Nephropathology
   
Case 33
Diagnosis
 
     
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Diagnosis: Oxalate crystals in a case of acute renal failure due to T-cell mediated rejection

Oxalate crystals are either yellowship-withe or display a wide range of colors, appear fan shaped, radially arranged or spiculated, and are birefringent on polarization as opposed to calcium phosphate crystals that do not polarize. Sometimes a giant cell reaction can be evidenced and later progressive tubular atrophy and fibrosis.

Oxalate crystals can be seen in many diseases with acute or chronic renal failure. They usually are evidenced in tubule lumens, but they can also be seen embedded within interstitial connective tissue or in the epithelium of tubules. Oxalate is normally excreted by the kidneys and plasm levels are increased with azotemia. Isolated oxalate cystals do not necessarily imply significant damage, but renal insufficiency of any nature will lead to increasing renal accumulation of oxalate. Extensive deposits of oxalate should suggest hyperoxaluria.

Hyperoxaluria can be divided into primary and secondary forms. Primary hyperoxaluria is subdivided into three types: Type I: increased excretion of glycolic acid related to deficit of alanine-glyoxalate aminotransferase. Type II is hyperoxaluria with L-glyceric acid, related to deficit of D-glycerate dehydrogenase. Type III is due to primary intestinal hyperabsortion of oxalate. Secondary Hyperoxaluria is due to (most of cases) enteric hyperabsortion in situations as Crohn's disease, celiac sprue, pancreatic insufficicncy, and small-intestinal bypass; other secondary causes are: diet everrich in oxalate, ethylene glycol intoxication, excess ascorbic acid intake, and adverse reaction to methoxyfluorane.

To diagnose hyperoxaluria (primary or secondary) is necessary a complete clinical analysis and paraclinic tests. In renal tissue Dr. R. Colvin wrote that the detection of axalate crystals in the walls of small arteries is "pathognomonic" of primary hyperoxaluria (Heptinstall's Pathology of the Kidney, 6th edition, Philadelphia, Wolters Kluwer - Lippincott Williams and Wilkins, 2007, pp. 1457-1458).

In our case there was not evidence of hyperoxaluria. Crystals were detected only in tubules, not in arteries or interstitium. Patient improved with antirejection treatment, but we does not have a posterior renal biopsy. This patient was losed of the follow-up.

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References

  • Yamaguchi S, Wiessner JH, Hasegawa AT, Hung LY, Mandel GS, Mandel NS. Study of a rat model for calcium oxalate crystal formation without severe renal damage in selected conditions. Int J Urol. 2005 Mar;12(3):290-8.[PubMed link]
  • Wiessner JH, Hasegawa AT, Hung LY, Mandel GS, Mandel NS. Mechanisms of calcium oxalate crystal attachment to injured renal collecting duct cells. Kidney Int. 2001 Feb;59(2):637-44. [PubMed link][Free full text]

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