Primary Nonfunction of Renal Allograft Secondary to Acute Oxalate Nephropathy

Parasuraman, Ravi; Zhang, Ping L.; Samarapungavan, Dilip; Pothugunta, Krishna; Reddy, Gopal; Rocher, Leslie L.; Dumler, Francis; Raofi, Vandad; Cohn, Steven; Koffron, Alan J.

doi:10.1155/2011/876906

Cited by 9 publications

(11 citation statements)

References 18 publications

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“… 12 , 14 , 15 , 16 Moreover, unrecognized or insufficiently treated hyperoxalemia pre- and post-transplantation can have severe implications for renal allograft survival. 8 , 17 , 18 , 19 …”

mentioning

confidence: 99%

Impact of Regular or Extended Hemodialysis and Hemodialfiltration on Plasma Oxalate Concentrations in Patients With End-Stage Renal Disease

Ermer

Kopp

Asplin

et al. 2017

Kidney International Reports

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IntroductionCalcium oxalate supersaturation is regularly exceeded in the plasma of patients with end-stage renal disease (ESRD). Previous reports have indicated that hemodialfiltration (HDF) lowers elevated plasma oxalate (POx) concentrations more effectively compared with hemodialysis (HD). We reevaluate the therapeutic strategy for optimized POx reduction with advanced dialysis equipment and provide data on the effect of extended treatment time on dialytic oxalate kinetics.MethodsFourteen patients with ESRD who underwent HDF 3 times a week for 4 to 4.5 hours (regular HDF; n = 8) or 7 to 7.5 hours (extended HDF; n = 6) were changed to HD for 2 weeks and then back to HDF for another 2 weeks. POx was measured at baseline, pre-, mid-, and postdialysis, and 2 hours after completion of the treatment session.ResultsBaseline POx for all patients averaged 28.0 ± 7.0 μmol/l. Intradialytic POx reduction was approximately 90% and was not significantly different between groups or treatment modes [F(1) = 0.63; P = 0.44]. Mean postdialysis POx concentrations were 3.3 ± 1.8 μmol/l. A rebound of 2.1 ± 1.9 μmol/l was observed within 2 hours after dialysis. After receiving 2 weeks of the respective treatment, predialysis POx concentrations on HD did not differ significantly from those on HDF [F(1) = 0.21; P = 0.66]. Extended treatment time did not provide any added benefit [F(1) = 0.76; P = 0.40].DiscussionIn contrast to earlier observations, our data did not support a benefit of HDF over HD for POx reduction. With new technologies evolving, our results emphasized the need to carefully reevaluate and update traditional therapeutic regimens for optimized uremic toxin removal, including those used for oxalate.

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mentioning

confidence: 99%

Impact of Regular or Extended Hemodialysis and Hemodialfiltration on Plasma Oxalate Concentrations in Patients With End-Stage Renal Disease

Ermer

Kopp

Asplin

et al. 2017

Kidney International Reports

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“… Early posttransplant accumulation of CaOx, which is usually characterized by few foci of CaOx and background of acute rejection and ATN; CRF, which is usually characterized by few foci of CaOx and background of chronic allograft nephropathy; Recurrent PH, which is characterized by extensive renal deposition of CaOx and chronic tubulointerstitial injury; and is associated with graft failure; and Secondary hyperoxaluria due to elevated enteric absorption of Ox or drugs that contain Ox. [ 2 3 4 14 ] …”

Section: Discussionmentioning

confidence: 99%

“…Secondary hyperoxaluria due to elevated enteric absorption of Ox or drugs that contain Ox. [ 2 3 4 14 ]…”

Section: Discussionmentioning

confidence: 99%

“…This leads to chronic injury of tubules and parenchyma that finally causes renal dysfunction and allograft failure, which is not reversible and specifies PH1 from other AON causes. [ 2 4 12 14 ] Another presentation of PH1 that differentiates it from the other causes of ESRD is that the bone Ox content among PH1 patients is higher than that in ESRD patients without PH1 (15-910 vs. 2-9 mmol Ox/g bony tissue). [ 18 ] The clinical manifestation of PH1 varies dramatically even among the family members who have the same AGXT mutations.…”

Section: Discussionmentioning

confidence: 99%

“…Acute Ox nephropathy (AON) is recognized by CaOx deposition in allograft, high serum Ox level, and massive deposition within renal parenchyma. [ 2 3 ] One of the causes of CaOx deposition in renal allograft is primary hyperoxaluria type 1 (PH1) which is a rare inborn metabolic disorder with autosomal recessive inheritance. [ 4 ] It is the most common form of primary hyperoxaluria (PH),[ 5 6 ] and is caused due to absolute or functional deficiency or mistargeting of peroxisomal alanine: Glyoxylate aminotransferase (AGT) in hepatic cells.…”

Section: Introductionmentioning

confidence: 99%

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Acute oxalate nephropathy following kidney transplantation: Report of three cases

Taheri¹,

Gheissari²,

Shaabani³

et al. 2015

J Res Med Sci

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Calcium oxalate (CaOx) crystal deposition is a common finding immediately after kidney transplantation. However, small depositions of CaOx could be benign while extensive depositions lead to poor graft outcome. Here we report three cases with end-stage renal disease (ESRD), bilateral nephrolithiasis, and unknown diagnosis of primary hyperoxaluria (PH) who underwent a renal transplant and experienced an early-onset graft failure. Although an acute rejection was suspected, renal allograft biopsies and subsequent allograft nephrectomies showed extensive CaOx deposition, which raised a suspicion of PH. Even though increased urinary excretion of CaOx was found in all patients, this diagnosis could be confirmed with further tests including genetic study and metabolic assay. In conclusion, massive CaOx deposition in kidney allograft is an important cause of poor allograft survival and needs special management. Furthermore, our cases suggest patients with ESRD and a history of nephrolithiasis should be screened for elevated urinary oxalate excretion and rule out of PH.

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Calcium oxalate crystal deposition in the kidney: identification, causes and consequences

2020

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Calcium oxalate (CaOx) crystal deposition within the tubules is often a perplexing finding on renal biopsy of both native and transplanted kidneys. Understanding the underlying causes may help diagnosis and future management. The most frequent cause of CaOx crystal deposition within the kidney is hyperoxaluria. When this is seen in native kidney biopsy, primary hyperoxaluria must be considered and investigated further with biochemical and genetic tests. Secondary hyperoxaluria, for example due to enteric hyperoxaluria following bariatric surgery, ingested ethylene glycol or vitamin C overdose may also cause CaOx deposition in native kidneys. CaOx deposition is a frequent finding in renal transplant biopsy, often as a consequence of acute tubular necrosis and is associated with poorer long-term graft outcomes. CaOx crystal deposition in the renal transplant may also be secondary to any of the causes associated with this phenotype in the native kidney. The pathophysiology underlying CaOx deposition is complex but this histological phenotype may indicate serious underlying pathology and should always warrant further investigation.

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Primary Nonfunction of Renal Allograft Secondary to Acute Oxalate Nephropathy

Cited by 9 publications

References 18 publications

Impact of Regular or Extended Hemodialysis and Hemodialfiltration on Plasma Oxalate Concentrations in Patients With End-Stage Renal Disease

Impact of Regular or Extended Hemodialysis and Hemodialfiltration on Plasma Oxalate Concentrations in Patients With End-Stage Renal Disease

Acute oxalate nephropathy following kidney transplantation: Report of three cases

Calcium oxalate crystal deposition in the kidney: identification, causes and consequences

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