Introduction:Pretransplant access varies, but whether pretransplant steps vary regionally across dialysis facilities remains unclear. Methods:We identified 62,467 adults (aged 18-80 years) referred from 2471 dialysis facilities and 27,171 initiating transplant evaluation from 2188 facilities in New England, New York, Southeast, and Ohio River Valley within the Early Steps to Transplant Access Registry (E-STAR) (January 1, 2015-December 31, 2023), linked with US Renal Data System (USRDS) and the Scientific Registry of Transplant Recipients data, followed-up through March 2, 2024. We examined dialysis facility-level proportions of evaluation start within 6 months of referral and waitlisting within 1 year of evaluation start. Descriptive statistics using analysis of variance and chi-square tests summarized outcome distributions and baseline characteristics within tertiles of outcome proportions, overall and by region. Results:Evaluation start within 6 months across 2471 facilities varied from 0% to 100%; median within-facility proportion was 50% (interquartile range: 33.3%-64.3%), ranging from 33.3% (18.2%-50%) in the Ohio River Valley to 66.7% (50%-76.7%) in New York. Waitlisting within 1 year of evaluation start varied from 0% to 100% across 2188 facilities; median within-facility proportion was 41.2% (26.0%-60%), lowest in the Southeast (31.9% [20%-43.8%]) and similar across other regions (50%). Facilities in the lowest tertile of evaluation start proportions (< 39.13%) more often treated patients from high-poverty neighborhoods (36.8% vs. 29.2%) and were for-profit (82.4% vs. 73.5%) than the highest tertile (> 58.33%). These characteristics varied by region. Facility-level clustering explained 12.2% (95% confidence interval [CI]: 10.5%-13.5%) of variation in evaluation and 8.2% (6.7%-9.2%) in waitlisting. Conclusion:Substantial regional variation in pretransplant access across dialysis facilities reinforces the need for region-specific strategies to improve access.
BK polyomavirus-associated nephropathy (PyVAN) remains a serious threat for renal dysfunction and graft loss in kidney transplant recipients on immunosuppressive medication. In this study, a pilot cohort of 16 kidney transplant recipients were recruited of which eight were with significant BKPV viremia (sBKPV) and the rest were controls matched to age, gender, and time since transplant. We used next-generation sequencing to characterize the miRNA expression profile in urine samples. In total, the expression of 8 miRNAs (miR-16-5p,miR-200c-3p,bkv-miR-B1-3p,let-7b-3p,miR-1269b,bkv-miR-B1-5p,miR-193a-3p,miR-944) were upregulated whereas 21miRNAs (miR-134-5p,miR-4724-5p,miR-127-3p,miR-6500-3p,miR-507,miR-378b,miR-3911,miR-211-5p,miR-486-5p,miR-143-3p,miR-3195,miR-1307-5p,miR-29a-5p,miR-378f,miR-12136,miR-378g,miR-144-3p,miR-378a-3p,let-7i-5p,miR-204-5p,miR-146a-5p) were downregulated with fold change > 2. We found that bkv-miR-B1-5p and bkv-miR-B1-3p have 19-fold and 5-fold higher expression values in BKPV viremia patient samples, respectively. A few earlier studies have reported BKV miRNA in urine and serum samples using the RT- PCR from PyVAN patients. Our results corroborated findings from earlier studies and highlighted the need for additional evaluation of the role of sequencing approaches for monitoring BKPV specific and host miRNAs to better understand the viral reactivation and disease pathogenesis.
Heavy metal toxicity has recently been described in solid organ transplant recipients. Allograft dysfunction or failure associated with arsenic, cadmium, chromium, cobalt and lead exposure have been reported, largely in renal transplant recipients, but also in small numbers of heart transplant recipients and a few liver and lung recipients. Conclusions: (1) In kidney transplant patients, highest tertile arsenic, cadmium and lead plasma levels were associated with increased allograft loss, compared to lower tertile levels; (2) Deteriorating metal hip prostheses may rarely cause heart failure due to cobalt and chromium cardiac toxicity in heart transplant and non-heart transplant patients, which resolves with prosthesis replacement; (3) Heavy metal testing should be considered in patients with multiple risk factors including occupational and environmental exposure, lower socioeconomic status, and multiple morbidities which could be associated with heavy metal toxicity; (4) Chelation therapy, used successfully in some non-transplant patients with chronic renal failure, has not been used systematically in transplant patients and studies are needed
Purpose of review The aim of this study was to describe recent developments in renal transplantation for HIV-positive recipients, especially the HIV Organ Policy Equity (HOPE) trial results. Recent findings HOPE trial data show that HIV-positive D+/R+ results are excellent and similar to D−/R+ in patients controlled on antiretroviral therapy (ART). Patients coinfected with hepatitis C or B virus now have effective treatment available. As pretransplant evaluation and post-transplant management is more complex in HIV-positive individuals early referral is important and coordination of evaluation and care with an infectious disease specialist is critical. HIV coordinated care services should be involved for best outcomes. HIV-positive renal transplant recipients have an increased risk of rejection and evidence suggests that standard lymphocyte depletion induction and maintenance immunosuppression be employed. Cardiovascular risk reduction and surveillance and attention to metabolic bone disease are important for HIV-positive renal transplant recipients. Summary HIV-positive to HIV-positive renal transplantation has been established as well tolerated and successful. Further efforts are needed to expand access to transplantation in this population. Video abstract http://links.lww.com/MOT/A29.
BACKGROUND:Compensation after living donor nephrectomy is well known, and a compensation prediction score (CPS) was made in Japan previously. The aim of this study was to perform external validation of CPS in the United States.METHODS:We studied retrospectively 78 living donor nephrectomies in our institution. We defined a favorable compensation as a postdonation estimated glomerular filtration rate (eGFR) at 1 year of >60% of the predonation eGFR. We analyzed the living donors' clinical characteristics and outcomes and validated CPS score.RESULTS:The median (range) donor age was 43 (21-63) years, and median body mass index was 26.9 (18.3-35.9) kg/m2. Forty-four percent of donors were White. The donor predonation eGFR was 105 (61-134) mL/min/1.73 m2, and the postdonation eGFR at 1 year was 73.2 (0-115) mL/min/1.73 m2. Eighty-three percent of donors had a favorable compensation. The CPS was 9.6 (1.6-15.6) and showed strong diagnostic accuracy for predicting favorable compensation (area under the curve, 0.788; 95% confidence interval, 0.652-0.924; P = .001). The CPS showed a significant positive correlation with the postdonation eGFR at 1 year (R = 0.54; P < .001).CONCLUSIONS:In the United States, the CPS would be a valid tool with which to predict a favorable compensation of remnant kidney function.
Clinical TransplantationVolume 35, Issue 4 e14245 LETTER TO THE EDITOR Bamlanivimab for treatment of COVID-19 in solid organ transplant recipients: Early single-center experience Abhay Dhand, Abhay Dhand orcid.org/0000-0003-3527-1938 Department of Medicine, Westchester Medical Center, NY, USASearch for more papers by this authorStephen A. Lobo, Stephen A. Lobo Department of Medicine, Westchester Medical Center, NY, USASearch for more papers by this authorKevin Wolfe, Kevin Wolfe Department of Surgery, Westchester Medical Center, NY, USASearch for more papers by this authorNicholas Feola, Nicholas Feola Department of Pharmacy, Westchester Medical Center, NY, USASearch for more papers by this authorChristopher Nabors, Christopher Nabors Department of Medicine, Westchester Medical Center, NY, USASearch for more papers by this author Abhay Dhand, Abhay Dhand orcid.org/0000-0003-3527-1938 Department of Medicine, Westchester Medical Center, NY, USASearch for more papers by this authorStephen A. Lobo, Stephen A. Lobo Department of Medicine, Westchester Medical Center, NY, USASearch for more papers by this authorKevin Wolfe, Kevin Wolfe Department of Surgery, Westchester Medical Center, NY, USASearch for more papers by this authorNicholas Feola, Nicholas Feola Department of Pharmacy, Westchester Medical Center, NY, USASearch for more papers by this authorChristopher Nabors, Christopher Nabors Department of Medicine, Westchester Medical Center, NY, USASearch for more papers by this author First published: 17 February 2021 https://doi.org/10.1111/ctr.14245Citations: 25 Correspondence Abhay Dhand, BHC-Transplant Center, Westchester Medical Center, Valhalla, NY 10595, USA Email: [email protected] Funding information There was no funding (research or employment) for this submission. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. REFERENCES 1Pereira MR, Mohan S, Cohen DJ, et al. COVID-19 in solid organ transplant recipients: Initial report from the US Epicenter. Am J Transplant. 2020; 20: 1800-1808. https://doi.org/10.1111/ajt.15941 10.1111/ajt.15941 CASPubMedWeb of Science®Google Scholar 2Kates OS, Haydel BM, Florman SS, et al. COVID-19 in solid organ transplant: a multi-center cohort study. Clin Infect Dis. 2020;ciaa1097: https://doi.org/10.1093/cid/ciaa1097 10.1093/cid/ciaa1097 PubMedWeb of Science®Google Scholar 3 Food and Drug Administration. Fact sheet for healthcare providers: emergency use authorization (EUA) of bamlanivimab; 2020. https://www.fda.gov/media/143603/download. Accessed November 14, 2020 Google Scholar 4Chen P, Nirula A, Heller B, et al. SARS-CoV-2 neutralizing antibody LY-CoV555 in outpatients with COVID-19. N Engl J Med. 2021; 384(3): 229-237. 10.1056/NEJMoa2029849 CASPubMedWeb of Science®Google Scholar 5Lundgren JD, Grund B, Barkauskas CE, et al. A Neutralizing Monoclonal Antibody for Hospitalized Patients with Covid-19. New England Journal of Medicine. 2020. http://dx.doi.org/10.1056/nejmoa2033130. Web of Science®Google Scholar Citing Literature Volume35, Issue4April 2021e14245 ReferencesRelatedInformation
Exposure to cadmium and lead is widespread, and is related to environmental contamination, occupational sources, food, tobacco and other consumer products. Lower socioeconomic status increases the risk of heavy metal exposure and the diseases associated with cadmium and lead toxicity. Concurrent toxicity with both cadmium and lead is likely but has not often been assessed. There is now substantial evidence linking cadmium and lead to many diseases including hypertension, diabetes mellitus, obesity, cancer, coronary artery disease, chronic kidney disease (CKD) and lung disease. Both chronic renal failure and ischemic heart disease patients have been treated separately in recent studies with calcium disodium ethylenediaminetetraacetic acid (Ca EDTA) chelation therapy. In patients with CKD, serum creatinine 1.5-4.0 mg/dL, and increased body lead burden, weekly low dose chelation with Ca EDTA slowed the rate of decline in renal function in diabetics and non-diabetics. In patients with a history of myocardial infarction, the Trial to Assess Chelation Therapy (TACT) study showed that Ca EDTA chelation decreased the likelihood of cardiovascular events, particularly in diabetics. Ca EDTA chelation administered carefully at lower dosage (<50 mg/kg per week) is generally safe. In the past, acute renal failure associated with much higher dosage was reported. We suggest that the preponderance of the evidence favors a more activist approach towards diagnosis and possible intervention in heavy metal toxicity.
Exposure to heavy metals is common. This exposure is related to environmental contamination of air, water and soil, occupational exposure, accumulation in food, tobacco, and other factors. Cadmium and lead are notable for their widespread contamination, long-lasting effects in the body, and renal as well as cardiovascular toxicity. Acute toxicity due to high-level exposure, as well as chronic low-level exposure are now well-established pathogenic entities. Both chronic renal failure and ischemic heart disease patients have been treated separately in recent studies with ethylenediaminetetraacetic acid (EDTA) chelation therapy. In patients with chronic kidney disease (serum creatinine: 1.5–4.0 mg/dL) and increased body lead burden, weekly low-dose chelation with calcium EDTA slowed the rate of decline in renal function in patients with diabetes and in non-diabetic patients. In patients with a history of myocardial infarction, the Trial to Assess Chelation Therapy study showed that EDTA chelation decreased the likelihood of cardiovascular events, particularly in patients with diabetes. However, heavy metal levels were not measured in this study. It is clear that more research is needed in this area. There is also a need to more frequently consider and test for the possibility of cadmium and lead toxicity in patients with increased risk, such as those with hypertension, diabetes mellitus, and chronic renal disease.
Obesity is now common among children and adults who are kidney transplant candidates and recipients. It is associated with an increased risk of cardiovascular disease and kidney failure. This also pertains to potential living kidney donors with obesity. Obese patients with end-stage renal disease benefit from transplantation as do nonobese patients, but obesity is also associated with more risk. A complicating factor is that obesity is also associated with increased survival on maintenance dialysis in adults, but not in children. The assessment of obesity and body habitus should be individualized. Body mass index is a common but imperfect indicator of obesity. The medical management of obesity in renal failure patients is often unsuccessful. Bariatric surgery, specifically laparoscopic sleeve gastrectomy, can result in significant weight loss with reduced morbidity, but many patients do not agree to undergo this treatment. The best approach to manage obese transplant candidates and recipients is yet unresolved.
Cardiovascular disease is the leading cause of death in patients with chronic renal disease and the most common cause of death and allograft loss among kidney transplant recipients. Transplant patients often have multiple cardiovascular risk factors antedating transplantation. Among the most prominent is hypertension (HTN), which affects at least 90% of transplant patients. Uncontrolled HTN is an independent risk factor for allograft loss. The etiology of HTN in transplant recipients is complex and multifactorial, including the use of essential immunosuppressive medications. Post-transplant HTN management requires a systematic and individualized approach with non-pharmacologic and pharmacologic therapies. There is no single ideal agent or treatment algorithm. Patients should regularly monitor and record their blood pressure at home. Often, multiple antihypertensive drugs are needed to achieve a goal blood pressure of 120-140/70-90 mm Hg. As transplant recipients commonly must take 8 to 12 different medications daily, adherence must be continually encouraged and monitored. Special attention must be paid to potential drug side effects and drug interactions with immunosuppressive medications.
Apparent treatment-resistant hypertension (aTRH) is defined as blood pressure (BP) >140/90 mmHg despite three different antihypertensive drugs including a diuretic. aTRH is associated with an increased risk of cardiovascular events, including stroke, chronic renal failure, myocardial infarction, congestive heart failure, aortic aneurysm, atrial fibrillation, and sudden death. Preliminary studies of renal nerve ablation as a therapy to control aTRH were encouraging. However, these results were not confirmed by the Symplicity 3 trial. Therefore, attention has refocused on drug therapy. Secondary forms of hypertension and associated conditions such as obesity, sleep apnea, and primary aldosteronism are common in patients with aTRH. The pivotal role of aldosterone in the pathogenesis of aTRH in many cases is well recognized. For patients with aTRH, the Joint National Committee-8, the European Society of Hypertension, and a recent consensus conference recommend that a diuretic, ACE inhibitor, or angiotensin receptor blocker and calcium channel blocker combination be used to maximally tolerated doses before starting a ‘fourth-line’ drug such as a mineralocorticoid receptor (MR) antagonist. Although the best fourth-line drug for aTRH has not been extensively investigated, a number of studies summarized here show that an MR antagonist is effective in reducing BP when added to the standard multi-drug regimen.
Resistant systemic hypertension in patients is defined as the inability to control blood pressure despite taking at least three antihypertensive drugs, one of which is a diuretic. Two nonpharmacologic approaches are being evaluated in resistant hypertensive patients. First, the Rheos® Baroreflex Hypertension Therapy system is an implantable device that activates the carotid baroreflex through electrical stimulation of the carotid sinus wall. Sustained and clinically lower blood pressure has been observed in patient clinical trials. The second approach is a catheter-based strategy which denervates the renal afferent and efferent autonomic nervous system. This strategy has also been shown to be effective in drug-resistant patients, and has also been shown to decrease renin production, preserve renal function, improve glucose tolerance, and reduce left ventricular hypertrophy. Both carotid sinus stimulation and renal denervation are now being evaluated in clinical trials for the long-term control of hypertension.
Cardiovascular disease (CVD) is the leading cause of death in dialysis patients and the most common cause of death and allograft loss among kidney transplant recipients. End-stage renal disease (ESRD) is associated with an increased incidence and prevalence of a wide range of CVDs including coronary artery disease, stroke, congestive heart failure, atrial fibrillation, sudden cardiac death, pulmonary hypertension, and valvular heart disease. CVD risk factors are very common in patients with ESRD, and most patients have multiple risk factors. Kidney transplantation is the treatment of choice for patients with ESRD, as a successful transplant improves longevity and quality of life, primarily by decreasing the incidence and severity of CVD. Correction of the uremic state and improved glomerular filtration rate seem to be the major mechanism of this benefit. Transplant candidates should undergo cardiovascular assessment, usually echocardiography and exercise stress testing, and may require formal cardiology consultation. Higher risk candidates, including those aged >50 years, hypertension, diabetes, established coronary artery disease or peripheral vascular disease, left ventricular hypertrophy, and dialysis duration >1 year, should have repeat cardiovascular assessment every 1-2 years. Transplant candidates and recipients should have individualized treatment for CVD and risk factors such as hypertension, diabetes, hyperlipidemia, and obesity. Special consideration should be given for statin therapy, as its use is associated with decreased cardiovascular death in dialysis and transplant patients. Prospective randomized, controlled trials are needed to determine the optimal approach to diagnosis and treat CVD in the transplant candidate and recipient population.
The incidence of End Stage Renal Disease (ESRD) is approximately 50% higher in men than women. In order to understand the molecular basis of this gender disparity, we examined sex specific gene expression patterns in control and diseased, human and murine kidney samples. Using the Affymetrix platform we performed comprehensive gene expression analysis on 42 microdissected human kidney samples (glomeruli and tubules). We identified 67 genes with gender biased expression in healthy human kidneys and 24 transcripts in diseased male and female human kidneys. Similar analysis performed in mice using male and female control and doxorubicin induced nephrotic syndrome kidneys identified significantly larger number of differentially expressed transcripts. The majority of genes showing gender biased expression either in diseased human and murine kidneys were different from those differentially expressed in healthy kidneys. Only 9 sexually dimorphic transcripts were common to healthy human and murine kidneys and five showed differential regulation in both human and murine diseased kidneys. In humans, sex biased genes showed statistical enrichment only to sex chromosomes while in mice they were enriched to sex chromosomes and various autosomes. Thus we present a comprehensive analysis of gender biased genes in the kidney. We show that sexually dimorphic genes in the kidney show species specific regulation. Our results also indicate that male and female kidneys respond differently to injury. These studies could provide the basis for the development of new treatment strategies for men and women with kidney disease.
This patient presented in 1976 with a creatinine of 2.8 mg/dL, and bilateral renal and ureteral stones requiring lithotomy. In 1983, he developed renal failure requiring hemodialysis. He received a living renal transplant in 1986, and was maintained on prednisone and cyclosporine immunosuppression. Routine ultrasonography in 1997 revealed hydronephrosis of the native right kidney. Follow-up studies showed a progressive increase in the size of the kidney and the development of cystic disease. Multiple urine cytologies were negative for malignant cells. Urine cultures were persistently positive for Escherichia coli and the patient was treated with multiple courses of antibiotics. In June 2003, the patient complained of back pain and weight loss. Sonography showed an enlarged, multiloculated cystic mass in the right renal fossa. CT scanning was notable for a new right hydroureter. He was admitted for an elective right nephrectomy. Gross examination revealed a 35× 20× 3 cm hydronephrotic kidney with multiple areas of necrosis and hemorrhage, and multiple mucosal masses, ranging from 0.5 to 2.5 cm, with one attached at the distal ureter lumen causing obstruction. Microscopy showed intestinal metaplasia throughout the renal pelvis and ureter, and multiple villous adenomas arising from metaplastic mucosa (Fig. 1), two with focal high grade dysplasia, and one with superficial stromal invasion. The mass in the distal ureter was also a villous adenoma. A swab of the kidney grew the same E. coli as in the previous positive urine cultures.FIGURE 1.: Example of an intestinal-type adenomatous polyp arising from metaplastic epitheliuam lining the renal pelvis (original magnification, 4×). Lower right hand corner insert shows intestinal-type epithelium at 40× magnification.A colonoscopy was performed to rule out metastasis from a colonic adenocarcinoma. Four polyps were identified and removed, all tubular adenomas. No villous adenomas or carcinomas were found. Intestinal-type villous adenoma is a rare tumor of the urinary tract. Patients typically present with hematuria, mucusuria, and irritative symptoms (1, 2). There is no predilection for age or sex (1–4). Villous adenomas of the urinary tract are identical to their colonic counterparts, with rounded projections of pseudostratified columnar epithelium and mucin producing cells (1, 2). Urothelium may undergo intestinal metaplasia in response to chronic irritation, such as from stones, chemical injury, or chronic inflammation (1). Our patient's multiple stones, urological procedures, and chronic infections may have led to persistent irritation of the renal pelvis and ureter, with intestinal metaplasia and subsequent villous adenoma development. Resection is curative, unless it is associated with underlying infiltrating adenocarcinoma. In two case series reviewing a combined 41 patients, none of the patients with isolated villous adenoma or with associated in situ adenocarcinoma had recurrence after local excision (1, 2). Intestinal-type villous adenomas of the urinary tract are most commonly found in the bladder, arising from metaplastic epithelium. In a series of 23 patients, one case was found in the ureter, and another in the ureteral orifice (1). Only one case of villous adenoma involving the renal pelvis has been reported (5). Our patient is unique in that he had multiple tumors involving the renal pelvis and ureter. This is also the first case that we could find of villous adenoma of the urinary system developing in a renal transplant patient. Krista G. Fudge Daniel Glicklich Ladan Golestaneh Division of Nephrology Department of Medicine Albert Einstein College of Medicine Montefiore Medical Center Bronx, NY James Pullman Department of Pathology Albert Einstein College of Medicine Montefiore Medical Center Bronx, NY
Seminars in DialysisVolume 9, Issue 1 p. 5-8 Should the Hepatitis C Positive End Stage Renal Disease Patient Be Transplanted? Daniel Glicklich, Corresponding Author Daniel Glicklich Division of Nephrology, Department of Medicine, Montefiore Medical Center and the Albert Einstein College of Medicine, Bronx, New YorkRenal Division, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467. Seminars in Dialysis–Vol 9, No 1 (Jan-Feb) 1996 pp 5–8Search for more papers by this authorToros Kapoian, Toros Kapoian Division of Nephrology, Department of Medicine, Montefiore Medical Center and the Albert Einstein College of Medicine, Bronx, New YorkSearch for more papers by this author Daniel Glicklich, Corresponding Author Daniel Glicklich Division of Nephrology, Department of Medicine, Montefiore Medical Center and the Albert Einstein College of Medicine, Bronx, New YorkRenal Division, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467. Seminars in Dialysis–Vol 9, No 1 (Jan-Feb) 1996 pp 5–8Search for more papers by this authorToros Kapoian, Toros Kapoian Division of Nephrology, Department of Medicine, Montefiore Medical Center and the Albert Einstein College of Medicine, Bronx, New YorkSearch for more papers by this author First published: January 1996 https://doi.org/10.1111/j.1525-139X.1996.tb00889.xCitations: 11AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Kirkman RL, Strom TB, Weir MR, Tilney NRL: Late mortality and morbidity in recipients of long-term renal allografts. Transplantation 34: 347–351, 1982. 10.1097/00007890-198212000-00007 PubMedWeb of Science®Google Scholar 2 Lefroncois N., Elmghabbar N., Chossegros P., Beutel H., Faure JL, Revillard JP, Traeger J., Duberhard JM, Torraine JL: Long term results in kidney transplantation: Patient and graft survival, causes of graft failure and mortality, renal function and complications after ten years. Transpl Proc 19: 3767–3768, 1987. Google Scholar 3 Rao KV, Anderson RC: Long-term results and complication in renal transplant recipients: observations in the second decade. Transplantation 45: 45–52, 1988. 10.1097/00007890-198801000-00011 CASPubMedWeb of Science®Google Scholar 4 Sengar DPS, Couture RA, Lazarovits AI: Long-term patient and renal allograft survival in HBsAg infection. Transpl Proc 21: 3358–3359, 1989. PubMedWeb of Science®Google Scholar 5 First MR: Long-term complications after transplantation. Am J Kidney Dis 22: 477–486, 1993. 10.1016/S0272-6386(12)70156-7 CASPubMedWeb of Science®Google Scholar 6 Caramelo C., Ortiz A., Aguilera B., Porres JC, Navas S., Marriott E., Alberola ML, Alamo C., Galera A., Garron MP, Gonzalez-Parra E., Fernandez de Gabriel MV, Oliva H., Carreno V.: Liver disease patterns in hemodialysis patients with antibodies to hepatitis C virus. Am J Kidney Dis 22: 822–828, 1993. 10.1016/S0272-6386(12)70341-4 PubMedWeb of Science®Google Scholar 7 Pol S., Romeo R., Zins B., Driss F., Lebkin B., Carnot F.: Hepatitis C virus RNA in anti-HCV positive hemodialyzed patients: significance and therapeutic implications. Kidney Int 44: 1097–1100, 1993. 10.1038/ki.1993.354 PubMedWeb of Science®Google Scholar 8 Kuhns M., de Medina M., McNamara A., Jeffers LJ, Reddy KR, Silva M., Ortiz L., Jiminez M., Schiff ER: Detection of hepatitis C virus RNA in hemodialysis patients. J Am Soc Nephrol 4: 1491–1497, 1994. CASPubMedWeb of Science®Google Scholar 9 Simon N., Courouce AM, Lemarreo N., Trepo C., Ducamp S.: A twelve year natural history of hepatitis C virus infection in hemodialyzed patients. Kidney Int 46: 504–511, 1994. 10.1038/ki.1994.301 CASPubMedWeb of Science®Google Scholar 10 Roth D.: Hepatitis C virus: The nephrologist's view. Am J Kidney Dis 25: 3–16, 1995. 10.1016/0272-6386(95)90617-7 PubMedWeb of Science®Google Scholar 11 Natov SN, Pereira BJG: Hepatitis C infection in patients on dialysis. Sem Dialysis 7: 360–368, 1994. 10.1111/j.1525-139X.1994.tb00855.x Web of Science®Google Scholar 12 Pereira BJG, Milford EL, Kirkman RL, Sayre KR, Johnson PJ, Wilber JL, Quan S., Levey AS: Prevalence of HCV RNA in hepatitis antibody positive cadaveric organ donors and their recipients. N Engl J Med 327: 910–915, 1992. 10.1056/NEJM199209243271302 PubMedWeb of Science®Google Scholar 13 Bukh J., Wantzin P., Krogsgaard K., Knudsen F., Purcell RH, Miller RH: High prevalence of hepatitis C virus RNA in dialysis patients: Significant number of patients with HCV infection. J Infect Dis 168: 1343–1348, 1993. 10.1093/infdis/168.6.1343 PubMedWeb of Science®Google Scholar 14 Chan T., Lok ASF, Chen IKP, Chan RT: A prospective study of hepatitis C virus infection among renal transplant recipients. Gastroenterology 104: 862–868, 1993. 10.1016/0016-5085(93)91023-B PubMedWeb of Science®Google Scholar 15 Alter MI, Margolis HS, Krawczynski K., Judson FN, Mares A., Alexander WJ, Hu Py, Miller JK, Gerber MA, Sampliner RE, Meeks EL, Beach MJ: The natural history of community-acquired hepatitis C in the United States. N Engl J Med 327: 1899–1905, 1992. 10.1056/NEJM199212313272702 CASPubMedWeb of Science®Google Scholar 16 Goffin E., Pirson Y., Cornu C., Gerbel A., Squifflet JP, Van Ypersele de Strihou C.: Outcome of HCV infection after renal transplantation. Kidney Int 45: 551–555, 1994. 10.1038/ki.1994.71 CASPubMedWeb of Science®Google Scholar 17 Meshari KA, Shaibani KA, Alfurayh O., Qunibi WY, Ali MA: Kidney Transplantation in HCV infected hemodialysis patients with mild hepatitis: a prospective controlled study of liver disease and graft function. J Am Soc Nephrol 5: 993, 1994. Google Scholar 18 Strauss RM, Gitlin N., Caudill M., Neylan IF, Nolte FS, Whelchel JD, Boyer TD: Chronic hepatitis C: A contraindication to renal transplantation? Hepatology 18: 344A, 1993. 10.1016/0270-9139(93)92900-K Web of Science®Google Scholar 19 Roth D., Zucker K., Cirocco R., DeMattos A., Burke GW, Nery J., Esquenazi V., Babischkin S., Miller J.: The impact of hepatitis C virus infection on renal allograft recipients. Kidney Int 45: 238–244, 1994. 10.1038/ki.1994.29 CASPubMedWeb of Science®Google Scholar 20 Dubois DB, Gretch D., del Rosa C., Lee W., Fine J., Blagg CR, Corey L.: Quantitation of hepatitis C viral RNA in sera of hemodialysis patients: Gender-related differences in viral load. Am J Kidney Dis 24: 795–801, 1994. 10.1016/S0272-6386(12)80673-1 PubMedWeb of Science®Google Scholar 21 Glicklich D., Reinus I., Greenstein S., Scheduler R., Mallis M., Clem-etson S., Tellis V.: Hepatitis C infection in renal transplant recipients: Histology and clinical features. J Am Soc Nephrol 5: 1007, 1994. Google Scholar 22 Kiyosawa K., Sodeyama T., Tanaka E., Gibo Y., Yoshikawa K., Nakano Y., Furuta S., Akahane Y., Nishioka K., Purcell RH, Alter HJ: Interrelations of blood transfusion, non-A non-B hepatitis and hepatocellular carcinoma: Analysis by detection of antibody to hepatitis C virus. Hepatology 12: 671–675, 1990. 10.1002/hep.1840120409 CASPubMedWeb of Science®Google Scholar 23 Tong MJ, El-Farra NS, Reikes AR, Co RL: Clinical outcomes after transfusion-associated Hepatitis C. N Engl J Med 332: 1463–1466, 1995. 10.1056/NEJM199506013322202 CASPubMedWeb of Science®Google Scholar 24 Stempel CA, Lake J., Kuo G., Vincenti F.: Hepatitis C–its prevalence in end-stage renal failure patients and clinical course after kidney-transplantation. Transplantation 55: 273–276, 1993. 10.1097/00007890-199302000-00008 CASPubMedWeb of Science®Google Scholar 25 Pol S., Legendre C., Saltiel C., Carnot F., Brechot C., Berthelot P., Mattlinger B., Kreis H.: Hepatitis C virus in kidney recipients: Epidemiology and impact on renal transplantation. J Hepatol 15: 202–206, 1992. 10.1016/0168-8278(92)90036-O CASPubMedWeb of Science®Google Scholar 26 Pol S., Hepatitis C virus infection in hemodialyzed patients and kidney allograft recipients. Advances in Nephrology 24: 315–330, 1995. CASPubMedGoogle Scholar 27 Pereira BJG, Milford EL, Kirkman RL, Levey AS: Transmission of hepatitis c virus by organ transplantation. N Engl J Med 325: 454–460, 1991. 10.1056/NEJM199108153250702 CASPubMedWeb of Science®Google Scholar 28 Alfurayh O., Sobh M., Buali AR, Ali MA, Barri Y., Qunibi W., Taher S.: Hepatitis C infection in chronic hemodialysis patients, a clinicopathologic study. Nephrol Dial Transplant 7: 327–332, 1992. 10.1093/oxfordjournals.ndt.a092137 PubMedWeb of Science®Google Scholar 29 Casanovas-Taltavull T., Baliellas C., Fernandez-Esparrach G., Rota R., Casas R., Benasco C., Grino JM, Andres E., Casais L., Liver biopsy in hemodialysis patients with chronic hepatitis C virus infection: A prospective study to determine the impact of liver injury severity on patients outcome. Hepatology 18: 326A, 1993. 10.1016/0270-9139(93)92829-O Web of Science®Google Scholar 30 Nieto J., Ferreras I., Mora F., Caparros G., Sanchez A., de la Torre M., Peces R.: Liver histopathological findings in hemodialysis patients with chronic hepatitis C virus infection. Nephrol Dial Transplant 8: 971, 1993. Google Scholar 31 Ozyilkan E., Akpolat T., Arik N., Koseoglo HT, Telatar H.: Characteristics of chronic hepatitis C virus infection in patients on maintenance hemodialysis. Nephrol Dial Transplant 9: 1697–1698 1994. CASPubMedWeb of Science®Google Scholar 32 Morales IM, Dominques P., Colina F., Lopez Carreira M., Castellano G., Fuertes A., Andres A., Fernandez G., Rodicio IL: Peculiarity of histological liver disease in hepatitis C infected kidney transplanted patients. J Am Soc Nephrol 5: 1025, 1994. Google Scholar 33 Morales IM, Munoz MA, Castellano G., Colina F., Fuertes A., Andres A., Campo C., Blasco A., Hernandez E., Rodicio IL: Impact of hepatitis C in long-functioning renal transplants–a clinicopathological follow up. Transplant Proc 25: 1450–1453, 1993. CASPubMedWeb of Science®Google Scholar 34 Chan TM, Wu PC, Lau JYN, Lai CL, Lok ASF, Cheng IKP: Clini-copathologic features of hepatitis C virus infection in renal allograft recipients. Transplantation 58: 996–1000, 1994. 10.1097/00007890-199411150-00004 CASPubMedWeb of Science®Google Scholar 35 Rao KV, Anderson WR, Kasiske BL: Value of liver biopsy in the evaluation and management of chronic liver disease in renal transplant recipients. Am J Med 94: 241–250, 1993. 10.1016/0002-9343(93)90055-T CASPubMedWeb of Science®Google Scholar 36 Simmonds P.: Variability of Hepatitis C virus. Hepatology 21: 570–583, 1995. 10.1002/hep.1840210243 CASPubMedWeb of Science®Google Scholar 37 Davis GL, Balart LA, Schiff ER, Lindsay K., Bodenheimer HC, Perrillo RP, Carey W., Jacobson IM, Payne J., Dienstag IL, Van Thiel DH, Tamburro C., Lefkowitch I., Albrecht I., Meschievitz C., Ortego TI, Gibas A.: Treatment of chronic hepatitis C with recombinant interferon alfa: a multicenter randomized controlled trial. N Engl J Med 321: 1501–1506, 1989. 10.1056/NEJM198911303212203 PubMedGoogle Scholar 38 Ohnishi K., Nomura F., Nakano M.: Interferon therapy for acute posttransfusion non-A, non-B hepatitis: Response with respect to anti-hepatitis C virus antibody status. Am J Gastroenterol 86: 1041–1049, 1991. PubMedWeb of Science®Google Scholar 39 Koenig P., Vogel W., UmLauft F., Weyrer K., Prommeggar R., Lhotta K., Neyer N., Stumavoll HK, Grunewald K.: Interferon treatment for chronic hepatitis C virus infection in uremic patients. Kidney Int 45: 1507–1509, 1994. 10.1038/ki.1994.197 PubMedWeb of Science®Google Scholar 40 Rao VK, Anderson WR: Effectiveness of alpha interferon treatment in altering the clinical and histological course of chronic viral hepatitis of ESRD patients awaiting renal transplantation. J Am Soc Nephrol 5: 1032, 1994. Web of Science®Google Scholar 41 Cerini R., Cozzolino G., Morante R., Lucariello A., De Rosa ML, Cacciatore F.: Relatively high dose for twelve months recombinant leukocyte interferon-alpha treatment in chronic hepatitis: A randomized controlled study. Hepatology 14: 70A, 1991. Web of Science®Google Scholar 42 Kovarik J., Mayer G., Pohanka E., Schwartz M., Traindl O., Graf H., Smolen I.: Adverse effect of low-dose prophylactic human recombinant leukocyte interferon-alpha treatment in renal transplant recipients. Transplantation 45: 402–405, 1988. 10.1097/00007890-198802000-00031 PubMedWeb of Science®Google Scholar 43 Kramer P., Ten Kate FWI, Bijnen AB, Jeekel J., Weimer W.: Recombinant leukocyte interferon A induces steroid-resistant acute vascular rejection episodes in renal transplant recipients. Lancet 1: 989–990, 1984. 10.1016/S0140-6736(84)92327-4 CASPubMedWeb of Science®Google Scholar 44 Rostaing L., Baron E., Modesto A., Girolami JP, Durand D., Sue JM: Renal failure in renal transplant patients treated with interferon A for chronic hepatitis C. J Am Soc Nephrol 5: 1034, 1994. Google Scholar 45 Rhodes J., Jones DH, Bleeher NM: Increased expression of human monocyte HLA-DR antigens and Fc receptors in response to human interferon in vivo. Clin Exp Immunol 53: 739–744, 1983. CASPubMedWeb of Science®Google Scholar Citing Literature Volume9, Issue1January 1996Pages 5-8 ReferencesRelatedInformation