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Publisher Summary This chapter discusses the biochemistry of the uremic syndrome. In recent years, the ability to treat uremia has outstripped the understanding of its pathogenesis. A precise understanding of the pathogenesis of the uremic syndrome, however, continues to elude people. Numerous substances have been isolated from the blood of uremic subjects and have been studied in vivo and in vitro . Increasingly clinicians appreciate the role of acidosis, hyponatremia and water intoxication, anemia, hyperkalemia, hypocalcemia, hyperphosphatemia, hypertension, and heart failure. Clinicians rely mainly on blood urea nitrogen (BUN) and serum creatinine measurements to evaluate patients with renal failure. The metabolic changes—retention of a legion of substances; the loss of vital renal hormones (e.g., erythropoietin) and enzymes (e.g., 1α-hydroxylase); the effect of the uremic environment on organ function, intermediary metabolism, and transport processes; dialysis-related problems; and exogenous toxins—observed in uremia result from the decline in renal excretory function. The chapter focuses on the retention of inorganic substances such as hyperkalemia, hydrogen ion and trace elements, and organic substances including oxalate, urea, guanidine, and polyamines. The chapter concludes with a discussion of dialysis related problems and related drugs and exogenous toxins.