OBJECTIVES: Based on a recently introduced mathematical model approach we show that uroliths located in the urinary tract (UT) can substantially deplete the urinary concentrations of lithogenic constituents by continuous growth. METHODS: To illustrate the influence of the urinary depletion effect on urinalysis, a "typical" calcium oxalate (CaOx) stone former, presently not stone-free, was investigated. Serum and urine samples were analyzed. Several metabolic tests were performed. Crystallization risk according to the BONN-Risk-Index (BRI) and the relative supersaturation in respect to CaOx (RS(CaOx)) were determined. X-ray films taken before and after a period of six months were evaluated in order to estimate stone size and average stone growth rate taken place within that period. RESULTS: Regarding CaOx urolithiasis the urine samples show a pathologically altered pH, a low 24h-citric acid excretion, and a low 24h-urine volume. Neither calcium nor oxalate excretion data reflect values indicating these substances as risk factors. However, BRI and RS(CaOx) reflect a high crystallization risk. The patient's intestinal oxalate absorption is high. Applying the depletion model, the patient's 24h-urine composition shifts from normooxaluric to hyperoxaluric. CONCLUSION: In the patient, a hitherto undetected hyperoxaluria is diagnosed when in-vivo stone growth is taken into account. This is a clear indication that the metabolic status can only be evaluated correctly in "stone-free" patients. Any stone material present in the UT must be considered in urinalysis interpretation as the stone-related urinary depletion effect is of high clinical relevance. A helpful nomogram is presented, allowing the estimation of the extent of urinary depletion caused by CaOx uroliths.
OBJECTIVES: Based on a recently introduced mathematical model approach we show that uroliths located in the urinary tract (UT) can substantially deplete the urinary concentrations of lithogenic constituents by continuous growth. METHODS: To illustrate the influence of the urinary depletion effect on urinalysis, a "typical" calcium oxalate (CaOx) stone former, presently not stone-free, was investigated. Serum and urine samples were analyzed. Several metabolic tests were performed. Crystallization risk according to the BONN-Risk-Index (BRI) and the relative supersaturation in respect to CaOx (RS(CaOx)) were determined. X-ray films taken before and after a period of six months were evaluated in order to estimate stone size and average stone growth rate taken place within that period. RESULTS: Regarding CaOx urolithiasis the urine samples show a pathologically altered pH, a low 24h-citric acid excretion, and a low 24h-urine volume. Neither calcium nor oxalate excretion data reflect values indicating these substances as risk factors. However, BRI and RS(CaOx) reflect a high crystallization risk. The patient's intestinal oxalate absorption is high. Applying the depletion model, the patient's 24h-urine composition shifts from normooxaluric to hyperoxaluric. CONCLUSION: In the patient, a hitherto undetected hyperoxaluria is diagnosed when in-vivo stone growth is taken into account. This is a clear indication that the metabolic status can only be evaluated correctly in "stone-free" patients. Any stone material present in the UT must be considered in urinalysis interpretation as the stone-related urinary depletion effect is of high clinical relevance. A helpful nomogram is presented, allowing the estimation of the extent of urinary depletion caused by CaOx uroliths.