Brad H Rovin

The Ohio State University, Columbus, Ohio, United States

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Publications (179)1153.39 Total impact

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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.
    American Journal of Nephrology 06/2015; 41(4-5):392-399. DOI:10.1159/000433568 · 2.65 Impact Factor
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    ABSTRACT: Idiopathic membranous nephropathy remains the leading cause of nephrotic syndrome in Caucasian adults. Immunosuppressive therapy with cyclosporine (CSA) is often successful in reducing proteinuria, but its use is associated with a high relapse rate. Rituximab, a monoclonal antibody that specifically targets CD20 on the surface of B-cells, is effective in achieving a complete remission of proteinuria in patients with idiopathic membranous nephropathy. However, whether rituximab is as effective as CSA in inducing and maintaining complete or partial remission of proteinuria in these patients is unknown. The membranous nephropathy trial of rituximab (MENTOR) hypothesizes that B-cell targeting with rituximab is non-inferior to CSA in inducing long-term remission of proteinuria. Patients with idiopathic membranous nephropathy, proteinuria ≥5 g/24 h, and a minimum of 3 months of Angiotensin-II blockade will be randomized into a 12-month treatment period with IV rituximab, 1,000 mg (2 infusions, 14 days apart; repeated at 6 months if a substantial reduction in proteinuria (equal to or >25%) is seen at 6 months) or oral CSA 3.5-5 mg/kg/day for 6 months (continued for another 6 months if a substantial reduction in proteinuria (equal to or >25%) is seen at 6 months). The efficacy of treatment will be assessed by the remission status (based on changes in proteinuria) at 24 months from randomization. Patient safety will be assessed via collection of adverse event data and evaluation of pre- and posttreatment laboratory data. At the 6-month post-randomization visit, patients who have been randomized to either CSA or rituximab but who do not have a reduction in proteinuria ≥25% (confirmed on repeat measurements within 2 weeks) will be considered treatment failures and exit the study. This study will test for the first time whether treatment with rituximab is non-inferior to CSA in inducing long-term remission (complete or partial) of proteinuria in patients with idiopathic membranous nephropathy. © 2015 S. Karger AG, Basel.
    06/2015; DOI:10.1159/000430849
  • Brad H Rovin, Jon B Klein
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    ABSTRACT: Proteomics has long been considered an ideal platform, and urine an ideal source for biomarker discovery in human autoimmune kidney diseases. A number of studies have examined the urine proteome to identify biomarkers of disease activity, kidney pathology, and response to therapy. Increasingly, proteomic studies of kidney disease have expanded to include blood, circulating cells and kidney tissue. Recently the clinical potential of renal proteomics has been realized through a handful of investigations whose results appear to be applicable to patient care. In this review, approaches to the proteomic evaluation of autoimmune kidney diseases will be considered in the context of developing clinically useful disease biomarkers. Copyright © 2015. Published by Elsevier Inc.
    Clinical Immunology 05/2015; DOI:10.1016/j.clim.2015.04.021 · 3.99 Impact Factor
  • Brad H Rovin, Isabelle Ayoub
    Nature Reviews Nephrology 04/2015; DOI:10.1038/nrneph.2015.65 · 8.37 Impact Factor
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    ABSTRACT: A spate of recent publications describes a newly recognized form of glomerulonephritis associated with active staphylococcal infection. The key kidney biopsy findings, glomerular immunoglobulin A (IgA) deposits dominant or codominant with IgG deposits, resemble those of IgA nephritis. Many authors describe this condition as "postinfectious" and have termed it "poststaphylococcal glomerulonephritis." However, viewed through the prism of poststreptococcal glomerulonephritis, the prefix "post" in poststaphylococcal glomerulonephritis is historically incorrect, illogical, and misleading with regard to choosing therapy. There are numerous reports describing the use of high-dose steroids to treat poststaphylococcal glomerulonephritis. The decision to use steroid therapy suggests that the treating physician believed that the dominant problem was a postinfectious glomerulonephritis, not the infection itself. Unfortunately, steroid therapy in staphylococcus-related glomerulonephritis can precipitate severe staphylococcal sepsis and even death and provides no observable benefits. Poststreptococcal glomerulonephritis is an authentic postinfectious glomerulonephritis; poststaphylococcal glomerulonephritis is not. Making this distinction is important from the perspective of history, pathogenesis, and clinical management. Copyright © 2015 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
    American Journal of Kidney Diseases 04/2015; 65(6). DOI:10.1053/j.ajkd.2015.01.023 · 5.76 Impact Factor
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    ABSTRACT: Significant advances are needed to improve the diagnosis, prognosis, and management of persons with CKD. Discovery of new biomarkers and improvements in currently available biomarkers for CKD hold great promise to achieve these necessary advances. Interest in identification and evaluation of biomarkers for CKD has increased substantially over the past decade. In 2009, the National Institute of Diabetes and Digestive and Kidney Diseases established the CKD Biomarkers Consortium (, a multidisciplinary, collaborative study group located at over a dozen academic medical centers. The main objective of the consortium was to evaluate new biomarkers for purposes related to CKD in established prospective cohorts, including those enriched for CKD. During the first 5 years of the consortium, many insights into collaborative biomarker research were gained that may be useful to other investigators involved in biomarkers research. These lessons learned are outlined in this Special Feature and include a wide range of issues related to biospecimen collection, storage, and retrieval, and the internal and external quality assessment of laboratories that performed the assays. The authors propose that investigations involving biomarker discovery and validation are greatly enhanced by establishing and following explicit quality control metrics, including the use of blind replicate and proficiency samples, by carefully considering the conditions under which specimens are collected, handled, and stored, and by conducting pilot and feasibility studies when there are concerns about the condition of the specimens or the accuracy or reproducibility of the assays. Copyright © 2015 by the American Society of Nephrology.
    Clinical Journal of the American Society of Nephrology 03/2015; 10(5). DOI:10.2215/CJN.11541114 · 5.25 Impact Factor
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    ABSTRACT: Patients with systemic lupus erythematosus (SLE) frequently develop lupus nephritis (LN), a complication frequently leading to end stage kidney disease. Immune complex deposition in the glomerulus is central to the development of LN. Using a targeted proteomic approach, we tested the hypothesis that autoantibodies targeting glomerular antigens contribute to the development of LN. Human podocyte and glomerular proteins were separated by SDS-PAGE and immunoblotted with sera from SLE patients with and without LN. The regions of those gels corresponding to reactive bands observed with sera from LN patients were analyzed using LC-MS/MS. LN reactive bands were seen at approximately 50 kDa in podocyte extracts and between 36-50 kDa in glomerular extracts. Those bands were analyzed by LC-MS/MS and 102 overlapping proteins were identified. Bioinformatic analysis determined that 36 of those proteins were membrane associated, including a protein previously suggested to contribute to glomerulonephritis and LN, annexin A2. By ELISA, patients with proliferative LN demonstrated significantly increased antibodies against annexin A2. Proteomic approaches identified multiple candidate antigens for autoantibodies in patients with LN. Serum antibodies against annexin A2 were significantly elevated in subjects with proliferative LN, validating those antibodies as potential biomarkers. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    PROTEOMICS - CLINICAL APPLICATIONS 03/2015; DOI:10.1002/prca.201400175 · 2.68 Impact Factor
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    ABSTRACT: Urinary monocyte chemoattractant protein-1 (MCP-1) and hepcidin are potential biomarkers of renal inflammation. We examined their association with development of diabetic nephropathy (DN) lesions in normotensive normoalbuminuric subjects with type 1 diabetes (T1D) from the Renin-Angiotensin System Study. Biomarker concentrations were measured in baseline urine samples from 224 subjects who underwent kidney biopsies at baseline and after 5 years. Fifty-eight urine samples below the limit of quantitation (LOQ, 28.8 pg/mL) of the MCP-1 assay were assigned concentrations of LOQ/√2 for analysis. Relationships between ln(MCP-1/Cr) or ln(hepcidin/Cr) and morphometric variables were assessed by sex using multiple linear regression after adjustment for age, T1D duration, HbA1c, mean arterial pressure, albumin excretion rate (AER) and glomerular filtration rate (GFR). In models that examined changes in morphometric variables, the baseline morphometric value was also included. Baseline mean age was 24.6 years, mean duration of T1D 11.2 years, median AER 6.4 µg/min and mean iohexol GFR 129 mL/min/1.73 m(2). No associations were found between hepcidin/Cr and morphometric variables. Higher MCP-1/Cr was associated with higher interstitial fractional volume at baseline and after 5 years in women (baseline partial r = 0.244, P = 0.024; 5-year partial r = 0.299, P = 0.005), but not in men (baseline partial r = -0.049, P = 0.678; 5-year partial r = 0.026, P = 0.830). MCP-1 was not associated with glomerular lesions in either sex. Elevated urinary MCP-1 concentration measured before clinical findings of DN in women with T1D was associated with changes in kidney interstitial volume, suggesting that inflammatory processes may be involved in the pathogenesis of early interstitial changes in DN. Published by Oxford University Press on behalf of ERA-EDTA 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US.
    Nephrology Dialysis Transplantation 02/2015; DOI:10.1093/ndt/gfv012 · 3.49 Impact Factor
  • New England Journal of Medicine 01/2015; 372(4):385. DOI:10.1056/NEJMc1414728#SA1 · 54.42 Impact Factor
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    ABSTRACT: Objective: There is a need to determine which response measures in lupus nephritis trials are most predictive of good long-term renal function. We utilized data from the Euro-Lupus Nephritis Trial (ELNT) to evaluate the performance of proteinuria, serum creatinine (SCr), and urine red blood cells (RBCs) as predictors of good long-term renal outcome. Methods: ELNT subjects with measures of proteinuria, SCr, and urine RBCs at 3, 6 or 12 months and a minimum 7 year follow-up were included (n=76). We assessed the ability of these clinical biomarkers at 3, 6, and 12 months after randomization to predict good long-term renal outcome (defined as SCr ≤ 1.0mg/dL) at 7 years. Receiver operating characteristic (ROC) curves were generated to assess parameter performance at these time points and to select the best cutoff for individual parameters; sensitivity and specificity were calculated for the parameters alone and in combination. Results: Proteinuria of <0.8g/day 12 months after randomization was the single best predictor of good long-term renal function (sensitivity=81%, specificity=78%). The addition of SCr to proteinuria did not improve performance; addition of urine RBCs significantly decreased sensitivity to 47%. Conclusions: This study demonstrates that the level of proteinuria at 12 months is the individual best predictor of long-term renal outcome. Inclusion of urine RBCs as part of a composite outcome measure actually undermines the predictive value of the trial data. We therefore suggest that urine RBCs should not be included as a component of clinical trial response criteria in lupus nephritis. This article is protected by copyright. All rights reserved. © 2015 American College of Rheumatology.
    01/2015; 67(5). DOI:10.1002/art.39026
  • Nephrology Dialysis Transplantation 11/2014; 30(1). DOI:10.1093/ndt/gfu348 · 3.49 Impact Factor
  • Wenrui Hao, Brad H Rovin, Avner Friedman
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    ABSTRACT: Lupus nephritis (LN) is an autoimmune disease that occurs when autoantibodies complex with self-antigen and form immune complexes that accumulate in the glomeruli. These immune complexes initiate an inflammatory response resulting in glomerular injury. LN often concomitantly affects the tubulointerstitial compartment of the kidney, leading first to interstitial inflammation and subsequently to interstitial fibrosis and atrophy of the renal tubules if not appropriately treated. Presently the only way to assess interstitial inflammation and fibrosis is through kidney biopsy, which is invasive and cannot be repeated frequently. Hence, monitoring of disease progression and response to therapy is suboptimal. In this paper we describe a mathematical model of the progress from tubulointerstitial inflammation to fibrosis. We demonstrate how the model can be used to monitor treatments for interstitial fibrosis in LN with drugs currently being developed or used for nonrenal fibrosis.
    Proceedings of the National Academy of Sciences 09/2014; 111(39). DOI:10.1073/pnas.1413970111 · 9.81 Impact Factor
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    ABSTRACT: Objective: In lupus nephritis (LuN), severe tubulointerstitial inflammation (TII) predicts progression to renal failure. Severe TII is associated with tertiary lymphoid neogenesis and in situ antigen-driven clonal B cell selection. The autoantigen(s) driving in situ B-cell selection in TII are not known. This study aimed to identify the dominant driving autoantigen(s).Methods: Single CD38+ or Ki-67+ B cells were laser captured from seven LuN diagnostic biopsies. Eighteen clonally expanded immunoglobulin heavy and light chain variable region pairs were cloned and expressed as monoclonal antibodies. Seven more antibodies were cloned from flow sorted CD38+ cells from an eighth biopsy. Antigen characterization was performed using a combination of confocal microscopy, ELISA, screening protoarrays, immunoprecipitation and mass spectrometry. Serum IgG titers to the dominant antigen were determined in 48 LuN and 35 non-nephritic lupus samples using purified antigen-coated arrays. Autoantigen expression was localized by immunohistochemistry and immunofluorescence on normal and LuN kidney.Results: Eleven of 25 antibodies reacted with cytoplasmic structures, four reacted with nuclei, and none with dsDNA. Vimentin was the only autoantigen identified by both mass spectrometry and by protoarray. Ten of the 11 anti-cytoplasmic TII antibodies directly bound vimentin. Vimentin was highly expressed by tubulointerstitial inflammatory cells, and tested TII antibodies preferentially bound inflamed tubulointerstitium. Finally, high-titers of serum anti-vimentin antibodies were associated with severe TII (p = 0.0001).Conclusion: Vimentin, an antigenic feature of inflammation, is a dominant autoantigen targeted in situ in LuN TII. This adaptive autoimmune response likely feeds forward to worsen TII and renal damage. © 2014 American College of Rheumatology.
    09/2014; DOI:10.1002/art.38888
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    ABSTRACT: The kidney biopsy is the standard of care for diagnosis of lupus nephritis and remains necessary to ensure accurate diagnosis and guide treatment. Repeat biopsy should be considered when therapy modifications are necessary, as in cases with incomplete or no response, or when stopping therapy for those in remission. There are several promising biomarkers of kidney disorders; however, these markers need to be validated in a prospective clinical trial before being applied clinically. Molecular analysis may provide the information presently lacking from current evaluation of kidney disorders and may better inform on prognosis and treatment considerations.
    Rheumatic Disease Clinics of North America 08/2014; 40(3). DOI:10.1016/j.rdc.2014.04.004 · 1.74 Impact Factor
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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.
    American Journal of Hypertension 07/2014; 28(2). DOI:10.1093/ajh/hpu129 · 3.40 Impact Factor
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    ABSTRACT: We present a unique case in which tubular epithelial crystalline deposits were initially overlooked on renal biopsy and thus the patient did not receive treatment for over a decade. Despite this, he had no progression of his renal disease. This case prompted a review of the literature to investigate how other patients with this rare renal disease have been treated, and what their outcomes were. Our review of the literature shows that for many patients with κ-light chain crystalline proximal tubulopathy and a plasma cell dyscrasia, chemotherapy does not seem to drastically improve renal function and may not be necessary in the absence of multiple myeloma. Watchful waiting may, in fact, be more beneficial.
    Clinical nephrology 05/2014; 83 (2015)(03). DOI:10.5414/CN108120 · 1.23 Impact Factor
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    ABSTRACT: Background/Purpose:Lupus nephritis (LN) is frequently associated with a poor long-term prognosis. Current non-invasive blood and urine tests do not reliably predict the course of LN. The objective of this study was to evaluate the performance of candidate urine biomarkers in predicting future kidney function in adults and children with LN. The biomarker candidates studies were liver-type fatty acid binding protein (L-FABP), albumin (Alb), monocyte chemoattractant protein 1 (MCP-1), Uromodulin, Transferrin and Hepcidin.Methods:L-FABP, Alb, MCP-1, Uromodulin, Transferrin and Hepcidin were measured by ELISA in urine from 70 adults and 42 children collected at the time of enrollment into prospective observational LN cohorts. Urine analytes were normalized to urine creatinine and logarithmically transformed. The association of each analyte to renal function loss (RFL), defined as a sustained increase of ≥25% in serum creatinine (SCr; adults) or a decrease in eGFR of ≥20% (children), was determined using a fixed effect model after adjusting for the age group (adult vs. child). In addition, the results were confirmed using Wilcoxon Rank Sum tests. Logistical models were used to predict the presence of RFL using each biomarker or a combination of the biomarkers. Biomarker performance in predicting RFL was assessed as the area under a ROC curve (AUC) corresponding to the logistical model.Results:13 children and 22 adults had RFL during the mean follow-up period of 6.1 months and 60 months, respectively. Overall patients with RFL showed significantly higher levels ALB than those without RFL (p < 0.05, 1). In addition, the levels of L-FABP, MCP-1, and Transferrin were also marginally higher in RFL (p-values < 0.1). The AUC using the combination of urine L-FABP, Alb, MCP-1 and Utransferrin was 0.66, slightly higher than those using any single biomarker as the predictor (ranging from 0.52–0.63).Table 1. Patient typeBiomarker/Cr$Renal function loss$Preserved renal function$p (Fixed effect model/Wilcoxon) N3577– LFABP1.75 ± 1.581.17 ± 1.620.084 / 0.066 Albumin5.58 ± 2.314.46 ± 2.190.017 / 0.030 MCP-15.77 ± 1.634.89 ± 2.450.064 / 0.034 UROMODULIN2.04 ± 1.302.14 ± 1.140.683 / 0.644 UTRANSFERRIN2.27 ± 2.271.49 ± 1.980.073 / 0.070All patients with LNHEPCIDIN3.85 ± 1.153.57 ± 1.670.378 / 0.656 N2248– LFABP1.69 ± 1.261.28 ± 1.690.326 / 0.229 Albumin5.90 ± 2.145.01 ± 2.010.100 / 0.147 MCP-15.98 ± 1.164.80 ± 2.700.061 / 0.057 UROMODULIN1.33 ± 1.061.65 ± 1.080.261 / 0.274 UTRANSFERRIN1.98 ± 1.781.41 ± 1.960.255 / 0.177Adults with LNHEPCIDIN3.80 ± 0.953.28 ± 1.710.197 / 0.368 N1329– LFABP1.84 ± 2.050.98 ± 1.500.136 / 0.218 Albumin5.05 ± 2.573.55 ± 2.210.060 / 0.116 MCP-15.38 ± 2.305.02 ± 2.020.634 / 0.402 UROMODULIN3.19 ± 0.682.96 ± 0.690.314 / 0.589 UTRANSFERRIN2.73 ± 2.941.64 ± 2.040.170 / 0.199Children with LNHEPCIDIN3.91 ± 1.454.02 ± 1.510.830 / 0.803Conclusion:Urine biomarkers L-FABP, Alb and MCP-1 are likely predictive to RFL. Other biomarkers such as Uromodulin, Transferrin and Hepcidin are markers of disease activity, but not predictive of RFL.
    03/2014; 66(S11). DOI:10.1002/art.38494
  • Annals of the Rheumatic Diseases 01/2014; 72(Suppl 3):A268-A268. DOI:10.1136/annrheumdis-2013-eular.830 · 9.27 Impact Factor
  • Brad H Rovin, Samir V Parikh
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    ABSTRACT: Immune complex accumulation in the kidney is the hallmark of lupus nephritis and triggers a series of events that result in kidney inflammation and injury. Cytotoxic agents and corticosteroids are standard of care for lupus nephritis treatment, but are associated with considerable morbidity and suboptimal outcomes. Recently, there has been interest in using novel biologic agents and small molecules to treat lupus nephritis. These therapies can be broadly categorized as anti-inflammatory (laquinamod, anti-tumor necrosis factor-like weak inducer of apotosis, anti-C5, and retinoids), antiautoimmunity (anti-CD20, anti-interferon α, and costimulatory blockers), or both (anti-interleukin 6 and proteasome inhibitors). Recent lupus nephritis clinical trials applied biologics or small molecules of any category to induction treatment, seeking short-term end points of complete renal response. These trials in general have not succeeded. When lupus nephritis comes to clinical attention during the inflammatory stage of the disease, the autoimmune stage leading to kidney inflammation will have been active for some time. The optimal approach for using novel therapies may be to initially target kidney inflammation to preserve renal parenchyma, followed by suppression of autoimmunity. In this review, we discuss novel lupus nephritis therapies and how they fit into a combinatorial treatment strategy based on the pathogenic stage.
    American Journal of Kidney Diseases 01/2014; 63(4). DOI:10.1053/j.ajkd.2013.11.023 · 5.76 Impact Factor
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    ABSTRACT: Renal flares are common in lupus nephritis. The impact of flares on the development of CKD in lupus nephritis was examined. A retrospective analysis of prospectively collected data from the Ohio Systemic Lupus Erythematosus (SLE) Study was conducted to determine if renal flares predispose to new CKD or progression of preexisting CKD. Patients in the Ohio SLE Study were followed from 2001 to 2009, with a median follow-up of 6 years. For this analysis, patients with biopsy-proven lupus nephritis and at least 3 years of follow-up were included (n=56). Frequency and duration of renal flares were compared between patients who never developed CKD (n=29) and patients who developed new CKD (n=12) and between patients with preexisting but stable CKD (n=7) and patients who progressed (n=8). Groups were also combined into good (no CKD and stable CKD) or poor (new CKD and progressive CKD) for analysis. The new CKD group had more renal flares per year compared with the no CKD group (median=0.56 flares/yr [range=0-2] versus median=0 flares/yr [range=0-1.4]; P<0.001). Additionally, the poor outcome group had more renal flares per year compared with the good outcome group (median=0.50 flares/yr [range=0-2] versus median=0 flares/yr [range=0-1.4]; P<0.001). New or progressive CKD was not preferentially associated with nephritic compared with proteinuric renal flares. Logistic regression showed that spending more than 30% of time in renal flare (odds ratio, 20; 95% confidence interval, 4.6 to 91.3; P<0.001) and age>35 years (odds ratio, 69; 95% confidence interval, 6.3 to 753.6; P<0.001) were independent predictors of the combined end point of developing new or progressive CKD. All four subjects over 35 years of age that spent over 30% of time in renal flare had a poor outcome. In patients with lupus nephritis, the relative duration of renal flare is an independent predictor of incident and progressive CKD.
    Clinical Journal of the American Society of Nephrology 11/2013; 9(2). DOI:10.2215/CJN.05040513 · 5.25 Impact Factor

Publication Stats

6k Citations
1,153.39 Total Impact Points


  • 1992–2015
    • The Ohio State University
      • • Pathology
      • • Department of Internal Medicine
      • • Division of Nephrology
      • • Division of Hospital Medicine
      Columbus, Ohio, United States
  • 2009
    • University of Louisville
      Louisville, Kentucky, United States
  • 2005
    • University of California, Los Angeles
      Los Angeles, California, United States
  • 2004
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1990–1991
    • Washington University in St. Louis
      • Department of Medicine
      San Luis, Missouri, United States