About

Sergey V. Brodsky is not mentioned in the provided page text, and there is no specific biographical or research information available about him on this page.

Research topics

• Medicine
• Internal medicine
• Endocrinology
• Immunology
• Gastroenterology
• Cardiology
• Pathology
• Urology
• Surgery
• Chemistry
• Mechanics
• Intensive care medicine
• Pharmacology
• Physics
• Biochemistry

Selected publications

• Disappearing glomeruli: loss of linear IgG in anti-GBM nephritis

  Kidney International · 2026-03-01

  article
  PublisherDOI

• Platelet Dysfunction in Chronic Kidney Disease Arises from Bone Marrow Remodeling and Megakaryocyte Reprogramming.

  UNC Libraries · 2026-03-21

  articleOpen access

  Chronic kidney disease (CKD) is associated with an increased risk of thrombotic events, yet the underlying mechanisms driving platelet dysfunction remain incompletely understood. Historically, platelet abnormalities in CKD have been attributed to circulating uremic toxins; however, the contribution of the bone marrow microenvironment and megakaryocyte (MK) biology has not been fully explored. In this study, we used a murine model of CKD induced by aristolochic acid (AA) to investigate the impact of CKD on megakaryopoiesis and platelet production. CKD mice developed hallmark features of kidney dysfunction, including anemia, proteinuria, hypertension, and elevated creatinine. Histological analysis revealed a hypocellularity and decreased MK density, while early hematopoietic progenitors were preserved. CKD-derived MKs displayed a distinct proteomic signature enriched for metabolic stress and hemostatic pathways. Functionally, bone marrow supernatant from CKD mice enhanced proplatelet formation in vitro, consistent with elevated platelet counts observed in vivo. Notably, CKD platelets exhibited a hyperreactive phenotype, characterized by increased integrin αIIbβ3 activation, degranulation, and enhanced aggregation in response to agonists. Together, these findings support a dual mechanism of platelet dysfunction in CKD: intrinsic reprogramming of MKs within the diseased bone marrow microenvironment and extrinsic priming by pro-thrombotic bone marrow factors. This study provides new insight into the hematopoietic origins of platelet abnormalities in CKD and underscores the importance of targeting bone marrow pathology to mitigate cardiovascular risk in this population.

  PublisherDOI

• Effects of Prothrombin on Podocytopathy and Proteinuria in Glomerular Disease

  Journal of the American Society of Nephrology · 2025-03-28 · 1 citations

  article

  Key Points Thrombin injures podocytes through its cognate receptors in vitro , and thrombin generation increases during proteinuric glomerular disease. In this study, plasma prothrombin levels modulated in vivo podocyte health and function in a rat model of glomerular disease. Thrombin antagonism may simultaneously prevent thrombosis and CKD progression due to glomerular disease. Background CKD is a leading cause of death; its progression is driven by glomerular podocyte injury and loss, manifesting as proteinuria. Proteinuria includes loss of coagulation zymogens, cofactors, and inhibitors resulting in a hypercoagulable state characterized by enhanced thrombin generation. Both CKD and proteinuria significantly increase the risk of thromboembolic disease. Meanwhile, anticoagulant medications (which antagonize thrombin and thereby prevent thromboembolism) have been shown to reduce proteinuria in rats, and thrombin has been shown to injure cultured human and rat podocytes. We thus aimed to directly determine the influence of circulating prothrombin, the zymogen precursor of thrombin, on glomerular pathobiology. We hypothesized that (pro)thrombin drives podocytopathy, podocytopenia, and proteinuria. Methods Glomerular proteinuria was induced with puromycin aminonucleoside in rats. Prothrombin was either knocked down using an antisense oligonucleotide–targeting prothrombin mRNA or elevated by serial intravenous prothrombin protein infusions, previously established methods to model hypoprothrombinemia and hyperprothrombinemia, respectively. After 10 days, plasma prothrombin levels were determined and kidneys were examined for (pro)thrombin colocalization to podocytes, histology, and electron microscopy. Podocytopathy, podocytopenia, proteinuria, and plasma albumin were measured. Results Antisense oligonucleotide–mediated prothrombin knockdown significantly reduced prothrombin colocalization to podocytes, tubular injury, podocyte foot process effacement, podocytopathy, and proteinuria, along with improved plasma albumin in the puromycin aminonucleoside glomerular disease model. By contrast, elevated prothrombin levels significantly increased podocytopathy and proteinuria. Podocytopenia was significantly improved in hypoprothrombinemic versus hyperprothrombinemic rats. Conclusions Thrombin generation is enhanced by glomerular proteinuria, and thrombin injures conditionally immortalized podocytes in vitro . In this study, prothrombin knockdown ameliorated in vivo podocyte injury and improved podocyte function in the rat puromycin aminonucleoside–induced glomerular disease model, whereas hyperprothrombinemia exacerbated podocyte injury and diminished podocyte function.

  PublisherDOI

• Cover Image

  Journal of the American Society of Nephrology · 2025-07-01

  paratext
  PublisherDOI

• “First do no harm”: Fundal pressure during labor—How safe is it?

  International Journal of Gynecology & Obstetrics · 2025-05-16 · 3 citations

  article

  OBJECTIVE: Fundal pressure (FP), a controversial obstetric maneuver due to its potential benefits and risks, lacks robust evidence concerning its effects. This study aimed to evaluate the maternal and neonatal outcomes associated with the application of FP during the second stage of labor. METHODS: Following our departmental protocol, FP is applied by obstetricians trained under the supervision of the head of the labor ward. Its implementation requires patient consent and documentation. This case-control study encompassed vaginal deliveries (VDs) involving FP (FP group) during the second stage of labor. The control group included subsequent deliveries matched 1:1 for gestational age, parity, and mode of delivery (vacuum extraction [VE] or VD). Maternal and neonatal outcomes were compared between the groups. Composite adverse outcomes included the presence of at least one of the following: grade 3-4 perineal tear, shoulder dystocia, postpartum hemorrhage, postpartum hospitalization exceeding 4 days, or postpartum use of analgesics exceeding five doses. RESULTS: Among 12 048 deliveries during the 3-year study period, 325 (2.7%) involved FP. There were no significant differences in maternal age, body mass index, or gestational age between the FP (n = 325) and control groups (n = 325). However, the FP group exhibited higher rates of labor induction (41.5% vs. 19.3%, P < 0.0001), oxytocin augmentation (52% vs. 23.6%, P < 0.0001), and prolonged duration of the second stage of labor (1.88 ± 1.2 vs. 1.57 ± 1.3 h, P = 0.003). There were no significant differences in the rate of postpartum hemorrhage, composite adverse maternal outcomes, or early neonatal outcomes between the groups. CONCLUSION: Fundal pressure, when administered by trained obstetricians, was not associated with adverse obstetric, maternal, or neonatal outcomes.

  PublisherDOI

• Genomewide Screen Identifies Peroxisomal Role in APOL1 Podocytopathy

  medRxiv · 2025-02-18 · 3 citations

  preprintOpen access

  The G1 and G2 variants of the APOL1 gene increase the risk of chronic kidney disease (CKD) in individuals of African descent. In the presence of secondary stressors such as inflammation and hypoxia, these gain-of-function variants can induce podocyte dysfunction and cell death through mechanisms that are not fully understood. To identify genes that influence the cytotoxic effects of APOL1 variants under hypoxic conditions, we conducted a comprehensive whole-genome RNA interference (RNAi) screen. We found that silencing several peroxisomal (PEX) genes significantly intensified the cytotoxicity associated with the G1 and G2 variants, revealing the previously unknown role of peroxisomes in APOL1-related cytotoxicity. Importantly, enhancing peroxisomal function through both genetic and pharmacological approaches led to a significant reduction in cytotoxicity linked to these variants. We also identified a peroxisomal targeting signal at the C-terminus of APOL1 that facilitates its translocation to peroxisomes during hypoxia, and mutations in this signal were found to reduce the cytotoxic effects of the variants. Collectively, our findings underscore the importance of peroxisomal function in the pathogenesis of CKD associated with APOL1 variants and suggest that targeting peroxisomes may represent an effective therapeutic strategy to mitigate CKD risk in vulnerable populations.

  PublisherOA PDFDOI

• Platelet dysfunction in chronic kidney disease arises from bone marrow remodeling and megakaryocyte reprogramming

  Blood Advances · 2025-12-18

  articleOpen access

  ABSTRACT: Chronic kidney disease (CKD) is associated with an increased risk of thrombotic events, yet the underlying mechanisms driving platelet dysfunction remain incompletely understood. Historically, platelet abnormalities in CKD have been attributed to circulating uremic toxins; however, the contribution of the bone marrow microenvironment and megakaryocyte biology has not been fully explored. In this study, we used a murine model of CKD induced by aristolochic acid to investigate the impact of CKD on megakaryopoiesis and platelet production. CKD mice developed hallmark features of kidney dysfunction, including anemia, proteinuria, hypertension, and elevated creatinine. Histological analysis revealed a hypocellularity and decreased megakaryocyte density, whereas early hematopoietic progenitors were preserved. CKD-derived megakaryocytes displayed a distinct proteomic signature enriched for metabolic stress and hemostatic pathways. Functionally, bone marrow supernatant from CKD mice enhanced proplatelet formation in vitro, consistent with elevated platelet counts observed in vivo. Notably, CKD platelets exhibited a hyperreactive phenotype, characterized by increased integrin αIIbβ3 activation, degranulation, and enhanced aggregation in response to agonists. Together, these findings support a dual mechanism of platelet dysfunction in CKD: intrinsic reprogramming of megakaryocytes within the diseased bone marrow microenvironment and extrinsic priming by prothrombotic bone marrow factors. This study provides new insight into the hematopoietic origins of platelet abnormalities in CKD and underscores the importance of targeting bone marrow pathology to mitigate cardiovascular risk in this population.

  PublisherDOI

• A Woman with Malignant Melanoma Who Developed Membranous Nephropathy After Treatment with a BRAF-MEK Inhibitor

  Journal of the American Society of Nephrology · 2025-10-01

  article

  Introduction: Membranous nephropathy (MN) is an immune complex-mediated disease characterized by subepithelial deposits along the glomerular basement membrane (GBM). Typically 70% of primary MN is anti-PLA2-receptor (PLA2R) positive. Secondary MN is often due to infection, drug exposure, and malignancy. We present a case of a young female diagnosed with metastatic melanoma and was found to have MN on kidney biopsy which complicated her treatment. Case Description: 47 year old Caucasian female with history of melanoma and hypothyroidism presented significant compressive right inguinal lymphadenopathy that was consistent with recurrent melanoma. She was initiated on a targeted BRAF/MEK inhibitor. One month later she had worsening bilateral lower extremity edema and new nephrotic range proteinuria (urine protein/creatinine of 5.9 g/g). She was then transitioned to PD-1 immunotherapy, but her malignancy progressed with persistent nephrotic range proteinuria. Five months later she had a 24 hour urine protein of 11.6 g, serum albumin 1.7 g/dL, serum creatinine of 1.0 mg/dL. Renal biopsy showed stage I-II MN with negative NELL1 and PLA2R stains. Due to progression of her disease on PD-1 immunotherapy, she was transitioned back to BRAF-MEK inhibitor therapy and given 2 doses of 1 gram of rituximab for her nephrotic syndrome. Four months later while on BRAF/MEK inhibitor therapy, she did have improvement in her nephrotic syndrome and melanoma markers. Serum albumin improved to 2.2 g/dL.Urine protein/creatinine ratio improved to 3.3 g/g. CD20+ B cells < 1%. One month later, she was hospitalized for complications from malignant pleural effusions and passed away. Discussion: This case highlights the lack of clarity of secondary MN in the oncologic patient and the need to avoid nephro-centric care. Her clinical course was suspicious of BRAF/MEK inhibitor induced secondary MN with nephrotic syndrome. Given the improvement in melanoma and proteinuria with continued therapy it is possible her MN was secondary to her malignancy. It is equally possible that she continued to have MN secondary to her BRAF/MEK inhibitor therapy, which was ameliorated by rituximab. This highlights the importance of focusing on cancer focused therapy for patients with concern for renal manifestations while on targeted chemotherapies.

  PublisherDOI

• Changes in the Glomerular Basement Membrane Thickness in Living-Donor Baseline Biopsies Within a 15-Year Period

  Journal of the American Society of Nephrology · 2025-10-01

  article
  PublisherDOI

• Utility of Different Anti-IgG Antibodies in Recognition of Punctate (Powdery) Podocyte Staining by Immunofluorescence in Patients with Diffuse Podocyte Foot Process Effacement

  2025-11-07

  articleOpen accessSenior author

  Circulating anti-nephrin autoantibodies recently were recognized as a possible pathogenic factor in patients with steroid-resistant minimal change disease. In a kidney biopsy, these patients have punctate ("powdery") staining in the podocytes by immunofluorescence. Previously published data described such pattern of staining by using anti-IgG Dako antibody. In the routine practice, different laboratories use different anti-IgG antibodies from a variety of vendors. The aim of this work was to compare the ability to recognize the punctate staining in the podocyte by two different anti-IgG antibodies (Dako and Kent) that are in use in our routine renal pathology practice. Our data indicates that both anti-IgG antibodies recognize the punctate ("powdery) staining in the podocytes in a subset of patients with minimal change disease.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R21DK090587

  NIH · $419k · 2013

• NIH Grant K01DK064863

  NIH · $141k · 2009

• Anticoagulant related nephropathy

  NIH · $1.9M · 2019–2024

Frequent coauthors

• Anjali A. Satoskar

  The Ohio State University

  286 shared

• Gyongyi Nadasdy

  The Ohio State University Wexner Medical Center

  230 shared

• Maryam M. Asgari

  Harvard University

  200 shared

• Alia Albawardi

  United Arab Emirates University

  131 shared

• Suresh T. Chari

  The University of Texas MD Anderson Cancer Center

  128 shared

• Stephen M. Bonsib

  Arkana Laboratories

  128 shared

• Nüket Bavbek

  128 shared

• Barbara Paul

  University of Pittsburgh

  128 shared

Labs

• AI4PathPI

  From Pixels to Prognosis: AI in Action!

Education

• M.D.

  North Ossetian State Medical Academy

  1992

• Ph.D.

  North Ossetian State Medical Academy

  1995

• Other, Anatomic Pathology

  New York Medical College at Westchester Medical Center

  2008

• Other, Renal Pathology

  The Ohio State University

  2009