Hyperoxaluria is characterized by an increased in excretion of oxalate by kidney.There are two distinct clinical expressions of hyperoxaluria, named primary and secondary hyperoxaluria. Primary hyperoxaluria is a genetic disorder due to defective enzyme activity .In contrast , secondary hyperoxaluria , is caused by increased dietary ingestion of oxalate or oxalate precursors. There are three main types of primary hyperoxaluria, each type is associated with specific metabolic defects. Type 1, is the most common form and accounting for about 80% of all cases. The defect in enzyme activity of the proxysomal hepatic enzyme L – alanine glyoxylate aminotransferase (AGT) , resulting in an increase of the glyoxylate pool, which is converted to oxalate. Type 2 is caused by deficiency of the enzyme activity glyoxylate  reductase / hydroxypyruvate reductase. Type 2 is characterized by recurrent nephrolithiasis , nephrocalcinosis , and end – stage renal disease. Type 3is characterized by recurring oxalate stones beginning in childhood or adolescence , and nephrocalcinosis or reduced kidney function. For treatment of hyperoxaluria manifestations, high oral fluid intake at all times and use of an inhibitor of calcium oxalate crystallization is commended.