Abnormalities of mineral metabolism are common early after renal TXP. An elevated serum Ca(adj) at three months post-TXP increases the risk for recipient death, while an elevated Ca(adj)P and Ca(adj) later in the first post-TXP year increases the risk of long-term death-censored graft loss.

Calcium and phosphorus homeostasis relies on a complex, tightly regulated system involving many ions and hormones. The regulation of calcium and phosphorus is controlled by the actions of these ions and hormones on the intestine, kidneys and bone. Disturbances in the serum level of calcium and/or phosphorus can lead to significant pathology, including kidney stones and bone disease. In addition to parathyroid hormone and vitamin D, recently identified factors such as fibroblast growth factors and klotho play an important role in maintaining mineral ion homeostasis. The identification of subfamily V transient receptor potential cation channels (TRPV channels), Na/P_i cotransporters, the vitamin D receptor and the calcium-sensing receptor have further advanced our understanding of this complex physiology. In this review we discuss the current understanding of the relationships between the ions, hormones, and transporters that maintain calcium and phosphorus homeostasis.

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Uric acid nephrolithiasis is typically found in individuals with a low urine pH and a normal concentration of urinary uric acid. Patients with a history of gout are at greater risk of forming uric acid stones, as are patients with obesity, diabetes, or the complete metabolic syndrome. The unifying renal tubular abnormality of these disorders appears to be the excretion of abnormally acidic urine. This article focuses on the relationship of these disorders to the development of uric acid stones. The diagnosis of uric acid stones can be elusive, because pure uric acid stones are radiolucent on plain radiographs. Ultrasound, or preferably noncontrast helical CT scanning, is required for their detection. The treatment of uric acid stones should focus on alkalinization of the urine with citrate or bicarbonate salts. Additional interventions such as increase in fluid intake and decrease in animal protein ingestion are often beneficial. Patients with documented hyperuricemia often require specific therapy to lower serum uric acid concentration and subsequent excretion.