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however&#44; it is thought to be associated with mitotic blockage linked to certain genotypes&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">A 51-year-old male patient with no cardiovascular risk factors&#44; was admitted to the Nephrology Department of our Hospital due to acute renal failure &#40;maximum creatinine 2&#46;49<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; CKD-EPI 28<span class="elsevierStyleHsp" style=""></span>ml&#47;min&#47;1&#46;73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>&#41;&#44; fever and elevated liver enzymes&#46; Urinalysis showed microhaematuria 5&#8211;10 red blood cells&#47;field&#44; proteinuria 350<span class="elsevierStyleHsp" style=""></span>mg&#47;24<span class="elsevierStyleHsp" style=""></span>h and absence of eosinophils&#46; A glomerular immunological study was performed&#44; with normal immunoglobulins&#44; negative antinuclear antibodies&#44; normal complement &#40;C3 and C4&#41;&#44; normal electrophoresis in blood and urine&#46; Given the persistent altered renal function without a clear cause&#44; we decided to perform a renal biopsy&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">This biopsy&#44; which included renal parenchyma consisting of cortex and medulla&#44; with 32 glomeruli&#59; 16 of them were sclerosed and the remaining showed slight segmental proliferation&#46; The characteristic lesion is observed in the interstitium&#44; at the level of the tubule cells&#44; which show large&#44; hyperchromatic and pleomorphic nuclei &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; In the rest of the interstitium&#44; histological lesions of acute tubular damage are observed &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#44; associated with a patchy lymphoplasmacytic inflammatory infiltrate of moderate intensity&#44; foci of fibrosis and tubular atrophy&#46; The immunohistochemistry study showed negativity for LMP-1 &#40;EBV&#41;&#44; CMV&#44; Herpes virus&#46; Ki67 &#40;cell proliferation index&#41; is negative in atypical cells and less than 5&#37; in tubular cells&#46; The direct immunofluorescence study shows no significant deposits with the antisera studied&#46; Electron microscopy showed a glomerulus with no significant lesions&#46; Based on these data&#44; the following diagnoses were made&#58; Histological lesion pattern&#58; &#40;1&#41; Global sclerosis in 50&#37; of the glomeruli&#44; with no defined lesion pattern in the non-sclerosed glomeruli&#46; &#40;2&#41; Acute tubular damage at different stages with marked nuclear atypia in tubular epithelial cells&#46; Note&#58; The negativity of Ki67 in most of the atypical cells rules out the possibility of regenerative changes and suggests investigating the following entities as aetiological causes&#58; heavy metal nephrotoxins&#44; infection by viruses other than those already studied and karyomegalic interstitial nephritis&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Given these results&#44; we proceeded to investigate possible infectious causes&#46; Microbiological and serological tests for hepatitis B&#44;C&#44; HIV&#44; toxoplasma&#44; syphilis&#44; rickettsia&#44; leishmania&#44; Herpes Simplex&#44; CMV and EBV were all negative&#46; Given that the patient worked in damp environments &#40;in basements&#41;&#44; we thought of Ochratoxin A&#44; derived from fungus&#44; this test was also negative&#46; The patient was then referred to the Clinical Genetics Unit of our hospital to investigate a possible genetic etiology&#46; With findings of homozygous mutation in the FAN1 gene &#40;associated with karyomegalic interstitial nephritis with an autosomal recessive inheritance pattern&#41;&#46; Carrier of the probably pathogenic variant c&#46;1578-1G&#62;T in homozygosis in the FAN1 gene&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">This is one of the rare cases of karyomegalic interstitial nephritis with confirmed genetic study published in the literature&#46; The prevalence of this entity is very low &#40;&#60;1&#47;1&#44;000&#44;000&#41; and there are very few cases described&#46; FAN 1 is considered an effector of the Fanconi pathway&#44; a DNA damage response signaling pathway dedicated to repair DNA inter-strand crosslink damage&#46; However&#44; no FAN1 mutations were detected in Fanconi anemia<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">6</span></a> because Fanconi anemia involves other nucleases in its pathogenesis&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">7</span></a> These differences in cellular phenotypes lines may explain the lack of apparent phenotypic similarities between FAN1-negative individuals&#44; compared to those who present karyomegalic interstitial nephritis&#44; and Fanconi individuals who have clinical disease&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">8</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">We would like to highlight the fact that there is a high percentage of individuals treated with renal replacement therapy&#44; diagnosed of fibrotic nephropathy&#44; of unknown cause&#44; in which a further study should be done as well as genetic causes should be considered&#46; Also&#44; to emphasize the importance of renal biopsy as a diagnostic tool&#44; and the importance of giving a name and surname to the renal diseases we treat&#46;</p></span>"
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Letter to the Editor
Karyomegalic nephropathy – Letter to the Editor
Nefritis kariomegálica – Carta al Editor
Rocio Gimena Muñoza,
Autor para correspondencia
rociogimu3@gmail.com

Corresponding author.
, Jessy Korina Peña Esparragozab, Carolina Castillo Torresc, Fuensanta Moreno Barriod
a Nephrology Department, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain
b Nephrology Department, Hospital Universitario La Paz, Madrid, Spain
c Pathology Department, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain
d Associate Professor, Universidad Alcalá de Henares, Nephrology Department, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Karyomegalic tubulointerstitial nephritis is a rare disease of uncertain etiology which has been linked to a genetic condition related to FAN1 gene&#46; It is characterized by chronic tubulointerstitial nephritis with karyomegalic tubular epithelial cells &#40;characteristic of the disease&#41; lining the proximal and distal tubules and with enlarged hyperchromatic nuclei&#46; It is a systemic entity that inevitably leads to end-stage renal disease&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">1</span></a> Involvement of other extrarenal organs may be present and is usually mild&#46; It may consist of recurrent upper respiratory tract infections and liver impairment&#44; as evidenced by elevated liver enzymes&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">2</span></a> The disease was first described by Burry in 1974&#44;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">3</span></a> and the term karyomegalic nephritis was coined by Mihatsch in 1979&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">4</span></a> The exact pathogenesis of this disorder is unknown&#59; however&#44; it is thought to be associated with mitotic blockage linked to certain genotypes&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">A 51-year-old male patient with no cardiovascular risk factors&#44; was admitted to the Nephrology Department of our Hospital due to acute renal failure &#40;maximum creatinine 2&#46;49<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; CKD-EPI 28<span class="elsevierStyleHsp" style=""></span>ml&#47;min&#47;1&#46;73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>&#41;&#44; fever and elevated liver enzymes&#46; Urinalysis showed microhaematuria 5&#8211;10 red blood cells&#47;field&#44; proteinuria 350<span class="elsevierStyleHsp" style=""></span>mg&#47;24<span class="elsevierStyleHsp" style=""></span>h and absence of eosinophils&#46; A glomerular immunological study was performed&#44; with normal immunoglobulins&#44; negative antinuclear antibodies&#44; normal complement &#40;C3 and C4&#41;&#44; normal electrophoresis in blood and urine&#46; Given the persistent altered renal function without a clear cause&#44; we decided to perform a renal biopsy&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">This biopsy&#44; which included renal parenchyma consisting of cortex and medulla&#44; with 32 glomeruli&#59; 16 of them were sclerosed and the remaining showed slight segmental proliferation&#46; The characteristic lesion is observed in the interstitium&#44; at the level of the tubule cells&#44; which show large&#44; hyperchromatic and pleomorphic nuclei &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; In the rest of the interstitium&#44; histological lesions of acute tubular damage are observed &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#44; associated with a patchy lymphoplasmacytic inflammatory infiltrate of moderate intensity&#44; foci of fibrosis and tubular atrophy&#46; The immunohistochemistry study showed negativity for LMP-1 &#40;EBV&#41;&#44; CMV&#44; Herpes virus&#46; Ki67 &#40;cell proliferation index&#41; is negative in atypical cells and less than 5&#37; in tubular cells&#46; The direct immunofluorescence study shows no significant deposits with the antisera studied&#46; Electron microscopy showed a glomerulus with no significant lesions&#46; Based on these data&#44; the following diagnoses were made&#58; Histological lesion pattern&#58; &#40;1&#41; Global sclerosis in 50&#37; of the glomeruli&#44; with no defined lesion pattern in the non-sclerosed glomeruli&#46; &#40;2&#41; Acute tubular damage at different stages with marked nuclear atypia in tubular epithelial cells&#46; Note&#58; The negativity of Ki67 in most of the atypical cells rules out the possibility of regenerative changes and suggests investigating the following entities as aetiological causes&#58; heavy metal nephrotoxins&#44; infection by viruses other than those already studied and karyomegalic interstitial nephritis&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Given these results&#44; we proceeded to investigate possible infectious causes&#46; Microbiological and serological tests for hepatitis B&#44;C&#44; HIV&#44; toxoplasma&#44; syphilis&#44; rickettsia&#44; leishmania&#44; Herpes Simplex&#44; CMV and EBV were all negative&#46; Given that the patient worked in damp environments &#40;in basements&#41;&#44; we thought of Ochratoxin A&#44; derived from fungus&#44; this test was also negative&#46; The patient was then referred to the Clinical Genetics Unit of our hospital to investigate a possible genetic etiology&#46; With findings of homozygous mutation in the FAN1 gene &#40;associated with karyomegalic interstitial nephritis with an autosomal recessive inheritance pattern&#41;&#46; Carrier of the probably pathogenic variant c&#46;1578-1G&#62;T in homozygosis in the FAN1 gene&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">This is one of the rare cases of karyomegalic interstitial nephritis with confirmed genetic study published in the literature&#46; The prevalence of this entity is very low &#40;&#60;1&#47;1&#44;000&#44;000&#41; and there are very few cases described&#46; FAN 1 is considered an effector of the Fanconi pathway&#44; a DNA damage response signaling pathway dedicated to repair DNA inter-strand crosslink damage&#46; However&#44; no FAN1 mutations were detected in Fanconi anemia<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">6</span></a> because Fanconi anemia involves other nucleases in its pathogenesis&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">7</span></a> These differences in cellular phenotypes lines may explain the lack of apparent phenotypic similarities between FAN1-negative individuals&#44; compared to those who present karyomegalic interstitial nephritis&#44; and Fanconi individuals who have clinical disease&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">8</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">We would like to highlight the fact that there is a high percentage of individuals treated with renal replacement therapy&#44; diagnosed of fibrotic nephropathy&#44; of unknown cause&#44; in which a further study should be done as well as genetic causes should be considered&#46; Also&#44; to emphasize the importance of renal biopsy as a diagnostic tool&#44; and the importance of giving a name and surname to the renal diseases we treat&#46;</p></span>"
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Nefrología
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¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?