an autosomal recessive disease, there have been previous reports of P482L heterozygous mutations greatly suppressing cystine reabsorption and causing cystinuria symptoms. Therefore, the highly influential P482L mutation of the SLC7A9 gene may have contributed to the onset of this autosomal recessive disease at an extremely young age.","Cystinuria là một rối loạn di truyền lặn trên nhiễm sắc thể thường, đặc trưng bởi sự giảm tái hấp thu cystine và các amino acid hai bazơ (lysine, ornithine và arginine) trong ống thận gần. Bệnh xuất hiện với triệu chứng sỏi thận tái phát. Cystinuria chiếm khoảng 6–8% tổng số sỏi thận ở trẻ em. Thời điểm khởi phát bệnh thường từ 10–30 tuổi. Trong nghiên cứu này, chúng tôi báo cáo một trường hợp cystinuria khởi phát sớm. Một bé gái 4 tháng tuổi đến khám với triệu chứng tiểu máu. Chúng tôi phát hiện nhiều sỏi thận qua siêu âm và chụp cắt lớp vi tính ổ bụng. Chẩn đoán là cystinuria thông qua phân tích sỏi tiểu và phân tích amino acid trong nước tiểu. Bệnh nhân được điều trị bằng cách kiềm hóa nước tiểu và sử dụng thuốc chelat cystine. Phân tích gen cho thấy một đột biến dị hợp tử P482L từ mẹ và một đột biến dị hợp tử A70V từ cha, trong gen SLC7A9. Gen này mã hóa cho một tiểu đơn vị dự đoán của protein vận chuyển amino acid trung tính và cơ bản, BAT1. Mặc dù cystinuria là một bệnh di truyền lặn trên nhiễm sắc thể thường, đã có những báo cáo trước đây cho thấy các đột biến dị hợp tử P482L làm giảm đáng kể sự tái hấp thu cystine và gây ra triệu chứng của cystinuria. Do đó, đột biến P482L có ảnh hưởng lớn của gen SLC7A9 có thể đã góp phần vào sự khởi phát của bệnh di truyền lặn này ở độ tuổi rất trẻ.",{"EN":1972,"VI":1973},"A case of early onset cystinuria in a 4-month-old girl","Trường hợp cystinuria khởi phát sớm ở bé gái 4 tháng tuổi",{"VI":1975},"Cystinuria, di truyền lặn, sỏi thận, đột biến gen, SLC7A9",{"VOID":1977},"Edvardsson VO, Ingvarsdottir SE, Palsson R, Indridason OS. Incidence of kidney stone disease in Icelandic children and adolescents from 1985 to 2013: results of a nationwide study. Pediatr Nephrol. 2018;33:1375–84.\nWard JB, Feinstein L, Pierce C, Lim J, Abbott KC, Bavendam T, Kirkali Z, Matlaga BR; NIDDK Urologic Diseases in America Project. Pediatric urinary stone disease in the United States: the urologic diseases in America project. Urology. 2019;129:180–7.\nEggermann T, Venghaus A, Zerres K. Cystinuria: an inborn cause of urolithiasis. Orphanet J Rare Dis. 2012;7:19.\nCalonge MJ, Gasparini P, Chillarón J, Chillón M, Gallucci M, Rousaud F, Zelante L, Testar X, Dallapiccola B, Di Silverio F. Cystinuria caused by mutations in rBAT, a gene involved in the transport of cystine. Nat Genet. 1994;6:420–5.\nFeliubadaló L, Font M, Purroy J, Rousaud F, Estivill X, Nunes V, Golomb E, Centola M, Aksentijevich I, Kreiss Y, Goldman B, Pras M, Kastner DL, Pras E, Gasparini P, Bisceglia L, Beccia E, Gallucci M, de Sanctis L, Ponzone A, Rizzoni GF, Zelante L, Bassi MT, George AL Jr, Manzoni M, De Grandi A, Riboni M, Endsley JK, Ballabio A, Borsani G, Reig N, Fernández E, Estévez R, Pineda M, Torrents D, Camps M, Lloberas J, Zorzano A, Palacín M; International Cystinuria Consortium. Non-type I cystinuria caused by mutations in SLC7A9, encoding a subunit (bo,+AT) of rBAT. Nat Genet. 1999;23:52–7.\nDello Strologo L, Pras E, Pontesilli C, Beccia E, Ricci-Barbini V, de Sanctis L, Ponzone A, Gallucci M, Bisceglia L, Zelante L, Jimenez-Vidal M, Font M, Zorzano A, Rousaud F, Nunes V, Gasparini P, Palacín M, Rizzoni G. Comparison between SLC3A1 and SLC7A9 cystinuria patients and carriers: a need for a new classification. J Am Soc Nephrol. 2002;13:2547–53.\nProt-Bertoye C, Lebbah S, Daudon M, Tostivint I, Bataille P, Bridoux F, Brignon P, Choquenet C, Cochat P, Combe C, Conort P, Decramer S, Doré B, Dussol B, Essig M, Gaunez N, Joly D, Le Toquin-Bernard S, Méjean A, Meria P, Morin D, N’Guyen HV, Noël C, Normand M, Pietak M, Ronco P, Saussine C, Tsimaratos M, Friedlander G, Traxer O, Knebelmann B, Courbebaisse M, French Cystinuria Group. CKD and Its Risk Factors among Patients with Cystinuria. Clin J Am Soc Nephrol. 2015;10:842–51.\nShigeta Y, Kanai Y, Chairoungdua A, Ahmed N, Sakamoto S, Matsuo H, Kim DK, Fujimura M, Anzai N, Mizoguchi K, Ueda T, Akakura K, Ichikawa T, Ito H, Endou H. A novel missense mutation of SLC7A9 frequent in Japanese cystinuria cases affecting the C-terminus of the transporter. Kidney Int. 2006;69:1198–206.\nYuen YP, Lam CW, Lai CK, Tong SF, Li PS, Tam S, Kwan EY, Chan SY, Tsang WK, Chan KY, Mak WL, Cheng CW, Chan YW. Heterogeneous mutations in the SLC3A1 and SLC7A9 genes in Chinese patients with cystinuria. Kidney Int. 2006;69:123–8.\nBisceglia L, Fischetti L, Bonis PD, Palumbo O, Augello B, Stanziale P, Carella M, Zelante L. Large rearrangements detected by MLPA, point mutations, and survey of the frequency of mutations within the SLC3A1 and SLC7A9 genes in a cohort of 172 cystinuric Italian patients. Mol Genet Metab. 2010;99:42–52.\nFont MA, Feliubadaló L, Estivill X, Nunes V, Golomb E, Kreiss Y, Pras E, Bisceglia L, d’Adamo AP, Zelante L, Gasparini P, Bassi MT, George AL Jr, Manzoni M, Riboni M, Ballabio A, Borsani G, Reig N, Fernández E, Zorzano A, Bertran J, Palacín M, International Cystinuria Consortium. Functional analysis of mutations in SLC7A9, and genotype-phenotype correlation in non-Type I cystinuria. Functional analysis of mutations in SLC7A9, and genotype-phenotype correlation in non-Type I cystinuria. Hum Mol Genet. 2001;10:305–16.\nServais A, Thomas K, Dello Strologo L, Sayer JA, Bekri S, Bertholet-Thomas A, Bultitude M, Capolongo G, Cerkauskiene R, Daudon M, Doizi S, Gillion V, Gràcia-Garcia S, Halbritter J, Heidet L, van den Heijkant M, Lemoine S, Knebelmann B, Emma F, Levtchenko E, Metabolic Nephropathy Workgroup of the European Reference Network for Rare Kidney Diseases (ERKNet) and eUROGEN. Cystinuria: clinical practice recommendation. Kidney Int. 2021;99:48–58.\nProt-Bertoye C, Lebbah S, Daudon M, Tostivint I, Jais JP, Lillo-Le Louët A, Pontoizeau C, Cochat P, Bataille P, Bridoux F, Brignon P, Choquenet C, Combe C, Conort P, Decramer S, Doré B, Dussol B, Essig M, Frimat M, Gaunez N, Joly D, Le Toquin-Bernard S, Méjean A, Meria P, Morin D, N’Guyen HV, Normand M, Pietak M, Ronco P, Saussine C, Tsimaratos M, Friedlander G, Traxer O, Knebelmann B, Courbebaisse M, French Cystinuria Group. 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