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- Title
Chronic respiratory alkalosis induces renal PTH-resistance, hyperphosphatemia and hypocalcemia in humans.
- Authors
Krapf, Reto; Jaeger, Philippe; Hulter, Henry N.; Fehlman, C.; Takkinen, R.
- Abstract
The effects of chronic respiratory alkalosis on divalent ion homeostasis have not been reported in any species. We studied four normal male subjects during a four-day control period (residence at 500 m), during six days of chronic respiratory alkalosis induced by hypobaric hypoxia (residence at 3450 m), followed by a six-day eucapnic recovery period (500 m) under metabolic balance conditions. Chronic respiratory alkalosis (ΔPaCO2, -8.4 mm Hg, Δ[H+] -3.2 nmol/liter) resulted in a sustained decrement in plasma ionized calcium concentration (Δ[loCa++]p, -0.10 mmol/liter, P < 0.05) and a sustained increment in plasma phosphate concentration (Δ[PO4]p, +0.14 mmol/liter, P < 0.005) associated with increased fractional excretion of Ca++ (+0.5%, P < 0.005), decreased phosphate clearance (-6.1 mI/min, P < 0.025) and decreased excretion of nephrogenous cAMP (-1.5 nmol/100 ml GFR, P < 0.0025). Urinary phosphate excretion decreased by 15.4 mmol/24 hr on day 1 of chronic respiratory alkalosis (P < 0.0025), but returned to control values by day 6 despite hyperphosphatemia. Serum intact [PTH] did not change. Sustained hypomagnesuria (-0.8 mmol/24 hr, P < 0.05) occurred during chronic respiratory alkalosis and was accounted for, at least in part, by decreased fractional excretion of Mg++ (-0.7%, P < 0.05) in the absence of change in plasma magnesium concentration. Serum 1,25(OH)2D levels were unchanged by chronic respiratory alkalosis. In conclusion, the decrease in nephrogenous cAMP generation despite unchanged serum intact PTH concentration suggests that chronic respiratory alkalosis results in impaired renal responsiveness to PTH as manifested by alterations in PTH-dependent renal calcium and phosphate transport. Hypomagnesuria in chronic respiratory alkalosis may be due, at least in part, to hypocalcemia-induced enhancement of renal magnesium reabsorption. The failure of [PTH] to increase during hypocalcemia may reflect defective PTH secretion.
- Subjects
ALKALOSIS; HYPOCALCEMIA; HYPOXEMIA; MAGNESIUM; CARBON dioxide; MINERAL metabolism
- Publication
Kidney International, 1992, Vol 43, Issue 3, p727
- ISSN
0085-2538
- Publication type
Article