The Experts below are selected from a list of 813 Experts worldwide ranked by ideXlab platform

Charles Y C Pak - One of the best experts on this subject based on the ideXlab platform.

  • alkali absorption and citrate excretion in calcium nephrolithiasis
    2009
    Co-Authors: M Khashayar D Sakhaee, Beverley Adamshuet, Russel H Williams, Paulette Padalino, Peggy A Whitson, Charles Y C Pak
    Abstract:

    The role of net gastrointestinal (GI) alkali absorption in the development of Hypocitraturia was investigated. The net GI absorption of alkali was estimated from the difference between simple urinary cations (Ca, Mg, Na, and K) and anions (Cl and P). In 131 normal subjects, the 24 h urinary citrate was positively correlated with the net GI absorption of alkali (r = 0.49, p < 0.001). In 11 patients with distal renal tubular acidosis (RTA), urinary citrate excretion was subnormal relative to net GI alkali absorption, with data from most patients residing outside the 95% confidence ellipse described for normal subjects. However, the normal relationship between urinary citrate and net absorbed alkali was maintained in 11 patients with chronic diarrheal syndrome (CDS) and in 124 stone-forming patients devoid of RTA or CDS, half of whom had "idiopathic" Hypocitraturia. The 18 stone-forming patients without RTA or CDS received potassium citrate (30-60 mEq/day). Both urinary citrate and net GI alkali absorption increased, yielding a significantly positive correlation (r = 0.62, p < 0.0001), with the slope indistinguishable from that of normal subjects. Thus, urinary citrate was normally dependent on the net GI absorption of alkali. This dependence was less marked in RTA, confirming the renal origin of Hypocitraturia. However, the normal dependence was maintained in CDS and in idiopathic Hypocitraturia, suggesting that reduced citrate excretion was largely dietary in origin as a result of low net alkali absorption (from a probable relative deficiency of vegetables and fruits or a relative excess of animal proteins).

  • pathophysiologic basis for normouricosuric uric acid nephrolithiasis
    2002
    Co-Authors: Khashayar Sakhaee, Orson W. Moe, Beverley Adamshuet, Charles Y C Pak
    Abstract:

    Pathophysiologic basis for normouricosuric uric acid nephrolithiasis. Background: Low urinary pH is the commonest and by far the most important factor in uric acid nephrolithiasis but the reason(s) for this defect is (are) unknown. Patients with uric acid nephrolithaisis have normal acid-base parameters according conventional clinical tests. Methods: We studied steady-state plasma and urinary parameters of acid-base balance in subjects with normouricosuric pure uric acid stones. We also tested the ability of these subjects to excrete ammonium in response to an acute acid load. We compared these parameters in patients with pure uric acid stones to patients with mixed uric acid/calcium oxalate stones, pure calcium stones, and normal volunteers. Results: Pure uric acid stone formers have a much higher incidence of either diabetes or glucose intolerance. After equilibration to a control diet, patients with uric acid stones have lower urinary pH and they excrete less of their acid as ammonium. This is compensated by higher titratable acidity and Hypocitraturia. Despite their low baseline urinary pH, uric acid stone formers further acidify their urine after an acid load because of a severely impaired ammonia excretory response. Their characteristics are significantly different from normal volunteers and pure calcium stone formers. Patients with mixed uric acid/calcium stones exhibit intermediate characteristics. Conclusion: We propose that certain patients with normouricosuric uric acid nephrolithiasis have a renal acidification disease. The primary defect lies in renal ammonium excretion, which may be linked to the insulin-resistant state. Although net acid excretion is maintained at the expense of increased titratable acidity and to some degree Hypocitraturia, the compromise is acid urine pH and may result in uric acid nephrolithiasis.

  • converting enzyme inhibition causes Hypocitraturia independent of acidosis or hypokalemia
    1998
    Co-Authors: Khashayar Sakhaee, Charles Y C Pak, Joel Z Melnick, Patricia A Preisig, Sharon Haynes
    Abstract:

    Converting enzyme inhibition causes Hypocitraturia independent of acidosis or hypokalemia Background Angiotensin II stimulates the proximal tubular Na/H antiporter and increases proximal tubular cell pH. Because intracellular pH may affect urinary citrate excretion and enzymes responsible for renal citrate metabolism, the present studies examined the effect of enalapril, an angiotensin converting enzyme inhibitor, on the activity of renal cortical ATP citrate lyase and urinary citrate excretion. Methods Enalapril was given to rats (15mg/kg/day) for seven days and to humans (10mg twice daily) for 10days. Blood and 24-hour urine samples were obtained in both groups. Renal cortical tissue from rats was analyzed for enzyme activity. Results In rats, enalapril decreased urinary citrate excretion by 88%. The change in urinary citrate was not associated with a difference in plasma pH, bicarbonate nor potassium concentration. However, similar to metabolic acidosis and hypokalemia, enalapril caused a 42% increase in renal cortical ATP citrate lyase activity. When given to humans, enalapril significantly decreased urinary citrate excretion and urine citrate concentration by 12% and 16%, respectively, without affecting plasma pH or electrolytes. Conclusions Enalapril decreases urinary citrate in rats and humans. This is due, at least in part, to increases in cytosolic citrate metabolism through ATP citrate lyase in rats similar to that seen with chronic metabolic acidosis and hypokalemia. The effects of enalapril on urinary citrate and renal cortical ATP citrate lyase occur independently of acidosis or hypokalemia but may be due to intracellular acidosis that is common to all three conditions.

  • randomized double blind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis
    1993
    Co-Authors: P Barcelo, O Wuhl, E Servitge, A Rousaud, Charles Y C Pak
    Abstract:

    In an attempt to document the efficacy of potassium citrate in stone formation, 57 patients with active lithiasis (2 or more stones during the preceding 2 years) and Hypocitraturia were randomly allocated into 2 groups, with 1 group taking 30 to 60 mEq. potassium citrate daily in wax matrix tablet formation and the other group receiving placebo. In 18 patients receiving potassium citrate for 3 years stone formation significantly declined after treatment from 1.2 +/- 0.6 to 0.1 +/- 0.2 per patient year (p < 0.0001), in 13 patients (72%) the disease was in remission and all patients showed a reduced stone formation rate individually. In contrast, 20 patients taking placebo medication for 3 years showed no significant change in stone formation rate (1.1 +/- 0.4 to 1.1 +/- 0.3 per patient year) and in only 4 patients (20%) was the disease in remission. The stone formation rate during potassium citrate treatment was significantly lower than during the placebo treatment (0.1 +/- 0.2 versus 1.1 +/- 0.3 per patient year, p < 0.001). Potassium citrate therapy caused a significant increase in urinary citrate, pH and potassium, whereas placebo did not. Adverse reactions to potassium citrate were mild causing only 2 patients in the potassium citrate group and 1 in the placebo group to withdraw from the study. In summary, our randomized trial showed the efficacy of potassium citrate in preventing new stone formation in idiopathic hypocitraturic calcium nephrolithiasis.

Khashayar Sakhaee - One of the best experts on this subject based on the ideXlab platform.

  • citrate therapy for calcium phosphate stones
    2019
    Co-Authors: Jeffrey D Rimer, Khashayar Sakhaee, Naim M. Maalouf
    Abstract:

    Purpose of reviewCalcium phosphate (CaP) stones represent an increasingly encountered form of recurrent nephrolithiasis, but current prophylactic medical regimens are suboptimal. Although Hypocitraturia is a well-described risk factor for CaP stones, strategies that enhance citrate excretion have no

  • Hypocitraturia and alkalinuria risk factors for nephrolithiasis in topiramate treated subjects
    2010
    Co-Authors: Sherry Soursbrothers, Khashayar Sakhaee, Naim M. Maalouf, Orson W. Moe
    Abstract:

    Topiramate (TPM) is widely prescribed for seizures and migraine prophylaxis. TPM has multiple and yet uncharacterized mechanisms of actions, including inhibition of carbonic anhydrase (CA), and its...

  • Hypocitraturia and hyperoxaluria after roux en y gastric bypass surgery
    2010
    Co-Authors: Naim M. Maalouf, P Tondapu, Eve S Guth, Edward H Livingston, Khashayar Sakhaee
    Abstract:

    Purpose: Roux-en-Y gastric bypass surgery is associated with an increased risk of nephrolithiasis but obesity itself is a known risk factor for kidney stones. To assess the mechanism(s) predisposing to nephrolithiasis after Roux-en-Y gastric bypass we compared urinary tract stone risk profiles in patients who underwent the procedure and normal obese individuals.Materials and Methods: In this cross-sectional study urine and serum biochemistry was evaluated in 19 nonstone forming patients after Roux-en-Y gastric bypass and in 19 gender, age and body mass index matched obese controls without a history of nephrolithiasis.Results: Compared with obese controls surgical patients had significantly higher mean ± SD urine oxalate (45 ± 21 vs 30 ± 11 mg daily, p = 0.01) and lower urine citrate (358 ± 357 vs 767 ± 307 mg daily, p <0.01). The prevalence of hyperoxaluria (47% vs 10.5%, p = 0.02) and Hypocitraturia (63% vs 5%, p <0.01) was significantly higher in surgical patients, who also had significantly lower urine...

  • pathophysiologic basis for normouricosuric uric acid nephrolithiasis
    2002
    Co-Authors: Khashayar Sakhaee, Orson W. Moe, Beverley Adamshuet, Charles Y C Pak
    Abstract:

    Pathophysiologic basis for normouricosuric uric acid nephrolithiasis. Background: Low urinary pH is the commonest and by far the most important factor in uric acid nephrolithiasis but the reason(s) for this defect is (are) unknown. Patients with uric acid nephrolithaisis have normal acid-base parameters according conventional clinical tests. Methods: We studied steady-state plasma and urinary parameters of acid-base balance in subjects with normouricosuric pure uric acid stones. We also tested the ability of these subjects to excrete ammonium in response to an acute acid load. We compared these parameters in patients with pure uric acid stones to patients with mixed uric acid/calcium oxalate stones, pure calcium stones, and normal volunteers. Results: Pure uric acid stone formers have a much higher incidence of either diabetes or glucose intolerance. After equilibration to a control diet, patients with uric acid stones have lower urinary pH and they excrete less of their acid as ammonium. This is compensated by higher titratable acidity and Hypocitraturia. Despite their low baseline urinary pH, uric acid stone formers further acidify their urine after an acid load because of a severely impaired ammonia excretory response. Their characteristics are significantly different from normal volunteers and pure calcium stone formers. Patients with mixed uric acid/calcium stones exhibit intermediate characteristics. Conclusion: We propose that certain patients with normouricosuric uric acid nephrolithiasis have a renal acidification disease. The primary defect lies in renal ammonium excretion, which may be linked to the insulin-resistant state. Although net acid excretion is maintained at the expense of increased titratable acidity and to some degree Hypocitraturia, the compromise is acid urine pH and may result in uric acid nephrolithiasis.

  • converting enzyme inhibition causes Hypocitraturia independent of acidosis or hypokalemia
    1998
    Co-Authors: Khashayar Sakhaee, Charles Y C Pak, Joel Z Melnick, Patricia A Preisig, Sharon Haynes
    Abstract:

    Converting enzyme inhibition causes Hypocitraturia independent of acidosis or hypokalemia Background Angiotensin II stimulates the proximal tubular Na/H antiporter and increases proximal tubular cell pH. Because intracellular pH may affect urinary citrate excretion and enzymes responsible for renal citrate metabolism, the present studies examined the effect of enalapril, an angiotensin converting enzyme inhibitor, on the activity of renal cortical ATP citrate lyase and urinary citrate excretion. Methods Enalapril was given to rats (15mg/kg/day) for seven days and to humans (10mg twice daily) for 10days. Blood and 24-hour urine samples were obtained in both groups. Renal cortical tissue from rats was analyzed for enzyme activity. Results In rats, enalapril decreased urinary citrate excretion by 88%. The change in urinary citrate was not associated with a difference in plasma pH, bicarbonate nor potassium concentration. However, similar to metabolic acidosis and hypokalemia, enalapril caused a 42% increase in renal cortical ATP citrate lyase activity. When given to humans, enalapril significantly decreased urinary citrate excretion and urine citrate concentration by 12% and 16%, respectively, without affecting plasma pH or electrolytes. Conclusions Enalapril decreases urinary citrate in rats and humans. This is due, at least in part, to increases in cytosolic citrate metabolism through ATP citrate lyase in rats similar to that seen with chronic metabolic acidosis and hypokalemia. The effects of enalapril on urinary citrate and renal cortical ATP citrate lyase occur independently of acidosis or hypokalemia but may be due to intracellular acidosis that is common to all three conditions.

Giovanni Gambaro - One of the best experts on this subject based on the ideXlab platform.

  • Medullary sponge kidney
    2016
    Co-Authors: Giovanni Gambaro
    Abstract:

    International audienceMedullary sponge kidney (MSK) is a renal malformation that mostly shows recurrent renal stones; renal concentration and acidification defects, hypercalciuria and Hypocitraturia are also common. Nephrocalcinosis and papillary duct ectasias are the morphological counterpart. Although MSK is frequently an apparently sporadic disorder, autosomal dominant inheritance has been observed in half of cases.The association of MSK with urinary tract developmental anomalies suggests that MSK belongs to the CAKUT disorders, and that its pathogenesis has to be investigated in one of the many steps of the kidney and urinary tract morphogenesis. Actually some rare GDNF variants have been observed in subjects with familial MSK. Since the GDNF-RET interaction has a critical role in the kidney-urinary tract development and nephronogenesis, it was proposed that those GDNF variants are disease causing mutations involved in at least some of the MSK cases. However, MSK is likely a heterogeneous genetic disorder and some of the sporadic cases are probably not genetic in origin. Data suggest that the distal acidification defect, that is frequently observed in MSK patients, plays a pivotal role in causing many of the clinical manifestations of MSK: defective bone mineralization, hypercalciuria, Hypocitraturia and stone formation. This hypothesis is supported by the finding that treatment with potassium citrate strongly improves bone mineralization, reduces calciuria and prevents renal stones. However, urinary stasis in the prepapillary ectasias is also a relevant condition for renal stone formation since lithogenesis occurs also in patients without defective acidification

  • long term treatment with potassium citrate and renal stones in medullary sponge kidney
    2010
    Co-Authors: Antonia Fabris, Antonio Nouvenne, Antonio Lupo, Patrizia Bernich, Cataldo Abaterusso, Nicola Marchionna, Giovanni Gambaro
    Abstract:

    Background and objectives: Medullary sponge kidney (MSK) is a renal malformation typically associated with nephrocalcinosis and recurrent calcium stones. Incomplete distal renal tubular acidosis, Hypocitraturia, and hypercalciuria are common. For stone prevention, patients with MSK generally receive the standard “stone clinic” recommendations and often receive potassium citrate (KC). However, the effect on stone recurrence of citrate treatment in these patients has never been studied. Design, setting, participants, & measurements: The issue was retrospectively analyzed on an outpatient basis in 97 patients with a radiologic diagnosis of MSK: 65 had at least one stone risk factor (SRF; hypercalciuria, Hypocitraturia, hyperuricosuria, hyperoxaluria) and received KC [29 ± 8 (SD) mEq/d]; 10 patients with SRF and 22 without received only general stone clinic suggestions. Follow-up was 78 ± 13, 72 ± 15, and 83 ± 14 months, respectively. The 24-hour urinary excretion of calcium, oxalate, uric acid, citrate, and morning urine pH were investigated at baseline and at the end of follow-up. Results: Parallel to a significant rise in urinary citrate and decreased urinary calcium (all P Conclusions: Treatment with KC is effective in preventing renal stones in the typical patient with MSK. It seems that two clinical phenotypes among patients showing typical MSK features during radiologic study exist.

  • bone disease in medullary sponge kidney and effect of potassium citrate treatment
    2009
    Co-Authors: Antonia Fabris, Antonio Nouvenne, Antonio Lupo, Patrizia Bernich, Cataldo Abaterusso, Nicola Marchionna, Chiara Canciani, Mauro Zamboni, Giovanni Gambaro
    Abstract:

    Background and objectives: In medullary sponge kidney (MSK)—a common malformative renal condition in patients with calcium nephrolithiasis—hypercalciuria, incomplete distal renal tubular acidosis, and Hypocitraturia are common. Clinical conditions with concomitant hypercalciuria and/or incomplete distal renal tubular acidosis are almost invariably associated with bone disease, making osteopathy highly likely in MSK, too. Patients with MSK have never been investigated for osteopathy; neither has the potential effect of potassium citrate administration (CA) on their urinary metabolic risk factors and on bone mineralization. Design, setting, participants, & measurements: These issues were retrospectively analyzed in 75 patients with MSK and primary stone risk factor (PSRF; hypercalciuria, Hypocitraturia, hyperuricosuria, and/or hyperoxaluria) on an outpatient basis; 65 received CA (2.9 ± 0.8 g/d), whereas 10 received only general “stone clinic” suggestions. The 24-h urinary excretion of calcium, phosphate, oxalate, uric acid, and citrate; morning urine pH; serum biochemistry; and bone mineral density were investigated at baseline and at the end of follow-up (78 ± 13 and 72 ± 15 mo in groups A and B, respectively). Results: CA led to a significant rise in urinary pH and citrate and decreased urinary calcium and phosphate (all P < 0.001). Patients with MSK and PSRF had reduced bone density. Bone density improved significantly in the group that was treated with oral CA. Conclusions: Bone disease is very frequent in patients with MSK and concomitant PSRF. Long-term CA improves bone density. The concurrent effects of treatment on PSRF suggest that the subtle acidosis plays a pivotal role in bone disease and hypercalciuria in patients with MSK.

Antonia Fabris - One of the best experts on this subject based on the ideXlab platform.

  • long term treatment with potassium citrate and renal stones in medullary sponge kidney
    2010
    Co-Authors: Antonia Fabris, Antonio Nouvenne, Antonio Lupo, Patrizia Bernich, Cataldo Abaterusso, Nicola Marchionna, Giovanni Gambaro
    Abstract:

    Background and objectives: Medullary sponge kidney (MSK) is a renal malformation typically associated with nephrocalcinosis and recurrent calcium stones. Incomplete distal renal tubular acidosis, Hypocitraturia, and hypercalciuria are common. For stone prevention, patients with MSK generally receive the standard “stone clinic” recommendations and often receive potassium citrate (KC). However, the effect on stone recurrence of citrate treatment in these patients has never been studied. Design, setting, participants, & measurements: The issue was retrospectively analyzed on an outpatient basis in 97 patients with a radiologic diagnosis of MSK: 65 had at least one stone risk factor (SRF; hypercalciuria, Hypocitraturia, hyperuricosuria, hyperoxaluria) and received KC [29 ± 8 (SD) mEq/d]; 10 patients with SRF and 22 without received only general stone clinic suggestions. Follow-up was 78 ± 13, 72 ± 15, and 83 ± 14 months, respectively. The 24-hour urinary excretion of calcium, oxalate, uric acid, citrate, and morning urine pH were investigated at baseline and at the end of follow-up. Results: Parallel to a significant rise in urinary citrate and decreased urinary calcium (all P Conclusions: Treatment with KC is effective in preventing renal stones in the typical patient with MSK. It seems that two clinical phenotypes among patients showing typical MSK features during radiologic study exist.

  • bone disease in medullary sponge kidney and effect of potassium citrate treatment
    2009
    Co-Authors: Antonia Fabris, Antonio Nouvenne, Antonio Lupo, Patrizia Bernich, Cataldo Abaterusso, Nicola Marchionna, Chiara Canciani, Mauro Zamboni, Giovanni Gambaro
    Abstract:

    Background and objectives: In medullary sponge kidney (MSK)—a common malformative renal condition in patients with calcium nephrolithiasis—hypercalciuria, incomplete distal renal tubular acidosis, and Hypocitraturia are common. Clinical conditions with concomitant hypercalciuria and/or incomplete distal renal tubular acidosis are almost invariably associated with bone disease, making osteopathy highly likely in MSK, too. Patients with MSK have never been investigated for osteopathy; neither has the potential effect of potassium citrate administration (CA) on their urinary metabolic risk factors and on bone mineralization. Design, setting, participants, & measurements: These issues were retrospectively analyzed in 75 patients with MSK and primary stone risk factor (PSRF; hypercalciuria, Hypocitraturia, hyperuricosuria, and/or hyperoxaluria) on an outpatient basis; 65 received CA (2.9 ± 0.8 g/d), whereas 10 received only general “stone clinic” suggestions. The 24-h urinary excretion of calcium, phosphate, oxalate, uric acid, and citrate; morning urine pH; serum biochemistry; and bone mineral density were investigated at baseline and at the end of follow-up (78 ± 13 and 72 ± 15 mo in groups A and B, respectively). Results: CA led to a significant rise in urinary pH and citrate and decreased urinary calcium and phosphate (all P < 0.001). Patients with MSK and PSRF had reduced bone density. Bone density improved significantly in the group that was treated with oral CA. Conclusions: Bone disease is very frequent in patients with MSK and concomitant PSRF. Long-term CA improves bone density. The concurrent effects of treatment on PSRF suggest that the subtle acidosis plays a pivotal role in bone disease and hypercalciuria in patients with MSK.

Naim M. Maalouf - One of the best experts on this subject based on the ideXlab platform.

  • citrate therapy for calcium phosphate stones
    2019
    Co-Authors: Jeffrey D Rimer, Khashayar Sakhaee, Naim M. Maalouf
    Abstract:

    Purpose of reviewCalcium phosphate (CaP) stones represent an increasingly encountered form of recurrent nephrolithiasis, but current prophylactic medical regimens are suboptimal. Although Hypocitraturia is a well-described risk factor for CaP stones, strategies that enhance citrate excretion have no

  • Full Review Salt and nephrolithiasis
    2016
    Co-Authors: Andrea Ticinesi, Naim M. Maalouf, Antonio Nouvenne, Loris Borghi, Tiziana Meschi
    Abstract:

    Dietary sodium chloride intake is nowadays globally known as one of the major threats for cardiovascular health. However, there is also important evidence that it may influence idiopathic calcium nephrolithiasis onset and recurrence. Higher salt intake has been associated with hypercalciuria and Hypocitraturia, which are major risk factors for calcium stone formation. Dietary salt restriction can be an effective means for secondary prevention of nephrolithiasis as well. Thus in this paper, we review the complex relationship between salt and nephrolithia-sis, pointing out the difference between dietary sodium and salt intake and the best methods to assess them, highlighting the main findings of epidemiologic, laboratory and intervention studies and focusing on open issues such as the role of dietary salt in secondary causes of nephrolithiasis

  • Salt and nephrolithiasis
    2014
    Co-Authors: Andrea Ticinesi, Naim M. Maalouf, Antonio Nouvenne, Loris Borghi, Tiziana Meschi
    Abstract:

    Dietary sodium chloride intake is nowadays globally known as one of the major threats for cardiovascular health. However, there is also important evidence that it may influence idiopathic calcium nephrolithiasis onset and recurrence. Higher salt intake has been associated with hypercalciuria and Hypocitraturia, which are major risk factors for calcium stone formation. Dietary salt restriction can be an effective means for secondary prevention of nephrolithiasis as well. Thus in this paper, we review the complex relationship between salt and nephrolithiasis, pointing out the difference between dietary sodium and salt intake and the best methods to assess them, highlighting the main findings of epidemiologic, laboratory and intervention studies and focusing on open issues such as the role of dietary salt in secondary causes of nephrolithiasis.

  • Hypocitraturia and alkalinuria risk factors for nephrolithiasis in topiramate treated subjects
    2010
    Co-Authors: Sherry Soursbrothers, Khashayar Sakhaee, Naim M. Maalouf, Orson W. Moe
    Abstract:

    Topiramate (TPM) is widely prescribed for seizures and migraine prophylaxis. TPM has multiple and yet uncharacterized mechanisms of actions, including inhibition of carbonic anhydrase (CA), and its...

  • Hypocitraturia and hyperoxaluria after roux en y gastric bypass surgery
    2010
    Co-Authors: Naim M. Maalouf, P Tondapu, Eve S Guth, Edward H Livingston, Khashayar Sakhaee
    Abstract:

    Purpose: Roux-en-Y gastric bypass surgery is associated with an increased risk of nephrolithiasis but obesity itself is a known risk factor for kidney stones. To assess the mechanism(s) predisposing to nephrolithiasis after Roux-en-Y gastric bypass we compared urinary tract stone risk profiles in patients who underwent the procedure and normal obese individuals.Materials and Methods: In this cross-sectional study urine and serum biochemistry was evaluated in 19 nonstone forming patients after Roux-en-Y gastric bypass and in 19 gender, age and body mass index matched obese controls without a history of nephrolithiasis.Results: Compared with obese controls surgical patients had significantly higher mean ± SD urine oxalate (45 ± 21 vs 30 ± 11 mg daily, p = 0.01) and lower urine citrate (358 ± 357 vs 767 ± 307 mg daily, p <0.01). The prevalence of hyperoxaluria (47% vs 10.5%, p = 0.02) and Hypocitraturia (63% vs 5%, p <0.01) was significantly higher in surgical patients, who also had significantly lower urine...