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No important features were found on his history except for his use of the azathioprine for a month&#46; Through a 24-hour urine analysis&#44; 4g&#47;day proteinuria was detected in the patient&#46; The patient was admitted to the clinic&#46; In physical examination is normal without arterial blood pressure of 140&#47;90 and the spleen was 5cm palpable&#46; Renal size and parenchyma were normal in abdominal ultrasonography&#46; Laboratory tests results and examinations of glomerular disease have been showed at Table 1&#46; Hence&#44; causes of nephrotic syndrome were excluded&#46; Renal biopsy was performed&#46; In light microscope were shown 29 glomeruli&#46; Global sclerosis and hyalinization were shown in five glomerule&#46; There was intensive segmental sclerosis in more small segments of the other two to three glomeruli&#46; The also remaining some glomeruli have mesengial cell proliferation and expansion&#46; In Bowmans capsule of one to two glomeruli presence of synechiae noted&#46; Tubulointerstitial area has been examined&#44; focal interstitial mononuclear cell infiltration has been observed&#46; In particular areas of inflammation have attenuation of some tubules epithelium and in the presence of eosinophilic material in the lumen characterized by atrophic changes were observed&#46; In vascular stuctures were normal except for a slight thickening of the wall&#46; Glomerulosclerosis&#44; segmental sclerotic areas and slight thickening of the glomerular basement membrane have been detected through the use of Trichome stain&#46; Furthermore&#44; amiloid staining and immunofluorescence study showed a negative&#46; All above these findings were indicative of FSGS&#46; In arterial blood pressure monitoring&#44; stage 1 hypertension was determined&#46; Perindopril&#44; azathioprine&#44; and ASA were prescribed and the patient was discharged&#46;</p><p class="elsevierStylePara">FSGS is a clinical and pathological disorder involving primarily the glomerulus&#46;<span class="elsevierStyleSup">2-3</span> Progressive glomerular scarring is the most important feature in this disease&#46; Early in the disease process&#44; glomerulosclerosis is both focal&#44; and segmental in nature&#46; Furhermore&#44; in later stages of the disease diffuse and global glomerulosclerosis develops&#46; The loss of filtration barrier&#44; depletion of podocytes and genetic susceptibility are the culprit factors in pathogenesis of FSGS&#46;<span class="elsevierStyleBold"> </span>The condition can be idiopathic or occur secondary to obesity&#44; intrarenal hemodynamic alterations&#44; conditions with glomerulomegaly&#44; the reduced number of nephron&#44; and renal atheroembolic disease&#46;<span class="elsevierStyleSup">2&#44;3 </span>The tendency to thromboses may occur in PV which one of the chronic myeloproliferative disorders&#46;<span class="elsevierStyleSup">1</span> It has been suggested that the increase level of red blood cells&#44; elevation of the platelet count&#44; increase in tissue factor&#44; polymorphonuclear leukocytes&#44; coagulation reactions related to the platelet surface and the presence of microparticles were culprit factors&#46;<span class="elsevierStyleSup">11 </span></p><p class="elsevierStylePara">In the light of these data&#44; we hypotezised that PV may cause of FSGS via recurrent thrombosis in microvascular level&#46; Furthermore&#44; it is well known that atheroembolic disease is a cause of FSGS&#46; Thus&#44; our case is important for present to develop of FSGS in the patient with PV&#46; In the existing literature&#44; a small number of cases of FSGS that are thought to be due to PV have been reported&#46;<span class="elsevierStyleSup">4-10</span> In addition&#44; 3&#46;6&#37; &#40;only two PV&#41; incidence of FSGS has been reported in patients with myeloproliferative disease&#46;<span class="elsevierStyleSup">10</span> It has been expressed in these case reports that hyperviscosity from increased hematocrit&#44; hypoperfusion&#44; predisposition to thrombosis related to elevated platelet counts and the continuation of these conditions in recurrent attacks may have a role on the development of FSGS&#46;<span class="elsevierStyleSup">9</span> The emergence of FSGS has been reported average three to seven years after the diagnosis of PV&#46;<span class="elsevierStyleSup">4-10 </span>In the case of the subject of our study&#44; considering that FSGS has been diagnosed with PV six years later is consistent with the literature&#46; The PV was thought to be the possible reason for FSGS&#46; Additionally&#44; FSGS may occur by occlusions due to the long term recurrent microvascular thrombosis and this also could disorder to glomerular hemodynamics&#46;</p><p class="elsevierStylePara">Consequently&#44; the co-existence of PV and FSGS seems to be a cause-effect relationship rather than a random combination&#46; Further studies will be needed to demonstrate for a better understanding of this association&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Acknowledgement</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">None of the authors has a financial interest in any of the products or methods mentioned in this article&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflict of interest</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><br></br></span>The authors declare that there is no conflict of interest associated with this manuscript&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11562&#95;108&#95;35467&#95;en&#95;t1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11562_108_35467_en_t1.jpg" alt="Haematological&#44; chemistrical&#44; serological and urinalysis findings of patient"></img></a></p><p class="elsevierStylePara">Table 1&#46; Haematological&#44; chemistrical&#44; serological and urinalysis findings of patient</p>"
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Development of Focal Segmental Glomerulosclerosis in a Patient with Polycythemia Vera: can Polycythemia Vera be a cause of Focal Segmental Glomerulosclerosis?
Development of Focal Segmental Glomerulosclerosis in a Patient with Polycythemia Vera: can Polycythemia Vera be a cause of Focal Segmental Glomerulosclerosis?
Erim Gulcana, Rahsan Yildirimb, Koray Uludagc, Mustafa Kelesa, Abdullah Uyanika
a Department of Nephrology, Ataturk University Medical Faculty, Erzurum, Turkey,
b Department of Hematology, Ataturk University Medical Faculty, Erzurum, Turkey,
c Department of Nephrology, Erzurum Research and Education Hospital, Erzurum, Turkey,
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          1 => array:3 [
            "entidad" => "Department of Hematology, Ataturk University Medical Faculty, Erzurum,  Turkey, "
            "etiqueta" => "<span class="elsevierStyleSup">b</span>"
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          2 => array:3 [
            "entidad" => "Department of Nephrology, Erzurum Research and Education Hospital, Erzurum,  Turkey, "
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      "en" => array:1 [
        "titulo" => "Development of Focal Segmental Glomerulosclerosis in a Patient with Polycythemia Vera&#58; can Polycythemia Vera be a cause of Focal Segmental Glomerulosclerosis&#63;"
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Dear Editor&#44;</span></p><p class="elsevierStylePara">Polycythemia vera &#40;PV&#41; is a myeloproliferative disorder of unknown etiology&#46; This condition is characterized by the abnormal proliferation of erythroid and myeloid series cells in the bone marrow&#46;<span class="elsevierStyleSup">1</span> Focal segmental glomerulosclerosis &#40;FSGS&#41; is a glomerular disease characterized by the presence of nephrotic syndrome&#44; hypertension&#44; and the progressive deterioration of the renal function&#46; Etiology is usually unknown&#44; but it may be seen in secondary conditions&#46;<span class="elsevierStyleSup">2-3 </span>PV in association with FSGS is rare&#46;<span class="elsevierStyleSup">4 </span>As far as we know&#44; only eight cases have been reported in the literature&#46;<span class="elsevierStyleSup">4-10</span> In the report&#44; we have presented a patient who development of FSGS associated with PV&#46;</p><p class="elsevierStylePara">A 46-year-old male patient diagnosed with PV six years earlier was referred to the nephrology clinic due to the detection of proteinuria on routine controls&#46; No important features were found on his history except for his use of the azathioprine for a month&#46; Through a 24-hour urine analysis&#44; 4g&#47;day proteinuria was detected in the patient&#46; The patient was admitted to the clinic&#46; In physical examination is normal without arterial blood pressure of 140&#47;90 and the spleen was 5cm palpable&#46; Renal size and parenchyma were normal in abdominal ultrasonography&#46; Laboratory tests results and examinations of glomerular disease have been showed at Table 1&#46; Hence&#44; causes of nephrotic syndrome were excluded&#46; Renal biopsy was performed&#46; In light microscope were shown 29 glomeruli&#46; Global sclerosis and hyalinization were shown in five glomerule&#46; There was intensive segmental sclerosis in more small segments of the other two to three glomeruli&#46; The also remaining some glomeruli have mesengial cell proliferation and expansion&#46; In Bowmans capsule of one to two glomeruli presence of synechiae noted&#46; Tubulointerstitial area has been examined&#44; focal interstitial mononuclear cell infiltration has been observed&#46; In particular areas of inflammation have attenuation of some tubules epithelium and in the presence of eosinophilic material in the lumen characterized by atrophic changes were observed&#46; In vascular stuctures were normal except for a slight thickening of the wall&#46; Glomerulosclerosis&#44; segmental sclerotic areas and slight thickening of the glomerular basement membrane have been detected through the use of Trichome stain&#46; Furthermore&#44; amiloid staining and immunofluorescence study showed a negative&#46; All above these findings were indicative of FSGS&#46; In arterial blood pressure monitoring&#44; stage 1 hypertension was determined&#46; Perindopril&#44; azathioprine&#44; and ASA were prescribed and the patient was discharged&#46;</p><p class="elsevierStylePara">FSGS is a clinical and pathological disorder involving primarily the glomerulus&#46;<span class="elsevierStyleSup">2-3</span> Progressive glomerular scarring is the most important feature in this disease&#46; Early in the disease process&#44; glomerulosclerosis is both focal&#44; and segmental in nature&#46; Furhermore&#44; in later stages of the disease diffuse and global glomerulosclerosis develops&#46; The loss of filtration barrier&#44; depletion of podocytes and genetic susceptibility are the culprit factors in pathogenesis of FSGS&#46;<span class="elsevierStyleBold"> </span>The condition can be idiopathic or occur secondary to obesity&#44; intrarenal hemodynamic alterations&#44; conditions with glomerulomegaly&#44; the reduced number of nephron&#44; and renal atheroembolic disease&#46;<span class="elsevierStyleSup">2&#44;3 </span>The tendency to thromboses may occur in PV which one of the chronic myeloproliferative disorders&#46;<span class="elsevierStyleSup">1</span> It has been suggested that the increase level of red blood cells&#44; elevation of the platelet count&#44; increase in tissue factor&#44; polymorphonuclear leukocytes&#44; coagulation reactions related to the platelet surface and the presence of microparticles were culprit factors&#46;<span class="elsevierStyleSup">11 </span></p><p class="elsevierStylePara">In the light of these data&#44; we hypotezised that PV may cause of FSGS via recurrent thrombosis in microvascular level&#46; Furthermore&#44; it is well known that atheroembolic disease is a cause of FSGS&#46; Thus&#44; our case is important for present to develop of FSGS in the patient with PV&#46; In the existing literature&#44; a small number of cases of FSGS that are thought to be due to PV have been reported&#46;<span class="elsevierStyleSup">4-10</span> In addition&#44; 3&#46;6&#37; &#40;only two PV&#41; incidence of FSGS has been reported in patients with myeloproliferative disease&#46;<span class="elsevierStyleSup">10</span> It has been expressed in these case reports that hyperviscosity from increased hematocrit&#44; hypoperfusion&#44; predisposition to thrombosis related to elevated platelet counts and the continuation of these conditions in recurrent attacks may have a role on the development of FSGS&#46;<span class="elsevierStyleSup">9</span> The emergence of FSGS has been reported average three to seven years after the diagnosis of PV&#46;<span class="elsevierStyleSup">4-10 </span>In the case of the subject of our study&#44; considering that FSGS has been diagnosed with PV six years later is consistent with the literature&#46; The PV was thought to be the possible reason for FSGS&#46; Additionally&#44; FSGS may occur by occlusions due to the long term recurrent microvascular thrombosis and this also could disorder to glomerular hemodynamics&#46;</p><p class="elsevierStylePara">Consequently&#44; the co-existence of PV and FSGS seems to be a cause-effect relationship rather than a random combination&#46; Further studies will be needed to demonstrate for a better understanding of this association&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Acknowledgement</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">None of the authors has a financial interest in any of the products or methods mentioned in this article&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflict of interest</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><br></br></span>The authors declare that there is no conflict of interest associated with this manuscript&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11562&#95;108&#95;35467&#95;en&#95;t1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11562_108_35467_en_t1.jpg" alt="Haematological&#44; chemistrical&#44; serological and urinalysis findings of patient"></img></a></p><p class="elsevierStylePara">Table 1&#46; Haematological&#44; chemistrical&#44; serological and urinalysis findings of patient</p>"
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