Hyperoxaluria in patients with recurrent calcium oxalate calculi: dietary and other risk factors.

The presence of mild hyperoxaluria in recurrent calcium oxalate stone formers is controversial. The aim of this study was to identify recurrent stone formers with mild hyperoxaluria and to classify them further by assessing their response to a low oxalate diet. In addition, the prevalence of other risk factors for stone formation in this group of patients was investigated. A total of 207 consecutive patients with recurrent renal calculi were screened and 40 (19%) were found to have mild hyperoxaluria. Of these, 18 (45%) responded to dietary oxalate restriction by normalising their urinary oxalate. The remaining 22 patients were classified as having idiopathic hyperoxaluria and were subdivided into those in whom urinary oxalate excretion was consistently elevated in all specimens measured and those in whom the elevation was intermittent in nature. Dietary oxalate restriction had a partially beneficial effect in lowering oxalate excretion in the patients with persistent hyperoxaluria. No difference in urinary oxalate excretion was found after dietary restriction in the patients with intermittent hyperoxaluria. Other risk factors, including dietary, absorptive and renal hypercalciuria and hypocitraturia, were documented, the prevalence of which (65%) was not significantly different from that (62.5%) found in 40 age- and sex-matched calcium stone formers without hyperoxaluria. The prevalence of hyperuricosuria was significantly greater in patients with hyperoxaluria when compared with stone controls. Further studies are required to elucidate the underlying mechanisms of hyperoxaluria in recurrent stone formers.     

Dietary risk factors for hyperoxaluria in calcium oxalate stone formers

BACKGROUND: Hyperoxaluria is a major predisposing factor in calcium oxalate urolithiasis. The aim of the present study was to clarify the role of dietary oxalate in urinary oxalate excretion and to assess dietary risk factors for hyperoxaluria in calcium oxalate stone patients. METHODS: Dietary intakes of 186 calcium oxalate stone formers, 93 with hyperoxaluria (>or=0.5 mmol/day) and 93 with normal oxalate excretion (<0.4 mmol/day), were assessed by a 24-hour weighed dietary record. Each subject collected 24-hour urine during the completion of the food record. Oxalate content of foods was measured by a recently developed analytical method. RESULTS: The mean daily intakes of energy, total protein, fat and carbohydrates were similar in both groups. The diets of the patients with hyperoxaluria were estimated to contain 130 mg/day oxalate and 812 mg/day calcium as compared to 101 mg/day oxalate and 845 mg/day calcium among patients without hyperoxaluria. These differences were not significant. The mean daily intakes of water (in food and beverages), magnesium, potassium, dietary fiber and ascorbic acid were greater in patients with hyperoxaluria than in stone formers with normal oxalate excretion. Multiple logistic regression analysis revealed that urinary oxalate excretion was significantly associated with dietary ascorbate and fluid intake, and inversely related to calcium intake. Differences of estimated diet composition of both groups corresponded to differences in urinary parameters. CONCLUSIONS: These findings suggest that hyperoxaluria predominantly results from increased endogenous production and from intestinal hyperabsorption of oxalate, partly caused by an insufficient supply or low availability of calcium for complexation with oxalate in the intestinal lumen.     

Renal oxalate excretion following oral oxalate load in patients with urinary calculus disease and healthy controls

Oral oxalate loading using sodium oxalate or a vegetable juice was done to evaluate the intestinal absorption of exogenous oxalate in 30 patients with renal stones and 13 healthy controls. Fifteen calcium oxalate stone formers, 7 non-oxalate stone formers and 10 healthy volunteers were given an oral loading of sodium oxalate (500 mg). Urinary oxalate increased promptly, reaching a peak value within 4 to 8 hours after administration of a synthetic oxalate orally in a fasting state. In calcium oxalate stone formers, the mean increment of urinary oxalate and the bioavailability following oral sodium oxalate load were significantly higher than in the healthy controls and non-oxalate stone formers. Furthermore, intestinal hyperabsorption of oxalate in our criterion was defined in six patients with calcium oxalate stones (40%). On the other hand, eight calcium oxalate stone formers and three healthy controls were given vegetable juice. Urinary oxalate was increased only slightly after the ingestion, and there was no difference between calcium oxalate stone formers and normal controls. These results suggest that a certain hyperoxaluria might be induced by intestinal absorption of exogenous oxalate, and that the hyperabsorption might indicate a possible risk factor for calcium oxalate stone formation.     

Hyperoxaluria in idiopathic calcium nephrolithiasis--what are the limits?

OBJECTIVE: The object of this study was to investigate the role for measurement of 24-h renal oxalate excretion in the evaluation of idiopathic calcium stone formers. MATERIALS AND METHODS: Renal excretion rates of oxalate and creatinine were measured in 24-h urines in 46 consecutive male recurrent idiopathic calcium stone formers and 61 healthy males. Furthermore, day-to-day variation in renal oxalate excretion in 10 male recurrent stone formers and 10 healthy males were evaluated by measuring 24-h oxalate excretion on 5 different days in each individual. Concentrations of oxalate in urine were measured using an enzymatic method without ascorbate interference. RESULTS: The cumulative frequency distribution curves of 24-h renal oxalate excretion rates of stone formers and controls were congruent, and there were no statistically significant differences in oxalate excretion rates between stone formers and controls. Mean 24-h oxalate excretion (95%-confidence intervals) was 0.22 (0.18-0.25) mmol and 0.21 (0.18-0.24) mmol in stone formers and controls, respectively (p = 0.9). The day-to-day variation study did not reveal any differences in renal oxalate excretion pattern between stone formers and controls, and the presence of intermittent hyperoxaluria could not be confirmed. The oxalate excretion rates were generally low. CONCLUSION: In our region, there appear to be no differences in 24-h renal excretion rates of oxalate between male recurrent idiopathic calcium stone formers and healthy males, and the syndrome of mild hyperoxaluric calcium nephrolithiasis could not be identified in our population of idiopathic stone formers. Hence, a limit of abnormal oxalate excretion that distinguishes an idiopathic stone former from a non-stone former could not be defined in our population. Therefore, the value of routine measurement of urinary oxalate in idiopathic urolithiasis is difficult to accept, and cannot be recommended.     

Prevalence of hyperoxaluria in idiopathic calcium oxalate kidney stone disease

Urinary excretion of oxalate, calcium and urate has been investigated in 88 patients affected by idiopathic calcium oxalate stone disease and in 20 normal subjects. Of these ions, only oxalate was found significantly higher in stone formers. Defining hyperoxaluria as urinary oxalate excretion greater than 2 SD above normal, 50% of stone-forming people were found to be hyperoxaluric. When stone formers were classified in normo- and hyperoxaluric, the prevalence of hypercalciuria, hyperuricuria, family history of stone disease and recurrencies in stone formation was the same in both groups. It is concluded that hyperoxaluria is a frequent finding in finding in idiopathic calcium oxalate renal stone disease.     

Intestinal Oxalobacter formigenes colonization in calcium oxalate stone formers and its relation to urinary oxalate

BACKGROUND AND PURPOSE: Oxalobacter formigenes is an anaerobic commensal colonic bacterium capable of degrading oxalate through the enzyme oxalyl-CoA decarboxylase. It has been theorized that individuals who lack this bacterium have higher intestinal oxalate absorption, leading to a higher urinary oxalate concentration and an increased risk of calcium oxalate urolithiasis. We performed a prospective, controlled study to evaluate O. formigenes colonization in calcium oxalate stone formers and to correlate colonization with urinary oxalate and other standard urinary stone risk factors. PATIENTS AND METHODS: Thirty-five first-time calcium oxalate stone formers were compared with 10 control subjects having no history of urolithiasis and a normal renal ultrasound scan. All subjects underwent standard metabolic testing by submitting serum and 24-hour urine specimens. In addition, all subjects submitted stool samples for culture and detection of O. formigenes by Xentr(ix) O. formigenes Monitor. RESULTS: Intestinal Oxalobacter was detected in only 26% of the stone formers compared with 60% of the controls (p < 0.05). Overall, the average urinary oxalate excretion by the two groups was similar (38.6 mg/day v 40.8 mg/day). Among stone formers, however, there were statistically higher urinary oxalate concentrations in O. formigenes-negative patients compared with those testing positive (41.7 mg/day v 29.4 mg/day) (p = 0.03). Furthermore, all 10 stone formers with hyperoxaluria (>44 mg/day) tested negative for O. formigenes (p < 0.05). CONCLUSIONS: Calcium oxalate stone formers have a low rate of colonization with O. formigenes. Among stone formers, absence of intestinal Oxalobacter correlates with higher urinary oxalate concentration and an increased risk of hyperoxaluria. Introduction of the Oxalobacter bacterium or an analog of its enzyme oxalyl-CoA decarboxylase into the intestinal tract may be a treatment for calcium oxalate stone disease.     

Intestinal oxalate and calcium absorption in recurrent renal stone formers and healthy subjects

The fractional intestinal absorption of oxalate and calcium was investigated by isotope techniques in 20 normal subjects and in 12 idiopathic calcium oxalate stone formers. The greatest amount of 14C-oxalate was excreted during the first six hour period in controls as well as in stone formers. The stone formers had a greater intestinal uptake of oxalate (11 +/- 5.1%) than the controls (6.2 +/- 3.7%; p less than 0.01). There was no significant relationship between the fractional absorption of oxalate and the total urinary oxalate excretion. The stone formers also had a higher fractional uptake of calcium compared to the controls (55 +/- 11% vs. 47 +/- 9.1%; p less than 0.05). There was a positive relationship (r = 0.47) between the urinary excretions of calcium and oxalate in the stone formers. During these conditions no correlation could be demonstrated between the fractional absorptions of oxalate and calcium, neither in the stone formers nor in the controls. In conclusion, patients with recurrent formation of calcium oxalate containing stones appear to have an enhanced intestinal uptake of both oxalate and calcium. This disturbance could be of primary pathogenic importance for their stone forming propensity.     

Urinary oxalate excretion in female calcium oxalate stone formers with and without a history of recurrent urinary tract infections

Therapy with antibiotics in recurrent urinary tract infections may destroy colonies of Oxalobacter formigenes in the intestinal tract. A lack of oxalate degradation caused by the absence of this bacterium is suggested to contribute to the hyperabsorption of dietary oxalate and to the increase in urinary oxalate excretion. The present study was performed to evaluate the effect of recurrent urinary tract infections and subsequent changes induced in the urinary excretion profile in female calcium oxalate stone formers. Serum biochemical profiles, 24-h urinary parameters, and the personal characteristics of 57 female calcium oxalate stone patients with recurrent urinary tract infections (RUTI) were compared with 78 female calcium oxalate stone patients without a history of urinary tract infection. All subjects were recruited during the same period. In female patients with RUTI, urinary oxalate excretion was significantly higher (0.374 mmol/day) than in females without urinary tract infection (0.308 mmol/day) (P < 0.05). Moreover, the mean 24-h pH value and urinary sodium excretion were significantly higher in women with RUTI than in women without a history of urinary tract infection. The significantly higher urinary oxalate excretion in female calcium oxalate stone formers with recurrent urinary tract infections may be associated with the application of antibiotics and a subsequent temporary or permanent decolonization of Oxalobacter formigenes.     

The efficacy of dietary intervention on urinary risk factors for stone formation in recurrent calcium oxalate stone patients

PURPOSE: Nutrition is suggested to be the major environmental risk factor in idiopathic calcium oxalate stone disease. The study was designed to evaluate the effect of dietary intervention on urinary risk factors for recurrence in calcium oxalate stone formers. MATERIALS AND METHODS: A total of 76 men and 31 women with idiopathic calcium oxalate stone disease collected 24-hour urine on their habitual, self-selected diets and after 7 days on a balanced standardized diet according to the recommendations for calcium oxalate stone formers. RESULTS: On the usual diet, a urine volume of less than 2.0 l per 24 hours was present in 57.9%, hypercalciuria in 25.2%, hypomagnesuria in 18.7%, hyperoxaluria in 14.0%, hyperuricosuria in 41.3% and hypocitraturia in 57.0% of patients. The frequency of metabolic abnormalities and the risk of calcium oxalate stone formation decreased significantly on the ingestion of the balanced diet, due to the significant increase in urinary volume, pH and citrate excretion and the significant decrease in urinary calcium and uric acid excretion. No change occurred in urinary oxalate and magnesium excretion. CONCLUSIONS: The evaluation of urinary risk profiles of the patients on their usual dietary habits revealed a high risk for calcium oxalate stone formation. A low fluid intake and an increased intake of protein and alcohol were identified as the most important dietary risk factors. The shift to a nutritionally balanced diet according to the recommendations for calcium oxalate stone formers significantly reduced the stone forming potential.     

Roux-en-Y gastric bypass is associated with early increased risk factors for development of calcium oxalate nephrolithiasis

BACKGROUND: Patients treated for obesity with jejunoileal bypass (JIB) experienced a marked increased risk of hyperoxaluria, nephrolithiasis, and oxalate nephropathy developing. Jejunoileal bypass has been abandoned and replaced with other options, including Roux-en-Y gastric bypass (RYGB). Changes in urinary lithogenic risk factors after RYGB are currently unknown. Our purpose was to determine whether RYGB is associated with elevated risk of developing calcium oxalate stone formation through increased urinary oxalate excretion and relative supersaturation of calcium oxalate. STUDY DESIGN: A prospective longitudinal cohort study of 24 morbidly obese adults (9 men and 15 women) recruited from a university-based bariatric surgery clinic scheduled to undergo RYGB between December 2005 and April 2007. Patients provided 24-hour urine collections for analysis 7 days before and 90 days after operation. Primary outcomes were changes in 24-hour urinary oxalate excretion and relative supersaturation of calcium oxalate from baseline to 3 months post-RYGB. RESULTS: Compared with their baseline, patients undergoing RYGB had increased urinary oxalate excretion (31 +/- 10 mg/d versus 41 +/- 18 mg/d; p = 0.026) and relative supersaturation of calcium oxalate (1.73 +/- 0.81 versus 3.47 +/- 2.59; p = 0.030) 3 months post-RYGB in six patients (25%). De novo hyperoxaluria developed. There were no preoperative patient characteristics predictive of development of de novo hyperoxaluria or the magnitude of change of daily oxalate excretion. CONCLUSIONS: This prospective study indicates that RYGB is associated with an earlier increase in urinary oxalate excretion and relative supersaturation of calcium oxalate than previously reported. Additional studies are needed to determine longterm post-RYGB changes in urinary oxalate excretion and identify patients that might be at risk for hyperoxaluria developing.     

Association of absence of intestinal oxalate degrading bacteria with urinary calcium oxalate stone formation

AIM: Urinary concentration of oxalate is considered an important factor in the formation of renal stones. Dietary oxalate is a major contributor to urinary oxalate excretion in most individuals. Furthermore, oxalate degrading bacteria have been isolated from human feces. We investigated the significance of oxalate degrading bacteria for urinary oxalate excretion and urinary stone formation. METHODS: Twenty-two known calcium oxalate stone-forming patients (stone formers) and 34 healthy volunteers (non-stone formers) were included in the study. Stool specimens were inoculated into pepton yeast glucose (PYG) medium supplemented with oxalate under anaerobic condition at 37 C for one week. After the incubation period, each colony was checked for the loss of oxalate from the culture medium. A 24-h urine sample was collected in 43 individuals and analyzed for oxalate excretion. RESULTS: Twenty-eight of 34 (82%) healthy volunteers and 10 of 22 (45%) calcium oxalate stone formers were colonized with oxalate degrading bacteria. Calcium oxalate stone formers were more frequently free of oxalate degrading bacteria (P < 0.01). Urinary excretion of oxalate in those with oxalate degrading bacteria was significantly less than in those without oxalate degrading bacteria (P < 0.05). Hyperoxaluria (> 40 mg/day) was found in four of 27 individuals (15%) with oxalate degrading bacteria compared to seven of 16 (44%) without oxalate degrading bacteria (P < 0.05), suggesting an association between the absence of oxalate degrading bacteria and the presence of hyperoxaluria. CONCLUSION: The absence of oxalate degrading bacteria in the gut could promote the absorption of oxalate, thereby increasing the level of urinary oxalate excretion. The absence of oxalate degrading bacteria from the gut appears to be a risk factor for the presence of absorptive hyperoxaluria and an increased likelihood of urolithiasis.     

Comparative study of 24-hour urinary excretion of glycosaminoglycans by renal stone formers and healthy adults

In order to find out the possible aetiological factors for urolithiasis in North-Western India, an endemic region for urinary calculi, we studied the 24-hour urinary excretion of glycosaminoglycans (GAGs), inhibitors of calcium oxalate crystallisation and/or crystal aggregation, in 58 healthy adults and in 100 stone formers. GAGs were colorimetrically estimated in urine in terms of glucuronic acid content after precipitation of GAGs by cetyl pyridinium chloride. The 24-hour urinary excretion of GAGs was significantly less in stone formers as compared to healthy adults (15.32 +/- 6.94 vs. 22.44 +/- 5.54 mumol/day; p less than 0.001). There was no significant difference in the 24-hour urinary excretion of GAGs between male and female stone formers, or between male and female healthy adults. There was no correlation between age and 24-hour urinary excretion of GAGs in any of the groups. In conclusion, 24-hour urinary excretion of GAGs is significantly less both in male and in female stone formers. The 24-hour urinary excretion of GAGs is not related to age or sex in both healthy adults as well as in stone formers.     

Clinical studies on the recurrence of urolithiasis: (1). Influence of diet on urinary excretion of the stone forming constituents

Twenty-four hour urinary excretion of the stone forming constituents, calcium, oxalate, uric acid, phosphate and magnesium were assayed either under the restricted diet (190 stone formers and 52 non-stone formers) or under the ambulatory free diet (93 stone formers and 14 non-stone formers). Under the ambulatory free diet, urinary excretion of calcium, uric acid and magnesium in the male stone formers, and urinary excretion of calcium and magnesium in the female stone formers was significantly higher than that under the restricted diet. Under the restricted diet, no difference in urinary excretion of calcium, oxalate, uric acid or phosphate was noted between the stone formers and non-stone formers. However, urinary magnesium excretion of the stone formers under the restricted diet was significantly lower than that of the non-stone formers. Under the free diet, no difference in urinary excretion of calcium, oxalate, uric acid, phosphate or magnesium was observed between the stone formers and non-stone formers. Also, there was no significant difference in urinary excretion of calcium, oxalate, uric acid, phosphate or magnesium between the unilateral urolithiasis patients without previous stone history and that of the bilateral or recurrent stone formers. We conclude that urinary excretion of calcium, oxalate, uric acid, phosphate and magnesium have no major role in the stone producing mechanism. However, reduction of urinary excretion of calcium, oxalate, uric acid and phosphate and augmentation of urinary excretion of magnesium are mandatory in preventing stone recurrence until a better understanding of the cause of urolithiasis is obtained.     

Influence of the calcium content of the diet on the incidence of mild hyperoxaluria in idiopathic renal stone formers

Urinary oxalate excretion was measured in 101 male idiopathic calcium (Ca) stone formers studied on 3 dietary conditions (free-choice, Ca-enriched, and low-Ca diet). The population consisted of 38 normocalciuric and 63 hypercalciuric patients. Mean oxalate excretion was similar in normocalciuric and in hypercalciuric patients, on free-choice as well as on Ca-enriched diet. In both conditions the incidence of hyperoxaluria (greater than or equal to 435 mumol/24 h) within each group of stone formers was also similar, ranging from 11 to 22%. On low-Ca diet, however, mean oxalate excretion increased significantly (p less than 0.01) in hypercalciurics but not in normocalciurics; on this diet, the incidence of hyperoxaluria was particularly high in the hypercalciurics (33%), compared with the normocalciurics (13%). On low-Ca diet, oxalate excretion was positively correlated with the estimated degree of intestinal absorption of calcium (p = 0.01). These results show that among idiopathic stone formers, mild hyperoxaluria is not a rare finding and that this disorder can be encountered in each group of patients; its incidence, however, is influenced by the calcium content of the diet. On a low-Ca diet, patients with intestinal Ca hyperabsorption are particularly prone to develop hyperoxaluria, an observation which leads to question the relevance of such a dietary advice unless oxalate intake is simultaneously reduced.     

Etiological role of estrogen status in renal stone formation

PURPOSE: Estrogen may protect against kidney stone formation since nephrolithiasis is more common in men than in women. Moreover, the incidence of stones rises after menopause in women. We examined the contribution of estrogen to kidney stone risk by comparing outpatient evaluations in the 2 genders, and in estrogen treated and untreated postmenopausal women. MATERIALS AND METHODS: We reviewed the results of the initial evaluation of 1,454 adult calcium oxalate stone formers, including 1,050 men and 404 women. Of the postmenopausal women 39 and 50 were estrogen treated and untreated, respectively. Samples of urine and blood were collected 1 week after the imposition of a diet restricted moderately in sodium and calcium, and modestly in oxalate and animal protein. RESULTS: Compared with men the daily excretion of urinary calcium, oxalate and uric acid was lower in women. Women had lower saturations of calcium oxalate and brushite as well as lower excretion of undissociated uric acid. Compared with men urinary calcium was lower in women until age 50 years, when it equaled that of men. Citrate was equal in the genders until the age 60 years, when it tended to decrease in women. Compared with nontreated postmenopausal women those treated with estrogen had lower mean 24-hour calcium plus or minus SD (155 +/- 62 versus 193 +/- 90 mg. per day, p <0.02), mean 2-hour fasting urine calcium (0.08 +/- 0.05 versus 0.12 +/- 0.09 mg./mg. creatinine, p <0.01) and mean calcium oxalate saturation (5.07 +/- 2.27 versus 6.48 +/- 3.44, p <0.05). CONCLUSIONS: The lower risk of stone formation in women may be due to the lower urinary saturation of stone forming salts. Estrogen treatment may decrease the risk of stone recurrence in postmenopausal women by lowering urinary calcium and calcium oxalate saturation.     

Oxalate loading test for outpatients with calcium oxalate stones

A spinach loading experiment was performed on 9 normal subjects, 25 outpatients who were single calcium oxalate stone formers and 25 recurrent calcium oxalate stone formers. The experimental diet contained 445 mg of total oxalate, 163 mg of soluble oxalate and 115 mg of calcium. Urinary oxalate excretion was observed 2 hrs before and 6 hrs after the experimental diet was consumed. There was no significant difference in urinary oxalate excretion in preloading urine of normal subjects and stone formers. However, urinary oxalate excretion in postloading urine was significantly elevated in stone formers. This loading test is recommended as a simple and valuable screening method of hyperabsorption of oxalate on outpatients with calcium oxalate stones.     

The relationship of 3' vitamin D receptor haplotypes to urinary supersaturation of calcium oxalate salts and to age at onset and familial prevalence of nephrolithiasis.

BACKGROUND: Idiopathic hypercalciuria (IHc) and idiopathic hypocitraturia are frequently associated with calcium nephrolithiasis. We investigated the relationship of vitamin D receptor (VDR) polymorphisms (BsmI, TaqI and FokI) to urinary supersaturation of calcium oxalate salts in recurrent calcium oxalate stone formers with IHc and the clinical relevance of this relationship. METHODS: The study included 110 Caucasian stone formers with IHc and 127 unrelated healthy controls without history of nephrolithiasis. Age at onset of nephrolithiasis, familial history score (FHS) and the ion activity product of calcium oxalate salts in urine (AP(CaOx)) were tabulated. BsmI, TaqI and FokI VDR polymorphisms were evaluated in all participants. RESULTS: Patients and controls were classified as homozygous (bbTT and BBtt) or heterozygous in relation to BsmI and TaqI polymorphisms. Compared with BBtt patients, bbTT homozygous stone formers showed lower citrate excretion (1.91+/-0.89 vs 3.46+/-1.39 mmol/24 h, P = 0.004) and higher AP(CaOx) (2.02+/-0.51 vs 1.53+/-0.53, P = 0.006). Among controls, there were similar differences in citrate excretion and AP(CaOx) between the two groups, but they were not statistically significant. Compared with BBtt, bbTT patients showed lower mean age at onset of nephrolithiasis (29.7+/-12.1 vs 38.1+/-12.7 years, P = 0.008) and higher values of FHS (2.45+/-1.9 vs 0.83+/-0.7, P = 0.006). Similar results were obtained for individual BsmI and TaqI alleles. The analysis of FokI alleles was not informative. CONCLUSIONS: Recurrent calcium oxalate stone formers with IHc and the bT VDR haplotype have more aggressive kidney stone diseases as indicated by a higher familial incidence and lower mean age at onset. This clinical severity is associated with the higher urinary supersaturation of calcium oxalate salts and abnormalities of renal citrate handling.     

Effect of dietary control of urinary uric acid excretion in calcium oxalate stone formers and non-stone-forming controls

BACKGROUND AND PURPOSE: Hyperuricosuria is a well-recognized risk factor for calcium oxalate urolithiasis. Some studies have demonstrated elevated urinary uric acid excretion in stone formers compared with non-stone-forming controls; nevertheless, these studies were limited by patient consumption of self-selected diets. With the recognition that dietary differences may induce variations in urinary uric acid excretion, we evaluated excretion of this compound in stone formers and controls consuming a standardized diet. SUBJECTS AND METHODS: A standardized formula diet was administered to 65 calcium oxalate stone formers and 61 age-matched non-stone-forming controls. During the 3 days of dietary intervention, 24-hour urine collections were obtained. Mean urinary uric acid excretion indexed to urinary creatinine was calculated for each subject, and the results in the two groups were compared. RESULTS: Stone-forming subjects did not have an elevation in urinary uric excretion compared with control subjects, with mean indexed urinary uric acid excretions of 337 +/- 64 mg/g of creatinine and 379 +/- 76 mg/g of creatinine, respectively. CONCLUSIONS: With dietary standardization, there was no observed increase in urinary uric acid excretion in our sampled populations. These findings emphasize the role of dietary factors in urinary uric acid excretion and highlight the potential value of dietary interventions.     

Value of routine citrate analysis and calcium/citrate ratio in calcium urolithiasis

24-hour urinary citrate excretion was measured in 176 calcium oxalate stone formers and 100 normal controls. A statistically significant difference (p less than 0.03) could be found between the two groups. When stone formers were divided into a group of 69 patients with recurrent calcium urolithiasis (RCU) and a group of 106 patients with a single stone episode, the latter did not differ from the control group, while in RCU a significantly lower citrate excretion compared with controls (p less than 0.005) could be found. Thus, patients with RCU could benefit from alkali citrate prophylaxis. A female-male difference in citrate excretion could not be found in either the control group or stone formers. Recurrent stone formers presented a significantly higher calcium/citrate ratio compared with controls, which would indicate an increased risk for stone formation. The value of routine citrate analysis is limited, however, by the great, variability of citrate levels in stone formers and controls.     

Dietary oxalate loads and renal oxalate handling

PURPOSE: Dietary oxalate makes a significant contribution to urinary oxalate excretion and, thus, may have a role in calcium oxalate kidney stone formation. Studies have indicated that the ingestion of oxalate rich foods results in transient increases in plasma oxalate concentrations and urinary oxalate excretion. We examined changes in plasma and urinary oxalate following oral crystalline oxalate loading under controlled dietary conditions to further define the renal handling of oxalate by normal adults. MATERIALS AND METHODS: Six normal adult subjects consumed controlled diets of known oxalate content for 1 week before ingesting loads of 0, 2, 4 and 8 mmol of oxalate. Urinary and plasma changes were measured to assess renal oxalate handling. Urinary excretion of proximal tubule derived enzymes and isoprostanes was monitored to assess for renal injury and oxidative stress. RESULTS: Time and dose dependent changes in plasma oxalate, urinary oxalate and in the clearance ratio of oxalate-to-creatinine were observed. A significant correlation (r=0.43, p <0.001) between the oxalate-to-creatinine clearance ratio and plasma oxalate levels was identified. No changes in urinary markers of oxidative stress or renal injury were observed following the 8 mmol oxalate load. CONCLUSIONS: Oxalate is rapidly absorbed and cleared by the kidney by filtration and secretion following an oral oxalate load. Renal oxalate secretion has a significant role in the renal handling of an oral oxalate load. There is no evidence of acute renal injury or oxidative stress with oral oxalate loads in these experimental conditions.