Sergey V Brodsky

The Ohio State University, Columbus, Ohio, United States

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Publications (92)400.99 Total impact

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    ABSTRACT: Immunofluorescence staining plays a vital role in nephropathology, but the panel of antibodies used has not changed for decades. Further classification of immunoglobulin (Ig)G-containing immune-type deposits with IgG subclass staining (IgG1, IgG2, IgG3, and IgG4) has been shown to be of diagnostic utility in glomerular diseases, but their value in the evaluation of renal biopsies has not been addressed systematically in large renal biopsy material. Between January 2007 and June 2014, using direct immunofluorescence, we stained every renal biopsy for the IgG subclasses if there was moderate to prominent glomerular IgG staining and/or IgG-predominant or IgG-codominant glomerular staining. The total number of biopsies stained was 1084, which included 367 cases of membranous glomerulonephritis, 307 cases of lupus nephritis, 74 cases of fibrillary glomerulonephritis, 53 cases of proliferative glomerulonephritis with monoclonal IgG deposits, and 25 cases of antiglomerular basement membrane disease, among others. We found that monoclonality of IgG deposits cannot always be reliably determined on the basis of kappa and lambda light chain staining alone, particularly if concomitant (frequently nonspecific) IgM staining is present. In IgG heavy and heavy and light chain deposition disease (3 cases), subclass staining is very helpful, and in proliferative glomerulonephritis with monoclonal IgG deposits subclass staining is necessary. IgG subclass staining is useful in differentiating primary from secondary membranous glomerulonephritis. In proliferative glomerulonephritis with polyclonal IgG deposition, IgG1 dominance/codominance with concomitant IgG3 and IgG2 but weak or absent IgG4 staining favors an underlying autoimmune disease. IgG subclass staining is a very useful diagnostic method in a selected cohort of renal biopsies, particularly in biopsies with glomerulonephritis with monoclonal IgG deposits.
    No preview · Article · Feb 2016 · The American journal of surgical pathology
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    ABSTRACT: Background: It is well-established from autopsy studies that gouty tophi can form in the kidney, particularly in the renal medulla. Recently hyperuricemia has been identified as a risk factor for progression of chronic kidney disease (CKD). Because each collecting duct serves more than 2,000 nephrons, we postulated that obstruction or disruption of collecting ducts by medullary tophi may explain, at least in part, the association between hyperuricemia and progressive CKD. This work was done to determine the prevalence of medullary tophi in CKD patients. Methods: We queried our nephropathology database over the last 10 years for native kidney biopsies that had medullary tophi. The presence or absence of CKD and uric acid levels around the time of biopsy were determined by chart review. Results: Predominant medullary tissue was reported in 796 of 7,409 total biopsies, and 572 of these were from patients with established CKD. Medullary tophi were seen in 36 patients, 35 of whom had CKD, suggesting a minimum prevalence of tophi in CKD and no-CKD of 6.11 and 0.45%, respectively Medullary tophi occurred with and without hyperuricemia or a history of gout. Conclusion: Medullary tophi appear to be far more likely to occur in CKD compared to no-CKD patients. This cross-sectional study cannot determine whether medullary tophi are a cause or consequence of CKD. However, given their location and bulk, it is possible that medullary tophi contribute to progression of established CKD by causing upstream nephron damage.
    No preview · Article · Dec 2015 · Clinical nephrology
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    ABSTRACT: Brodifacoum (BDF) is a superwarfarin that is used primarily as a rodenticide. There have been increasing numbers of reports of human cases of accidental or intentional BDF ingestion with high mortality rate. Its broad availability and high lethality suggest that BDF should be considered a potential chemical threat. Currently, there is no biomarker for early detection of BDF ingestion in humans; patients typically present with severe coagulopathy. Since we demonstrated earlier that warfarin can induce acute kidney injury with hematuria, we tested whether BDF would also lead to change in urinary biomarkers. BDF was administered to Sprague Dawley rats via oral gavage. N-acetylcysteine (NAC) was given per os in drinking water 24 h prior to BDF. Urinalysis was performed at different times after BDF administration. Anticoagulation and serum creatinine levels were analyzed in the blood. We observed that within a few hours the animals developed BDF-dose-dependent transient hemoglobinuria, which ceased within 24 h. This was accompanied by a transient decrease in hematocrit, gross hemolysis and an increase in free hemoglobin in the serum. At later times, animals developed true hematuria with red blood cells in the urine, which was associated with BDF anticoagulation. NAC prevented early hemoglobinuria, but not late hematuria associated with BDF. We propose that transient early hemoglobinuria (associated with oxidative stress) with consecutive late hematuria (associated with anticoagulation) are novel biomarkers of BDF poisoning, and they can be used in clinical setting or in mass casualty with BDF to identify poisoned patients. © 2015 S. Karger AG, Basel.
    No preview · Article · Jun 2015 · American Journal of Nephrology
  • I. Ayoub · L. Hebert · B. Rovin · S. Brodsky · T. Nadasdy

    No preview · Conference Paper · Apr 2015
  • Source
    Sergey V. Brodsky
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    ABSTRACT: We have recently identified a new clinical syndrome in patients receiving warfarin for anticoagulation therapy. This syndrome has been named warfarin-related nephropathy (WRN), and patients with chronic kidney disease (CKD) appear to be particularly susceptible. WRN is defined as an acute increase in international normalized ratio (INR) to > 3.0, followed by evidence of acute kidney injury (AKI) within 1 week of the INR increase. AKI was defined as a sustained increase in serum creatinine of greater than or equal to 0.3 mg/dL. The AKI cannot be explained by any other factors, and the kidney biopsy demonstrates extensive glomerular hemorrhage with tubular obstruction by red blood cells (RBCs). Beyond AKI, WRN is a significant risk factor for mortality within the first 2 months of diagnosis and it accelerates the progression of CKD. We demonstrated that 5/6 nephrectomy in rats is a suitable experimental model to study WRN. Animals treated with warfarin showed an increase in serum creatinine and morphologic findings in the kidney similar to those in humans with WRN. Our recent evidence suggests that novel oral anticoagulants may induce AKI. Diagnosis of WRN may be challenging for a renal pathologist. A few cases with suspected WRN and pathologic considerations are described.
    Preview · Article · Nov 2014
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    ABSTRACT: Background: Hypertension is a common comorbidity in patients with chronic kidney disease (CKD). We reported earlier that oral anticoagulants, including warfarin and dabigatran, may induce acute kidney injury. No effects of oral anticoagulants on blood pressure (BP) have been previously reported. The aim of this study was to examine in detail the relationship of anticoagulant therapy and BP in rats. Methods: Sham-operated and 5/6 nephrectomy rats were treated with different doses of oral anticoagulants (warfarin and dabigatran), superoxide scavenger N-acetylcysteine (NAC), vitamin K, and protease activated receptor 1 (PAR-1) inhibitor SCH79797. BP was measured by a tail cuff daily. Results: Warfarin and dabigatran both increased systolic BP in sham-operated and 5/6 nephrectomy rats in a dose-dependent manner. SCH79797 also increased systolic BP in a dose-dependent manner. Vitamin K prevented warfarin-induced increase in BP but did not affect BP when administered alone. NAC delayed the warfarin-associated increase in BP. Warfarin effects on BP were similar in 5/6 nephrectomy rats with different CKD stages. Conclusions: Both warfarin and dabigatran increase systolic BP in rats. The mechanism of this effect is not clear, but our data suggest that it is related to decreased thrombin activity associated with anticoagulant treatment. The superoxide scavenger NAC delayed, but did not prevent, warfarin-induced hypertension.
    No preview · Article · Jul 2014 · American Journal of Hypertension
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    ABSTRACT: Background: Endothelial microparticles (EMPs) are membrane vesicles shed from endothelial cell in response to injury, activation or apoptosis. Kidney transplantation (KTx) is the treatment of choice for patients with end stage kidney disease (ESKD). The aim of this study was to analyze changes in EMP and serum creatinine (SCr) in patients following KTx. Methods: Blood was periodically collected from patients before (pre-KTx) and after KTx for two months. EMPs were identified as CD31(+)/CD42b(-) microparticles and quantified by fluorescence-activated cell scanning. Results: This study included 213 KTx, 14 kidney/pancreas (KPTx) recipients and 60 healthy donors prior to donation. The recipients were divided into 5 groups based on the cause of ESKD. No differences in the quantity of circulating EMP were seen in the pre-KPTx or KTx recipient sera and healthy donor sera. Patients with ESKD secondary to diabetes mellitus, obstructive/inherited kidney disease and autoimmune disease had a decrease in both circulating EMP and SCr by day 60 after KTx. Conclusion: Reduction in both circulating EMP and SCr was seen after kidney KTx in patients with selective ESKD.
    No preview · Article · Jul 2014 · Transplant Immunology
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    ABSTRACT: Owing to the need of lifelong immunosuppression, solid-organ transplant recipients are known to have an increased risk of posttransplant malignancies including lung cancer. Posttransplant neoplastic transformation of donor-derived cells giving rise to hematopoietic malignancies, Kaposi sarcoma, and basal cell carcinoma in nongraft tissues has been reported. The goal of this study was to assess the cell origin (donor versus recipient derived) of posttransplant non-small cell lung carcinomas (NSCLCs) in kidney and heart transplant recipients. An institutional database search identified 2557 kidney and heart transplant recipients in 8 consecutive years. Among this cohort, 20 (0.8%) renal and 18 (0.7%) heart transplant recipients developed NSCLC. The study cohort comprised 6 of 38 NSCLCs arising in donor-recipient sex-mismatched transplant patients. The tumor cell origin was evaluated by chromogenic in situ hybridization with Y-chromosome probe on formalin-fixed, paraffin-embedded tissues. Y-chromosome was identified in 97% ± 1% (range from 92% to 99%) of all types of nucleated cells in male control tissues. In all 5 NSCLCs from male recipients of female donor organ, Y-chromosome was identified in 97% ± 2% (range from 92% to 100%) of tumor cells, statistically equivalent to normal control (P < .001). No Y-chromosome was identified in NSCLC cells from a female recipient of male kidney. These findings suggest a recipient derivation of NSCLC arising in kidney and heart transplant recipients. A combination of histologic evaluation and chromogenic in situ hybridization with Y-chromosome analysis allows reliable determination of tissue origin in sex-mismatched solid-organ transplant recipients and may aid in management of posttransplant malignancy in such cases.
    No preview · Article · May 2014 · Human pathology
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    ABSTRACT: Acute pyelonephritis (APN) versus acute rejection (AR) is a frequently encountered diagnostic and therapeutic dilemma in kidney transplants. Variable culture results, overlapping histologic features, and persistent graft dysfunction despite antibiotics are frequently encountered. Therefore, we explored the utility of intragraft microRNA profiles to distinguish between allograft APN and AR. Between 2003 and 2011, we identified 49 patients with biopsy features of APN, within the first 2 years posttransplant. MicroRNA profiling was performed on 20 biopsies (normal kidney, n=4; unequivocal AR, n=5; features of APN, n=11). Only 32% (16/49) of the patients had concomitant positive urine cultures at biopsy, and in 8 of 16 patients, colony count was less than 10 CFU/mL. In 14 of 49 patients, positive urine culture did not coincide with the biopsy, and in 19 of 49 patients, urine cultures were negative. On microRNA profiling, good clustering was seen among the normal kidneys and among AR biopsies. Among the 11 biopsies with features of APN, 4 biopsies showed good clustering with a pattern distinct from AR; (these patients recovered graft function with antibiotics); 7 of 11 biopsies showed heterogeneity in microRNA profiles and variable outcomes with antibiotic treatment. We identified a panel of 25 microRNAs showing statistical difference in expression between AR and APN. MiR-99b, miR-23b let-7b-5p, miR-30a, and miR-145 were validated using qPCR. Allograft pyelonephritis can be a diagnostic and therapeutic challenge. A gestalt approach is required. In addition to histology and cultures, differential intragraft microRNA expression may prove helpful to distinguish APN from AR in renal allograft biopsies.
    No preview · Article · Feb 2014 · Transplantation
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    ABSTRACT: We utilized mouse models to elucidate the immunologic mechanisms of functional graft loss during mixed antibody-mediated rejection of renal allografts (mixed AMR), in which humoral and cellular responses to the graft occur concomitantly. Although the majority of T cells in the graft at the time of rejection were CD8 T cells with only a minor population of CD4 T cells, depletion of CD4 but not CD8 cells prevented acute graft loss during mixed AMR. CD4 depletion eliminated antidonor alloantibodies and conferred protection from destruction of renal allografts. ELISPOT revealed that CD4 T effectors responded to donor alloantigens by both the direct and indirect pathways of allorecognition. In transfer studies, CD4 T effectors primed to donor alloantigens were highly effective at promoting acute graft dysfunction, and exhibited the attributes of effector T cells. Laser capture microdissection and confirmatory immunostaining studies revealed that CD4 T cells infiltrating the graft produced effector molecules with graft destructive potential. Bioluminescent imaging confirmed that CD4 T effectors traffic to the graft site in immune replete hosts. These data document that host CD4 T cells can promote acute dysfunction of renal allografts by directly mediating graft injury in addition to facilitating antidonor alloantibody responses.
    No preview · Article · Jan 2014 · American Journal of Transplantation

  • No preview · Article · Jan 2014
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    ABSTRACT: Excessive anticoagulation with warfarin can result in acute kidney injury (AKI) by causing glomerular hemorrhage and renal tubular obstruction by red blood cell (RBC) casts in some patients, especially in those with chronic kidney disease (CKD). This condition was described as warfarin-related nephropathy (WRN). Recent evidence suggests that WRN-like syndromes are not confined to anticoagulation with warfarin, but may be seen with other anticoagulants, such as dabigatran. The aim of this study was to investigate dabigatran effects on kidney function in an animal model of CKD and possible pathogenic mechanisms of AKI. Control and 5/6 nephrectomy rats were treated with different doses of dabigatran and protease-activated receptor 1 (PAR-1) inhibitor SCH79797. Dabigatran resulted in changes in coagulation in rats similar to those in humans at 50 mg/kg/day. Dabigatran resulted in a dose-dependent increase in serum creatinine (Scr) and hematuria in both control and 5/6 nephrectomy rats. SCH79797 also increased Scr and hematuria, more prominent in animals with CKD. Morphologically, numerous RBC tubular casts were seen in 5/6 nephrectomy rats treated with either dabigatran or SCH79797 and only occasional RBC casts in control rats. Our data indicate that WRN represents part of a broader syndrome, anticoagulant-related nephropathy (ARN). ARN, at least partially, is mediated via PAR-1. Our findings suggest that not only CKD patients, but other patients as well, are at high risk of developing AKI if the therapeutic range of anticoagulation with dabigatran is exceeded. Close monitoring of kidney function in patients on dabigatran therapy is warranted.
    No preview · Article · Sep 2013 · Nephrology Dialysis Transplantation
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    ABSTRACT: Amyloid light chain amyloidosis involving the kidneys is not uncommon in patients with monoclonal gammopathy. The mainstay of treatment of amyloid light chain amyloidosis is autologous hematopoietic stem cell transplantation. Evidence that the autologous hematopoietic stem cell transplantation has been successful is the absence of free monoclonal light chains in serum and urine. Herein, we report 2 cases of progressive renal amyloid light chain amyloidosis after autologous hematopoietic stem cell transplantation, documented by kidney biopsy, despite the absence of monoclonal protein in the serum and urine. Kidney function declined progressively in both patients. During that time, numerous immunofixation and protein electrophoresis test results were negative for monoclonal protein, both in serum and urine, concealing the progression of the amyloidosis. We conclude that close monitoring of kidney function is warranted following autologous hematopoietic stem cell transplantation in patients with amyloid light chain amyloidosis, even with negative results from monoclonal protein testing. Unexplained, worsening renal function warrants a kidney biopsy to assess whether retreatment of the monoclonal gammopathy is indicated.
    No preview · Article · Sep 2013 · Archives of pathology & laboratory medicine
  • S. Brodsky · A. Satoskar · L. Hebert · T. Nadasdy

    No preview · Article · Aug 2013 · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin
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    ABSTRACT: Warfarin related nephropathy (WRN) occurs under conditions of over-anticoagulation with warfarin. WRN is characterized by glomerular hemorrhage with occlusive tubular red blood cell (RBC) casts and acute kidney injury (AKI). Herein we test the hypothesis that oxidative stress plays a role in the AKI of WRN. 5/6 nephrectomy rats were treated with either warfarin (0.04 mg/kg/day) alone or with 4 different doses of the antioxidant N-acetylcysteine (NAC). Also, tested was the ability of our NAC regimen to mitigate AKI in a standard ischemia/reperfusion model in the rat. Warfarin resulted in a 3-fold or greater increase in PT in each experimental group. Scr increased progressively in animals receiving only warfarin + vehicle. However, in animals receiving warfarin + NAC, the increase in Scr was lessened, starting at NAC 40 mg/kg/day, and completely prevented at NAC 80 mg/kg/day. NAC did not decrease hematuria or obstructive RBC casts, but mitigated acute tubular injury. Oxidative stress in the kidney was increased in animals with WRN and it was decreased by NAC. The NAC regimen used in the WRN model preserved kidney function in the ischemia/reperfusion model. Treatment with deferoxamine (iron chelator) did not affect WRN. No iron was detected in tubular epithelial cells. In conclusion, this work taken together with our previous work in WRN models shows that glomerular hematuria is a necessary but not sufficient explanation for the AKI in WRN. The dominant mechanism of the AKI of WRN is tubular obstruction by RBC casts with increased oxidative stress in the kidney.
    Preview · Article · Apr 2013 · AJP Renal Physiology
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    ABSTRACT: Background: Kidney biopsy is a vital tool in the diagnosis of kidney disease. Although it has become a routine procedure, it is not complication-free. Some serious complications of percutaneous kidney biopsy include retroperitoneal hemorrhage and death. There is an increased belief that smaller biopsy needle size results in a lower complication rate. As renal pathologists, we witness an increased number of kidney biopsies performed with a small needle size (as low as gauge 22), which results in inadequate tissue sampling and often non-diagnostic biopsy results. Herein we report the diagnostic value of kidney biopsies according to the size of the biopsy needles. Methods: We performed kidney biopsies from nephrectomy specimens using biopsy needles of different sizes. Morphologic parameters were analyzed. Results: We found that biopsies performed by small needles (gauges 20 and 22) contain significantly lower numbers of glomeruli and blood vessels, which limits pathologic evaluation. Data from our institution do not show differences in kidney biopsy complication rates between 16- and 18-gauge needles. Conclusions: Our data indicate that small biopsy needles do not provide sufficient material for diagnosis, and they increase the likelihood for a repeat biopsy.
    No preview · Article · Mar 2013 · American Journal of Nephrology
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    ABSTRACT: Recent breakthrough findings revealed that most patients with idiopathic (primary) membranous glomerulonephritis have IgG4 antibodies to the phospholipase A2 receptor (PLA2R). These IgG4 antibodies can be detected in the glomerular immune complexes and they colocalize with PLA2R. In secondary forms of membranous glomerulonephritis, such IgG4 antibodies are absent or less prevalent. There are no studies addressing the IgG subclass distribution across different stages of membranous glomerulonephritis. During a 25-month period, we identified 157 consecutive biopsies with membranous glomerulonephritis with adequate tissue for light, immunofluorescence and electron microscopy. Of the 157 membranous glomerulonephritis cases, 114 were primary membranous glomerulonephritis and 43 were secondary membranous glomerulonephritis. We compared the intensity of IgG subclass staining (on a semiquantitative scale of 0 to 3+) and the IgG subclass dominance between primary and secondary membranous glomerulonephritis and between the different stages of membranous glomerulonephritis. In primary membranous glomerulonephritis most (76% of cases) were IgG4 dominant. In contrast, in secondary membranous glomerulonephritis IgG1 was dominant in 60% of biopsies (P=0.0018). Interestingly, in early stage (stage 1) primary membranous glomerulonephritis, IgG1 was the dominant IgG subclass (64% of cases); in all later stages IgG4 dominated (P=0.0493). It appears that there is an inverse relationship between the intensity of glomerular capillary IgG4 and C1q staining. In secondary forms of membranous glomerulonephritis (heterogeneous group with low case numbers), we did not find such associations. Our data indicate that in early stage membranous glomerulonephritis, antibody response is different from later stages, with IgG1 dominant deposits. It is possible that early on, antigens other than PLA2R have an important role, Alternately, there may be an IgG subclass switch in the antibody response with IgG4 taking over later as the dominant immunoglobulin.Modern Pathology advance online publication, 18 January 2013; doi:10.1038/modpathol.2012.237.
    No preview · Article · Jan 2013 · Modern Pathology
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    ABSTRACT: Background: In children and adults, Henoch-Schönlein purpura (HSP) has a characteristic clinical presentation that includes a purpuric lower extremity skin rash, IgA-dominant glomerulonephritis, and abdominal and joint pain. A similar clinical presentation can be seen in adults who have a systemic infection with methicillin-resistant Staphylococcus aureus. It is critically important to distinguish the IgAdominant glomerulonephritis of HSP from the IgA-dominant glomerulonephritis of staphylococcal infection, because HSP may need to be treated with corticosteroids and immunosuppressives, while Staphylococcus infection-associated glomerulonephritis requires antibiotics. Design: We searched our renal biopsy database for cases of Staphylococcus infection-associated IgA-dominant glomerulonephritis, to identify those with an HSP-like presentation. Their clinical, laboratory, and biopsy findings are reviewed. Results: Between 2004 and 2011, we identified 37 patients with culture-proven Staphylococcus infection-associated glomerulonephritis. Of these, 8 (22%) had an HSP-like presentation manifested by lower extremity purpuric skin rash. Mesangial IgA and C3 deposits were consistent findings on kidney biopsy. Crescents were uncommon. Four of the 8 patients received glucocorticoid (steroid) therapy for a presumed diagnosis of HSP. Renal function worsened in 3 patients, and 1 patient ultimately improved but developed sepsis during the course. Overall, renal outcome was poor in 71% of the cases despite mild chronic renal injury in the biopsy. Conclusion: In adult patients with an HSPlike presentation, a high index of suspicion for underlying Staphylococcal infection is warranted. Blood cultures are frequently negative. Cultures from the site of infection should be performed. Steroid treatment did not improve outcomes. Renal outcomes were frequently poor.
    No preview · Article · Jan 2013 · Clinical nephrology
  • Anthony S Alvarado · Sergey V Brodsky · Tibor Nadasdy · Neeraj Singh
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    ABSTRACT: We report 3 cases of Clostridium difficile-associated hemolytic uremic syndrome (HUS) with biopsy proven renal thrombotic microangiopathy. Two patients with acute renal failure were kidney transplants recipients whereas the third patient developed renal failure in the native kidneys. The presentation was preceded by acute diarrhea and stool. Clostridium difficile toxin was detected in all the 3 patients. Stool studies were negative for Escherichia coli, Shigella dysenteriae and other enteric pathogens. The diagnosis of Clostridium difficile-associated hemolytic uremic syndrome was suspected due to presence of thrombocytopenia, microangiopathic hemolytic anemia and biopsy proven renal thrombotic microangiopathy without another clinically apparent cause. This case series suggest that Clostridium difficile infection may cause renal failure due to thrombotic microangiopathy (TMA) and should be considered in the differential diagnosis of diarrhea-associated HUS.
    No preview · Article · Jan 2013 · Clinical nephrology
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    ABSTRACT: The use of digital whole slide images (WSI) in the field of pathology has become feasible for routine diagnostic purposes and has become more prevalent in recent years. This type of technology offers many advantages but must show the same degree of diagnostic reliability as conventional glass slides. Several studies have examined this issue in various settings and indicate that WSI are a reliable method for diagnostic pathology. Since transplant pathology is a highly specialized field that requires not only accurate but rapid diagnostic evaluation of biopsy materials, this field may greatly benefit from the use of WSI. In this study, we assessed the reliability of using WSI compared to conventional glass slides in renal allograft biopsies. We examined morphologic features and diagnostic categories defined by the Banff 07 Classification of Renal Allograft Pathology as well as additional morphologic features not included in this classification scheme. We found that intraobserver scores, when comparing the use of glass slides versus WSI, showed substantial agreement for both morphologic features (κ = 0.68) and acute rejection diagnostic categories (κ = 0.74). Furthermore, interobserver reliability was comparable for morphologic features (κ = 0.44 [glass] vs 0.42 [WSI]) and acute rejection diagnostic categories (κ = 0.49 [glass] vs 0.51 [WSI]). These data indicate that WSI are as reliable as glass slides for the evaluation of renal allograft biopsies.
    No preview · Article · Nov 2012 · Human pathology

Publication Stats

4k Citations
400.99 Total Impact Points


  • 2008-2015
    • The Ohio State University
      • Pathology
      Columbus, Ohio, United States
  • 2002-2009
    • New York Medical College
      • • Department of Medicine
      • • Department of Pathology
      New York City, New York, United States
    • Vrije Universiteit Brussel
      • Cell Biology and Histology (CYTO)
      Bruxelles, Brussels Capital, Belgium
    • Kawasaki Medical University
      • Department of Medical Engineering
      Kurasiki, Okayama, Japan
  • 2004-2008
    • Renal Research Institute
      New York, New York, United States
    • Cornell University
      Итак, New York, United States
  • 2003
    • Yale University
      New Haven, Connecticut, United States
  • 2000-2002
    • State University of New York
      New York City, New York, United States
  • 2001
    • The University of Tokyo
      • Department of Neurology
      白山, Tōkyō, Japan