|Values are valid only on day of printing.|
Evaluation of hypo- or hyper-phosphatemic states
Evaluation of patients with nephrolithiasis
Approximately 80% of filtered phosphorus is reabsorbed by renal proximal tubule cells. The regulation of urinary phosphorus excretion is principally dependent on regulation of proximal tubule phosphorus reabsorption. A variety of factors influence renal tubular phosphate reabsorption, and consequent urine excretion. Factors which increase urinary phosphorus excretion include high phosphorus 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 phosphorus excretion include low dietary phosphorus intake, insulin, high dietary potassium intake, and decreased intestinal absorption of phosphorus (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.
<1,100 mg/24 hours
Interpretation of urinary phosphorus excretion is dependent upon the clinical situation, and should be interpreted in conjunction with the serum phosphorus 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