Changes in serum and urinary calcium during phosphate depletion: studies on mechanisms

Abstract

ABSTRA CT The changes in serum calcium and the renal handling of this ion were evaluated during phosphate depletion. 96 renal clearance studies were carried out in 10 dogs before and after prolonged phosphate depletion (30-160 days) and after repletion. Depletion was produced by reducing phosphate intake and administering aluminum hydroxide gel while intakes of sodium, calcium, and magnesium were constant. With phosphate depletion, serum phosphorus fell to less than 1.0 mg/100 ml and diffusible serum calcium either remained unchanged or rose transiently. Glomerular filtration rate (GFR) fell by 15 to 53%. Despite the reduced filtered load of calcium, its fractional excretion increased in most experiments. This hypercalciuria was not dependent upon changes in sodium or magnesium excretion, or the urinary concentration of complexing anions, and persisted after sodium restriction. Phosphate repletion reversed the effects on GFR and calcium excretion. The intravenous infusion of small quantities of phosphate (0.04 mmole/min) into either intact or thyroparathyroidectomized (T-PTX), phosphate-depleted animals caused a significant reduction in fractional excretion of calcium, but the intrarenal infusion of 0.02 mmole/min of phosphate into one kidney failed to produce an ipsilateral effect. The administration of parathyroid extract reduced fractional calcium excretion, but the latter remained significantly elevated. After T-PTX, fractional calcium excretion did not increase in the phosphate-depleted animals. Furthermore, serum calcium was normal after T-PTX until serum phosphorus increased slightly, and

Epithelial magnesium transport and regulation by the kidney

“…It is evident from clearance experiments that the urinary excretion of divalent cations of phosphate-depleted subjects is inappropriate for the plasma concentration, supporting the notion of defective tubular transport (153). Using micropuncture, we have demonstrated that defective magnesium absorption occurred in the loop of Henle and the distal tubule of phosphate-depleted dogs (156).…”

“…One of the hallmarks of hypophosphatemia and cellular phosphate-depletion is the striking increase in urinary excretion of calcium and magnesium (153). Magnesium excretion may be sufficiently large to lead to hypomagnesemia (154,155).…”

“…The increase in divalent ion excretion in both human and animals occurs within hours following initiation of dietary phosphate restriction. Three mechanisms have been proposed to account for the increased renal excretion: 1) mobilization of calcium and magnesium from bone, 2) suppression of parathyroid hormone secretion, and 3) aberrant tubular transport (153).…”

Renal Bicarbonate Wasting during Phosphate Depletion A POSSIBLE CAUSE OF ALTERED ACID-BASE HOMEOSTASIS IN HYPERPARATHYROIDISM

“…There is indirect evidence to indicate that the activity of the parathyroid glands is inhibited during phosphate depletion. Thus, rats show hypoplasia of the parathyroid glands during phosphate depletion (26); also serum calcium levels remain normal or slightly elevated after removal of the parathyroid glands in phosphate depleted rats (26,27) and dogs (20,28), indicating that serum so 7.10.…”

Orthopaedic · Radiology · Pathology Conference: Chronic Multifocal Chest and Leg pain in a 34-year-old Woman

“…The aluminum or magnesium component of these drugs binds dietary phosphate, preventing its intestinal absorption and causing a negative phosphate balance typically within 3 to 4 weeks. The resulting hypophosphatemia is thought to prevent proper nucleation of mineral salts into the bone matrix, causing osteomalacia [6,11]. In addition, hypercalciuria can appear within 2 weeks [25] and, if not adequately supplemented in the diet, can lead to increased bone resorption via parathyroid hormone [2].…”