A glomerular filtration rate below 30 ml/min is associated with reduced ability to excrete H + ions due to impaired generation of ammonia and failure to excrete endogenously produced acid. This leads to a metabolic acidosis with increased anion gap as sulfates, phosphates, and organic anions accumulate. When severe, the acidosis may cause dyspnea and require correction by bicarbonate administration.
Kaliuresis is impaired in chronic renal failure with normal plasma levels maintained by an adaptive increase in secretion by the remaining nephrons and by increased colonic excretion under the influence of aldosterone. Potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, and non-steroidal anti-inflammatory drugs can precipitate hyperkalemia, and the composition of fluid replacement and feeding should be considered with care.
Phosphate retention with reciprocal hypocalcemia and reduced dihydroxylation of 25-hydroxyvitamin D are triggers for the development of secondary hyperparathyroidism. Parathyroid hormone stimulates osteoclastic activity and liberates calcium from the bones in an effort to normalize serum calcium levels, and over time a minority of patients will develop hypercalcemia due to autonomous or tertiary hyperparathyroidism. The adverse neuromuscular effects of hypocalcemia are offset by the acidosis of renal failure which increases the ionized component of the total plasma calcium. Acute correction of the acidosis can precipitate tetany and fits during which bones weakened by renal osteodystrophy can fracture.
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