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Approximately 80% of filter phosphorous is reabsorbed by renal proximal tubule cells. The regulation of urinary phosphorous excretion is principally dependent on regulation of proximal tubule phosphorous reabsorption. A variety of factors influence renal tubular phosphate reabsorption, and consequent urine excretion. Factors which increase urinary phosphorous excretion include high phosphorous diet, parathyroid hormone, extracellular volume expansion, low dietary potassium intake and proximal tubule defects (eg, Fanconi Syndrome, X-linked hypophosphatemic Rickets, tumor-induced osteomalacia). Factors which decrease, or are associated with decreases in, urinary phosphorous excretion include low dietary phosphorous intake, insulin, high dietary potassium intake, and decreased intestinal absorption of phosphorous (eg, phosphate-binding antacids, vitamin D deficiency, malabsorption states).
A renal leak of phosphate has also been implicated as contributing to kidney stone formation in some patients.
Evaluation of hypo- or hyper-phosphatemic states
Evaluation of patients with nephrolithiasis
Interpretation of urinary phosphorous excretion is dependent upon the clinical situation, and should be interpreted in conjunction with the serum phosphorous concentration.
No significant cautionary statements
Agarwal R, Knochel JP: Hypophosphatemia and hyperphosphatemia. In The Kidney. Sixth edition. Edited by Barry M Brenner. WB Saunders Company, Philadelphia, PA, 2000, pp 1071-1125