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• W2890680912 abstract "Acute kidney injury (AKI) is common in patients with severe hepatic failure and is associated with significant morbidity and mortality. Ischemia and inflammation are the hallmarks of the pathophysiology of kidney injury in cirrhosis.1Gines P. Schrier R.W. Renal failure in cirrhosis.N Engl J Med. 2009; 361: 1279-1290Crossref PubMed Scopus (602) Google Scholar Additionally, an important nonvasomotor mechanism of AKI in cirrhosis is the toxicity of cholephiles, often known as bile cast nephropathy, with histological evidence of tubular bile cast formation and tubular epithelial injury. Recently, an increasing number of cases have been described from kidney biopsies, although most cases included other causes of AKI, such as hepatorenal syndrome. Here, we report a case of bile cast nephropathy in a patient with obstructive cholestasis caused by choledocholithiasis, without evidence of hepatorenal syndrome. This is an excellent teaching case, particularly to the nephrology trainee, and the teaching points are highlighted in Table 1.Table 1Distinct teaching points for kidney trainee audience• Bile cast nephropathy has been a largely forgotten diagnosis as a cause of acute kidney injury and is diagnosed via a kidney biopsy.• Bile cast nephropathy is promoted by associated kidney ischemia, but severe isolated cholestasis is sufficient to induce its occurrence.• Bile cast nephropathy represents a spectrum of renal injury from proximal tubulopathy to intrarenal bile cast formation found in patients with severe liver dysfunction.• The management of bile cast nephropathy is through normalization of bilirubinemia, which may require time on renal replacement therapy. Open table in a new tab A 61-year-old man was admitted to the Royal Brisbane and Women’s Hospital in April 2018, with fatigue, anorexia, and severe jaundice. He had a background of T3N0 transitional cell bladder carcinoma, bilateral retinoblastoma, and multiple malignant melanomas. Before his admission, his baseline kidney function was normal with a serum creatinine of 86 μmol/l (normal 60 μmol/l to 120 μmol/l) (corresponding to estimated glomerular filtration rate of greater than 90 ml/min per 1.73 m2 as calculated by the Chronic Kidney Disease Epidemiology Collaboration creatinine equation, which is the normal reference range). Blood pressure on admission was 110/70 mm Hg and heart rate was 68 beats per minute regularly regular. He had no fever but was oliguric. His skin was markedly jaundiced and scleral icterus was present, but he demonstrated no peripheral stigmata of chronic liver disease. His abdomen was not tender or peritonitic and there was no evidence of ascites. Laboratory tests revealed a cholestatic picture with increased total bilirubin (260 mg/dl) (normal <20 mg/dl), alkaline phosphatase (1070 IU/l) (normal 30–110 IU/l), and γ-glutamyltranspeptidase (450 IU/l) (normal <38 IU/l) levels. Serum creatinine level was elevated at 463 μmol/l (estimated glomerular filtration rate 11 ml/min per 1.73 m2 as calculated by the Chronic Kidney Disease Epidemiology Collaboration creatinine equation). C-reactive protein level was 4.5 mg/l (normal <5 mg/l). Autoimmune and infectious causes were excluded. Proteinuria was measured at protein excretion of 1.1 g per 24 hours (normal <15 mg per 24 hours). There was no microhematuria. Computed tomography of the abdomen and pelvis without injection of iodine contrast did not reveal an etiology. A magnetic resonance cholangiopancreatography showed obstructive cholestasis with intrahepatic and extrahepatic dilated bile ducts caused by common bile duct stones. In the absence of signs of portal hypertension and with preserved natriuresis (sodium urinary excretion, 95 mmol/l), hepatorenal syndrome was excluded. The patient’s kidney dysfunction progressed, and he became acidemic and oliguric, requiring commencement of hemodialysis via a central catheter. A kidney biopsy was subsequently performed. The renal cortical tissue sample measured 0.7 cm and included 23 glomeruli of which 3 were globally sclerosed (Figure 1). The remaining glomeruli were normal by light microscopy. They did not show mesangial or endocapillary hypercellularity. There were no crescents or necrotizing lesions, and no lesions of segmental sclerosis were identified. Arterial vessels showed mild fibro-intima thickening. There was no vasculitis. There was no discernible tubular atrophy or interstitial fibrosis. Many of the tubules contained yellow to green casts, some of which were birefringent when viewed under polarized light. There were additional features of tubular injury with epithelial flattening, detachment of cells into the lumen, and occasional mitotic figures. The interstitium was edematous and contained a relatively mild but diffuse infiltrate of chronic inflammatory cells, including eosinophils. In addition, there appeared to be a few small non-necrotizing granulomata. There was no immunofluorescence directed against IgG, IgA, IgM, complement components C3 and C1q, or κ and λ light chains. The diagnosis of bile cast nephropathy in the setting of obstructive cholestasis, most likely caused by common bile duct stones, was made. Endoscopic retrograde cholangiopancreatography with sphincterotomy and stent insertion was performed with extensive sludge noted but no stones were found at the time of the procedure. A significant decrease in serum bilirubin levels occurred after the stent insertion, accompanied by a reduction in serum creatinine (Figure 2). Three months after the occurrence of the AKI, kidney function had recovered to close to baseline, with a serum creatinine level of 115 μmol/l (corresponding estimated glomerular filtration rate 67 ml/min per 1.73 m2, as calculated by Chronic Kidney Disease Epidemiology Collaboration creatinine equation). This case is a histologic description of bile cast nephropathy in the setting of cholestasis without underlying hepatopathy. The mechanism by which bile cast nephropathy occurs is controversial, but has been reported in the literature. Kidney injury combined with marked cholestasis may result from the precipitation of cholephiles in renal tubules with toxicity on the epithelial cells.2Rafat C. Burbach M. Brocheriou I. et al.Bilirubin-associated acute tubular necrosis in a kidney transplant recipient.Am J Kidney Dis. 2013; 61: 782-785Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar The formation of casts may be secondary to the poor water solubility of cholephiles and/or the limits of absorption in the proximal tubules, above which casts may form and cause tubular obstruction.3Kaler B. Karram T. Morgan W.A. et al.Are bile acids involved in the renal dysfunction of obstructive jaundice? An experimental study in bile duct ligated rats.Ren Fail. 2004; 26: 507-516Crossref PubMed Scopus (39) Google Scholar Bile casts are conventionally found in the distal tubule, classically at the level of the aquaporin 2−positive collecting duct,4Krones E. Wagner M. Eller K. et al.Bile acid-induced cholemic nephropathy.Dig Dis. 2015; 33: 367-375Crossref PubMed Scopus (36) Google Scholar, 5Fickert P. Krones E. Pollheimer M.J. et al.Bile acids trigger cholemic nephropathy in common bile-duct-ligated mice.Hepatology. 2013; 58: 2056-2069Crossref PubMed Scopus (100) Google Scholar which may be the result of a higher urinary concentration caused by water reabsorption or lower urinary pH, subsequently decreasing bile cast solubility.6Hofmann A.F. Mysels K.J. Bile acid solubility and precipitation in vitro and in vivo: the role of conjugation, pH, and Ca2+ ions.J Lipid Res. 1992; 33: 617-626PubMed Google Scholar Fajers7Fajers C.M. Experimental studies in cholemic nephrosis. 3. The effect of cholemia by itself and combined with ten minutes' unilateral renal ischemia on the kidneys of hydrated rabbits as judged by some renal function tests.Acta Pathol Microbiol Scand. 1957; 41: 44-55Crossref PubMed Scopus (7) Google Scholar studied the effects of cholemia with or without renal ischemia and showed that 2 days of isolated cholemia induced only slight and insignificant morphologic changes in the kidneys and that lesions were more severe with concomitant ischemia. Hyperbilirubinemia has additionally been shown to attenuate the development of angiotensin II−induced arterial hypertension by reducing the production of superoxide8LeBlanc R.M. Navar L.G. Botros F.T. Bilirubin exerts renoprotective effects in angiotensin II-hypertension.Am J Med Sci. 2010; 340: 144-146Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar and sodium reabsorption in the thick ascending loop of Henle.8LeBlanc R.M. Navar L.G. Botros F.T. Bilirubin exerts renoprotective effects in angiotensin II-hypertension.Am J Med Sci. 2010; 340: 144-146Abstract Full Text Full Text PDF PubMed Scopus (16) Google Scholar, 9Brem A.S. Cashore W.J. Pacholski M. et al.Effects of bilirubin on transepithelial transport of sodium, water, and urea.Kidney Int. 1985; 27: 51-57Abstract Full Text PDF PubMed Scopus (8) Google Scholar Bilirubin may also cause deleterious effects on kidney cells. Using cortical slices of kidney, another study showed that bilirubin was taken up by renal epithelial cells via the organic anion transport system and, within the cell, inhibit adenosine triphosphate production.9Brem A.S. Cashore W.J. Pacholski M. et al.Effects of bilirubin on transepithelial transport of sodium, water, and urea.Kidney Int. 1985; 27: 51-57Abstract Full Text PDF PubMed Scopus (8) Google Scholar Lower adenosine triphosphate levels were in turn associated with mitochondrial structural defects, which led to increased permeability of cell membranes, resulting in modified electrolyte content and cell volume.9Brem A.S. Cashore W.J. Pacholski M. et al.Effects of bilirubin on transepithelial transport of sodium, water, and urea.Kidney Int. 1985; 27: 51-57Abstract Full Text PDF PubMed Scopus (8) Google Scholar In summary, bile cast nephropathy appears to be promoted by associated kidney ischemia, but severe isolated cholestasis may be sufficient to induce its occurrence. AKI in these cases is most likely due to epithelial cell damage and tubular obstruction caused by bile casts. Normalization of bilirubinemia in the aforementioned patient may have led to complete kidney function recovery." @default.
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• W2890680912 title "Bile Cast Nephropathy in a Patient With Obstructive Jaundice" @default.
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• W2890680912 doi "https://doi.org/10.1016/j.ekir.2018.09.008" @default.
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