Abstract

Studies on erythrocytes from stone forming patients1 and on renal papillary cells from stone forming rats2 demonstrated abnormally high rates of oxalate transport, and it has been suggested that increased oxalate uptake plays an important role in urolithiasis. Understanding how a change in oxalate uptake affects oxalate excretion is difficult, however, because information on renal oxalate handling is limited. Available data from micropuncture studies indicate that oxalate undergoes both reabsorption and secretion within the kidney with net secretion occurring in the proximal tubule3. Such studies are technically quite difficult and provide only limited control of the composition of extracellular space such that it is difficult to predict the magnitude and direction of oxalate flux under physiological and pathophysiological conditions. These difficulties led us to examine vectorial oxalate flux using a simpler model system, LLC-PK1 cells. These cells retain many of the characteristics of normal renal epithelial cells and form intact monolayers that can be used for examination of vectorial transport4. Moreover, studies in our laboratory have demonstrated that these cells express different transport systems for oxalate at the luminal and abluminal membrane surfaces: a C1-/oxalate exchanger at the luminal surface and a SO4 2-(oxalate)/HCO3- exchanger at the abluminal surface. Thus, the present studies examined the magnitude and direction of vectorial oxalate flux across confluent monolayers of LLC-PK1 cells.

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