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    "textoCompleto" => "<p class="elsevierStylePara">Macroscopic haematuria due to the rupture of renal cysts is a common manifestation of autosomal dominant polycystic kidney disease &#40;ADPKD&#41;&#46; Many patients with ADPKD have frequent episodes of haematuria or evidence of intracystic haemorrhage throughout the progression of the disease&#46;<span class="elsevierStyleSup">1</span> The presence of sickle cell trait &#40;Hb AS&#41; is also accompanied by manifestations in the kidney&#44; particularly haematuria&#44; and papillary necrosis is the most frequent cause of macroscopic haematuria in heterozygous carriers of this haemoglobinopathy&#46;<span class="elsevierStyleSup">2-6</span> In one study&#44; macroscopic haematuria was the cause for 4&#37; of all hospital admissions of Afro-Americans with sickle cell trait&#46;<span class="elsevierStyleSup">7</span> As such&#44; it is not surprising that the simultaneous inheritance of both genetic diseases can create a synergy with regard to the appearance of these haemorrhagic complications&#46; Despite the fact that the association of these two hereditary diseases&#44; ADPKD and sickle cell trait&#44; was first recorded in the 1990&#8217;s&#44; when a study suggested that Afro-American patients with ADPKD and sickle cell trait could develop chronic renal failure &#40;CRF&#41; early in life&#44;<span class="elsevierStyleSup">8&#44;9</span> only recently was it pointed out that sickle cell trait is a risk factor for the development of chronic kidney disease in a population of Afro-Americans with CRF&#46;<span class="elsevierStyleSup">10&#44;11</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Haemoglobin S is the result of glutamic acid being replaced by valine as the sixth amino acid in the beta globin chain&#44; which produces a haemoglobin tetramer &#40;alpha2&#47;beta S2&#41; that is poorly soluble when deoxygenated&#46;<span class="elsevierStyleSup">4</span> Polymerisation of this type of deoxyhaemoglobin &#40;HB S&#41; is essential to vaso-occlusive phenomena&#46;<span class="elsevierStyleSup">4&#44;7&#44;12&#44;13</span> The polymer assumes the form of an elongated fibre that becomes aligned with other fibres&#44; resulting in the distortion of the erythrocyte into the classic crescent-moon or sickle shape&#44; and a drastic reduction in the flexibility of the cell&#46; The common renal manifestations of this disease in homozygous individuals &#40;Hb SS&#41; include defects in urine concentrations &#40;altered counter current mechanism&#41;&#44; distal renal tubular acidosis&#44; abnormal proximal tubular function&#44; and in early stages&#44; increased glomerular filtration rate&#46;<span class="elsevierStyleSup">14&#44;15</span> The primary cause of these symptoms appears to be the deformation of erythrocytes &#40;which adopt the sickle shape&#41; in the <span class="elsevierStyleItalic">vasa recta</span> capillaries of the renal medulla&#46; It is well established that dehydration&#44; acidosis&#44; decreased oxygen pressure&#44; and high osmolarity are the primary triggers for erythrocytes to adopt the sickle shape&#46; The normal medullary medium plays an important role in this process&#44; as it has a low oxygen pressure and high osmolarity&#46; Furthermore&#44; blood flow in <span class="elsevierStyleItalic">vasa recta</span> capillaries is much slower than in cortical vessels&#44; leading to a longer transit time&#46; Congestion and stasis in <span class="elsevierStyleItalic">vasa recta</span> capillaries can cause focal haemorrhage and necrosis&#46; Finally&#44; these processes can lead to interstitial inflammation and fibrosis&#44; tubular atrophy&#44; and papillary infarctions due to vascular lesions&#46; These lesions are more severe in patients with Hb SS genotypes than in Hb AS carriers&#46; In very early stages&#44; the physiopathology of hyperfiltration is believed to be attributed to the vasculopathy associated with haemolysis more than vaso-occlusive processes related to viscosity&#46;<span class="elsevierStyleSup">14&#44;15</span> In order to control haematuria resulting from papillary necrosis&#44; several different medical treatments have been used&#44; such as administering vasopressin&#44; tranexamic acid&#44; and oral urea&#44; or direct haemostasis over the affected papillae&#44; which includes the use of laser treatment&#46;<span class="elsevierStyleSup">4&#44;16-19</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Sickle cell disease &#40;Hb SS&#41; affects approximately 300 000 live births per year&#46;<span class="elsevierStyleSup">4&#44;7</span> The prevalence of sickle cell trait is approximately 8&#37;-10&#37; in Afro-Americans&#44;<span class="elsevierStyleSup">4</span> and can be as high as 25&#37;-30&#37; in certain areas of western Africa&#46;<span class="elsevierStyleSup">4&#44;7</span> Roughly 2&#46;5 million people in the USA and 30 million people in the world are heterozygous for the gene that causes sickle cell disease&#46; The presence of sickle cell trait Hb AS&#41;&#44; the most common haemoglobinopathy in the United States&#44; is estimated to be 40 to 50 times more common than sickle cell anaemia &#40;Hb SS&#41;&#44; and is particularly prevalent among individuals that descend from Sub-Saharan Africa&#44;India&#44; Saudi Arabia and Mediterranean countries<span class="elsevierStyleSup">4&#44;7</span> With the current patterns of global migration&#44; the number of carriers of the sickle cell haemoglobin gene is increasing in Europe&#44; and is estimated to be around 1&#37; of the total population&#46; As such&#44; many European countries have introduced early detection programmes for haemoglobinopathies in newborn infants&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Sickle cell trait is a benign disorder with no haematological manifestations in the heterozygous carrier&#44; since the morphology of the erythrocytes&#44; red blood cell indices&#44; reticulocyte count&#44; and peripheral blood smears are normal&#46; In spite of the generally benign nature of Hb AS&#44; several different potentially severe complications have been described&#46; For instance&#44; Hb AS carriers can develop rhabdomyolysis&#44; heat stroke&#44; acute renal failure&#44; papillary necrosis&#44; splenic infarction&#44; and sudden death&#46;<span class="elsevierStyleSup">4&#44;7&#44;12&#44;13&#44;20</span> Some of these events can occur during conditions of extreme physical stress&#44; and are occasionally attributed to vaso-occlusive crises&#44; suggesting that&#44; although sickle cell trait is usually quiescent&#44; it is not always benign&#46; Sickle cell trait is associated with health deterioration in terms of urine concentration&#44; haematuria&#44; and renal papillary necrosis&#46;<span class="elsevierStyleSup">21 </span>A less common cause of haematuria in these cases is renal medullary carcinoma&#44; which is a tumour that is almost exclusively found in Hb AS patients&#46;<span class="elsevierStyleSup">22</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Although sickle cell trait alone may not be sufficient for the development of chronic kidney disease&#44; it could contribute to the progression of CRF in the presence of additional factors such as ADPKD&#44; diabetes&#44; and hypertension&#46; Since patients with sickle cell trait and diabetes mellitus are prone to suffering from papillary necrosis and episodes of haematuria&#44;<span class="elsevierStyleSup">23&#44;24</span> it is possible that the pathophysiological factors induced by sickle cell trait could exacerbate the microvascular complications that arise from diabetes mellitus&#46; Meanwhile&#44; it is unknown if sickle cell trait patients have an increased risk of developing microvascular complications associated with diabetes mellitus&#46; Recently&#44; association with sickle cell trait has been recognised as an indicator of poor prognosis in diabetic patients&#44; and patients with African heritage develop renal failure on average 10 years earlier than Caucasian patients&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">KEY CONCEPTS</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">1&#46; Sickle cell trait &#40;Hb AS&#41; is a benign disorder carried by heterozygous individuals&#44; with no haematological manifestations&#46; The morphology of erythrocytes&#44; red blood cell indices&#44; reticulocyte counts&#44; and peripheral blood smears are all normal&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">2&#46; Dehydration&#44; acidosis&#44; reduced O<span class="elsevierStyleInf">2</span> pressure&#44; and high osmolarity are the primary triggers for the sickle shape taken by erythrocytes in the <span class="elsevierStyleItalic">vasa recta</span> capillaries&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">3&#46; Hb AS is associated with deteriorating urine concentrations&#44; haematuria&#44; and renal papillary necrosis&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">4&#46; Simultaneous inheritance of sickle cell trait and ADPKD can create a synergy&#44; causing recurrent haematuria&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">5&#46; In Afro-American patients with ADPKD&#44; sickle cell trait must be ruled out&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">6&#46; Although the existence of sickle cell trait alone may not be enough for developing chronic kidney disease&#44; it could contribute to the progression of CRF in the presence of other factors such as ADPKD&#44; diabetes&#44; and arterial hypertension&#46;</p>"
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Autosomal dominant polycystic kidney disease and sickle cell trait
Poliquistosis renal autosómica dominante y hemoglobina con rasgo falciforme
, R.. Pecesb, C.. Pecesc
b Servicio de Nefrología, Hospital Universitario La Paz. IdiPAZ, Madrid
c Área de Tecnología de la Información, SESCAM, Toledo,
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    "textoCompleto" => "<p class="elsevierStylePara">Macroscopic haematuria due to the rupture of renal cysts is a common manifestation of autosomal dominant polycystic kidney disease &#40;ADPKD&#41;&#46; Many patients with ADPKD have frequent episodes of haematuria or evidence of intracystic haemorrhage throughout the progression of the disease&#46;<span class="elsevierStyleSup">1</span> The presence of sickle cell trait &#40;Hb AS&#41; is also accompanied by manifestations in the kidney&#44; particularly haematuria&#44; and papillary necrosis is the most frequent cause of macroscopic haematuria in heterozygous carriers of this haemoglobinopathy&#46;<span class="elsevierStyleSup">2-6</span> In one study&#44; macroscopic haematuria was the cause for 4&#37; of all hospital admissions of Afro-Americans with sickle cell trait&#46;<span class="elsevierStyleSup">7</span> As such&#44; it is not surprising that the simultaneous inheritance of both genetic diseases can create a synergy with regard to the appearance of these haemorrhagic complications&#46; Despite the fact that the association of these two hereditary diseases&#44; ADPKD and sickle cell trait&#44; was first recorded in the 1990&#8217;s&#44; when a study suggested that Afro-American patients with ADPKD and sickle cell trait could develop chronic renal failure &#40;CRF&#41; early in life&#44;<span class="elsevierStyleSup">8&#44;9</span> only recently was it pointed out that sickle cell trait is a risk factor for the development of chronic kidney disease in a population of Afro-Americans with CRF&#46;<span class="elsevierStyleSup">10&#44;11</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Haemoglobin S is the result of glutamic acid being replaced by valine as the sixth amino acid in the beta globin chain&#44; which produces a haemoglobin tetramer &#40;alpha2&#47;beta S2&#41; that is poorly soluble when deoxygenated&#46;<span class="elsevierStyleSup">4</span> Polymerisation of this type of deoxyhaemoglobin &#40;HB S&#41; is essential to vaso-occlusive phenomena&#46;<span class="elsevierStyleSup">4&#44;7&#44;12&#44;13</span> The polymer assumes the form of an elongated fibre that becomes aligned with other fibres&#44; resulting in the distortion of the erythrocyte into the classic crescent-moon or sickle shape&#44; and a drastic reduction in the flexibility of the cell&#46; The common renal manifestations of this disease in homozygous individuals &#40;Hb SS&#41; include defects in urine concentrations &#40;altered counter current mechanism&#41;&#44; distal renal tubular acidosis&#44; abnormal proximal tubular function&#44; and in early stages&#44; increased glomerular filtration rate&#46;<span class="elsevierStyleSup">14&#44;15</span> The primary cause of these symptoms appears to be the deformation of erythrocytes &#40;which adopt the sickle shape&#41; in the <span class="elsevierStyleItalic">vasa recta</span> capillaries of the renal medulla&#46; It is well established that dehydration&#44; acidosis&#44; decreased oxygen pressure&#44; and high osmolarity are the primary triggers for erythrocytes to adopt the sickle shape&#46; The normal medullary medium plays an important role in this process&#44; as it has a low oxygen pressure and high osmolarity&#46; Furthermore&#44; blood flow in <span class="elsevierStyleItalic">vasa recta</span> capillaries is much slower than in cortical vessels&#44; leading to a longer transit time&#46; Congestion and stasis in <span class="elsevierStyleItalic">vasa recta</span> capillaries can cause focal haemorrhage and necrosis&#46; Finally&#44; these processes can lead to interstitial inflammation and fibrosis&#44; tubular atrophy&#44; and papillary infarctions due to vascular lesions&#46; These lesions are more severe in patients with Hb SS genotypes than in Hb AS carriers&#46; In very early stages&#44; the physiopathology of hyperfiltration is believed to be attributed to the vasculopathy associated with haemolysis more than vaso-occlusive processes related to viscosity&#46;<span class="elsevierStyleSup">14&#44;15</span> In order to control haematuria resulting from papillary necrosis&#44; several different medical treatments have been used&#44; such as administering vasopressin&#44; tranexamic acid&#44; and oral urea&#44; or direct haemostasis over the affected papillae&#44; which includes the use of laser treatment&#46;<span class="elsevierStyleSup">4&#44;16-19</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Sickle cell disease &#40;Hb SS&#41; affects approximately 300 000 live births per year&#46;<span class="elsevierStyleSup">4&#44;7</span> The prevalence of sickle cell trait is approximately 8&#37;-10&#37; in Afro-Americans&#44;<span class="elsevierStyleSup">4</span> and can be as high as 25&#37;-30&#37; in certain areas of western Africa&#46;<span class="elsevierStyleSup">4&#44;7</span> Roughly 2&#46;5 million people in the USA and 30 million people in the world are heterozygous for the gene that causes sickle cell disease&#46; The presence of sickle cell trait Hb AS&#41;&#44; the most common haemoglobinopathy in the United States&#44; is estimated to be 40 to 50 times more common than sickle cell anaemia &#40;Hb SS&#41;&#44; and is particularly prevalent among individuals that descend from Sub-Saharan Africa&#44;India&#44; Saudi Arabia and Mediterranean countries<span class="elsevierStyleSup">4&#44;7</span> With the current patterns of global migration&#44; the number of carriers of the sickle cell haemoglobin gene is increasing in Europe&#44; and is estimated to be around 1&#37; of the total population&#46; As such&#44; many European countries have introduced early detection programmes for haemoglobinopathies in newborn infants&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Sickle cell trait is a benign disorder with no haematological manifestations in the heterozygous carrier&#44; since the morphology of the erythrocytes&#44; red blood cell indices&#44; reticulocyte count&#44; and peripheral blood smears are normal&#46; In spite of the generally benign nature of Hb AS&#44; several different potentially severe complications have been described&#46; For instance&#44; Hb AS carriers can develop rhabdomyolysis&#44; heat stroke&#44; acute renal failure&#44; papillary necrosis&#44; splenic infarction&#44; and sudden death&#46;<span class="elsevierStyleSup">4&#44;7&#44;12&#44;13&#44;20</span> Some of these events can occur during conditions of extreme physical stress&#44; and are occasionally attributed to vaso-occlusive crises&#44; suggesting that&#44; although sickle cell trait is usually quiescent&#44; it is not always benign&#46; Sickle cell trait is associated with health deterioration in terms of urine concentration&#44; haematuria&#44; and renal papillary necrosis&#46;<span class="elsevierStyleSup">21 </span>A less common cause of haematuria in these cases is renal medullary carcinoma&#44; which is a tumour that is almost exclusively found in Hb AS patients&#46;<span class="elsevierStyleSup">22</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Although sickle cell trait alone may not be sufficient for the development of chronic kidney disease&#44; it could contribute to the progression of CRF in the presence of additional factors such as ADPKD&#44; diabetes&#44; and hypertension&#46; Since patients with sickle cell trait and diabetes mellitus are prone to suffering from papillary necrosis and episodes of haematuria&#44;<span class="elsevierStyleSup">23&#44;24</span> it is possible that the pathophysiological factors induced by sickle cell trait could exacerbate the microvascular complications that arise from diabetes mellitus&#46; Meanwhile&#44; it is unknown if sickle cell trait patients have an increased risk of developing microvascular complications associated with diabetes mellitus&#46; Recently&#44; association with sickle cell trait has been recognised as an indicator of poor prognosis in diabetic patients&#44; and patients with African heritage develop renal failure on average 10 years earlier than Caucasian patients&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">KEY CONCEPTS</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">1&#46; Sickle cell trait &#40;Hb AS&#41; is a benign disorder carried by heterozygous individuals&#44; with no haematological manifestations&#46; The morphology of erythrocytes&#44; red blood cell indices&#44; reticulocyte counts&#44; and peripheral blood smears are all normal&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">2&#46; Dehydration&#44; acidosis&#44; reduced O<span class="elsevierStyleInf">2</span> pressure&#44; and high osmolarity are the primary triggers for the sickle shape taken by erythrocytes in the <span class="elsevierStyleItalic">vasa recta</span> capillaries&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">3&#46; Hb AS is associated with deteriorating urine concentrations&#44; haematuria&#44; and renal papillary necrosis&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">4&#46; Simultaneous inheritance of sickle cell trait and ADPKD can create a synergy&#44; causing recurrent haematuria&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">5&#46; In Afro-American patients with ADPKD&#44; sickle cell trait must be ruled out&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">6&#46; Although the existence of sickle cell trait alone may not be enough for developing chronic kidney disease&#44; it could contribute to the progression of CRF in the presence of other factors such as ADPKD&#44; diabetes&#44; and arterial hypertension&#46;</p>"
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Article information
ISSN: 20132514
Original language: English
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Idiomas
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