Acid-base disorders and the kidney

In the normal human body, the extracellular fluid pH of 7.40 is closely protected. Any increase in acidity or alkalinity summons forth three lines of defense, starting immediately with the blood buffers, followed soon by the respiratory system's control of CO2, and finally purged by the renal excretion of the excess acid or base. The complex interrelated processes of the renal responses require a few days to accomplish maximum compensation. We have presented the fundamental principles governing maintenance of the acid-base equilibrium to provide a conceptual framework for understanding the clinical disorders of hydrogen ion metabolism. The somewhat elusive concepts of endogenous acid production and net acid balance have also been reviewed to help reveal the pathophysiology of metabolic acidosis caused by renal tubular acidosis, chronic renal failure, certain infant feedings, and total parenteral nutrition. The development and perpetuation of metabolic alkalosis in relationship to chloride and potassium deficiency have been examined. In the delineation of a clinical acid-base disorder, the clinician must bear in mind the continual interactions of electrolytes and hormonal systems and should be prepared to reevaluate frequently the elected therapy against the changing responses, based on a thorough understanding of physiology. The various types of renal tubular acidosis have manifold facets but the basic understanding of their pathophysiology begins with the concept of the "anion gap," a point of reference that can be used in the differential diagnosis and treatment. In this chapter a number of new causes of type IV renal tubular acidosis--currently considered to be the most common form of renal tubular acidosis--have been pointed out, along with special reference to the mineral, electrolyte, and aldosterone metabolism in the various acidoses and current means of reversing growth failure in the child, especially through bicarbonate treatment. The mechanism of metabolic acidosis in chronic renal failure including metabolic acidosis in children undergoing dialysis and in recipients of kidney transplantation, and its relationships to mineral and electrolyte metabolism have been presented. The pathophysiology of the acidosis related to certain infant formulas and the acidogenic properties of some amino acid solutions employed in total parenteral nutrition have been briefly reviewed. Finally, the metabolic alkalosis seen in a variety of chloride deficiency syndromes, such as Bartter's syndrome and dietary chloride deprivation, has been discussed and a rational approach to evaluation and treatment outlined.