Gut-kidney axis in oxalate homeostasis.

Purpose Of Review: The gut-kidney axis plays a critical role in oxalate homeostasis, and better understanding of oxalate transport regulatory mechanisms is essential for developing novel therapies.

Recent Findings: Oxalate potentially contributes to chronic kidney disease (CKD) progression, CKD - and end stage renal disease (ESRD)-associated cardiovascular diseases, polycystic kidney disease (PKD) progression, and/or poor renal allograft survival, emphasizing the need for plasma and urinary oxalate lowering therapies. One promising strategy would be to enhance the bowel's ability to secrete oxalate, which might be facilitated by the following findings.

Extracellular nucleotides inhibit oxalate transport by human intestinal Caco-2-BBe cells through PKC-δ activation.

Nephrolithiasis remains a major health problem in Western countries. Seventy to 80% of kidney stones are composed of calcium oxalate, and small changes in urinary oxalate affect risk of kidney stone formation. Intestinal oxalate secretion mediated by the anion exchanger SLC26A6 plays an essential role in preventing hyperoxaluria and calcium oxalate nephrolithiasis, indicating that understanding the mechanisms regulating intestinal oxalate transport is critical for management of hyperoxaluria.

Cholinergic signaling inhibits oxalate transport by human intestinal T84 cells.

Urolithiasis remains a very common disease in Western countries. Seventy to eighty percent of kidney stones are composed of calcium oxalate, and minor changes in urinary oxalate affect stone risk. Intestinal oxalate secretion mediated by anion exchanger SLC26A6 plays a major constitutive role in limiting net absorption of ingested oxalate, thereby preventing hyperoxaluria and calcium oxalate urolithiasis.

Regulation of anion exchanger Slc26a6 by protein kinase C.

SLC26A6 (CFEX, PAT1) is an anion exchanger expressed in several tissues including renal proximal tubule, pancreatic duct, small intestine, liver, stomach, and heart. It has recently been reported that PKC activation inhibits A6-mediated Cl/HCO(3) exchange by disrupting binding of carbonic anhydrase to A6. However, A6 can operate in HCO(3)-independent exchange modes of physiological importance, as A6-mediated Cl/oxalate exchange plays important roles in proximal tubule NaCl reabsorption and intestinal oxalate secretion.

Effect of reversal of catheter ports on recirculation: comparison of the PermCath with Tesio Twin Catheter.

To study the effect of the reversal of the blood ports on blood flow rate (QB), percentage recirculation, and blood urea nitrogen (BUN) clearance, we compared 12 well functioning chronic hemodialysis catheters (7 PermCaths and 5 Tesio Twin Catheters) in both standard and reversed blood flow setups. The reversal of PermCath ports caused no change in the QB (307+/-20 ml/min vs. 314+/-9 ml/min, standard vs.