Abstract
ABSTRACTIntroduction:Secondary hyperoxalemia is a multifactorial disease that affects several organs and tissues in patients with native or transplanted kidneys. Plasma oxalate may increase during renal failure because it is cleared from the body by the kidneys. However, there is scarce evidence about the association between glomerular filtration rate and plasma oxalate, especially in the early stages of chronic kidney disease (CKD).Methods:A case series focuses on the description of variations in clinical presentation. A pilot study was conducted using a cross-sectional analysis with 72 subjects. The glomerular filtration rate (GFR) and plasma oxalate levels were measured for all patients. Results: Median (IQR) GFR was 70.50 [39.0; 91.0] mL/min/1.73 m2. Plasma oxalate was < 5.0 µmol/L in all patients with a GFR > 30 mL/min/1.73m2. Among the 14 patients with severe CKD (GFR < 30 mL/min/1.73 m2) only 4 patients showed a slightly increased plasma oxalate level (between 6 and 12 µmol/L).Conclusion:In non-primary hyperoxaluria, plasma oxalate concentration increases when GFR < 30mL/min/1.73 m2 and, in our opinion, values greater than 5 µmol/L with a GFR > 30 mL/min/1.73 m2 are suggestive of primary hyperoxaluria. Further studies are necessary to confirm plasma oxalate increase in patients with low GFR levels (< 30mL/min/1.73 m2).
Highlights
Secondary hyperoxalemia is a multifactorial disease that affects several organs and tissues in patients with native or transplanted kidneys
chronic kidney disease (CKD)-EPI equation had a mean error of -3.0 (95%CI, -7.0 to -0.5) mL/min/1.73 m2 without statistical difference to glomerular filtration rate (GFR)
The use of CKD-EPI in patients without mGFR could be adequate for evaluation of plasma oxalate (POx) levels
Summary
Secondary hyperoxalemia is a multifactorial disease that affects several organs and tissues in patients with native or transplanted kidneys. There is scarce evidence about the association between glomerular filtration rate and plasma oxalate, especially in the early stages of chronic kidney disease (CKD). The glomerular filtration rate (GFR) and plasma oxalate levels were measured for all patients. Further studies are necessary to confirm plasma oxalate increase in patients with low GFR levels (< 30mL/ min/1.73 m2). Increase of POx and oxalosis, i.e., calcium oxalate deposition in tissues, can result in primary (PH) or secondary hyperoxaluria (SH).[1,2] PHs are a group of rare autosomal recessive. In patients with chronic kidney disease (CKD), POx accumulates 10-30 times above normal levels as a result of its reduced excretion. Neither hemodialysis nor peritoneal dialysis can normalize POx levels in CKD patients; a 60% reduction is expected after a usual hemodialysis procedure, but POx was found to return to pre-dialysis levels within 48 h.7 In contrast to PH, clinical manifestations of uremic oxalosis, such as nephrolithiasis, fractures, and bone pain, are uncommon.[1,7]
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