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T R Wandzilak

Publications and source records attributed to T R Wandzilak.

7 recordsLinked to original sources
PubMed1995

Effect of second messenger systems on oxalate uptake in renal epithelial cells.

The oxalate transport system along with protein phosphorylation appears to be deranged in stone formers. This study was undertaken to characterize in LLC-PK1 cells in culture the effect of altering specific intracellular second messenger systems on oxalate uptake. Cellular uptake experiments were performed at 37 degrees C in buffer [265 mM mannitol, 5 mM NaOH, 5 mM KOH, 10 mM Ca-EGTA, 25 mM HEPES/TRIS, pH = 7.4 or in Hank's balanced salt solution (HBSS)] containing 200 microM labeled oxalate (1-14C, 0.3 microCi). Cells were preincubated with DAG (final concentration of 100 microM), phorbol myristate acetate (10 microM), forskolin (50 microM), 8-bromo-cyclic AMP (50 microM), trifluoroperazine (20 microM) and low molecular weight heparin (1 mg/ml) for 10 min in the presence and absence of the anion transport inhibitor DIDS (100 microM) and the effect(s) on oxalate uptake at 10, 25 and 45 min incubation were determined. Chemicals (DAG, forskolin, TPA and 8-bromo-cAMP) which stimulate protein kinase A or C activity resulted in an increased uptake of oxalate while inhibitors of these systems (trifluoroperazine and low molecular weight heparin) resulted in decreased oxalate uptake. The results demonstrate that oxalate uptake in renal tubular cells is modulated by protein kinase C and A dependent mechanisms.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1994

Effect of high dose vitamin C on urinary oxalate levels.

The effect of high dose ascorbate on urinary oxalate levels in healthy adults was investigated using a modified ion chromatography method. Subjects ingested 1, 5 and 10 gm. supplemental ascorbate per day for 5 days, separated by 5 days of no supplementation. Urine ascorbate levels demonstrated variable increases with ascorbate supplementation. Ascorbate added directly to urine in vitro resulted in statistically significant but modest increases in measured oxalate. Addition of 5.68 mmol./l. ascorbate increased measured urinary oxalate by 36 mumol./l., implying conversion of ascorbate to oxalate during analysis. Measurement of 24-hour urinary oxalate levels with 5 and 10 gm. ascorbate per day showed similar, modest increases, which could be entirely accounted for by oxalate production during analytical procedures. Thus, no genuine increase in urinary oxalate was demonstrable despite a greatly increased ascorbate intake.

Adult↗
PubMed1992

Oxalate transport in cultured porcine renal epithelial cells.

Oxalate-containing kidney stones are the most common type (75%) of renal stones. In order to control oxalate excretion in the urine, a basic understanding of the cellular transport of oxalate is imperative. We have utilized the technique of continuous cell culture to establish and characterize a model system to study renal epithelial cell (LLCPK1) oxalate transport. Our data demonstrate that oxalate uptake in these cells is dependent on time, concentration and energy. The Km for oxalate uptake was 200 microM. Oxalate uptake was decreased at lower temperatures and elevated in an acidic extracellular environment. Both anion exchange inhibitors DIDS and SITS inhibited oxalate uptake. Sulfate, chloride, and bicarbonate decreased oxalate uptake, as did the diuretics bumetanide and furosemide. There was no evidence for the co-transport of oxalate with sodium. Our data show that monolayers of cultured kidney epithelial cells are a valuable model system for study of the basic cellular mechanisms of oxalate transport.

Animals↗
PubMed1990

The hyperoxaluric syndromes.

Oxalate is a major component of renal stones and an important determinant of calcium oxalate solubility in urine. Although the well-defined hyperoxaluric states are relatively uncommon, a significant number of patients with calcium oxalate stones have some degree of hyperoxaluria. For these reasons an understanding of both the causes of hyperoxaluria and methods of controlling oxalate synthesis and excretion is important. This review focuses on methods for the measurement of oxalate, the metabolic pathways of oxalate synthesis, the transport and excretion of oxalate, and the hyperoxaluric syndromes.

Erythrocytes↗
PubMed1989

The quantitation of oxalate in amniotic fluid by ion-chromatography.

Calcium oxalate is the predominant constituent of most kidney stones. The rare genetic disorder, primary hyperoxaluria, is characterized by the continuous excessive synthesis and urinary excretion of oxalic acid, leading to stone formation and renal insufficiency. The earliest measurement of oxalate in suspected cases of primary hyperoxaluria is advantageous and would lend support for continued analysis and eventual confirmation of the disease. Therefore, we quantitated oxalate levels in amniotic fluid (AF) using medium pressure ion-exchange chromatography. The mean concentration of oxalate in amniotic fluid was 1.67 mg/l +/- 0.8 (SD); (range 0.64 to 5.11 mg/l). The mean oxalate/creatinine ratio (O/C) was 0.23 +/- 0.11 (SD); (range 0.07 to 0.53). This ratio is similar to that found in the urine of infants less than 1 year (0.19 +/- 0.10; n = 17). There was no significant difference between males and females in oxalate concentration or O/C ratio. Regression analysis showed no significant correlation of fetal age with oxalate, O/C or creatinine. Studies in 13 sets of di-amnionic twins showed no statistical difference in oxalate or O/C between twin A and B. This study demonstrates the ability to accurately quantitate oxalate in amniotic fluid by ion-chromatography, and suggests that this may have a potential application in the initial screening process for the prenatal detection of primary hyperoxaluria.

Amniotic Fluid↗
PubMed1989

Oxalate synthesis, transport and the hyperoxaluric syndromes.

This article reviews the mechanisms involved in the synthesis, absorption, excretion and transport of oxalic acid, and the factors controlling these processes in man. The clinical syndromes associated with hyperoxaluria and recurrent calcium oxalate stone disease are reviewed, including new studies that raise the possibility of a generalized oxalate transport abnormality in some patients with renal stone disease. The important role of oxalate in the determination of calcium oxalate solubility in patients with calcium oxalate stone disease is emphasized and future directions for research in the prevention of recurrent calcium oxalate stone disease are discussed.

Animals↗