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						<title>Crystals in the Renal Tubules?</title>
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							<teaser>Can crystallization in the renal tubules occur in the absence of crystals in urine and cause graft dysfunction?</teaser>
							<articleType>profAskTheExpert</articleType>
							<keywords>transplantation</keywords>
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						<authors></authors>
						<authorBios>Flavio Vincenti, MD, Clinical Professor of Medicine, University of California, San Francisco, San Francisco, CA</authorBios>
						<authorDisclosures></authorDisclosures>
						<citation>
							<publisher>Medscape</publisher>
							<publication>Medscape Transplantation</publication>
							<publicationDate>01/03/2002</publicationDate>
							<volume>3</volume>
							<issue>1</issue>
							<pages></pages>
							<copyright></copyright>
							<publicationDisclaimer></publicationDisclaimer>
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							<extraCitation></extraCitation>
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						<body>&lt;h3&gt;Question&lt;/h3&gt;

					&lt;FONT SIZE=&quot;2&quot;&gt;

					The case is an 8-year-old male with recurrent bladder stones (calcium oxalate mono and dihydrate), questionable chronic interstitial nephropathy, chronic renal failure, and end-stage renal disease (native kidney biopsy not done) who underwent live-related renal allograft transplantation. His immunosuppressive regimen is cyclosporine (CsA) at 8 mg/kg, azathioprine, and &lt;i&gt;Wysolone&lt;/i&gt; (corticosteroid). Diuresis occurred immediately and his serum creatinine level decreased to 1.8 mg/dL. On the seventh postoperative day, his serum creatinine level began rising and his urine output fell slightly. By postoperative day 16, his serum creatinine level was 4.7 mg/dL. A biopsy done on the eighth day showed no evidence of rejection or acute tubular necrosis. There was heavy interstitial infiltration by polymorphonuclear neutrophils and crystal deposition in the tubule lumens. The glomeruli were normal. A repeat biopsy 2 weeks later showed decreased inflammation and increased crystals. Repeated urinalyses showed acidic pH with no evidence of crystals, and urine culture and sensitivities were repeatedly negative. His ultrasound was normal. The trough CsA level is 295 ng/mL. He has received antirejection therapy (3 g solumedrol) and antibiotics empirically, but with no response.&lt;p&gt;Can crystallization in the renal tubules occur in the absence of crystals in urine and cause graft dysfunction?

					&lt;b&gt;Mukut Minz, MD&lt;/b&gt;&lt;P&gt;

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					&lt;H3&gt;Response&lt;/H3&gt;

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					&lt;b&gt;from , 01/03/2002&lt;/b&gt;&lt;br&gt;
					&lt;FONT SIZE=&quot;2&quot;&gt;A review of the history, the course, and the pathology of this patient suggests that this patient may have had primary oxalosis and developed rapid recurrence of oxalosis in the transplanted kidney. The presentation and the biopsy findings are characteristics and unfortunately, the prognosis for this kidney is poor. Crystallization in the renal tubules can occur in the absence of crystals in the urine and indeed lead to graft failure. To minimize recurrence of oxalosis in the transplanted graft, patients should be dialyzed aggressively prior to transplantation and then treated with neutrophosphate, magnesium, and pyridoxine. Some patients may in fact benefit from receiving combined kidney-liver transplantation, which would insure complete correction of the metabolic abnormality.&lt;p&gt;&lt;/font&gt;&lt;p&gt; &lt;/font&gt;</body>
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						<suggestedReading>Casale AJ, Leichter HE, Sheth KJ, Segura AD, Lawson RK. Renal transplantation in a child with primary oxalosis. Child Nephrol Urol. 1990;19:103-106.&lt;p&gt;Ellis SR, Hulton S-A, McKiernan PJ, de Ville de Goyet J, Kelly DA. Combined liver-kidney transplantation for primary hyperoxaluria type 1 in young children. Nephrol Dial Transplant. 2001;16:348-354.&lt;p&gt;Scheinman JI, Najarian JS, Mauer SM. Successful strategies for renal transplantation in primary oxalosis. Kidney Int. 1984;25:804-811.&lt;p&gt;</suggestedReading>
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