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Objective: This study evaluated the role of body mass index (BMI) and dietary potential renal acid load (PRAL) with urinary saturation for calcium oxalate (US-CaOx), calcium phosphate (US-CaP) and uric acid (US-UA) in renal stone formers. Materials and methods: A retrospective analysis was conducted of laboratory data collected on 442 renal stone-forming patients. Demographic information, BMI and 24 h urinary samples were collected from patients on their regular diets. PRAL was calculated as the Load of Acid to Kidney Evaluation (LAKE) score through a short questionnaire. Results: Urinary risk factors, but also inhibitors of calcium stone formation such as magnesium, tended to increase in relation to BMI (p = .000). Urinary pH (p = .002) and ammonium/sulfate ratio (p = .000) were negatively related to BMI. This resulted in a positive correlation between BMI and US-UA (p = .000), whereas US-CaOx and US-CaP were not influenced by BMI. LAKE score was positively correlated with US-CaOx (p = .022) and US-CaP (p = .000) as a consequence of the inverse relationship between LAKE score and citrate (p = .000). Multiple linear regression analysis identified BMI (p = .009) and male gender (p = .002) as independent predictors of US-UA, and LAKE score (p = .004) and age (p = .001) as independent predictors of US-CaP. Conclusions: BMI, which depends on excessive intake of energy from food, is not related to an increased biochemical risk of calcium stone formation, which is more dependent on the renal acid load of the diet. In contrast, obesity is associated with an increased risk of uric acid stone formation due to insulin resistance, impaired ammoniagenesis and low urinary pH. [ABSTRACT FROM AUTHOR]

Objective To assess (i) the extent to which urinary supersaturation ( SS) has successfully discriminated between stone formers and healthy individuals ( N), (ii) whether absolute SS has diagnostic worth and (iii) whether high SS is the fundamental cause of stone formation per se., Materials and Methods Google Scholar was used to identify studies in which urinary compositional data had been determined., In those cases where SS values were not given, or where other risk indices had been reported, they were (re-)calculated., Collected data were termed 'global' but were then 'filtered' according to stone type and protocols used for SS calculations., SS distribution plots for calcium oxalate, brushite and uric acid were constructed., Data were statistically analysed using the unpaired t-test and Mann- Whitney test., Results In all, 47 studies yielded 123 SS values for healthy individuals and 122 values for stone formers., The mean and median SS values were significantly greater in stone formers compared with healthy individuals in all but one of the comparisons., Wide variations in SS occurred for healthy individuals and stone formers. The two groups could not be separated., Conclusions Absolute SS has no diagnostic worth. It is impossible to quantify the meaning of a 'high' SS value. Urines cannot be identified as originating from healthy individuals or stone formers based on their SS., SS should be determined in clinical and research settings for relative comparisons during the assessment of treatment efficacies., This study provides a compelling argument for SS being a casual factor rather than a causal one. [ABSTRACT FROM AUTHOR]

Introduction: In lithogenesis, for a stone to form it is necessary that the urine is supersaturated with respect to the salt that will constitute the future stone. The objective was to analyze the urinary saturations of Calcium Oxalate (CaOxa), brushite (calcium phosphate), struvite (ammonium-magnesium phosphate) and uric acid (UA) in children with and without lithiasis. Correlate them with the different parameters involved in the lithiasic process. And compare saturations in children with or without overweight., Material and Methods: We examined 108 healthy children and 53 patients diagnosed with lithiasis. In 24-h urine, the different biochemical parameters involved in lithiasis and the saturation levels of CaOxa, brushite, struvite and UA., Results: We studied 108 healthy children with a mean age of 9.5 ± 3.9 years. Renal lithiasis was diagnosed in 53 patients with an average age of 10.5 ± 5.8 years. Children with lithiasis had higher saturation values of CaOxa (4.86 ± 2.71 vs. 3.15 ± 1.99, p < 0.01) and brushite (1.58 ± 1.23 vs. 0.86 ± 0.81, p < 0.001) compared to non-lithiasic children. UA saturation was higher in children with body mass index greater than 22 (5.25 ± 3.52 vs. 3.84 ± 3.5, p < 0.04). Finally, urinary pH, ammonium concentration and uricosuria influenced UA saturation. that the urinary pH regression coefficient in the uric acid saturation regression analysis was -4.5., Conclusions: The mean values of calcium oxalate and brushite saturations were higher in children with lithiasis. Uric acid saturation was elevated in overweight children. Finally, urinary pH greatly influenced uric acid saturation.

Because dietary ingredients and feeding patterns influence the volume, pH and solute concentration of urine, diet can contribute to the etiology, management or prevention of recurrence of some causes of lower urinary tract disease. Most research assessing the effect of diet has focused on the latter two aspects, primarily because of interest in struvite urolithiasis. Manipulation of urine pH through dietary means has proven an effective tool for the management and prevention of struvite urolithiasis; acidification of urine, however, may be a risk factor for calcium oxalate urolithiasis, which now appears to occur with approximately equal frequency in cats. Prediction of urine pH from dietary analysis would thus be a valuable tool, but considerable further research is required before this can be achieved with commercial canned foods. With the growing importance of urolith types other than struvite, alternatives to the measurement of urine pH are required to assess critically the likely beneficial (or detrimental) effects of manipulation of nutrient profile. Measurement of urinary saturation may permit the development and fine tuning of nutrient profiles aimed at controlling lower urinary tract diseases in cats that are associated with a range of different mineral types. The majority of cats with signs of lower urinary tract disease do not, however, have urolithiasis; indeed, no specific cause can be established in most of these cats. Recent observations suggest that recurrence rates of signs in cats classified as having idiopathic lower urinary tract disease may be more than halved if affected animals are maintained on high, rather than low moisture content diets. J. Nutr. 2753S-2757S, 1998 [ABSTRACT FROM AUTHOR]

It has been suggested recently that the first step in the formation of calcium oxalate stones appears to be crystallisation. This step is said to depend on the state of saturation of the urine. This hypothesis was checked in cystine stone formers. Cystine crystalluria was found in 83% of 24 urine samples from cystine stone formers (CSF) but in none of the 400 control samples and appears to be a good guide in the diagnosis of cystine lithiasis. Urinary cystine saturations was constantly higher in CSF than in non-cystine stone formers (NCSF) who exhibited undersaturated urine with respect to cystine. There was almost no overlap between these 2 groups. Crystals were never found in undersaturated urine and were always present when the saturation was above 1. There appears to be a good correlation between the level of urinary saturation and the presence of crystalluria and there is no need for any additional factor such as a defective inhibitor. The study underlines the limits of a therapeutic regimen of a high fluid intake and alkalinisation of the urine. [ABSTRACT FROM AUTHOR]

This paper describes a simple method to measure the capacity of undiluted urine and of other inhibitor containing solutions (PPi and EHDP) to protect a given mass of calcium oxalate crystals from growth. The method has also been used to determine relative urinary saturation with respect to calcium oxalate. It is based on titration with oxalate and measures the critical changes of concentration necessary to reach saturation or to induce crystal growth. From these changes inhibitory capacity as well as the level of urinary saturation can be calculated in terms of differences of concentration products. The use of the methods at present available to measure urinary oxalate are thereby avoided. In order to compare the results from different urines without the need for cumbersome calculations of activity products we have introduced a saturation-inhibition ratio. [ABSTRACT FROM AUTHOR]

The physico-chemical basis for the action of various drugs in calcium nephrolithiasis may be described in terms of changes produced in the urinary state of saturation (APR), limit of metastability (FPR), or in crystal growth. The validation of this scheme for drug action requires further correlation of objective responses to drug therapy, described in terms of urinary crystallisation, with the clinical response. [ABSTRACT FROM AUTHOR]

Objective To produce an index of lithogenic risk which identifies patients at risk of stone recurrence and facilitates the monitoring of prophylactic treatments. Patients and methods The EQUIL2, program provides an evaluation of the state of urinary saturation, particularly of calcium oxalate, based on the pH and total concentrations (mmol/l) of sodium, potassium, calcium, magnesium, uric acid, chloride, ammonium, citrate, phosphate, sulphate, oxalate, pyrophosphate and carbon dioxide. The morning urinary calcium oxalate saturation coefficient was thus calculated for 30 stone-formers (Group 1) and 30 normal control subjects (Group 2). Results Urine from the majority of individuals was saturated, with no significant difference between the two groups. There appeared to be a correlation between the state of saturation and the urinary calcium oxalate molar product in both stone-formers (r =0.931) and controls (r=0.914). Conclusion In future studies on urinary calcium oxalate saturation, it should be possible to supplement the sophisticated coefficient determined by the EQUIL, program with the molar product, except in cases where monitoring therapies have little or no effect on urinary oxalate or urinary calcium levels. [ABSTRACT FROM AUTHOR]