A BASIC computer program for the calculation of urinary supersaturation with respect to the common kidney stone components is described. In vitro and in vivo tests show that the program described accurately calculates supersaturation. The application of this computer program to urolithiasis research is discussed.

Mineralization of bone matrix may be influenced by the presence of specific, noncollagenous bone proteins. The quantitative influence of two bone-specific proteins--bone gamma-carboxyglutamic acid (Gla) protein and osteonectin--and other proteins that decreased the rate of crystal growth was measured by adding seed crystals of hydroxyapatite to a solution of CaCl2 and KH2PO4, pH 7.4 at 37 degrees C. The molar concentrations of proteins needed to inhibit the rate of crystal growth by 50% were as follows: osteonectin, 0.15 microM; bone Gla protein, 0.8 microM; prothrombin, 0.9 microM; prothrombin fragment 1, 1.0 microM; soybean trypsin inhibitor, 3 microM; prethrombin 1, 9 microM; cytochrome c, 30 microM. Calmodulin and parvalbumin were found to be less active than prothrombin fragment 1 and had no activity in the micromolar range. The combination of two inhibitors resulted in a mixture with an inhibitory activity that was the sum of the two inhibitors. Decarboxylation of bone Gla protein significantly reduced its inhibitory activity. These results indicate that the inhibitory activity of a protein does not correlate with Ca2+-binding affinity under these conditions, that the mixture of inhibitors has an additive effect, and that gamma-carboxyglutamic acid residues enhance the ability of a protein to inhibit hydroxyapatite-seeded crystal growth.

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Alimentary phosphorus deprivation due to a low-phosphorus diet (LPD) elicits a profound antiphosphaturia and an increase in sodium-dependent inorganic phosphate (Pi) uptake by renal cortical brush border membrane (BBM) vesicles. But, in alimentary phosphorus deprivation due to total fasting, high urinary excretion of Pi persists. In the present study, we determined whether low tubular reabsorption of Pi in fasting is due to a diminished capacity of the specific Pi transport system with the renal cortical luminal BBM or whether it is due to a reduced transepithelial reabsorption of Pi because of metabolic conditions occurring in proximal tubule cells during fasting. Sodium-dependent Pi transport in compared with fasted rats or rats fed a normal phosphorus diet. Sodium-dependent uptake of D-glucose was significantly lower in LPD rats, compared with fast animals or animals fed a normal diet. Thus, in contrast to LPD, fasting does nt elicit an increase in Pi transport and a decrease in D-glucose transport across the isolated renal BBM. The same differences in BBM transport of Pi were present also in thyroparathyroidectomized rats. Further experiments demonstrated that the adaptation of renal function and the renal BBM transport to LPD are overridden by a subsequent period of total fasting. Results of the present study show that fasting both prevents and reverses the renal response of rats to alimentary phosphorus deprivation. The differences in Pi excretion between fasted rats, LPD rats, and LPD rats subsequently fasted are attributed, at least in part, to specific adaptive changes in sodium-dependent Pi transport across the luminal BBM, rather than to alterations in other cellular (metabolic) components of transepithelial Pi reabsorption in the proximal tubule.

Factors that promote the formation of calcium oxalate dihydrate (COD) in urine were investigated. Crystals resulting from the incubation of 25-ml aliquots of the solution to be tested and 1 ml of 0.05 M ammonium oxalate were examined by infrared spectrophotometry. With reference spectra of known mixtures, the fractional content of COD could be estimated. At pH 6.5, only COD formed in human urine. In a supersaturated inorganic solution of calcium oxalate, the percentage of COD was 7.5 +/- 1.4. Pyrophosphate (1 to 8 X 10(-5) M), citrate (10(-4) to 2 X 10(-3) M), RNA from yeast (5 X 10(-9) to 0.5 X 10(-7) M), or heparin (2 X 10(-9) to 2 X 10(-7) M) added to a supersaturated solution of calcium oxalate increased the percentage of COD proportional to the concentration of the additives. Chondroitin sulfate and magnesium had no effect. An increase in pH increased the formation of COD in inorganic solutions containing citrate, pyrophosphate, and heparin and in undiluted urine. RNA-citrates and citrate-pyrophosphate mixtures showed additivity. Urine showed an effect that was inversely proportional to its dilution. Substances that promote COD formation in this system had their phase-stabilizing effects at concentrations normally found in urine. Further, these same substances are known inhibitors of calcium oxalate crystal formation. With both inhibition and phase stabilization, there is additivity of effects, and changes in pH alter the response.

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