Plasma Level and Renal Clearance of Oxalate in Normal Subjects and in Patients with Primary Hyperoxaluria or Chronic Renal Failure or Both

Abstract

1. Plasma oxalate has been measured by a radioisotopic method applicable to all concentrations of plasma oxalate and renal function, and also by an enzymatic method which was only applicable to raised concentrations of plasma oxalate. 2. Where the two methods could be applied simultaneously, the agreement between them was good. 3. Plasma oxalate was 86% ultrafiltrable at concentrations of up to 44 micromol/l. 4. Oxalate clearance and the exchangeable oxalate pool were also measured. The ratio of oxalate clearance to creatinine clearance was greater than unity in most normal subjects and patients. 5. These methods were used in normal subjects and in patients with primary hyperoxaluria and/or chronic renal failure. A raised plasma oxalate concentration was found in both conditions. Chronic renal failure is probably the most common cause of a raised plasma oxalate.

Evidence that serum calcium oxalate supersaturation is a consequence of oxalate retention in patients with chronic renal failure.

“…Serum oxalate concentration increases during chronic renal failure (1,2), and is above normal in virtually all patients who require chronic dialysis (3)(4)(5), because oxalate is removed from the body almost entirely by filtration at the renal glomerulus (6)(7)(8) and by secretion in the early portions of the proximal tubules (9-1 1). In some patients with chronic renal failure, crystals of calcium oxalate have been identified in kidney, blood vessels, myocardium, thyroid, synovia, cartilage, bone, and periodontium (12)(13)(14)(15)(16)(17).…”

Atypical Features of Primary Hyperoxaluria in End-Stage Renal Disease

“…In this situation, increased plasma oxalate levels have proven to be of value. Whilst raised plasma oxalate levels were documented in case 1 on two occasions neither value exceeded levels associated with the degree of renal failure [9], Oxalate deposits in the bone marrow aspirate has been an infrequent finding in PH [1,2], as was the case in our patients. In these cir cumstances, bone wedge biopsy or transcutaneous bone biopsy is the procedure of choice, being more represen tative than aspirate to confirm the diagnosis [14].…”

“…A presumptive diagnosis of PH was made on histological findings and the cardiological manifestation of com plete heart block [8]. However, two subsequent pre-dialysis samples taken 3 months apart revealed plasma oxalate levels of 3.0 pg/ml (33 pmol/l) [serum creatinine 7.9 mg/dl (700 pmol/l)] and 3.64 pg/ ml (40 pmol/l), [serum creatinine 1 1.8 mg/dl (1,045 pmol/l)]; oxalate/creatinine ratios: 0.047 and 0.038 subsequently; these levels are normal for the degree of renal failure [9] and were therefore consid ered to be inconsistent with PH. The patient received a cadaveric transplant in February 1986. and immunosuppression with ciclosporin and prednisolone.…”

Plasma Oxalate in Chronic Renal Failure and Normal Subjects: Methodological Problems

“…The results of serum oxalate determinations in normal subjects reported by Borland et al [1] in their recent paper (0-55 um ol/l) are far out of the range found in normal subjects as determined by in vivo isotope clearance meth ods (below 3 pm ol/l) [2], The reason why in many earlier studies in which chemical methods were used concentra tions are reported exceeding these low values by one order of magnitude is not clear [3), but in more recent studies [2,3,[6][7][8][9][10][11][12][13] normal values much closer to the true value were found, i.e. at least lower than 6 pm ol/l (table 1).…”