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enteric hyperoxaluria is another potential cause of kidney stones and interstitial nephritis in patients with short bowel syndrome or other causes of fat malabsorption in patients without colectomy&#46;<span class="elsevierStyleSup">3&#44;4</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">We report the case of a 59-year old patient who underwent surgery for a Bismuth type IIIB hilar cholangiocarcinoma in September 2009&#46; There were a number of complications after the intervention&#58; ischaemic necrosis of the right hepatic lobe anterior segments&#44; a biliary fistula and abscesses in the surgical site&#46; The patient was therefore eventually discharged wearing a drain in the surgical site&#46; In January 2010&#44; the patient was admitted due to acute renal failure with serum creatinine of 9&#46;6mg&#47;dl&#44; vomiting and increased cardiac output due to drainage&#46; Urine sodium was 34meq&#47;l&#46; Additional tests also highlighted the presence of a proteinuria of 0&#46;6g&#47;24h and urine sediment with 10 red cells per field without leukocyturia&#46; The patient had a beta-2-microglobulin level of 548&#46;72&#956;g&#47;g and NAG of 9U&#47;l in the urine&#46; The renal function continued to deteriorate despite volume replacement and a renal biopsy was performed to investigate the origin of the acute renal failure&#46;</p><p class="elsevierStylePara">The renal biopsy showed varying degrees of shrinkage with fibrous thickening of the capsule in some glomeruli&#46; Diffuse fibrosis was observed in the interstitial area&#44; with focal tubular atrophy affecting approximately 25&#37; of the parenchyma&#46; Predominantly lymphoplasmacytic inflammatory infiltrate was detected in various areas&#44; with occasional presence of eosinophils&#46; Some tubules had necrotic cylinders in the lumen&#46; The lumen of many tubules was occupied by birefringent crystals consistent with oxalate &#40;Figure 1&#41;&#46;</p><p class="elsevierStylePara">The oxalate in urine was 47&#46;70mg&#47;24h &#40;up to 40mg&#47;24h with normal renal function&#41;&#46; After hydration&#44; correction of acidosis&#44; treatment with calcium carbonate and low oxalate diet&#44; the patient presented a successful evolution&#44; with a progressive decline in serum creatinine to 2mg&#47;dl prior to discharge&#46;</p><p class="elsevierStylePara">Under normal conditions&#44; the daily load of endogenous and exogenous oxalate is completely excreted by the kidneys&#46; When renal function is altered&#44; renal and extrarenal deposits of oxalate begin to appear&#44; which is known as systemic oxalosis&#46; When there is a high oxalate load&#44; hyperoxaluria is produced&#44; increasing the risk of nephrolithiasis and nephrocalcinosis&#46; In addition&#44; acute renal failure may be triggered in patient with a precipitating factor&#44; such as dehydration and&#47;or metabolic acidosis&#46;</p><p class="elsevierStylePara">Hyperoxaluria is defined as the presence of urinary oxalate values greater than 40mg&#47;day&#46; It is frequently observed in patients with fat malabsorption due to digestive hyperabsorption of oxalate&#44; unlike primary hyperoxaluria due to enzyme deficiencies associated with a hyperproduction of oxalate in the liver&#46;<span class="elsevierStyleSup">5</span></p><p class="elsevierStylePara">The patient in question presented an enteric hyperoxaluria in relation to malabsorption of fats&#46; The main mechanism involved is the binding of calcium in the intestine by fatty acids&#44; which decreases the calcium oxalate in the digestive tract and increases the ionised oxalic acid absorbed in the intestine&#46; These patients may benefit from conservative treatment based on reducing oxalate and fat in the diet&#44; the administration of calcium carbonate as an oxalate binder&#44; and an increased intake of fluids and administration of bases&#44; such as sodium citrate&#44; in order to increase urinary calcium oxalate solubility&#46; Likewise&#44; it has yet to be confirmed if recolonisation with <span class="elsevierStyleItalic">Oxalobacter formigenes</span> also reduces urinary oxalate excretion&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">In conclusion&#44; 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Acute renal failure due to oxalate crystal deposition and enteric hyperoxaluria
Insuficiencia renal aguda por depósito de cristales de oxalato e hiperoxaluria de origen entérico
, A.. Sentísb, L.F.. Quintanab, E.. Massób, N.S.. Perézb, A.. Botey Puigb, J.M.. Campistol Planab
b Servicio de Nefrología y Trasplante Renal, Hospital Clínic i Provincial, Barcelona,
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44; </span></p><p class="elsevierStylePara">Acute renal failure associated with intratubular crystal precipitation is a common cause of renal injury which may occur in the context of a wide variety of clinical situations&#46; The most common are those associated with uric acid nephropathy and with intravenous acyclovir&#44; sulphonamides&#44; methotrexate&#44; and indinavir treatment&#46; Most patients affected by this type of renal disease have a variety of predisposing risk factors&#44; notable among which are effective intravascular volume depletion and previous chronic renal failure&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara">Ingestion of ethylene glycol and&#44; exceptionally&#44; the administration of ascorbic acid at high doses can cause hypercalcaemia and acute renal failure due to deposition of oxalate crystals&#46;<span class="elsevierStyleSup">2</span> However&#44; enteric hyperoxaluria is another potential cause of kidney stones and interstitial nephritis in patients with short bowel syndrome or other causes of fat malabsorption in patients without colectomy&#46;<span class="elsevierStyleSup">3&#44;4</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">We report the case of a 59-year old patient who underwent surgery for a Bismuth type IIIB hilar cholangiocarcinoma in September 2009&#46; There were a number of complications after the intervention&#58; ischaemic necrosis of the right hepatic lobe anterior segments&#44; a biliary fistula and abscesses in the surgical site&#46; The patient was therefore eventually discharged wearing a drain in the surgical site&#46; In January 2010&#44; the patient was admitted due to acute renal failure with serum creatinine of 9&#46;6mg&#47;dl&#44; vomiting and increased cardiac output due to drainage&#46; Urine sodium was 34meq&#47;l&#46; Additional tests also highlighted the presence of a proteinuria of 0&#46;6g&#47;24h and urine sediment with 10 red cells per field without leukocyturia&#46; The patient had a beta-2-microglobulin level of 548&#46;72&#956;g&#47;g and NAG of 9U&#47;l in the urine&#46; The renal function continued to deteriorate despite volume replacement and a renal biopsy was performed to investigate the origin of the acute renal failure&#46;</p><p class="elsevierStylePara">The renal biopsy showed varying degrees of shrinkage with fibrous thickening of the capsule in some glomeruli&#46; Diffuse fibrosis was observed in the interstitial area&#44; with focal tubular atrophy affecting approximately 25&#37; of the parenchyma&#46; Predominantly lymphoplasmacytic inflammatory infiltrate was detected in various areas&#44; with occasional presence of eosinophils&#46; Some tubules had necrotic cylinders in the lumen&#46; The lumen of many tubules was occupied by birefringent crystals consistent with oxalate &#40;Figure 1&#41;&#46;</p><p class="elsevierStylePara">The oxalate in urine was 47&#46;70mg&#47;24h &#40;up to 40mg&#47;24h with normal renal function&#41;&#46; After hydration&#44; correction of acidosis&#44; treatment with calcium carbonate and low oxalate diet&#44; the patient presented a successful evolution&#44; with a progressive decline in serum creatinine to 2mg&#47;dl prior to discharge&#46;</p><p class="elsevierStylePara">Under normal conditions&#44; the daily load of endogenous and exogenous oxalate is completely excreted by the kidneys&#46; When renal function is altered&#44; renal and extrarenal deposits of oxalate begin to appear&#44; which is known as systemic oxalosis&#46; When there is a high oxalate load&#44; hyperoxaluria is produced&#44; increasing the risk of nephrolithiasis and nephrocalcinosis&#46; In addition&#44; acute renal failure may be triggered in patient with a precipitating factor&#44; such as dehydration and&#47;or metabolic acidosis&#46;</p><p class="elsevierStylePara">Hyperoxaluria is defined as the presence of urinary oxalate values greater than 40mg&#47;day&#46; It is frequently observed in patients with fat malabsorption due to digestive hyperabsorption of oxalate&#44; unlike primary hyperoxaluria due to enzyme deficiencies associated with a hyperproduction of oxalate in the liver&#46;<span class="elsevierStyleSup">5</span></p><p class="elsevierStylePara">The patient in question presented an enteric hyperoxaluria in relation to malabsorption of fats&#46; The main mechanism involved is the binding of calcium in the intestine by fatty acids&#44; which decreases the calcium oxalate in the digestive tract and increases the ionised oxalic acid absorbed in the intestine&#46; These patients may benefit from conservative treatment based on reducing oxalate and fat in the diet&#44; the administration of calcium carbonate as an oxalate binder&#44; and an increased intake of fluids and administration of bases&#44; such as sodium citrate&#44; in order to increase urinary calcium oxalate solubility&#46; Likewise&#44; it has yet to be confirmed if recolonisation with <span class="elsevierStyleItalic">Oxalobacter formigenes</span> also reduces urinary oxalate excretion&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">In conclusion&#44; calcium oxalate deposition associated with enteric hyperoxaluria is a rare cause of acute renal failure in the native and transplanted kidney&#46;<span class="elsevierStyleSup">5&#44;7&#44;8</span> Patients with fat malabsorption are at high risk and should be identified and treated early to prevent loss of kidney function&#46; If parenchymal acute renal failure is seen in a patient with fat malabsorption&#44; urinary oxalate excretion should be measured&#44; deterioration of the acid-base balance reversed and early hydration provided&#46;</p><p class="elsevierStylePara"><a href="grande&#47;10644&#95;108&#95;13129&#95;en&#95;10644&#95;f1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10644_108_13129_en_10644_f1.jpg" alt="Renal biopsy&#46; 1A&#41; Diffuse interstitial fibrosis with focal tubular atrophy and interstitial foci of inflammatory infiltrate&#59; 1B&#41; Glomerulus with fibrous thickening of the capsule&#59; 1C&#41; Expansion and mesangial sclerosis&#59; 1D&#41; Tubules with lumen occupied by b"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Renal biopsy&#46; 1A&#41; Diffuse interstitial fibrosis with focal tubular atrophy and interstitial foci of inflammatory infiltrate&#59; 1B&#41; Glomerulus with fibrous thickening of the capsule&#59; 1C&#41; Expansion and mesangial sclerosis&#59; 1D&#41; Tubules with lumen occupied by b</p>"
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