Letter to the Editor
A case report of cyanotic nephropathy
Nefropatía por cianosis. A propósito de un caso
Mayra Ortega-Díaz, Marta Puerta Carretero, Elena Corchete, Juan A. Martín Navarro
, M. Teresa Jaldo, Marta Albalate, Patricia de Sequera, Roberto Alcázar Arroyo
Corresponding author
Servicio de Nefrología, Hospital Universitario Infanta Leonor, Madrid, Spain
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A propósito de un caso" "tienePdf" => "es" "tieneTextoCompleto" => "es" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "96" "paginaFinal" => "98" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "A case report of cyanotic nephropathy" ] ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figura 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1571 "Ancho" => 2161 "Tamanyo" => 419923 ] ] "descripcion" => array:1 [ "es" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Fisiopatología de la nefropatía por cianosis.</p> <p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">FF: fracción de filtración; FSR: flujo sanguíneo renal; GEFyS: glomerulosclerosis focal y segmentaria; GLM: glomérulo; GNCM: glomerulonefritis de cambios mínimos; HFG: hiperfiltración glomerular; HT: hipertrofia; PDGF: factor de crecimiento derivado de las plaquetas; TCP: túbulo contorneado proximal; TGFβ: factor de crecimiento tumoral β; VSD AA: vasodilatación arteriola aferente.</p> <p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Línea continua: vía de daño vascular; línea quebrada: vía de daño proliferativo; doble cuadrícula: vía de daño final.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Mayra Ortega-Díaz, Marta Puerta Carretero, Elena Corchete, Juan A. 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Martín Navarro, M. Teresa Jaldo, Marta Albalate, Patricia de Sequera, Roberto Alcázar Arroyo" "autores" => array:8 [ 0 => array:2 [ "nombre" => "Mayra" "apellidos" => "Ortega-Díaz" ] 1 => array:2 [ "nombre" => "Marta" "apellidos" => "Puerta Carretero" ] 2 => array:2 [ "nombre" => "Elena" "apellidos" => "Corchete" ] 3 => array:4 [ "nombre" => "Juan A." "apellidos" => "Martín Navarro" "email" => array:1 [ 0 => "juanmartinnav@hotmail.com" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 4 => array:2 [ "nombre" => "M. Teresa" "apellidos" => "Jaldo" ] 5 => array:2 [ "nombre" => "Marta" "apellidos" => "Albalate" ] 6 => array:2 [ "nombre" => "Patricia" "apellidos" => "de Sequera" ] 7 => array:2 [ "nombre" => "Roberto" "apellidos" => "Alcázar Arroyo" ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Servicio de Nefrología, Hospital Universitario Infanta Leonor, Madrid, Spain" "identificador" => "aff0005" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "<span class="elsevierStyleItalic">Corresponding author</span>." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Nefropatía por cianosis. A propósito de un caso" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1567 "Ancho" => 2157 "Tamanyo" => 349216 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Pathophysiology of cyanotic nephropathy.</p> <p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">FF: filtration fraction; RBF: renal blood flow; FSGE: focal and segmental glomerulosclerosis; GLM: glomerulus; MCGN: minimal change glomerulonephritis; GHF: glomerular hyperfiltration; HT: hypertrophy; PDGF: platelet derived growth factor; PCT: proximal convoluted tubule; TGFβ: tumor growth factor β; AA VSD: arteriolar afferent vasodilation.</p> <p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Continuous line: pathway of vascular damage; broken line: path of proliferative damage; double grid: path of final damage.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Cyanosis nephropathy is an infrequent and not well known condition, so the description of a case should be of interest.</p><p id="par0010" class="elsevierStylePara elsevierViewall">A 49-year-old man attended outpatient clinic for proteinuria. He was diagnosed with tricuspid atresia in his early childhood, treated surgically with classic Glenn intervention (anastomosis of the superior vena cava to the right pulmonary artery) at 20 months of age, and in a second intervention by means of Blalock-Taussig pulmonary systemic fistula left (GORE-TEX<span class="elsevierStyleSup">®</span> graft prosthesis from the subclavian artery to the homolateral pulmonary artery), which subsequently had to be repaired with an endovascular stent due to stenosis. He had moderate left ventricular dysfunction with chronic cyanosis, with habitual Hb values of 17<span class="elsevierStyleHsp" style=""></span>g/dl and Hct of 60%. Moderate thrombocytopenia and transient ischemic attack 10 years earlier, after which antiaggregation with ASA was replaced by clopidogrel. Regular treatment included clopidogrel, allopurinol and bosentan. In addition, he had periodic phlebotomies until 2 years ago when they were suspended at the discretion of their cardiologists. The patient consulted for a proteinuria of unknown time of evolution. Normal blood pressure with a BMI of 23<span class="elsevierStyleHsp" style=""></span>kg/m<span class="elsevierStyleSup">2</span>. In the analytic, Cr 0.78<span class="elsevierStyleHsp" style=""></span>mg/dl with estimated glomerular filtration rate by CKD-EPI greater than 90<span class="elsevierStyleHsp" style=""></span>ml/min/1.73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>, Hb 23.8<span class="elsevierStyleHsp" style=""></span>g/dl; Hct of 80.8%; platelets 89,000/ml; uric acid 7.9<span class="elsevierStyleHsp" style=""></span>mg/dl; cholesterol 257<span class="elsevierStyleHsp" style=""></span>mg/dl; systematic urine with minimal microhematuria; MAu/Cru 3371.4<span class="elsevierStyleHsp" style=""></span>mg/g and proteinuria of 6.21<span class="elsevierStyleHsp" style=""></span>g/24<span class="elsevierStyleHsp" style=""></span>h of mixed type. Negative viral serology. Negative immunology tests including complement, ANA, ANCA, anti-DN, anti-phospholipase and anti-PLA2R antibodies. Immunoglobulins and proteinogram were normal. Abdominal ultrasound with kidneys of conserved size and bilateral diffuse hyper echogenicity as the only finding that that was noteworthy.</p><p id="par0015" class="elsevierStylePara elsevierViewall">Since 1960,<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">1</span></a> it has been known that between 30 and 50% of cyanotic heart diseases can be the cause of a secondary glomerulopathy known as cyanosis nephropathy.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">2</span></a> It is a correlate of cardiorenal syndrome type 2. It is produced trough to different mechanisms (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>)<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">3–5</span></a> initiated by hyperviscosity syndrome secondary to extreme polycythemia and cyanosis, which cause an increase in shear stress by passing a high number of red blood cells through the capillary unit in the glomerulus. The subsequent decrease in renal blood flow and filtration fraction induce hypoxia, with an angiogenic response mediated by the release of nitric oxide, selective vasodilatation of the afferent arteriole and increased capillary pressure, which determines glomerular hyperfiltration. The decrease in peritubular capillary blood flow also contributes to increase in capillary pressure. In parallel, cyanosis triggers an angiogenic stimulus with an increase in the number of capillaries per glomerulus, glomerulomegaly due to endothelial proliferation and an increase in the surface area of the glomerular capillary, the podocyte stretches and it is hypertrophied due to stress and there is a damage that mimics glomerulonephritis due to minimal changes and subsequently to segmental glomerulosclerosis.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">6</span></a></p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">It is accepted that the initial damage is in the tubule,<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">7–9</span></a> especially in the proximal tubule, as reflected by an increase in urinary N-acetyl glucosamine and α1-microglobulin that usually occurs in the first decade of life and continue in the next decade with a glomerular damage (albuminuria, proteinuria and decrease in glomerular filtration). As the mechanism of compensating glomerular hyperfiltration is exhausted, a glomerular hyalinosis develops with glomerulosclerosis and interstitial fibrosis that will condition the midterm prognosis. A different injury is distinguished in small vessels resulting from capillary dilation, thickening or endothelial destruction, glomerulosclerosis and periglomerular fibrosis mediated by a non-vascular proliferative mechanism, resulting from the shunt in the pulmonary circulation. Under normal conditions, after being released from the spleen and bone marrow, a population of megakaryocytes are retained in the interstitium and in the pulmonary vasculature<a class="elsevierStyleCrossRefs" href="#bib0095"><span class="elsevierStyleSup">5,10,11</span></a> where they disaggregate forming active platelets at a rate of 10<span class="elsevierStyleSup">6</span>/h. However in conditions of right/left shunt this step is avoided and the megakaryocytes pass intact to the systemic circulation making possible that their alpha granules, rich in PDGF and in TGFβ, reach the renal glomerulus and be released, producing 2 effects. A peripheral thrombocytopenia that indirectly quantifies the degree of shunt (the greater thrombocytopenia, the greater shunt) and an increase of proliferative platelet factors that will cause an increase in mesangial juxtaglomerular cells, mesangial matrix and focal interstitial fibrosis.</p><p id="par0025" class="elsevierStylePara elsevierViewall">The hematocrit level, the delay until shunt surgery and a platelet level of less than 250,000/ml are risk factors for the appearance of nephropathy.<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">3,12,13</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The treatment consists of reducing surgical waiting times, periodic phlebotomies and inhibition of the renin–angiotensin–aldosterone axis with ACE inhibitors.<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">14</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Renal prognosis is unfavorable if the cause is not resolved. In our case, we began treatment with statins and ACEIs, and periodic phlebotomies were again recommended without sufficient follow-up to evaluate the response at the present time.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Ortega-Díaz M, Puerta Carretero M, Corchete E, Martín Navarro JA, Jaldo MT, Albalate M, et al. Nefropatía por cianosis. A propósito de un caso. Nefrologia. 2019;39:96–98.</p>" ] ] "multimedia" => array:1 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1567 "Ancho" => 2157 "Tamanyo" => 349216 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Pathophysiology of cyanotic nephropathy.</p> <p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">FF: filtration fraction; RBF: renal blood flow; FSGE: focal and segmental glomerulosclerosis; GLM: glomerulus; MCGN: minimal change glomerulonephritis; GHF: glomerular hyperfiltration; HT: hypertrophy; PDGF: platelet derived growth factor; PCT: proximal convoluted tubule; TGFβ: tumor growth factor β; AA VSD: arteriolar afferent vasodilation.</p> <p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Continuous line: pathway of vascular damage; broken line: path of proliferative damage; double grid: path of final damage.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:14 [ 0 => array:3 [ "identificador" => "bib0075" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Glomerular alterations in cyanotic congenital heart disease" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "G.S. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 17 | 7 | 24 |
| 2024 October | 103 | 48 | 151 |
| 2024 September | 98 | 43 | 141 |
| 2024 August | 90 | 70 | 160 |
| 2024 July | 123 | 31 | 154 |
| 2024 June | 73 | 51 | 124 |
| 2024 May | 70 | 52 | 122 |
| 2024 April | 98 | 46 | 144 |
| 2024 March | 89 | 33 | 122 |
| 2024 February | 89 | 43 | 132 |
| 2024 January | 84 | 31 | 115 |
| 2023 December | 75 | 40 | 115 |
| 2023 November | 112 | 57 | 169 |
| 2023 October | 84 | 87 | 171 |
| 2023 September | 100 | 75 | 175 |
| 2023 August | 91 | 31 | 122 |
| 2023 July | 111 | 63 | 174 |
| 2023 June | 109 | 33 | 142 |
| 2023 May | 205 | 55 | 260 |
| 2023 April | 144 | 55 | 199 |
| 2023 March | 139 | 44 | 183 |
| 2023 February | 105 | 42 | 147 |
| 2023 January | 102 | 44 | 146 |
| 2022 December | 153 | 73 | 226 |
| 2022 November | 140 | 45 | 185 |
| 2022 October | 130 | 54 | 184 |
| 2022 September | 86 | 58 | 144 |
| 2022 August | 87 | 41 | 128 |
| 2022 July | 100 | 69 | 169 |
| 2022 June | 105 | 58 | 163 |
| 2022 May | 108 | 34 | 142 |
| 2022 April | 111 | 55 | 166 |
| 2022 March | 89 | 65 | 154 |
| 2022 February | 95 | 55 | 150 |
| 2022 January | 127 | 49 | 176 |
| 2021 December | 91 | 66 | 157 |
| 2021 November | 113 | 52 | 165 |
| 2021 October | 117 | 69 | 186 |
| 2021 September | 94 | 58 | 152 |
| 2021 August | 71 | 66 | 137 |
| 2021 July | 93 | 43 | 136 |
| 2021 June | 78 | 44 | 122 |
| 2021 May | 67 | 45 | 112 |
| 2021 April | 291 | 163 | 454 |
| 2021 March | 134 | 54 | 188 |
| 2021 February | 109 | 46 | 155 |
| 2021 January | 63 | 32 | 95 |
| 2020 December | 61 | 28 | 89 |
| 2020 November | 78 | 27 | 105 |
| 2020 October | 73 | 25 | 98 |
| 2020 September | 81 | 30 | 111 |
| 2020 August | 43 | 26 | 69 |
| 2020 July | 52 | 16 | 68 |
| 2020 June | 67 | 38 | 105 |
| 2020 May | 59 | 48 | 107 |
| 2020 April | 130 | 27 | 157 |
| 2020 March | 51 | 20 | 71 |
| 2020 February | 88 | 33 | 121 |
| 2020 January | 111 | 44 | 155 |
| 2019 December | 70 | 38 | 108 |
| 2019 November | 61 | 39 | 100 |
| 2019 October | 69 | 26 | 95 |
| 2019 September | 55 | 25 | 80 |
| 2019 August | 42 | 14 | 56 |
| 2019 July | 48 | 33 | 81 |
| 2019 June | 57 | 27 | 84 |
| 2019 May | 51 | 29 | 80 |
| 2019 April | 60 | 45 | 105 |
| 2019 March | 36 | 37 | 73 |
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