Influence of gender and age on calcium oxalate crystal growth inhibition by urine from relatives of stone forming patients

PURPOSE: We define the relationships between urine inhibition of calcium oxalate crystal growth and age, gender, urine chemistries and stone formation among relatives of calcium stone forming patients. MATERIALS AND METHODS: We collected 24-hour urine samples from 366 first degree relatives of calcium stone formers. Calcium oxalate crystal growth inhibition was studied using a constant amount of dialyzed urine protein in a seeded crystallization system. Standard stone risk measurements were also performed on the urine, including supersaturation for calcium oxalate, calcium phosphate and uric acid. RESULTS: By multivariate analysis crystal growth inhibition is strongly inversely related to the amount of protein excreted per day, and the age of the subject. When corrected for protein excretion and age, urine proteins from nonstone forming male subjects inhibited crystal growth more strongly than those from corresponding female subjects. Among stone formers the sex difference was not present. CONCLUSIONS: Inhibition of calcium oxalate crystal growth is influenced by a complex combination of gender, age, stone formation and assay conditions. The effect of daily protein excretion is most likely a consequence of using a fixed amount of urine protein per assay. The influence of age is significant and unexplained, with the urine of young people (less than 20 years) demonstrating a vigorous ability to inhibit crystallization. In addition, the urine of nonstone forming male relatives appears to have a greater ability to inhibit crystallization than that of nonstone forming female relatives. Further use of this assay in clinical investigations must take age and gender into proper account.     

A porcine model of calcium oxalate kidney stone disease

PURPOSE: The pig has been extensively used in biomedical research because of the similarities in organ structure and function to humans. It is desirable to have an animal model of oxaluria and urolithiasis with physiological, anatomical and nutritional characteristics that more closely resemble those of man. In this study we determined if feeding pigs trans-4-hydroxy-l-proline (HP) increased urine oxalate levels and if it would serve as a model for human hyperoxaluria and stone disease. MATERIALS AND METHODS: Male Yorkshire-Durox cross-bred pigs were fed HP for up to 20 days. Urine was periodically collected and analyzed for oxalate levels and the presence of crystalluria. After 20 days of feeding the kidneys were removed and examined grossly and microscopically for indications of injury, crystal deposition and stone formation. RESULTS: Feeding pigs 10% HP (weight per weight HP/food) produced hyperoxaluria, which reached a maximum and leveled off by day 6. Urine oxalate remained near this level until the study ended at 20 days regardless of the further increase in HP to 20% of the weight of the food. When the kidneys were removed and grossly examined, calcium oxalate encrustations were observed on multiple papillary tips. Histopathological observation of the papillary tissue showed tissue injury and crystal deposition. CONCLUSIONS: Pigs fed HP have hyperoxaluria and calcium oxalate crystalluria, and calcium oxalate papillary deposits form that may be precursors of kidney stones. The use of the pig as a model of human hyperoxaluria and stone formation should prove ideal for studies of these human diseases.     

Effect of high and low calcium diets on stone forming risk during liberal oxalate intake

PURPOSE: Recent studies suggest that a high calcium diet protects against calcium oxalate stone formation. We compared the effect of high and low calcium diets on urinary saturation of calcium oxalate during liberal oxalate intake. MATERIALS AND METHODS: A total of 10 healthy subjects (5 male, 5 female) participated in a 2-phase, randomized, crossover study comparing high (1,000 mg daily) and low (400 mg daily) calcium intake on a liberal oxalate diet (200 mg daily). During each phase subjects adhered to an instructed diet for 3 days followed by a controlled, metabolic diet for 4 days. Blood and 24-hour urine specimens collected on the last 2 days of each phase were analyzed for serum biochemistry studies and stone risk factors, respectively. RESULTS: Urinary calcium was higher (mean +/- SD 171 +/- 64 vs 124 +/- 49 mg daily, p = 0.002) and oxalate was lower (25 +/- 4.8 vs 27 +/- 4 mg daily, p = 0.02) on the high vs low calcium diet. Overall, the urinary relative saturation ratio of calcium oxalate was higher on the high compared with the low calcium diet (3.3 vs 2.5, p <0.0001) even after adjusting for confounding variables. CONCLUSIONS: In normal subjects urinary saturation of calcium oxalate was higher on a high calcium diet than a low calcium diet during liberal oxalate intake because the decrease in urinary oxalate did not overcome the effect of increased calcium. A high calcium diet during liberal oxalate intake may pose an increased risk of calcium oxalate stone formation.     

Conversion of calcium oxalate to calcium phosphate with recurrent stone episodes

PURPOSE: We have extended our previous observation that the percent occurrence of calcium oxalate stones decreased while that of calcium phosphate stones increased with each new stone event. MATERIALS AND METHODS: The National VA Crystal Identification Center has analyzed veteran patient urinary tract stones from VA hospitals throughout the United States since 1983. We reviewed the composition of 33,198 stones with emphasis on the changes in composition. More than 11,786 stones came from 5,088 recurrent stone formers. Stones were analyzed using high resolution x-ray powder diffraction and Fourier transform infrared spectroscopic techniques. When the stones were investigated as a function of time, it was determined that there was greater variability when samples were more than 30 days apart. RESULTS: The percent occurrence of whewellite, weddelite, apatite, brushite and uric acid in stones increased between 1.0% and 5.9% since our previous study. The percent occurrence of struvite decreased by 2.6%. The percent of calcium oxalate stones decreased while that of calcium phosphate stones increased with each new event. However, the total percent occurrence of all calcium containing stones did not significantly change with recurrent stone events. CONCLUSIONS: Our study suggests a strong trend for the conversion of stone disease from calcium oxalate to calcium phosphate containing stones, which could influence the progression and severity of disease.     

Prevention of stone formation and bone loss in absorptive hypercalciuria by combined dietary and pharmacological interventions

PURPOSE: We determined whether dietary restriction of calcium and oxalate, combined with thiazide and potassium citrate treatment, would prevent stone formation and avert bone loss in 18 men and 10 women with type I absorptive hypercalciuria. MATERIALS AND METHODS: Patients were treated with thiazide (20) or indapamide (8) and potassium citrate (average dose 35 mEq. daily) for 1 to 11 years (mean 3.7) while maintained on low calcium oxalate diet. Serum and urinary chemistry studies and bone mineral density were measured at baseline and at the end of treatment. New stones formed were quantitated during 3 years before and during treatment. RESULTS: During treatment urinary calcium significantly decreased (346 +/- 85 to 248 +/- 79 mg. daily, p <0.001) but urinary oxalate did not change. Urinary pH and citrate significantly increased, and urinary saturation of calcium oxalate significantly decreased by 46%. Stone formation rate decreased significantly from 2.94 to 0.05 per year (p <0.001). L2-L4 bone mineral density increased significantly by 5.7% compared to normal peak value, and by 7.1% compared with normal age and gender matched value. Femoral neck bone mineral density also increased significantly. CONCLUSIONS: Dietary restriction of calcium and oxalate, combined with thiazide and potassium citrate, satisfactorily controlled hypercalciuria, prevented the secondary increase in urinary oxalate, reduced urinary saturation of calcium oxalate, virtually eliminated recurrent stone formation, and increased bone density of the spine and femoral neck. Thus, this dietary pharmacological program controlled stone formation as well as bone loss that often accompany type 1 absorptive hypercalciuria.     

高血糖在高草酸尿环境下促进肾草酸钙结石形成的机制研究

目的通过细胞及动物实验,探究高血糖促进草酸钙结石形成的机制。方法八周龄Wistar雄性大鼠(共40只)随机分为4组:阴性对照组、高草酸尿模型组,高血糖模型组,高血糖合并高草酸尿模型组;每组10只。采用q RT-PCR检测在含有不同浓度葡萄糖培养基下HK2细胞中OPN、MCP-1、Cbfa1、BMP-2 m RNA的表达;酶联免疫吸附测定(ELISA)检测OPN与MCP-1在培养基中的浓度;钙盐染色检测各组大鼠肾组织中草酸钙结石晶体;细胞凋亡试验检测各组大鼠肾组织中肾小管上皮细胞凋亡。免疫组织化学染色法(IHC)检测OPN在各组大鼠肾组织中的表达;ELISA检测MCP-1在各组大鼠24小时尿液中的含量。结果高浓度葡萄糖环境中,HK-2细胞的OPN与MCP-1表达上调。高血糖合并高草酸尿模型组肾组织中有大量草酸钙沉积,大量肾小管上皮细胞凋亡,OPN表达显著增加,其尿液中MCP-1总量明显增加,与其他组相比有统计学差异(P0.05)。结论高血糖能促使肾小管上皮细胞炎症趋化因子OPN、MCP-1表达增加。在高草酸尿环境中,高血糖能促进肾小管上皮细胞凋亡及草酸钙结石形成。高血糖可能是通过炎症趋化因子加重局部炎症反应,促进肾小管上皮细胞凋亡及草酸钙结石形成。     

Jejunoileal bypass reversal: effect on renal function, metabolic parameters and stone formation

PURPOSE: While the effect of jejunoileal bypass (JIB) reversal has been well studied regarding hepatic function, there is little information regarding the effect of reversal on renal function and even less data regarding the metabolic urinary stone environment. We evaluated the results of JIB reversal on renal function, the urinary stone milieu and the clinical development of recurrent calculi in affected patients. MATERIALS AND METHODS: From 1995 to 2003, 4 female patients with a mean age of 48.2 years underwent JIB reversal primarily for refractory stone disease. The clinical and metabolic courses prior to and following bypass reversal were reviewed specifically to evaluate renal function, serum and urinary metabolic stone profiles, and clinical stone formation. RESULTS: At initial presentation following JIB all 4 patients had significantly increased 24-hour urinary oxalate (range 80 to 160 mg, mean 112.5, normal less than 50) and significantly low 24-hour urinary citrate (range 5 to 62 mg, mean 21.5, normal greater than 320). Following reversal 24-hour urinary oxalate normalized to between 31 and 36 mg (mean 33.75). However, 24-hour urinary citrate continued to be low (range 215 to 248 mg, mean 226.5). After JIB reversal all 4 patients continued to have new stones until the commencement of urinary alkalization, following which only 1 had 1 calculus, which occurred 47 months after reversal. After JIB mean serum creatinine was 1.48 mg/dl (range 0.8 to 1.9) and mean urinary creatinine excretion was 0.91 mg per hour (range 0.69 to 1.15). After JIB reversal mean serum creatinine was 1.28 mg/dl (range 0.6 to 2.0) and mean urinary creatinine excretion was 1.0 mg per hour (range 0.85 to 1.10). CONCLUSIONS: JIB reversal normalizes 24-hour urinary oxalate. While urinary citrate improves, it continues to be low and such patients are at high risk for recurrent stone formation. However, in this setting appropriate replacement therapy has a significant and positive impact on that propensity.     

The urinary response to an oral oxalate load in recurrent calcium stone formers

PURPOSE: Dietary oxalate may contribute up to 50% to 80% of the oxalate excreted in urine. We studied the urinary response to an oral oxalate load in male and female idiopathic recurrent calcium oxalate stone formers with and without mild hyperoxaluria to evaluate the potential pathophysiological significance of dietary oxalate. MATERIALS AND METHODS: A total of 60 recurrent calcium stone formers underwent an oral oxalate load test. Urine samples were obtained after an overnight fast. Each patient then received an oral oxalate load (5 mM. sodium oxalate dissolved in 250 ml. distilled water) and 3, 2-hour urine samples were obtained 2, 4 and 6 hours after the oxalate load. We compared the response to the oxalate load in patients with and without mild hyperoxaluria, and in male and female patients without hyperoxaluria. RESULTS: The peak urinary response occurred 4 hours after the oral oxalate load in all patients. Those with mild hyperoxaluria had a mean fasting urinary oxalate-to-creatinine ratio +/- SE of 0.027 +/- 0.003 and a mean peak urinary oxalate-to-creatinine ratio of 0.071 +/- 0.006. In comparison, patients with normal oxalate excretion had a fasting and peak urinary oxalate-to-creatinine ratio of 0.018 +/- 0.001 and 0.056 +/- 0.004, respectively (p <0.05). The mean 6-hour increment for urinary oxalate excretion after the oxalate load for patients with hyperoxaluria versus those with normal urinary oxalate excretion was 17.2 +/- 1.9 versus 12.1 +/- 0.98 mg. (p <0.05). In the subset of patients with normal urinary oxalate excretion mean 6-hour cumulative urinary oxalate excretion was 16.8 +/- 1.3 and 13.3 +/- 1.4 mg. in males and females, respectively (p not significant). CONCLUSIONS: Recurrent calcium stone formers with mild hyperoxaluria have higher fasting urinary oxalate and an exaggerated urinary response to an oral oxalate load compared with recurrent calcium stone formers with normal urinary oxalate excretion. Men and women stone formers without hyperoxaluria excrete similar fractions of an oral oxalate load. Increased gastrointestinal absorption and renal excretion of dietary oxalate may be a significant pathophysiological mechanism of stone formation in patients with mild hyperoxaluria.     

Decreased renal expression of the putative calcium oxalate inhibitor Tamm-Horsfall protein in the ethylene glycol rat model of calcium oxalate urolithiasis

PURPOSE: Tamm-Horsfall protein is believed to inhibit calcium oxalate crystallization, aggregation or adhesion to the renal epithelium. We determined whether ethylene glycol induced urolithiasis changes the expression of renal and urinary Tamm-Horsfall protein. For comparison the expression of another calcium oxalate inhibitor, osteopontin, was also analyzed. MATERIALS AND METHODS: Male rats were treated with 0.75% ethylene glycol plus an AIN-76 diet (Dyets, Bethlehem Pennsylvania) (ethylene glycol group) or standard rat chow and water (control group) for up to 8 weeks (6 per group for 8 weeks and 3 per group for 3 days to 6 weeks). Kidneys and urine (8 weeks only) were harvested and analyzed by Northern and Western blot analysis, and immunohistochemistry. RESULTS: Tamm-Horsfall protein message and protein (membrane bound form) were decreased, while those of osteopontin were increased in the kidneys of rats treated with ethylene glycol for 8 weeks. As judged by immunochemistry Tamm-Horsfall protein and osteopontin were consistently present in a few tubules in rats in the ethylene glycol and control groups, respectively. In urine expression of the free form of Tamm-Horsfall protein (approximately 75 kDa.) was decreased but detectable in ethylene glycol treated rats. Although readily detected in tissue, osteopontin was not detected in the urine of control or ethylene glycol treated rats. In the time course experiment Tamm-Horsfall protein did not decrease until 4 weeks, when calcium oxalate crystals were detectable in the kidneys of treated rats. In contrast, osteopontin was increased, although inconsistently, beginning at 3 days. CONCLUSIONS: Unlike other calcium oxalate inhibitors, such as osteopontin, renal message and protein for Tamm-Horsfall protein was decreased in ethylene glycol treated rats. Tamm-Horsfall protein expression did not decrease until aggregates of crystals had been deposited in the kidneys, while osteopontin expression began to increase almost immediately. Comparisons of the data on kidneys and urine obtained by RNA or protein blot analysis and immunochemistry underscore the need to examine tissue and urine by multiple techniques to obtain the most accurate assessment of how protein expression is changed by a given treatment.     

苄丙酮香豆素对实验性大鼠肾草酸钙结石形成的影响

目的：探讨Vit．K拮抗剂苄丙酮香豆素(商品名华法令)对大鼠肾草酸钙结石形成的影响。方法：采用乙二醇饮水和氯化铵灌胃作成石剂，30只Wistar大鼠随机分为对照组(A组)、成石组(B组)、华法令组(C组)。饲养4周后，检测大鼠肾组织钙含量和草酸钙晶体形成、24h尿钙、尿草酸含量及血生化指标。结果：成石组和华法令组肾组织中钙、镁含量，24h尿草酸及尿钙、镁排泄量差异无显著性意义；镜下观察发现：华法令组大鼠肾脏草酸钙结晶形成多于成石组，但组间比较差异无显著性意义。结论：苄丙酮香豆素对大鼠肾草酸钙结石的形成无显著影响。     

Influence of cranberry juice on the urinary risk factors for calcium oxalate kidney stone formation

Cranberry juice is popular remedy for many ills; apart from the pleasant tasting many people drink it to help in preventing UTIs and stones. Authors from Cape Town (where there is the added benefit of an excellent climate) assessed the influence of cranberry juice on urinary risk factors for calcium oxalate calculi in a randomized crossover trial, showing that it has anti‐lithogenic properties. In the second paper, authors from Jerusalem report on 14 patients with distal ureteric strictures after kidney transplantation, all of whom were treated endourologically. They found transurethral incision of the distal ureteric stricture to be effective.

OBJECTIVE

To investigate the potential influence of cranberry juice on urinary biochemical and physicochemical risk factors associated with the formation of calcium oxalate kidney stones, as this product might affect the chemical composition of urine.

SUBJECTS AND METHODS

Urinary variables were assessed in a randomized cross‐over trial in 20 South African men (students) with no previous history of kidney stones. The first group of 10 subjects drank 500 mL of cranberry juice diluted with 1500 mL tap water for 2 weeks, while the second group drank 2000 mL of tap water for the same period. This was followed by a 2‐week ‘washout’ period before the two groups crossed over. During the experimental phase subjects kept a 3‐day food diary to assess their dietary and fluid intakes; 24‐h urine samples were collected at baseline and on day 14 of the trial periods, and analysed using modern laboratory techniques. Urine analysis data were used to calculate the relative urinary supersaturations of calcium oxalate, uric acid and calcium phosphate. Data were assessed statistically by analysis of variance.

RESULTS

The ingestion of cranberry juice significantly and uniquely altered three key urinary risk factors. Oxalate and phosphate excretion decreased while citrate excretion increased. In addition, there was a decrease in the relative supersaturation of calcium oxalate, which tended to be significantly lower than that induced by water alone.

CONCLUSION

Cranberry juice has antilithogenic properties and, as such, deserves consideration as a conservative therapeutic protocol in managing calcium oxalate urolithiasis.

     

Estrogen replacement increased the citrate and calcium excretion rates in postmenopausal women with recurrent urolithiasis.

PURPOSE: Epidemiological data indicate a sharp increase in urinary calcium stone formation after menopause. We investigated the role of menopausal estrogen replacement therapy on the urinary constituents and characteristics that may influence recurrent calcium oxalate stone disease. MATERIALS AND METHODS: Urinary constituents in 28 postmenopausal women on estrogen replacement therapy for more than 6 months were compared with those in 41 women who had never been exposed to estrogen after menopause. These 2 groups had a history of recurrent calcium oxalate urolithiasis. A group of age matched, nonstone forming volunteers who were and were not on estrogen served as controls. RESULTS: The 24-hour urine collection revealed significantly higher mean calcium plus or minus standard deviation (188.8 +/- 101.5 versus 129.2 +/- 80.9 mg./24 hours, p <0.01), citrate (576.6 +/- 237.9 versus 306.2 +/- 209.9 mg./24 hours, p <0.001) and agglomeration inhibition (203 +/- 106 versus 159 +/- 81 minutes, p <0.05) in stone forming women who were versus were not on estrogen. CONCLUSIONS: Higher urinary citrate and higher agglomeration inhibition in women exposed to estrogen may decrease the risk of subsequent calcium stone formation.     

Effects of 5 different diets on urinary risk factors for calcium oxalate kidney stone formation: evidence of different renal handling mechanisms in different race groups

PURPOSE: Since the incidence of renal calculi in the South African black population is extremely rare while in white subjects it occurs at the same rate as elsewhere in the western world, we investigated the possibility that different renal handling mechanisms in response to different dietary challenges might occur in the 2 race groups. MATERIALS AND METHODS: We administered 5 different dietary protocols, including low calcium, high oxalate, vitamin C, high salt and lacto-vegetarian, to 10 healthy male subjects from each race group. We collected 24-hour urine at baseline and after 4 days on the prescribed diet which were analyzed for biochemical and physicochemical risk factors. Dietary intake was controlled throughout the experimental period. A 24-hour dietary recall questionnaire was recorded at baseline and analyzed using food composition tables. Statistical analysis of variance was performed on all the data. RESULTS: The low calcium diet caused statistically significant changes only in black subjects, which consisted of urinary oxalate increase (0.17 to 0.23 mmol./24 hours, p = 0.01), relative supersaturation of calcium oxalate decrease (1.88 to 0.97, p = 0.03) and relative supersaturation of brushite increase (0.85 to 1.69, p = 0.03). The high oxalate diet caused statistically significant changes in both race groups but these changes were different in the 2 groups. In white subjects urinary pH increased (6.24 to 6.62, p = 0.01), potassium excretion increased (40.01 to 73.49, p = 0.01) and relative supersaturation of brushite increased (1.34 to 2.12, p = 0.05). In black subjects urinary citrate increased (1.94 to 2.99 mmol./24 hours, p = 0.01). Clinically unimportant changes occurred in both race groups after the other 3 diets. CONCLUSIONS: Renal handling of dietary calcium and oxalate in South African black and white subjects is different and may explain the different stone incidence in the 2 race groups.     

The role of Randall's plaques in the pathogenesis of calcium stones

PURPOSE: Knowledge of the inciting lesion in kidney stone formation has remained rudimentary until quite recently. Randall theorized that areas of apatite plaque on the renal papillae would be an ideal site for an overgrowth of calcium oxalate to develop into a calculus. We reviewed in vivo data that have further defined the role of Randall's plaques in stone disease. MATERIALS AND METHODS: We examined a set of literature that tested 2 hypotheses, that is 1) Randall's plaques are a specialized disease that begins as apatite in a unique region of the kidney due to local driving forces and anatomy, and 2) stones that arise from causes different from common calcium oxalate stones do not necessarily arise on plaque. RESULTS: Intraoperative papillary and cortical biopsy specimens obtained during percutaneous nephrolithotomy from the kidneys of 3 types of stone formers (idiopathic calcium stone formers, patients with stones due to bariatric procedures and brushite stone formers) showed unique histopathological findings. CONCLUSIONS: The metabolic and surgical pathological findings in 3 distinct groups of stone formers demonstrate that the histology of the renal papillae from a stone former is particular to the clinical setting.     

碘海醇对实验性大鼠草酸钙结石形成的影响

目的探讨造影剂碘海醇对大鼠草酸钙结石形成的影响。方法将40只Wister大鼠随机分为成4组：空白对照组（A）、单纯诱石组（B）、单纯碘海醇组（C）、诱石＋碘海醇组（D）。用乙二醇法诱导建立大鼠草酸钙结石模型,C、D组尾静脉注射碘海醇。实验第4周末检测肾组织中丙二醛（MDA）含量及超氧化物歧化酶（SOD）活力,镜下观察肾内草酸钙晶体沉积情况。结果A、B、C、D4组肾脏组织MDA含量（nmol／mg蛋白）分别为2．74±0．48、4．51±1．47、6．92±2．18、8．87±2．31,SOD活力（U／mg蛋白）分别195．21±11．01、170．24±13．59、140．86±25．91、121．54±25．50,各组间差异有统计学意义（P〈0．05）。B、D组结晶等级评分高于A组,D组结晶等级评分高于B组（P〈1．05）。培论碘海醇促进了大鼠肾小管内草酸结晶量的增加,其机制与碘海醇诱导的肾小管上皮氧化应激损伤有关。     

Acute caffeine effects on urine composition and calcium kidney stone risk in calcium stone formers

PURPOSE: Caffeine increases urinary calcium (ca) excretion in nonstone formers. We designed a study to determine the effect of caffeine consumption on urinary composition in stone formers. MATERIALS AND METHODS: A total of 39 normocalcemic patients with calcium stones consumed caffeine (6 mg/kg lean body mass) after 14 hours of fasting. Urinary composition was compared 2 hours before and 2 hours after caffeine consumption. Control subjects included 9 nonstone formers studied contemporaneously with patients plus data from 39 nonstone formers from previous studies matched to each patient by level of fasting calcium/creatinine (Cr), gender and age. RESULTS: Caffeine increased urinary Ca/Cr, magnesium/Cr, citrate/Cr and sodium/Cr but not oxalate/Cr in stone formers and controls. The Tiselius stone risk index for calcium oxalate precipitation increased from 2.4 to 3.1 in stone formers and from 1.7 to 2.5 in nonstone formers. Of the 39 stone formers 32 had an increased Tiselius risk index after caffeine. Post-caffeine increases in Ca/Cr and Na/Cr were highly correlated. CONCLUSIONS: Caffeine consumption may modestly increase risk of calcium oxalate stone formation.     

Physicochemical metabolic characteristics for calcium oxalate stone formation in patients with gouty diathesis

PURPOSE: We determined why calcium oxalate stones instead of uric acid stones form in some patients with gouty diathesis. MATERIALS AND METHODS: Gouty diathesis was diagnosed from absence of secondary causes of uric acid stones or low urinary pH, and reduced fractional excretion of urate with discriminant score of the relationship between urinary pH and fractional excretion of urate less than 80. From the stone registry 163 patients with gouty diathesis were identified, including 62 with uric acid stones (GD + UA) and 101 patients with calcium oxalate stones (GD + Ca). Metabolic data and 24-hour urinary chemistry study were compared between the 2 groups. RESULTS: Compared with GD + UA, GD + Ca had significantly greater urinary calcium (196 +/- 96 mg per day vs 162 +/- 82 mg per day, p <0.05) and significantly lower urinary citrate (430 +/- 228 vs 519 +/- 288 mg per day, p <0.05), resulting in higher urinary saturation of calcium oxalate. Both groups had low urinary pH (less than 5.5) and high urinary undissociated uric acid (greater than 100 mg/dl). Urinary calcium post-oral calcium load was significantly higher in GD + Ca than in GD + UA (0.227 vs 0.168 mg/dl glomerular filtrate, p <0.001). CONCLUSIONS: Calcium oxalate stones may form in some patients with gouty diathesis due to increased urinary excretion of calcium and reduced excretion of citrate. Relative hypercalciuria in GD + Ca may be due to intestinal hyperabsorption of calcium.