Oxalate Nephropathy

Abstract

The exact function of oxalate in the body is unknown. Eighty percent of blood oxalate is synthesized by enzymes in the liver and the rest is derived from diet. Factors that influence oxalate absorption from the intestine include dietary calcium and fat intake and intestinal microflora. The main route of oxalate excretion is through the kidney. In the situation where oxalate metabolism is impaired such as hereditary disorder or disorders of the gastrointestinal tract, urinary oxalate excretion increases to compensate for the increase in circulating oxalate. The increase in oxalate concentration in renal parenchyma and tubules can result in many forms of kidney dysfunction including acute and chronic oxalate nephropathy or calcium oxalate urolithiasis. Prolonged exposure to oxalate can cause permanent kidney damage and chronic kidney disease. Further impairment in oxalate excretion leads to oxalate accumulation in other organs such as eyes, bone and heart. Kidney biopsy can reveal the presence of oxalate crystals in renal
parenchyma and tubules accompanied by tubular injury and damage. Current evidence suggest that calcium oxalate crystal may trigger interleukin-1β-dependent innate immunity via the NLRP3 in intrarenal mononuclear phagocytes and directly damage tubular cells. Specific treatments including liver and/or kidney transplantation or pancreatic enzyme supplementation can eliminate oxalate accumulation. Other supportive care include increased water intake, calcium supplement and dietary fat and oxalate restriction. Among patients who receive hemodialysis, blood oxalate should be kept at the lowest level in order to prevent oxalate accumulation in other organs.