Low-oxalate Diet Research Articles

Vitamin C-induced hyperoxaluria causing reversible tubulointerstitial nephritis and chronic renal failure: a case report

Vitamin C is a precursor of oxalate and promoter of its absorption, potentially causing hyperoxaluria. Malabsorption causes Calcium (Ca) chelation with fatty acids, producing enteric hyperoxaluria.CaseA 73-year-old man with both risk factors was hospitalized with serum creatinine of 8.4 mg/dL (versus 1.2 mg/dL four months earlier) (normal 0.6–1.3 mg/dL). Given his oxalate-rich diet, chronic diarrhea, and daily 680 mg vitamin C and furosemide, we postulated Ca oxalate-induced nephropathy, a diagnosis confirmed by documenting hyperoxaluria, and finding of diffuse intraluminal crystals and extensive interstitial fibrosis on biopsy. He was hemodialysed 6 times to remove excess oxalate. Two weeks off vitamin C, his creatinine spontaneously fell to 3.1 mg/dL. Three months later, on low oxalate diet and 100 mg vitamin B6, urine oxalate to creatinine ratio decreased from 0.084 to 0.02 (normal < 0.035), while creatinine fell and stayed at 1.8 mg/dL.Conclusion1) High-dose vitamin C can induce hyperoxaluric nephropathy and progressive renal failure, especially if aggravated by diarrhea, oxalate-rich diet, metabolic acidosis, and dehydration. 2) The diagnosis should be suspected in unexplained renal insufficiency when associated with these risk factors. 3) Since prompt treatment could avert end-stage renal disease, we recommend monitoring urinary oxalate in patients on high-dose vitamin C and renal biopsy if necessary.

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

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. 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. 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. 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.

Influence of a high-oxalate diet on intestinal oxalate absorption

Hyperoxaluria is a major risk factor for renal stones. In most cases, it is sustained by increased dietary loads. In healthy individuals with a normal Western diet, the majority of urinary oxalate is usually derived from endogenous metabolism. However, up to 50% may be derived from the diet. We were interested in the effect of a high-oxalate diet on oxalate absorption, not merely on the frequently studied increased oxalate excretion. In study I, 25 healthy volunteers were tested with the [13C2]oxalate absorption test once while following a low-oxalate (63 mg) and once while following a high-oxalate (600 mg) diet for 2 days each. In study II, four volunteers repeated study I, and afterwards continued with a high-oxalate diet (600 mg oxalate/day) for 6 weeks. In the last week, the [13C2]oxalate absorption test was repeated. After 4 weeks of individual normal diet, the oxalate absorption test with a high-oxalate diet was performed again. The results of study I show that the mean [13C2]oxalate absorption under low-oxalate diet was 7.9 +/- 4.0%. In the presence of oxalate-rich food, the percent absorption for the soluble labelled oxalate almost doubled (13.7 +/- 6.3%). The results of study II show that the mean [13C2]oxalate absorption of the four volunteers under low-oxalate diet was 7.3 +/- 1.4%. The absorption increased to 14.7+/-5.2% under 600 mg oxalate. After 6 weeks under a high-oxalate diet, the [13C2]oxalate absorption was significantly decreased (8.2 +/- 1.7%). After the wash-out phase, the absorption was again high (14.1 +/- 2.2%) under the 600 mg oxalate challenge.

Diätetische und medikamentöse Therapie des Kurzdarmsyndroms

Diarrhoea, malabsorption and malnutrition characterise the short bowel syndrome. The underlying gastrointestinal disorders, the types of intestinal resections performed and the subsequent pathophysiological situations are reviewed. Recommended therapeutic measures in the postoperative period as well as in the rehabilitation of patients with short bowel syndrome are discussed in more detail. In the postoperative period, parenteral nutrition is essential followed by an enteral diet to stimulate bowel adaptation, reduce fluid loss and increase nutrient absorption. The final diet should be based on the anatomy of the retained bowel (presence or absence of a colon and ileum). The importance of the colon as a digestive organ in patients with short bowel and the need of a low-oxalate diet are underlined. The possible benefit of new treatment options (glutamine, growth hormone and glucagon-like peptide 2) is discussed. Both typical complications of the short bowel syndrome and management of these complications are presented.

Hepatobiliary, renal and bone complications of intestinal failure

Abnormal liver function tests in patients with intestinal failure (IF) may be due to the underlying disease, IF or the treatments given (including parenteral nutrition (PN)). PN-related liver disease in children usually relates to intrahepatic cholestasis and in adults to steatosis. Steatosis may be consequent upon an excess of carbohydrate, lipid or protein, or upon a deficiency of a specific molecule. Pigment-type gallstones are common in adults and children with IF; these develop from biliary sludge that forms during periods of gallbladder stasis. Ileal disease/resection, parenteral nutrition, surgery, rapid weight loss and drugs all increase the risk of developing gallstones. Gallstone formation may be prevented by reducing gallbladder stasis (oral/enteral feeding or prokinetic agents), altering bile composition, or by means of a prophylactic cholecystectomy. Calcium oxalate renal stones are common in patients with a short bowel and retained functioning colon and are consequent upon increased absorption of dietary oxalate; they are prevented by a low-oxalate diet. An osteopathy may occur with long-term parenteral nutrition.

The relative effects of supplemental dietary calcium and oxalate on urine composition and calcium oxalate relative supersaturation in healthy adult dogs

The aim of this study was to establish the relative effects of dietary calcium and oxalate (in the form of oxalic acid) on the composition of urine produced by healthy adult Cairn Terriers and Miniature Schnauzers. A nutritionally complete dry dog food was fed to 7 dogs (4 Cairn terriers and 3 Miniature schnauzers) for 24 weeks. The dogs were fed the diet alone, or supplemented with six different combinations of dietary calcium (as carbonate and sulphate) and oxalate (as oxalic acid) commonly found in dry commercially prepared dog foods. Urine pH, volume, specific gravity, and concentrations of 12 analytes were measured for each dog; urinary relative supersaturation (RSS) with calcium oxalate (CaOx) was calculated from these values. The effects of supplemental calcium and oxalate were established using two-way analysis of variance and multiple range tests (least significant difference); P<0.05 was considered significant. The lowest level of dietary calcium and oxalate resulted in the lowest CaOx RSS. The high calcium, low oxalate diet resulted in the highest CaOx RSS, a low calcium diet with increased dietary oxalate also tended to increase CaOx RSS although results were highly variable. Urinary calcium concentration increased significantly with dietary calcium; urinary oxalate increased, although inconsistently, with dietary oxalic acid only when dietary calcium was low. Measures to reduce both calcium and oxalate should be considered when implementing dietary changes to reduce the risk of calcium oxalate formation in dogs. A reduction in dietary calcium without a concomitant decrease in dietary oxalate may increase the risk of CaOx crystallisation in susceptible dogs.

Pure versus Complicated Vulvar Vestibulitis: A Randomized Trial of Fluconazole Treatment

Objective: To examine the effectiveness of a 6-month treatment consisting of a weekly oral dose of 150 mg fluconazole for women with vestibulitis, and to explore the causes of treatment failure. Methods: Forty women with vestibulitis were randomized to either of two treatment groups. One group received a 6-month low oxalate diet with calcium citrate complement, as a placebo, and the second group the same diet and calcium citrate with the addition of a weekly oral tablet of 150 mg fluconazole. The women were examined 3 months after completing treatment, for response to therapy. Results: The addition of intensive 6-month fluconazole treatment did not lead to an outcome better than that attained by maintaining a low oxalate diet with calcium citrate supplementation. The satisfactory response rate was 15 and 30%, respectively. The presence of ‘complicated vestibulitis’, candidiasis concomitant with vestibulitis, decreases the satisfactory response rate regardless of the type of treatment administered (odds ratio 19.9, 95% CI 1.6, 250). Conclusion: Prolonged oral fluconazole is an ineffective treatment of vestibulitis, whether pure or complicated by concomitant vulvovaginal candidiasis. The coexistence of candidiasis and vestibulitis – complicated vestibulitis – might represent a subset of vestibulitis that is resistant to the currently available medical therapy.

EFFECTS OF CALCIUM AND MAGNESIUM ON URINARY OXALATE EXCRETION AFTER OXALATE LOADS

Urinary oxalate is a primary determinant of the level of calcium oxalate saturation and the formation of calcium oxalate crystals, a key event in kidney stone formation. The primary objective of this study was to compare the effects of calcium carbonate and magnesium oxide on oxalate absorption. An experimental model was used that allowed differentiation between endogenously and oxalate load-derived urinary oxalate. Twenty-four healthy subjects (10 males, 14 females) participated in three oxalate load (OL) tests: control (OL alone), calcium carbonate (OL with concomitant calcium carbonate ingestion), and magnesium oxide (OL with concomitant magnesium oxide ingestion). Oxalate loads consisted of 180 mg. unlabeled and 18 mg. 1,2[13C2] oxalic acid. Timed urine samples were collected after the OL for analysis of oxalate, calcium, magnesium, and creatinine. Both the calcium carbonate and magnesium oxide treatments were associated with significantly lower load-derived oxalate levels at all time points within the initial 24-hour post-oxalate ingestion period compared with levels observed for the control treatment. There were no treatment effects on endogenous oxalate levels. The efficiency of oxalate absorption for the calcium carbonate (5.1%) and magnesium oxide (7.6%) treatments was significantly lower than that for the control treatment (13.5%). The results suggested that magnesium was nearly as effective as calcium in reducing oxalate absorption and urinary excretion. Higher levels of urinary oxalate, calcium, and magnesium in males appeared to be largely a function of body size since gender differences either disappeared or were reversed when a correction was made for urinary creatinine excretion.

Persistent Vulvar Vestibulitis: The Continuing Challenge

A continuing challenge in the management of women with vulvar vestibulitis is the patient who has not responded to surgical treatment. The main reason for persistent dyspareunia is failure to excise the sensitive periurethral tissue in the primary operation. In other cases, the Bartholin’s glands may be the source of the pain. A low oxalate diet, the administration of interferon, and biofeedback training of the lower pelvic muscles—treatments that are used as a first-choice approach for vulvar vestibulitis, may all work in the postoperative patient. The management of a patient with residual vestibulitis should be conservative, and only when medical measures fail, do we consider additional surgical methods such as Bartholin’s gland resection or repeat perineoplasty.

A pilot study of the use of a low oxalate diet in the treatment of vulval vestibulitis

Thirty-one women with vulval vestibulitis were evaluated for evidence of abnormal dietary oxalate intake and a wide range of dietary intakes was recorded. No woman was found to have abnormal urinary excretion. Sixteen women agreed to undertake a low oxalate diet and there was an apparent response in six (37%).

Urinary Oxalate Excretion and its Role in Vulvar Pain Syndrome

Abstract Objective: This study was undertaken to determine the urinary oxalate excretion patterns in patients with vulvodynia compared with controls and to evaluate antioxalate therapy in women with vulvar pain syndrome (vulvodynia). Study design: A total of 130 consecutive patients with vulvar pain syndrome and 23 volunteers without symptoms collected urine specimens for 24 hours; each voiding was saved in individual labeled containers and refrigerated. The specimens were analyzed individually for oxalate and calculated according to 24-hour concentration, volume, and peak oxalate by hour. A total of 59 patients were treated with low-oxalate diets and calcium citrate for 3 months and evaluated for objective relief of vulvar pain. Results: The 24-hour excretion of oxalate was almost identical in controls and vulvodynia patients. The total 24-hour excretion was directly proportional to the volume of urine excreted ( p p 1 mg/40 dl) were treated with an antioxalate regimen. Fourteen (24%) demonstrated an objective response, but only 6 (10%) could have pain-free sexual intercourse. Conclusions: Urinary oxalates may be nonspecific irritants that aggravate vulvodynia; however, the role of oxalates as instigators is doubtful.

Persistent vulvar vestibulitis: the continuing challenge.

A continuing challenge in the management of women with vulvar vestibulitis is the patient who has not responded to surgical treatment. The main reason for persistent dyspareunia is failure to excise the sensitive periurethral tissue in the primary operation. In other cases, the Bartholin's glands may be the source of the pain. A low oxalate diet, the administration of interferon, and biofeedback training of the lower pelvic muscles-treatments that are used as a first-choice approach for vulvar vestibulitis, may all work in the postoperative patient. The management of a patient with residual vestibulitis should be conservative, and only when medical measures fail, do we consider additional surgical methods such as Bartholin's gland resection or repeat perineoplasty.

Urinary oxalate excretion and its role in vulvar pain syndrome

Objective: This study was undertaken to determine the urinary oxalate excretion patterns in patients with vulvodynia compared with controls and to evaluate antioxalate therapy in women with vulvar pain syndrome (vulvodynia). Study design: A total of 130 consecutive patients with vulvar pain syndrome and 23 volunteers without symptoms collected urine specimens for 24 hours; each voiding was saved in individual labeled containers and refrigerated. The specimens were analyzed individually for oxalate and calculated according to 24-hour concentration, volume, and peak oxalate by hour. A total of 59 patients were treated with low-oxalate diets and calcium citrate for 3 months and evaluated for objective relief of vulvar pain. Results: The 24-hour excretion of oxalate was almost identical in controls and vulvodynia patients. The total 24-hour excretion was directly proportional to the volume of urine excreted ( p < 0.001). No significant differences were found in peak oxalate excretion (95% confidence intervals). The number of voidings was higher in the vulvodynia cohort ( p < 0.02). The 59 women with elevated oxalate concentrations (>1 mg/40 dl) were treated with an antioxalate regimen. Fourteen (24%) demonstrated an objective response, but only 6 (10%) could have pain-free sexual intercourse. Conclusions: Urinary oxalates may be nonspecific irritants that aggravate vulvodynia; however, the role of oxalates as instigators is doubtful.

Nutritional Management of an Infant with Primary Oxalosis:: from Dialysis to Kidney/Liver Transplantation

LEARNING OUTCOME: To describe nutritional needs of an infant with primary oxalosis (PHO) while on dialysis and after kidney/liver transplantation.Primary hyperoxaluria type 1 (PHO) is a rare autosomal recessive inborn error of glyoxylate metabolism in which excessive oxalate synthesis and lack of excretion cause nephrocalcinosis, renal failure and systemic oxalate deposition. Infants with PHO have a significant morbidity and mortality, and therefore nutritional management is important to help diminish this oxalate burden. Described is an infant with PHO. A five month old infent was admitted with problems of failure to thrive, and increased emesis. Lab data revealed a BUN of 150 mg/dl, creatinine of 9.0 mg/dl, phosphorus of 8.5 mg/dl. A 24-hour urine collection and renal ultrasound confirmed the diagnosis of PHO. Aggressive management included a thallium fundoplication, gastric feeding tube, hemodialysis 6 days/week, and daily peritoneal dialysis. Calorie and protein needs were met 100% by formulas with sodium chloride added, providing 100-115 calories/kg/day and 3.5–3.8 grams of protein/kg/day. Oral baby food intake was minimal. Since vitamin C intake is contraindicated as it increases oxalate formation, a non-vitamin C containing super potency B-complex vitamin was used along with an iron supplement. At one year of age, the infant underwent a combined kidney-liver transplant. Weight was at the 75th percentile, height at the 50-75th percentile and head circumference at the 50th percentile. Gastrostomy feedings were started post-transplant at a high volume rate to provide 100% of calories, protein and phosphorus. A high fluid intake is crucial to minimize oxalate deposition in the transplanted kidney. Parents were instructed to provide a low oxalate diet as solid food was introduced, and a regular multivitamin/day. The infant was discharged 2 months post-transplant with motor skills appropriate for age and maintaining growth parameters. It will take years to mobilize the total body stores of oxalate; therefore, fluid and nutritional management will continue to play a significant role in this infant's care.

Vulvar vestibulitis?A complex clinical entity

Objective This study aims to determine the pathophysiology of vulvar vestibulitis and to evaluate currently used treatment options. Methods Two hundred twenty women with vulvar vestibulitis were seen between October 1987 and March 1995. Every patient had vulvar pain when they attempted intercourse, 75% had excessive vaginal discharge, 36.4% had constant or recurring vulvar burning, and 10.9% had symptoms suggestive of cystitis. All were cultured for the presence of Candida albicans. One hundred sixty-one (73.2%) were also tested for vaginal IgE and prostaglandin E2 (PGE2); 72 (32.7%) had a vulvar biopsy performed as well. Results A wide range of variants were noted: 53 (24.1%) had a human papilloma virus (HPV) infection, 25 (11.4%) had a Candida vulvovaginitis, 43 (19.5%) had a vaginal allergy, 15 (6.8%) had vaginal PGE2 present, 14 (6.4%) had elevated urinary oxalate excretion, and 29 (13.2%) had a variety of diagnosed variants. In 81 (36.8%) no underlying diagnosis was made. This understates the numbers and varieties of vulvar vaginal diagnoses, for not all patients received a vaginal fluid analysis, a vulvar biopsy, or a 24 h urine screen for oxalates. A variety of medical and operative interventions was used. Symptoms were relieved in 65.9% of patients. The degree of success varied. Successful outcomes were achieved in 14.3% of patients using a low oxalate diet and calcium citrate supplementation, 16% with anti-Candida treatment, 48.1% with antihistamines, 77% with vulvar injection of interferon, 83% with operative removal of inflamed vulvar tissue, and a posterior colporrhaphy used to cover the cutaneous defect. Conclusions The diagnosis of vulvar vestibulitis is easy to make. An etiology for this chronic condition will not be achieved in every patient. A majority of patients can get relief by a variety of medical and operative interventions. Infect. Dis. Obstet. Gynecol. 4:269–275, 1996. © 1997 Wiley-Liss, Inc.

Vulvar Vestibulitis—A Complex Clinical Entity

Objective: This study aims to determine the pathophysiology of vulvar vestibulitis and to evaluate currently used treatment options. Methods: Two hundred twenty women with vulvar vestibulitis were seen between October 1987 and March 1995. Every patient had vulvar pain when they attempted intercourse, 75% had excessive vaginal discharge, 36.4% had constant or recurring vulvar burning, and 10.9% had symptoms suggestive of cystitis. All were cultured for the presence of Candida albicans. One hundred sixty-one (73.2%) were also tested for vaginal IgE and prostaglandin E2 (PGE2); 72 (32.7%) had a vulvar biopsy performed as well. Results: A wide range of variants were noted: 53 (24.1%) had a human papilloma virus (HPV) infection, 25 (11.4%) had a Candida vulvovaginitis, 43 (19.5%) had a vaginal allergy, 15 (6.8%) had vaginal PGE2 present, 14 (6.4%) had elevated urinary oxalate excretion, and 29 (13.2%) had a variety of diagnosed variants. In 81 (36.8%) no underlying diagnosis was made. This understates the numbers and varieties of vulvar vaginal diagnoses, for not all patients received a vaginal fluid analysis, a vulvar biopsy, or a 24 h urine screen for oxalates. A variety of medical and operative interventions was used. Symptoms were relieved in 65.9% of patients. The degree of sueeess varied. Successful outcomes were achieved in 14.3% of patients using a low oxalate diet and calcium citrate supplementation, 16% with anti-Candida treatment, 48.1% with antihistamines, 77% with vulvar injection of interferon, 83% with operative removal of inflamed vulvar tissue, and a posterior colporrhaphy used to cover the cutaneous defect. Conclusions: The diagnosis of vulvar vestibulitis is easy to make. An etiology for this chronic condition will not be achieved in every patient. A majority of patients can get relief by a variety of medical and operative interventions.

Oxalate depletion from leafy vegetables using alginate entrapped banana oxalate oxidase

The feasibility of depleting the high oxalate content of spinach (Spinacia oleracea), amaranthus (Amaranthus gangeticus), and paruppu keerai (Portulaca oleracea) using alginate entrapped banana oxalate oxidase is demonstrated for the first time. The relevance of this work to low-oxalate diet preparation for hyperoxaluric patients is discussed.

Medical Management of Vulvar Vestibulitis: Results of a Sequential Treatment Plan

Objective: The objectives of this study were to assess the efficacy of medical management for vulvar vestibulitis and to examine several historical variables and determine their predictive values as to which treatments will be most successful. Methods: Seventy-four patients diagnosed with vulvar vestibulitis were evaluated. Each patient was treated using a sequence of consecutive medical therapies for vulvar vestibulitis. These therapies were topical aqueous 4% lidocaine with intercourse, topical corticosteroid therapy, oral amitriptyline, topical low-dose 5-fluorouracil (5-FU) cream, intralesional alpha-interferon, and a low-oxalate diet in combination with oral calcium citrate. The patients were followed over 3–30 months and their responses to therapy were assessed. In addition, a statistical analysis was performed to determine the positive predictive values of certain historical variables and specific treatment successes. Results: Forty-nine patients reported positive responses to one of the initiated therapies. More specifically, 18.1% of the patients who used lidocaine, 33.8% who used topical corticosteroids, 57.1% who used amitriptyline, 16.7% who used 5-FU, none who received interferon, and 50% who tried a low-oxalate diet had positive responses to therapy. No historical variables were predictive of which therapies would have the most successful outcome. Conclusions: Medical management is effective in alleviating the symptoms of vulvar vestibulitis. Various aspects of a patient's history are not helpful in selecting the therapy that will be most effective.

Practical management of the short bowel

A shortened small intestine may end at a stoma or be anastomosed to the colon. Patients with a jejunostomy, but not those with a colon, lose large amounts of sodium. The intake and absorption of sodium can be increased by sipping a sodium-glucose solution; stomal loss can be reduced by restricting water or low-sodium drinks. If a stoma is situated less than 100 cm along the jejunum, a constant negative sodium balance may necessitate parenteral saline supplements. Gastric anti-secretory drugs or a somatostatin analogue reduce jejunostomy losses in such patients but do not restore a positive sodium balance. Loperamide or codeine phosphate benefit some patients. Magnesium deficiency can usually be corrected by oral magnesium oxide supplements. An elemental or hydrolysed diet is not beneficial. Patients with a jejunostomy can maintain a normal diet without fat reduction. When the colon is present, unabsorbed carbohydrate is fermented to absorbable short chain fatty acids. Unabsorbed long chain fatty acids and bile salts cause watery diarrhoea and increased colonic oxalate absorption with hyperoxaluria. Such patients benefit from a high carbohydrate, low-fat and low-oxalate diet. Parenteral nutrition is needed only by the few patients unable to maintain health or avoid socially disabling diarrhoea despite these measures.

Effect of calcium citrate supplementation on urinary calcium oxalate saturation in female stone formers: implications for prevention of osteoporosis

In 14 women aged 37-68 y with a history of renal calcium calculi, bone densities were 12.0% below those of age-matched control subjects at the L2-4 lumbar spine (P = 0.007) and 6.4% less at the femoral neck (P = 0.095). A low-oxalate diet was supplemented with 1 g Ca/d as citrate. In 6 mo, plasma 1,25(OH)2D concentrations fell from 53.2 +/- 18.8 to 41.9 +/- 15.2 ng/L (P = 0.02) and parathyroid hormone from 39.1 +/- 17.0 to 30.8 +/- 12.5 ng/L (P = 0.02). Calcium oxalate saturation was 2.15 +/- 1.38 at baseline, 2.27 +/- 1.00 at 1 mo, and 2.06 +/- 1.57 at 6 mo. The increase in urinary calcium at 1 mo from 4.411 +/- 1.87 to 6.514 +/- 2.82 mmol/24 h (P = 0.01) was offset by a parallel increase in citrate excretion from 2.909 +/- 1.45 to 3.455 +/- 1.34 mmol/24 h (P = 0.03). Calcium citrate supplementation did not increase the lithogenicity of the women in this protocol.