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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44;</span></p><p class="elsevierStylePara">Primary sclerosing cholangitis &#40;PSC&#41; is a chronic cholestatic liver disease characterised by inflammation and fibrosis in the intrahepatic and extrahepatic bile ducts&#44; which primarily affects middle-age males&#46;<span class="elsevierStyleSup">1&#44;2</span> It can occur as an isolated entity or in association with inflammatory bowel disease&#46; The aetiopathogenesis of PSC has not been established&#44; although growing evidence points towards genetic and immunological causes&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara">Associated interstitial nephropathy in patients with chronic cholestatic liver disease was first described in the medical literature during the 1990s in paediatric patients&#44; and it was suggested that this association might represent a new syndrome&#46;<span class="elsevierStyleSup">3&#44;4</span></p><p class="elsevierStylePara">Recently&#44; the existence of a new disease&#44; called &#8220;IgG4-related sclerosing disease&#8221; has been proposed&#46;<span class="elsevierStyleSup">5&#44;6</span></p><p class="elsevierStylePara">Here&#44; we describe the case of a female patient diagnosed with PSC with severe interstitial nephropathy&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">A 77 year-old female was referred to the nephrology department due to plasma creatinine values of 2&#46;4mg&#47;dl&#46; The patient&#8217;s history included several surgical procedures&#58; meniscus in 1985&#44; thymoma with benign histology in 1999&#44; nasal sinus polyps more than 20 years ago and again in 2008&#44; varicose veins in 2006&#44; cystocele in 2008&#44; and hip fracture in July 2010&#46; She was diagnosed with primary sclerosing cholangitis in 2003&#44; and was under treatment with ursodeoxycholic acid&#46; On several occasions&#44; the patient had been placed retrograde biliary catheters and undergone sphincterotomy and dilation of the areas of stenosis&#46; Inflammatory bowel disease had also been diagnosed around the same time&#46; In later follow-up sessions&#44; she underwent several colonoscopies&#44; which occasionally produced normal results&#44; and at other times revealed small ileocaecal and colonic ulcers&#46; The patient also suffered an episode of pericarditis of unknown cause in January 2010&#44; and had bilateral gonarthrosis&#46; The patient was intolerant to oral iron supplements&#44; and had no toxic habits&#46;</p><p class="elsevierStylePara">At the first visit&#44; the patient was taking zolpidem 10mg&#47;day&#44; ursodeoxycholic acid 1250mg&#47;day&#44; pantoprazole 40mg&#47;day&#44; mirtazapine 15mg&#47;day&#44; and occasional paracetamol and dextropropoxyphene&#46;</p><p class="elsevierStylePara">The patient complained of intense fatigue&#44; dyspnoea after moderate exercise&#44; reduced appetite&#44; occasional nausea associated with coughing&#44; periodical constipation lasting 48 hours and alternating with diarrhoea that produced 3 or 4 evacuations per day&#44; but with no pathological signs&#44; nocturia twice per day for several months&#44; diurnal urination every 3-4 hours&#44; and no history of reno-ureteral lithiasis or haematuria&#46;</p><p class="elsevierStylePara">As regards family background&#44; the patient&#8217;s parents both died at an elderly age&#44; and three brothers had died as a result of tumours&#46;</p><p class="elsevierStylePara">The physical examination revealed the following values for standard parameters&#58; height&#58; 159cm&#59; weight&#58; 53kg&#59; blood pressure&#58; 137&#47;72mm Hg&#59; heart rate&#58; 95bpm&#46; We did not observe jugular vein engorgement&#44; carotid pulses were rhythmic and symmetrical&#44; cardiopulmonary auscultation normal&#44; and we observed hepatomegaly of approximately 4 finger-widths in the right lobe&#44; with no pain or abdominal murmurs&#46; The limbs were without oedema&#44; and distal pulses were present&#46;</p><p class="elsevierStylePara">The patient&#8217;s plasma creatinine values were 2&#46;4-2&#46;5mg&#47;dl in November 2010&#44; 2&#46;9mg&#47;dl in December 2010&#44; and 2&#46;7mg&#47;dl in January 2011&#46;</p><p class="elsevierStylePara">Complementary tests in January and February 2011 revealed the following&#58; cholesterol&#58; 204mg&#47;dl&#59; glutamic-oxaloacetic-transaminase &#40;GOT&#41;&#58; 37U&#47;l&#59; glutamic-pyruvic-transaminase &#40;GPT&#41;&#58; 23U&#47;l&#59; gamma-glutamyl transferase &#40;GGT&#41;&#58; 431U&#47;l&#59; alkaline phosphatase&#58; 483U&#47;l&#59; lactate dehydrogenase &#40;LDH&#41;&#58; 646U&#47;l&#59; ferritin&#58; 399ng&#47;ml&#59; transferrin saturation index&#58; 11&#37;&#46; All other biochemical parameters were normal&#46; The results of a haemogram were&#58; haematocrit&#58; 35&#46;1&#37;&#59; haemoglobin&#58; 11&#46;3g&#47;dl&#44; and all other values were normal&#46; The results of a blood clotting test were&#58; activated partial thromboplastin time&#58; 45 seconds&#46; The patient was anticardiolipin IgM positive&#58; 21&#46;80U MPL&#47;ml &#40;normal&#58; 0&#46;5-11&#41;&#46;</p><p class="elsevierStylePara">The results of a 24-hour urine test were&#58; proteinuria&#58; 0&#46;53g&#47;24 hours&#59; creatinine clearance&#58; 17ml&#47;min&#46; The urine resulted negative&#46;</p><p class="elsevierStylePara">An immunological analysis was positive for anti-neutrophil cytoplasmic antibodies &#40;ANCA&#41; &#40;anti-MPO and anti-PR3 negative&#41;&#59; the test was negative for anti-nuclear antibodies &#40;ANA&#41;&#44; anti-DNA antibodies&#44; anti-smooth muscle antibodies&#44; and anti-mitochondrial antibodies&#46; We also detected a decrease in immunoglobulins&#58; IgG&#58; 253mg&#47;dl &#40;normal&#58; 751-1560mg&#47;dl&#41;&#59; IgM&#58; 10mg&#47;dl &#40;normal&#58; 46-304mg&#47;dl&#41;&#59; IgA&#58; 81mg&#47;dl &#40;normal&#58; 82-453mg&#47;dl&#41;&#46; Complement&#44; rheumatoid factor&#44; C-reactive protein&#44; and ceruloplasmin were all within normal ranges&#46;</p><p class="elsevierStylePara">Serology for hepatitis B and C and HIV were all negative&#46;</p><p class="elsevierStylePara">Thyroid hormones and anti-thyroid antibodies were within normal levels&#46; Intact parathyroid hormone was 149pg&#47;ml&#46;</p><p class="elsevierStylePara">Electrophoresis revealed decreased immunoglobulins in a blood sample&#44; and non-selective proteinuria in a urine sample&#46; A Bence-Jones proteinuria test was negative&#46;</p><p class="elsevierStylePara">In imaging tests &#40;renal ultrasound&#41;&#44; we observed kidneys with normal size&#44; morphology&#44; and echogenicity&#44; with no lithiasis or dilation&#46;</p><p class="elsevierStylePara">Given the deteriorated renal function of unknown cause &#40;we had no previous reference values to compare with&#41;&#44; we performed a percutaneous renal biopsy with the following findings&#58; 4 glomeruli&#44; 2 of which were completely sclerosed&#44; and the other 2 progressing towards sclerosis&#46; An immunofluorescence study was negative for IgG&#44; IgA&#44; IgM&#44; and C3&#46; We observed dense lymphocyte infiltration expanding throughout the interstitial tissue&#44; destroying the normal architecture of the renal parenchyma &#40;Figure 1A and Figure 1B&#41;&#46; We could not properly assess fibrosis due to the high level of infiltration&#46; Figure 2A displays the immunohistochemical results using CD3 &#40;monoclonal antibody that marks all T-lymphocytes&#41;&#44; demonstrating that the majority of the infiltration is due to T-lymphocytes&#44; and Figure 2B shows the results of the immunohistochemical analysis using CD4&#46; The final histological diagnosis was severe tubulointerstitial nephropathy &#40;interstitial infiltration was predominantly by CD4-positive T-lymphocytes&#41;&#46;</p><p class="elsevierStylePara">The biopsy findings indicated treatment with prednisone 50mg&#47;day in a progressively decreasing prescription&#46;</p><p class="elsevierStylePara">Eight months later&#44; the patient has stable renal function &#40;plasma creatinine&#58; 2&#46;2mg&#47;dl&#59; creatinine clearance&#58; 20ml&#47;min&#59; proteinuria&#58; 0&#46;49g&#47;24h&#41;&#46; Current liver function values are&#58; GOT&#58; 24U&#47;l&#59; GPT&#58; 18U&#47;l&#59; GGT&#58;172U&#47;l&#59; alkaline phosphatase&#58; 342U&#47;l&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">PSC is a disease of an unknown aetiology&#44; with a progressive clinical presentation that affects the bile ducts and causes cirrhosis&#46;<span class="elsevierStyleSup">1</span> Patients with PSC can have a number of serological findings&#44; including hyper-gamma-globulinaemia and positive tests for atypical ANCA and other auto-antibodies such as anti-nuclear&#44; anti-smooth muscle&#44; anti-thyroid&#44; anti-cardiolipin&#44; and rheumatoid factor antibodies&#46;<span class="elsevierStyleSup">7</span> Elevated IgG4 levels &#40;a characteristic marker of autoimmune pancreatitis&#41; have also been described in some patients with PSC&#46;<span class="elsevierStyleSup">8</span> In fact&#44; IgG4-related sclerosing cholangitis is also included in the group of idiopathic sclerosing cholangitis&#46;<span class="elsevierStyleSup">5</span></p><p class="elsevierStylePara">Recently&#44; &#8220;IgG4-related sclerosing disease&#8221; has been classified as a new pathological&#47;clinical entity&#46;<span class="elsevierStyleSup">5-7</span> It is a systemic disease characterised by infiltration of plasma IgG4-positive and T-lymphocyte cells into several different organs&#58; pancreas&#44; bile ducts&#44; salivary glands&#44; retroperitoneum&#44; kidneys lungs&#44; and prostate&#46; The histological findings in affected organs include fibrosis&#44; sclerosis&#44; destroyed glandular architecture&#44; and lymphoplasmacytic infiltration&#46;</p><p class="elsevierStylePara">Tubulointerstitial nephropathy is also related to certain medications&#44; infections&#44; and autoimmune processes&#46; Several cases of interstitial nephropathy have been associated with sclerosing cholangitis&#44; leading to speculation about a new syndrome&#46;</p><p class="elsevierStylePara">We have described a new case of interstitial nephritis in a female patient with PSC&#46; In our case&#44; we evaluated whether this could be in the context of IgG4-related sclerosing disease&#44; but could not show such an association&#58; firstly&#44; because plasma IgG levels were 1mg&#47;dl &#40;although the patient did have an overall decrease in all immunoglobulins&#41;&#44; and secondly&#44; because the renal histological analysis did not report positivity for IgG4&#46; However&#44; the levels of IgG4 alone are insufficient to include or exclude the diagnosis of IgG4-related systemic disease&#46;<span class="elsevierStyleSup">9</span> In fact&#44; we observed dense interstitial infiltration of predominantly CD4-positive T-lymphocytes&#44; which practically destroyed all renal structures&#46;</p><p class="elsevierStylePara">There is no standardised treatment protocol for this new entity&#44; although the majority of studies have prescribed 30-60mg&#47;day of prednisolone in a progressively decreasing prescription&#44; with good responses&#46;<span class="elsevierStyleSup">5-7 </span>In our case&#44; the severe level of interstitial damage led us to indicate treatment with oral steroids&#58; although we did not reach a complete recovery of renal function &#40;possibly because the deterioration was already several months progressed before the biopsy&#44; with severe histological damage&#41;&#44; we did manage to stabilise renal function&#46;</p><p class="elsevierStylePara">In conclusion&#44; we have described the case of severe interstitial nephritis in a woman with primary sclerosing cholangitis&#58; in these patients&#44; we should examine whether this association could be referred to as an emerging pathology&#58; &#8220;IgG4-related systemic disease&#46;&#8221;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors affirm that they have no conflicts of interest related to the content of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11305&#95;16025&#95;30573&#95;en&#95;f1&#95;1111305&#46;jpg" class="elsevierStyleCrossRefs"><img src="11305_16025_30573_en_f1_1111305.jpg" alt="Haematoxylin eosin staining &#40;x10&#41;&#58; dense interstitial lymphocyte infiltration that destroyed most recognisable structures"></img></a></p><p class="elsevierStylePara">Figure 1A&#46; Haematoxylin eosin staining &#40;x10&#41;&#58; dense interstitial lymphocyte infiltration that destroyed most recognisable structures</p><p class="elsevierStylePara"><a href="grande&#47;11305&#95;16025&#95;30574&#95;en&#95;f1&#95;1111305&#46;jpg" class="elsevierStyleCrossRefs"><img src="11305_16025_30574_en_f1_1111305.jpg" alt="Haematoxylin eosin staining &#40;x20&#41;&#58; dense interstitial lymphocyte infiltration that destroyed most recognisable structures"></img></a></p><p class="elsevierStylePara">Figure 1B&#46; Haematoxylin eosin staining &#40;x20&#41;&#58; dense interstitial lymphocyte infiltration that destroyed most recognisable structures</p><p class="elsevierStylePara"><a href="grande&#47;11305&#95;16025&#95;30575&#95;en&#95;f2&#95;1111305&#46;jpg" class="elsevierStyleCrossRefs"><img src="11305_16025_30575_en_f2_1111305.jpg" alt="Immunohistochemical staining &#40;x20&#41; with CD3"></img></a></p><p class="elsevierStylePara">Figure 2A&#46; Immunohistochemical staining &#40;x20&#41; with CD3</p><p class="elsevierStylePara"><a href="grande&#47;11305&#95;19157&#95;30576&#95;en&#95;ref&#46;1130513962&#95;11305&#95;19115&#95;27645&#95;es&#95;11305&#95;figura2b&#46;jpg" class="elsevierStyleCrossRefs"><img src="11305_19157_30576_en_ref.1130513962_11305_19115_27645_es_11305_figura2b.jpg" alt="Immunohistochemical staining &#40;x20&#41; with CD4"></img></a></p><p class="elsevierStylePara">Figure 2B&#46; Immunohistochemical staining &#40;x20&#41; with CD4</p>"
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