Publications by authors named "Marjan Afrouzian"

14 Publications

  • Page 1 of 1

Case Report: Renal Failure due to Focal Segmental Glomerulosclerosis in a Patient with Murine Typhus.

Am J Trop Med Hyg 2020 09;103(3):1017-1019

Division of General Medicine, Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas.

Murine typhus is a flea-borne rickettsiosis caused by . When severe, endothelial dysfunction can lead to acute kidney injury secondary to prerenal azotemia or acute tubular necrosis. Here, we describe an unusual cause of kidney injury during the course of murine typhus-focal segmental glomerulosclerosis.
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http://dx.doi.org/10.4269/ajtmh.20-0116DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7470532PMC
September 2020

The Banff 2019 Kidney Meeting Report (I): Updates on and clarification of criteria for T cell- and antibody-mediated rejection.

Am J Transplant 2020 09 28;20(9):2318-2331. Epub 2020 May 28.

Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Canada.

The XV. Banff conference for allograft pathology was held in conjunction with the annual meeting of the American Society for Histocompatibility and Immunogenetics in Pittsburgh, PA (USA) and focused on refining recent updates to the classification, advances from the Banff working groups, and standardization of molecular diagnostics. This report on kidney transplant pathology details clarifications and refinements to the criteria for chronic active (CA) T cell-mediated rejection (TCMR), borderline, and antibody-mediated rejection (ABMR). The main focus of kidney sessions was on how to address biopsies meeting criteria for CA TCMR plus borderline or acute TCMR. Recent studies on the clinical impact of borderline infiltrates were also presented to clarify whether the threshold for interstitial inflammation in diagnosis of borderline should be i0 or i1. Sessions on ABMR focused on biopsies showing microvascular inflammation in the absence of C4d staining or detectable donor-specific antibodies; the potential value of molecular diagnostics in such cases and recommendations for use of the latter in the setting of solid organ transplantation are presented in the accompanying meeting report. Finally, several speakers discussed the capabilities of artificial intelligence and the potential for use of machine learning algorithms in diagnosis and personalized therapeutics in solid organ transplantation.
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http://dx.doi.org/10.1111/ajt.15898DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7496245PMC
September 2020

Lymphoma-Associated Monoclonal Cryoglobulinemic Glomerulonephritis and Relationship with Hepatitis C Virus Infection: A Case Report.

Case Rep Nephrol 2019 18;2019:7940291. Epub 2019 Aug 18.

Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX, USA.

We report a case of type I cryoglobulinemic glomerulonephritis in a patient with chronic hepatitis C who presented with acute renal failure. The renal biopsy revealed membranoproliferative GN (MPGN) due to cryoglobulinemia with unexpected monoclonal Kappa restriction on immunofluorescence microscopy, suggesting an underlying hematopoietic malignancy. The bone marrow biopsy revealed presence of marginal zone lymphoma. Our case raises awareness regarding possibility of monoclonality in the renal biopsy of HCV-infected patients and exemplifies the crucial role the renal biopsy plays in detecting lymphoid malignancies where clinical features are ambiguous.
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http://dx.doi.org/10.1155/2019/7940291DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6719345PMC
August 2019

The Impact of Renal Tissue Procurement at Bedside on Specimen Adequacy and Best Practices.

Am J Clin Pathol 2019 01;151(2):205-208

Department of Pathology, University of Texas Medical Branch, Galveston.

Objectives: Renal biopsy is the gold standard for the diagnosis of both native and allograft renal diseases. We studied the impact of tissue procurement at bedside (TPB) omission on the adequacy of renal biopsies.

Methods: We compared 120 renal biopsies collected during 2015 using TPB with 111 renal biopsies collected during 2016 when TPB was discontinued. Adequacy criteria were applied as follows: by light microscopy, 10 glomeruli and two arteries for allograft biopsies and seven glomeruli for native biopsies. At least one glomerulus was considered adequate for immunofluorescence and electron microscopy in both groups.

Results: The rate of inadequacies in allograft biopsies increased significantly, from 12.50% to 21.61% (P < .05), when TPB was discontinued.

Conclusions: Elimination of TPB service had a negative impact on allograft specimen adequacy. Repeat biopsies add cost and delay patient care. Institutions should take this into consideration when considering omission of TPB.
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http://dx.doi.org/10.1093/ajcp/aqy120DOI Listing
January 2019

Role of the efflux transporters BCRP and MRP1 in human placental bio-disposition of pravastatin.

Biochem Pharmacol 2018 10 12;156:467-478. Epub 2018 Sep 12.

Maternal-Fetal Pharmacology and Bio-Development Laboratories, Department of Obstetrics & Gynecology, University of Texas Medical Branch, Galveston, TX 77555, USA. Electronic address:

The expression and activity of human placental transporters during pregnancy could be altered by several factors including pathological changes associated with preeclampsia. The aims of this study were to identify the placental efflux transporters involved in the bio-disposition of pravastatin, determine the protein expression of these transporters and their encoding genes as well as the activity of pravastatin uptake in placentas obtained from patients with preeclampsia. ATP-dependent uptake of [3H]-pravastatin by trophoblast tissue apical and basal membrane vesicles exhibited sigmoidal kinetics. The curved shapes of Eadie-Hofstee plots indicate that more than one placental transporter are involved in the uptake of pravastatin. ATP-dependent uptake of [3H]-pravastatin into vesicles expressing MRP1-5, BCRP, and P-gp, as well as the results of inhibition studies suggest that BCRP and MRP1 are the major placental efflux transporters responsible for the in vitro uptake of pravastatin. Compared to placentas from healthy pregnancies, preeclamptic placentas had increased number of syncytial knots with increased expression of BCRP in their apical membrane and increased expression of MRP1 in the cytoplasm of the syncytiotrophoblast and in cytoplasm of syncytial knots. There was a concomitant increase in ABCC1 but not in ABCG2 gene expressions in preeclamptic placentas. ATP-dependent uptake of [3H]-pravastatin by vesicles prepared from apical membranes of preeclamptic placentas was similar to the uptake by vesicles prepared from placentas obtained after uncomplicated pregnancies (13.9 ± 6.5 vs 14.1 ± 5.8 pmol·mg protein min). The transporter-specific changes in the expression of BCRP and MRP1 in preeclamptic placentas did not affect the efflux activity of transporters localized on the apical membrane of the syncytiotrophoblast.
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http://dx.doi.org/10.1016/j.bcp.2018.09.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6502225PMC
October 2018

Florid Proliferation of Hyalinized Vessels in a Spermatic Cord STAT6 Positive Solitary Fibrous Tumor and Its Potential Clinical Implications.

Case Rep Pathol 2018 28;2018:7462032. Epub 2018 Jun 28.

Department of Pathology, University of Texas Medical Branch, Galveston, TX, USA.

A solitary fibrous tumor (SFT) arising in the paratesticular region is a rare event. Typically most SFTs present as a lung mass and have a characteristic microscopic appearance. Although uncommon, SFTs may present at just about any anatomical site. Here we present a case of a SFT arising along the right spermatic cord, with histologic features mimicking a cellular angiofibroma. We describe the diagnostic immunohistochemical markers useful for arriving at its diagnosis. We also summarize our current understanding of the structural and molecular features that make up SFTs and discuss how these features may help us better understand the pathophysiology of pluripotent mesenchymal stem cell differentiation.
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http://dx.doi.org/10.1155/2018/7462032DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046177PMC
June 2018

Bile Cast Nephropathy in Cirrhotic Patients: Effects of Chronic Hyperbilirubinemia.

Am J Clin Pathol 2017 May;147(5):525-535

Department of Pathology.

Objectives: The aim of this study was to determine the prevalence of bile cast nephropathy (BCN) in autopsied cirrhotic patients and to correlate BCN with clinical and laboratory data to direct attention to this underrecognized renal complication of liver failure.

Methods: We assessed 114 autopsy cases of cirrhosis for the presence of renal intratubular bile casts using Hall stain for bile. Presence of bile casts was correlated with etiology of cirrhosis, clinical and laboratory data, and histologic findings.

Results: Bile casts were identified in 55% of cases. The most common etiology of cirrhosis was hepatitis C virus (HCV) infection (52%), and serum creatinine ( P  = .02) and serum urea nitrogen ( P  = .01) were significantly higher in the Hall-positive group. Conjugated bilirubin was below 20 mg/dL in 90%, and levels below 10 mg/dL were noted in 80% of cases.

Conclusions: To our knowledge, this is the largest study of BCN in human subjects and a first report describing the association of BCN with HCV-related cirrhosis. We demonstrated that in the face of protracted chronic hyperbilirubinemia, bile casts are formed at much lower bilirubin levels than previously thought. Furthermore, we proposed an algorithm to assist in better identification of bile casts.
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http://dx.doi.org/10.1093/ajcp/aqx030DOI Listing
May 2017

Levamisole-Adulterated Cocaine Nephrotoxicity:  Ultrastructural Features.

Am J Clin Pathol 2016 May;145(5):720-6

Department of Pathology

Objectives: The issue of levamisole-adulterated cocaine is emerging as a rapidly growing public health concern due to an increasing number of reports describing its role in cutaneous vasculitis and agranulocytosis. Of note, levamisole is recognized as a contaminant in 69% of the cocaine used within the United States.

Methods: We describe a patient who was a chronic cocaine user and developed systemic vasculitis characterized by polyarthralgia, bullous skin lesions, agranulocytosis, and antineutrophil cytoplasmic antibody-positive rapidly progressive glomerulonephritis.

Results: The skin biopsy specimen demonstrated leukocytoclastic vasculitis. The renal biopsy specimen revealed pauci-immune necrotizing and crescentic glomerulonephritis and unusual deposits with medium electron density composed of granules, microspherules, and rare single fibrils on electron microscopy.

Conclusions: The electron microscopic features of levamisole-adulterated cocaine toxicity are novel findings that are presented for the first time, to our knowledge, in this report.
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http://dx.doi.org/10.1093/ajcp/aqw029DOI Listing
May 2016

Four miniature kidneys: supernumerary kidney and multiple organ system anomalies.

Hum Pathol 2014 May 12;45(5):1100-4. Epub 2013 Dec 12.

Department of Pathology, Division of Surgical Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.

More than 350 years after Martius's first reported case in 1656, supernumerary kidney (SNK) continues to fascinate the world of medicine, generating new ideas in the domain of embryogenesis. Association of a normal kidney with a second or third ipsilateral smaller kidney is an extremely rare anomaly with only a total of 81 cases reported until today. We are reporting a case of SNK, clinically diagnosed as right hydronephrosis, associated with an ipsilateral ectopic ureter, a contralateral partially duplicated ureter, and a multiseptate gallbladder. Pathologic examination of the nephrectomy revealed 4 miniature kidneys, joining a dilated ureter through 4 separate conduits. Our patient is the first reported case of SNK with absent ipsilateral normal kidney, presence of more than 3 kidneys on 1 side, and associated anomaly in the gallbladder. This case represents a unique combination of rarities, suggesting insights in the domain of molecular embryology.
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http://dx.doi.org/10.1016/j.humpath.2013.11.015DOI Listing
May 2014

Evaluating the accuracy of functional biomarkers for detecting histological changes in chronic allograft nephropathy.

Transpl Int 2007 Jul 22;20(7):608-15. Epub 2007 May 22.

Division of Transplantation, Department of Surgery, University of Calgary, Foothills Medical Centre, 1403-29 Street NW, Calgary, Alberta, Canada.

The most common cause of late kidney transplant failure is chronic allograft nephropathy (CAN). Much research has focused on identifying biomarkers (or correlates) that would predict subsequent CAN and allow timely intervention. Functional biomarkers such as serum creatinine and estimated glomerular filtration rate (eGFR) have been widely adopted, even though they have not been rigorously evaluated as surrogate markers. This study evaluated serum creatinine and eGFR for predicting the early histopathological changes seen in transplant protocol biopsies (TPB). We prospectively followed 289 kidney transplant patients in the Southern Alberta Transplant Program who had TPB at 6-12 months post-transplant. Tissue samples (n = 280) were independently examined by renal pathologists. The ability of serum creatinine or eGFR to predict the threshold level for abnormal histopathology was evaluated by calculating the area under the receiver operator characteristic curve. Serum creatinine and eGFR had poor predictive value (most confidence intervals included 0.5, indicating no predictive ability) for ten individual histological measurements (Banff 97 scores), and the Chronic Allograft Damage Index. We conclude that serum creatinine and eGFR have a limited clinical role in predicting the early histopathological changes that precede CAN and should not be used for this purpose.
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http://dx.doi.org/10.1111/j.1432-2277.2007.00494.xDOI Listing
July 2007

Renal medullary carcinoma as an incidental finding in a horseshoe kidney: case report and literature review.

Can J Urol 2005 Oct;12(5):2837-40

Department of Pathology and Laboratory Medicine, Calgary Laboratory Services, University of Calgary, Alberta, Canada.

Renal medullary carcinoma is rare and extremely aggressive neoplasm that typically affects young patients of African decent who demonstrate sickle cell trait or disease. Since the original description in 1995, only few cases have been reported outside the United States. A 29 year-old Canadian male of Afro-Caribbean decent with sickle cell trait developed right-sided hemiparesis due to brain infarct. During the clinical work-up, a 3 cm renal tumor was detected in a horseshoe kidney. The patient died suddenly 2 weeks after the presentation of massive non-neoplastic pulmonary thromboembolism, confirmed at autopsy. The final diagnosis of renal medullary carcinoma was established after the autopsy. Due to the small size of the tumor and the limited metastatic spread only to the regional lymph nodes, the tumor was considered an incidental finding, and not the primary cause of patient's death.
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October 2005

The effects of systemic hypoxia on colon anastomotic healing: an animal model.

Dis Colon Rectum 2005 Jul;48(7):1460-70

GI Research Group, Department of Surgery, University of Calgary, Calgary, Alberta, Canada.

Purpose: Acute postoperative systemic hypoxia occurs frequently in the clinical setting following intestinal resection, as a result of complications such as pneumonia, pulmonary edema, or the acute respiratory distress syndrome. Although it is well established that oxygen is essential for metabolism in general and intestinal anastomotic healing, the mechanisms by which systemic hypoxia affect this process are not clear. The purpose of this study was to establish an animal model to simulate acute systemic hypoxia and to examine the effects on anastomotic healing. We investigated the hypothesis that systemic hypoxia impairs anastomotic healing in the colon by disrupting revascularization via changes in the expression of two putative angiogenic factors: inducible nitric oxide synthase and vascular endothelial growth factor.

Methods: Phase I: Juvenile male Sprague-Dawley rats underwent carotid artery cannulation. In a controlled environment the FiO2 was incrementally decreased from 21 to 9 percent and the resultant PaO2 measured. Phase II: Animals underwent colonic transection with immediate reanastomosis and were placed in either a normoxic (FiO2 21 percent) or hypoxic (FiO2 11 percent) environment for seven days. Perianastomotic in vivo tissue oxygen saturation was measured before segmental colon resection in each of the animals and at seven days before measurement of anastomotic bursting pressure. Perianastomotic tissue samples were assessed by Western blot assay for the expression of vascular endothelial growth factor and inducible nitric oxide synthase protein. Sections from each tissue sample were taken and evaluated by a pathologist blinded to treatment group for determination of anastomotic healing score.

Results: Phase I: Incrementally decreasing the FiO2 resulted in a progressive decrease in PaO2 (r2 = 0.77). Phase II: Animals maintained in a hypoxic environment had a significant decrease in tissue oxygen saturation (73 +/- 9 percent vs. 94 +/- 3 percent; P < 0.0001) and anastomotic bursting pressure (118 +/- 18 mmHg vs. 207 +/- 30 mmHg; P < 0.0001) compared with normoxic controls. Systemic hypoxia induced a significant increase, when compared with normoxic controls, in vascular endothelial growth factor (247.1 +/- 9.5 vs. 142.2 +/- 10.6; P < 0.0001) and inducible nitric oxide synthase (259.6 +/- 21.1 vs. 120.2 +/- 10.9; P < 0.0001) protein expression and led to a significant decrease in the overall wound-healing score.

Conclusion: This study validates a new animal model to study the effects of acute systemic hypoxia on colonic anastomotic healing. In this model, systemic hypoxia directly translated into local tissue hypoxia, and anastomotic healing was impaired. Contrary to our original hypothesis, hypoxia led to a significant increase in vascular endothelial growth factor and inducible nitric oxide synthase protein expression at the colonic anastomotic site. Impairment in anastomotic integrity despite upregulation of these angiogenic factors could be a result of the inability of wounded tissue to respond to vascular endothelial growth factor and inducible nitric oxide synthase or alternatively, hypoxia may adversely affect collagen synthesis and deposition directly.
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http://dx.doi.org/10.1007/s10350-005-0047-3DOI Listing
July 2005

Heterogeneity in the evolution and mechanisms of the lesions of kidney allograft rejection in mice.

Am J Transplant 2003 Dec;3(12):1501-9

1st Department of Internal Medicine, University of Luebeck School of Medicine, Luebeck, Germany.

The natural history and pathogenesis of the pathologic lesions that define rejection of kidney transplants have not been well characterized. We studied the evolution of the pathology of rejection in mouse kidney allografts, using four strain combinations across full major histocompatibility complex (MHC) plus nonMHC disparities, to permit more general conclusions. Interstitial infiltrate, MHC induction, and venulitis appeared by day 5, peaked at day 7-10, then stabilized or regressed by day 21. In contrast, tubulitis, arteritis, and glomerulitis were absent or mild at days 5 and 7, but progressed through day 21, indicating separate regulation and homeostatic control of these lesions. Edema, hemorrhage, and necrosis also increased through day 21. All lesions were T-dependent, failing to develop in T-cell-deficient hosts. Allografts into immunoglobulin-deficient hosts manifested typical infiltration, MHC induction, and tubulitis at days 7 and 21, indicating that these lesions are alloantibody-independent. However at day 21 kidneys rejecting in immunoglobulin-deficient hosts showed decreased edema, arteritis, venulitis, and necrosis. Thus the three groups of lesions are: T-cell-mediated interstitial infiltration, MHC induction, and venulitis, which develops rapidly then stabilizes; slower but progressive T-cell-mediated tubulitis and arteritis; and late antibody-mediated endothelial injury, which contributes to late edema, arteritis, and venulitis.
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http://dx.doi.org/10.1046/j.1600-6135.2003.00269.xDOI Listing
December 2003

Transcription factor IRF-1 in kidney transplants mediates resistance to graft necrosis during rejection.

J Am Soc Nephrol 2002 May;13(5):1199-209

Department of Medicine, Division of Nephrology and Immunology, and Department of Surgery, University of Alberta, Edmonton, Alberta, Canada.

In many circumstances kidney transplants remain viable despite extensive inflammation, permitting rejection episodes to be reversed. The mechanisms by which the kidney resists host effector mechanisms are not known. In mouse kidney transplants, resistance requires interferon-gamma (IFN-gamma), which acts on the graft to protect the graft from necrosis during the first days of rejection as well as inducing major histocompatibility complex (MHC) expression. Because some effects of IFN-gamma are mediated by transcription factor IRF-1, the role of IRF-1 in the donor tissue early phases of rejection of mouse kidney allografts was studied. H-2(b) kidneys were transplanted from mice with wild-type IRF-1 genes (WT) or mice with disrupted IRF-1 genes (IRF-1KO) into CBA (H-2(k)) recipients. At day 5 and day 7, IRF-1KO and WT kidneys were functioning despite typical rejection pathology: interstitial infiltration and tubulitis. However, function deteriorated rapidly in rejecting IRF-1KO allografts, associated with widespread epithelial necrosis, peritubular capillary congestion, glomerulitis, and fibrin thrombi in small veins by day 7. At day 21, WT kidneys were viable despite severe tubulitis and arteritis, whereas IRF-1KO kidneys showed massive necrosis of the epithelium despite patent large vessels. Compared with WT kidneys, rejecting IRF-1KO kidneys showed less induction of donor MHC yet had similar mRNA levels of perforin, granzyme B, and Fas ligand and evoked host alloantibody responses. Thus in rejecting kidney transplants, IRF-1 in the graft mediates MHC induction, but it also mediates resistance to necrosis, an effect that could be crucial to permit success in interventions against rejection.
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http://dx.doi.org/10.1097/01.asn.0000013302.11876.a5DOI Listing
May 2002