Electrolyte excretion in polycystic kidney disease: interrelationship between sodium, calcium, magnesium, and phosphate

The ability to regulate the excretion of sodium and its relation to the excretion of calcium, magnesium, and phosphate were examined in 13 patients with PCK, seven without azotemia (GFR 29 to 83 ml/min) and six with azotemia (GFR ≤20 ml/min). Studies were conducted while the subjects were on a high-sodium (100 mEq) or a low-sodium (10 mEq) diet. All patients attained balance on a high-sodium diet, and all were able to reduce urinary sodium excretion on a low sodium intake. Azotemic patients (group II) were unable, however, to lower urine sodium concentration below 34 ± 10 mEq/day (S.D.), in contrast to nonazotemic subjects (group 1) who achieved a daily sodium excretion of 13 ± 8 mEq/day. The minimum sodium excretion attained by group II patients is not different from that seen in patients with renal disease of other etiologies. This indicates that the salt-losing tendency in patients with polycystic kidneys is not an inherent manifestation of the disease but rather a consequence of the adaptation to chronic renal failure. Regardless of the diet, a relationship could be found between sodium and calcium excretion but not between sodium and magnesium or phosphate excretion in group 1 patients. In group II patients the excretion of calcium, magnesium, and phosphate bore a significant relationship to that of sodium. Since secondary hyperparathyroidism was probably present in both groups, these results are compatible with the suggestion that depression of tubular reabsorption of Na⁺, Ca⁺⁺, Mg⁺⁺, and phosphate in advanced renal failure is the result of a common mechanism.