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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2007  |  Volume : 18  |  Issue : 2  |  Page : 253-256
Oxalosis Presenting as Early Renal Allograft Failure

Department of Nephrology, King Fahd Medical city, Riyadh, Saudi Arabia

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Hyperoxaluria can result in the deposition of oxalate in bones, arteries, eyes, heart, nerves, kidneys and other structures when there is a reduction in glomerular filtration rate. Liver and kidney transplantation is curative for patients with Type I primary hyperoxaluria. Here we report a case of recurrent oxalosis in a post-transplant kidney with early graft failure in an adult male.

Keywords: Oxalosis, Renal transplantation

How to cite this article:
Alsuwaida A, Hayat A, Alwakeel JS. Oxalosis Presenting as Early Renal Allograft Failure. Saudi J Kidney Dis Transpl 2007;18:253-6

How to cite this URL:
Alsuwaida A, Hayat A, Alwakeel JS. Oxalosis Presenting as Early Renal Allograft Failure. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2022 Jan 18];18:253-6. Available from: https://www.sjkdt.org/text.asp?2007/18/2/253/32319

   Introduction Top

Hyperoxaluria is a rare disorder. It can be primary (an inborn error of oxalate metabolism) or secondary to bowel disease or decreased excretion. Primary oxaluria usually leads to renal failure due to the deposition of oxalate crystals in kidneys and the formation of renal stones. Interstitial deposits of oxalate induce an inflammatory reaction with formation of granulomas, resulting in chronic interstitial nephritis and chronic renal failure. Hyperoxaluria can also cause intratubular obstruction which results from a heavy load of oxalate excretion post-transplant, causing tubular obstruction and renal failure. Oxalate deposition can also occur in other tissues such as bone, blood vessels, heart, nerves and eyes. [1],[2]

Diagnosis of oxalosis is missed in many patients initially and cases may be detected during evaluation of renal failure or, at times, even in the post-transplant period. Positive family history and proper physical examination and urinalysis may yield strong clues for proper diagnosis. Here we report a case of hyperoxaluria with negative family history, which was diagnosed only following kidney allograft failure and biopsy of the renal allograft.

   Clinical Summary Top

A 31-year-old male patient was referred to King Fahd Medical City (KFMC), Riyadh, Saudi Arabia on 20/02/2006 for evaluation of a non-functioning renal allograft. The patient had undergone an unrelated renal transplant in Pakistan on 12 th January 2006. The cause of renal failure was not known and there was no history of similar illness in his family. He had no history of recurrent kidney stones. He was declared to have end-stage renal disease (ESRD) on January 1999, and since then he had been on maintenance hemo­dialysis (HD) three times a week through the left arterio-venous fistula. He was stable on HD with no history of passage of stones or thrombosis.

The patient underwent kidney transplant in January 2006. The donor was a young healthy man with a negative tissue cross match. There was no history of prolonged cold/warm ischemia. Immediately following the surgery, the patient had good urine output and his renal functions improved; however, six hours after surgery, the patient developed oliguria and his renal functions deteriorated.

Doppler and DTPA scans of the allograft showed no evidence of renal artery or renal vein thrombosis; however, there was poor perfusion of the transplant kidney. Ultrasound of the abdomen revealed the transplant kidney measured 14 cms with increased cortical echogenicity and no hydronephrosis. Allo­graft biopsy was done which revealed five glomeruli with depositions of large oxalate crystals in the tubules encroaching the glomeruli, mild tubulitis, and no evidence of cortical necrosis, hyper acute/acute rejection or fibrinoid necrosis. The interstitium showed scattered granulomas with birefringnent oxalate crystals. Bone marrow biopsy was normal with no oxalate deposits. The patient was restarted on daily HD. Possibility of primary hyperoxaluria was considered and the patient is scheduled for graft nephrectomy. The following medicines were added to his treatment protocol: pyridoxine, magnesium oxide and orthophosphate, while immuno­supressive medications were stopped.

   Discussion Top

Primary hyperoxaluria (PH) is a heterogenous disease with variability in the age of onset and a variable progression to kidney failure. As a group, PH comprise three inborn errors of metabolism with recessive inheritance, characterized by oxalate deposition in kidneys, bone marrow, bold vessels, eyes and other tissues.[1],[2] Kidney involvement can present with recurrent urinary calculi, interstitial nephritis and/or chronic renal failure. Recently, more cases of oxalosis are being reported to cause acute renal failure in both native and transplanted kidneys.[3],[4] In cases of early renal allograft failure, it is most likely related to oxalate mobilized from previous tissue deposits. We have demonstrated in this case that progression to ESRD is possible without apparent nephrocalcinosis on a renal ultra-sound of native kidneys.

Typically, plasma oxalate is elevated even when the glomerular filtration rate (GFR) is within the normal range. The main symptoms at diagnosis are urolithiasis (54%) and nephrocalcinosis (30%). PH Type I is due to the deficiency of hepatic­specific peroxisomal enzyme alanine-glycolate amino transferase (AGT) which utilizes pyridoxine (Vit B6) as a co-enzyme. The metabolic defect in Type II PH is a deficiency in the activity of D-Glycerate dehydrogenase, and often follows a more benign course than the Type I disease. Type III PH is due to increased intestinal absorption of oxalate of unknown patho­physiology.[5],[6],[7] All three types of hyper­oxaluria have the same clinical features and may be differentiated biochemically on the basis of urinary organic acid excretion. Patients with Type I disease excrete an excess of glycolic acid while those with Type II excrete an excess of L-glyceric acid. PH Type III does not show any elevation of organic acid excretion. About 30% of patients are diagnosed only after reaching ESRD. Diagnosis is usually based on history and urinary oxalate excretion. Glycolate and L-glyceric acid excretion and liver biopsy for enzyme defects are confirmatory.

Historically, renal transplantation has yielded very poor results in patients with PH Type I because of recurrent oxalosis of the graft. In the last 10 years, simulta­neously combined hepatorenal transplan­tation has been successfully applied correcting the metabolic lesion in the liver and replacing the damaged kidneys. [1],[8] However, few successful cases of selective renal transplan­tation with excellent renal function have been reported in patients with PH Type I. [9] This is especially the case in patients without significant systemic oxalosis and with evidence of residual AGT activity.

Studies have also shown that it is possible to perform successful renal transplantation in small children and adults with primary oxalosis and completely prevent the deposition of oxalate in renal allografts.[10] A specialized strategy for medical manage­ment known as the Sheinmann protocol, which includes intensive pre-transplant HD, post-transplant long-term diuresis and admini­stration of neutral phosphate, magnesium and pyridoxine has been shown to improve the outcome of renal transplantation in these patients [9]

   Conclusion Top

Renal transplantation with a strict medical protocol would appear to be the initial treatment of choice for renal failure due to primary oxalosis in centers where liver transplantation facilities are not well developed. Overall, renal transplantation is better than dialysis except in cases in which the nephrologist knows before hand the cause of primary renal failure and follows strict protocols of treatment (Sheinmann protocol) before transplantation

   References Top

1.Leumann E, Hoppe B. The primary hyperoxalurias. J Am Soc Nephrol 2001; 12: 1986-93.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Hoppe B, Langman CB. A United States survey on diagnosis, treatment and outcome of primary hyperoxaluria. Pediatr Nephrol 2003; 18: 986-91.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Kim HH, Koh HI, Ku BI, Lee HS. Late onset primary hyperoxaluria diagnosed after renal transplantation presented with early recurrence of disease. Nephrol Dial Transplant 2005; 20(8):1738-40.  Back to cited text no. 3    
4.Wong PN, Tong MW, Mak SK et al. Late-onset primary hyperoxaluria type 1 in a Chinese individual with absent alanine: glyoxylate aminotransferase activity. Chin Med J 2004; 117(12): 1889-90.  Back to cited text no. 4    
5.Singh DR, Sagade SN, Kamat MH, Deshpande RB Shah BV. Oxalosis with nephrocalcinosis. Nephrol Dial Transplant 2000; 15: 124-5.  Back to cited text no. 5    
6.Cochat P, Deloraine A, Rotily M, et al. Epidemiology of primary hyperoxaluria type-1. Nephrol Dial Transplant 1995; 10: 3-7.  Back to cited text no. 6    
7.van Woerden CS, Groothoff JW, Wanders RJ, Davin JC, Wijburg FA. Primary hyperoxaluria type 1 in the Netherlands: prevalence and outcome. Nephrol Dial Transplant 2003; 18: 273-9.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Jamieson NV on behalf of the European PH I Transplantation Study Group. The European primary hyperoxaluria type 1 transplant registry report on the results of combined liver/ kidney transplantation for primary hyperoxaluria 1984-1994.Nephrol Dial Transplant 1995; 10 Suppl 8: 33-7.  Back to cited text no. 8    
9.Saborio P, Scheinman JI. Transplantation for primary hyperoxaluria in the United States. Kidney Int 1999; 56:1094-100.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Milliner DS, Eickholt JT, Bergstralh EJ, Wilson DM, Smith LH. Results of long­term treatment with ortho-phosphate and pyridoxine in patients with primary hyperoxaluria. N Engl J Med 1994; 331: 1553-8.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]

Correspondence Address:
Abdulkareem Alsuwaida
P.O. Box 11525 Riyadh 59046
Saudi Arabia
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PMID: 17496404

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