Interactions of Starvation and Selective Phosphorus Depletion on Renal Phosphate Reabsorption

Abstract

Renal phosphate (Pi) wastage following 7 days of starvation was investigated in normal rats (HI-P) and others previously stabilized on a low phosphorus (LO-P) diet. In LO-P animals, P_i excretion increased after starvation, but was significantly less than in starved HI-P rats. After thyroparathyroidectomy, the increase in Pi excretion after parathyroid hormone (PTH) was significantly greater in nonacidotic starved HI-P rats than in LO-P animals. However, PTH elicited a 31-fold increase in P_i excretion in both of these groups. Starved LO-P and HI-P rats responded equivalently to dibutyryl cyclic AMP. The renal response to phosphate depletion normally promotes P_i conservation, but is attenuated markedly by 7 days of subsequent starvation. This results from at least partial restoration of phosphaturic responsiveness to PTH during starvation.

Efforts to establish an animal model of Fanconi syndrome after ifosfamide administration to rats

“…Similar results have been described for starvation. It resulted in a significant decrease in the urinary content of potassium, magnesium, phosphate, and calcium (Olsson and Kallner, 1995;Stele, 1982) as well as in a decrease in renal plasma flow and GFR. A short polyuric phase was followed by distinct oliguria (Thompson et al, 1987;Boim et al, 1992).…”

The phosphatonins and the regulation of phosphorus homeostasis

“…In states of phosphate equilibrium or balance and normal renal function, the amount of phosphorus appearing in urine is remarkably similar to that absorbed in the intestine and can serve as a rough approximation of the amount absorbed in the intestine. In states of phosphate deprivation resulting from inadequate intake of phosphorus or low absorption of phosphorus from the intestine, urinary phosphorus concentrations are low and serve as appropriate indicators of altered phosphorus regulation (39,114,115,117).…”