Biochemistry of renal failure.

The term uremia is used clinically to describe that state associated principally with the retention of nitrogenous metabolic products and is characterized by a raised blood urea concentration. The increase in the blood urea concentration is perhaps the most striking abnormality of the body fluids in renal failure, although it is not the most important functionally. The clinical syndrome of uremia involves all the systems of the body as a result of biochemical alterations in the constitution of the internal environment. The alterations in the latter compartment are due not only to the retained metabolic products but also to associated changes in water, electrolyte, and acid-base homeostasis. There are also features of the clinical syndrome of uremia which are attributable to variations in the rates of secretion and metabolism of a number of hormones in which the kidney is recognized to play a role, either directly or indirectly. This brief review deals with the retained uremic metabolites and their biochemical significance in the clinical syndrome of uremia. The metabolites discussed include urea, creatinine, guanidines and related compounds, uric acid, dimethylamine, and the middle molecule hypothesis. The potential role of some of these metabolites is discussed with regard to their potential toxic role as enzyme inhibitors. The biochemical aspects of uremic neuropathy are reviewed to highlight the biochemical complexity of the investigation of the uremic syndrome.