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James E Lingeman - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms of human kidney Stone formation
Urolithiasis, 2014Co-Authors: Andrew P. Evan, F. L. Coe, Elaine M. Worcester, James Williams, James E LingemanAbstract:The precise mechanisms of kidney Stone formation and growth are not completely known, even though human Stone disease appears to be one of the oldest diseases known to medicine. With the advent of the new digital endoscope and detailed renal physiological studies performed on well phenotyped Stone formers, substantial advances have been made in our knowledge of the pathogenesis of the most common type of Stone former, the idiopathic Calcium Oxalate Stone former as well as nine other Stone forming groups. The observations from our group on human Stone formers and those of others on model systems have suggested four entirely different pathways for kidney Stone formation. Calcium Oxalate Stone growth over sites of Randall's plaque appear to be the primary mode of Stone formation for those patients with hypercalciuria. Overgrowths off the ends of Bellini duct plugs have been noted in most Stone phenotypes, do they result in a clinical Stone? Micro-lith formation does occur within the lumens of dilated inner medullary collecting ducts of cystinuric Stone formers and appear to be confined to this space. Lastly, cystinuric Stone formers also have numerous small, oval, smooth yellow appearing calyceal Stones suggestive of formation in free solution. The scientific basis for each of these four modes of Stone formation are reviewed and used to explore novel research opportunities
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Three pathways for human kidney Stone formation
Urological Research, 2010Co-Authors: Andrew P. Evan, Elaine M. Worcester, James E LingemanAbstract:No single theory of pathogenesis can properly account for human kidney Stones, they are too various and their formation is too complex for simple understanding. Using human tissue biopsies, intraoperative imaging and such physiology data from ten different Stone forming groups, we have identified at least three pathways that lead to Stones. The first pathway is overgrowth on interstitial apatite plaque as seen in idiopathic Calcium Oxalate Stone formers, as well as Stone formers with primary hyperparathyroidism, ileostomy, and small bowel resection, and in brushite Stone formers. In the second pathway, there are crystal deposits in renal tubules that were seen in all Stone forming groups except the idiopathic Calcium Oxalate Stone formers. The third pathway is free solution crystallization. Clear examples of this pathway are those patient groups with cystinuria or hyperoxaluria associated with bypass surgery for obesity. Although the final products may be very similar, the ways of creation are so different that in attempting to create animal and cell models of the processes one needs to be careful that the details of the human condition are included.
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in idiopathic Calcium Oxalate Stone formers unattached Stones show evidence of having originated as attached Stones on randall s plaque
BJUI, 2010Co-Authors: Nicole L Miller, Elaine M. Worcester, Andrew P. Evan, James C Williams, Fredric L Coe, Sharon B Bledsoe, Larry C Munch, Shelly E Handa, James E LingemanAbstract:Study Type – Diagnostic (exploratory cohort) Level of Evidence 2b OBJECTIVE To analyse the structure and composition of unattached Stones in idiopathic Calcium Oxalate (CaOx) Stone-formers (ICSF) and compare them to attached Stones from the same cohort, to investigate whether there is more than one pathogenic mechanism for Stone formation in ICSF. PATIENTS AND METHODS ICSF undergoing percutaneous nephrolithotomy or ureteroscopy for the treatment of nephrolithiasis gave consent to participate in this study. All accessible renal papillae were endoscopically imaged using a digital endoscope. All Stones were removed and determined by the operating surgeon to be attached or unattached to the underlying papilla. Micro-computed tomography (micro-CT), which provides three-dimensional analysis of entire Stones, was used to compare the structure and composition of attached and unattached Stones. RESULTS Of 115 Stones collected from nine patients (12 renal units), only 25 Stones were found not to be attached to renal papillae. Of these 25 Stones, four were lost and 12 showed definite morphological evidence of having been attached to tissue, probably having been displaced from papillae during access. For the remaining nine Stones, micro-CT analysis showed at least one internal region of Calcium phosphate within each of these unattached CaOx Stones, i.e. the internal structure of the unattached Stones is consistent with their having originated attached to Randall’s plaque, and then having become detached but retained in the kidney, with new layers of CaOx eventually covering the original attachment site. CONCLUSIONS Micro-CT analysis supports the hypothesis that in ICSF, both attached and unattached Stones occur as a result of a common pathogenic mechanism, i.e. in this type of Stone former, CaOx Stones, even those not showing morphology that betrays attachment, all originate attached to interstitial plaque on the renal papilla.
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renal intratubular crystals and hyaluronan staining occur in Stone formers with bypass surgery but not with idiopathic Calcium Oxalate Stones
Anatomical Record-advances in Integrative Anatomy and Evolutionary Biology, 2008Co-Authors: Andrew P. Evan, James E Lingeman, Fredric L Coe, Sharon B Bledsoe, Daniel L Gillen, Elaine M. WorcesterAbstract:Whether idiopathic Calcium Oxalate (CaOx) Stone formers form inner medullary collecting duct (IMCD) crystal deposits bears on pathogenetic mechanisms of Stone formation. In prior work, using light and transmission electron microscopy, we have found no IMCD crystal deposits. Here, we searched serial sections of papillary biopsies from a prior study of 15 idiopathic Calcium Oxalate Stone formers, 4 intestinal bypass patients with CaOx Stones, and 4 non-Stone-forming subjects, and biopsies from an additional hitherto unreported 15 idiopathic Calcium Oxalate Stone formers and 1 bypass patient using polarized light oil immersion optics, for deposits overlooked in our original study. We found no IMCD deposits in any of 1,500 serial sections from the 30 idiopathic Calcium Oxalate Stone formers, nor in 87 additional sections from a frozen idiopathic Calcium Oxalate Stone former biopsy sample processed without exposure to aqueous solutions. Among 4 of the 5 bypass patients but in none of the 30 idiopathic Calcium Oxalate Stone formers or 4 normal Stone formers, we found tiny birefringent thin crystalline overlays on scattered IMCD cell membranes. We also found IMCD lumen deposits in two bypass patients that contained mixed birefringent and nonbirefringent crystals, presumably CaOx and apatite. In the bypass patients, we observed focal apical IMCD cell hyaluronan staining, which was absent in idiopathic Calcium Oxalate Stone formers. The absence of any IMCD deposits in 1,500 serial sections of biopsies from 30 idiopathic Calcium Oxalate Stone formers allows us to place the upper limit on the probability of their occurrence at approximately 0.002 and place the lower limit of their size at the resolution of the optics (<0.2 mu). The tiny deposits in bypass patients may be the initial crystal lesion.
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role of interstitial apatite plaque in the pathogenesis of the common Calcium Oxalate Stone
Seminars in Nephrology, 2008Co-Authors: Andrew P. Evan, James E Lingeman, Fredric L Coe, Elaine M. WorcesterAbstract:By using intraoperative papillary biopsy material from kidneys of idiopathic Calcium Oxalate, intestinal bypass for obesity, brushite, cystine, and distal renal tubular acidosis Stone formers during percutaneous nephrolithotomy, we have determined that idiopathic Calcium Oxalate Stone formers appear to be the special case, although the most commonly encountered one, in which Stones form external to the kidney and by processes that do not involve the epithelial compartments. It is in this one group of patients that we find not only abundant interstitial plaque, but also strong evidence that the plaque is essential to Stone formation. The initial site of plaque formation is always in the papillary tip, and must be in the basement membrane of the thin loop of Henle. With time, plaque spreads throughout the papilla tip to the urothelium, which under conditions we do not understand is denuded and thereby exposes the apatite deposits to the urine. It is on this exposed apatite that a Stone forms as an overgrowth, first of amorphous apatite and then layers of Calcium Oxalate. This process generates an attached Stone fixed to the side of a papilla, allowing the ever-changing urine to dictate Stone growth and composition.
A Hesse - One of the best experts on this subject based on the ideXlab platform.
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effect of n 3 fatty acid supplementation on urinary risk factors for Calcium Oxalate Stone formation
The Journal of Urology, 2011Co-Authors: Roswitha Siener, Brigitte Jansen, Bernhard Watzer, A HesseAbstract:Purpose: Findings are inconsistent in a few studies of the effect of n-3 fatty acid supplementation on urinary Calcium and Oxalate excretion in Stone formers. We evaluated the physiological effects of supplementation with eicosapentaenoic acid and docosahexaenoic acid on urinary risk factors for Calcium Oxalate Stone formation under standardized conditions.Materials and Methods: We studied 15 healthy subjects initially while consuming a standardized diet for 5 days (control phase). During consecutive intervention phases 1—5-day standardized diet, 2—20-day free diet and 3—5-day standardized diet participants received 900 mg eicosapentaenoic acid and 600 mg docosahexaenoic acid daily. While ingesting the standardized diets, daily 24-hour urine samples were collected.Results: After short-term supplementation with eicosapentaenoic acid and docosahexaenoic acid in phase 1 we noted no changes in urinary parameters compared to the control phase. After 30-day supplementation with eicosapentaenoic acid and docosah...
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intestinal Oxalate absorption is higher in idiopathic Calcium Oxalate Stone formers than in healthy controls measurements with the 13c2 Oxalate absorption test
The Journal of Urology, 2006Co-Authors: Susanne Voss, A Hesse, Diana J Zimmermann, T Sauerbruch, G.e. Von UnruhAbstract:Purpose: We assessed the importance of Oxalate hyperabsorption for idiopathic Calcium Oxalate urolithiasis, Oxalate absorption in healthy volunteers and recurrent Calcium Oxalate Stone formers was compared.Materials and Methods: The [13C2]Oxalate absorption test, a standardized, radioactivity-free test, was performed. On 2 days 24-hour urine was collected and an identical standard diet containing 800 mg Ca daily was maintained. On the morning of day 2 a capsule containing 0.37 mmol sodium [13C2]Oxalate was ingested. A total of 120 healthy volunteers (60 women and 60 men) and 120 patients (30 women and 90 men) with idiopathic CaOx urolithiasis (60% or greater CaOx) were tested.Results: Mean intestinal Oxalate absorption in the volunteers was 8.0 ± 4.4%, and in the patients was 10.2 ± 5.2% (p <0.001). There was no significant difference in mean absorption values between men and women within both groups. A high overlap between the absorption values of volunteers and patients was found. Only in the patient gr...
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the efficacy of dietary intervention on urinary risk factors for Stone formation in recurrent Calcium Oxalate Stone patients
The Journal of Urology, 2005Co-Authors: Roswitha Siener, G.e. Von Unruh, Claudia Nicolay, Natalie Schade, A HesseAbstract:ABSTRACT 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.
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dependence of Oxalate absorption on the daily Calcium intake
Journal of The American Society of Nephrology, 2004Co-Authors: G.e. Von Unruh, Susanne Voss, T Sauerbruch, A HesseAbstract:Two to 20% of ingested Oxalate is absorbed in the gastrointestinal tract of healthy humans with a daily 800 mg Calcium intake. Calcium is the most potent modifier of the Oxalate absorption. Although this has been found repeatedly, the exact correlation between Calcium intake and Oxalate absorption has not been assessed to date. Investigated was Oxalate absorption in healthy volunteers applying 0.37 mmol of the soluble salt sodium [(13)C(2)]Oxalate in the Calcium intake range from 5 mmol (200 mg) Calcium to 45 mmol (1800 mg) Calcium. Within the range of 200 to 1200 mg Calcium per day, Oxalate absorption depended linearly on the Calcium intake. With 200 mg Calcium per day, the mean absorption (+/- SD) was 17% +/- 8.3%; with 1200 mg Calcium per day, the mean absorption was 2.6% +/- 1.5%. Within this range, reduction of the Calcium supply by 70 mg increased the Oxalate absorption by 1% and vice versa. Calcium addition beyond 1200 mg/d reduced the Oxalate absorption only one-tenth as effectively. With 1800 mg Calcium per day, the mean absorption was 1.7% +/- 0.9%. The findings may explain why a low-Calcium diet increases the risk of Calcium Oxalate Stone formation.
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The role of overweight and obesity in Calcium Oxalate Stone formation.
Obesity Research, 2004Co-Authors: Roswitha Siener, Sara Glatz, Claudia Nicolay, A HesseAbstract:Objective: The aim of the study was to assess the influence of overweight and obesity on the risk of Calcium Oxalate Stone formation. Research Methods and Procedures: BMI, 24-hour urine, and serum parameters were evaluated in idiopathic Calcium Oxalate Stone formers (363 men and 164 women) without medical or dietetic pretreatment. Results: Overweight and obesity were present in 59.2% of the men and in 43.9% of the women in the study population. Multiple linear regression analysis revealed a significant positive relationship between BMI and urinary uric acid, sodium, ammonium, and phosphate excretion and an inverse correlation between BMI and urinary pH in both men and women, whereas BMI was associated with urinary Oxalate excretion only among women and with urinary Calcium excretion only among men. Serum uric acid and creatinine concentrations were correlated with BMI in both genders. Because no association was established between BMI and urinary volume, magnesium, and citrate excretion, inhibitors of Calcium Oxalate Stone formation, the risk of Stone formation increased significantly with increasing BMI among both men and women with urolithiasis (p = 0.015). The risk of Calcium Oxalate Stone formation, median number of Stone episodes, and frequency of diet-related diseases were highest in overweight and obese men. Discussion: Overweight and obesity are strongly associated with an elevated risk of Stone formation in both genders due to an increased urinary excretion of promoters but not inhibitors of Calcium Oxalate Stone formation. Overweight and obese men are more prone to Stone formation than overweight women.
Andrew P. Evan - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms of human kidney Stone formation
Urolithiasis, 2014Co-Authors: Andrew P. Evan, F. L. Coe, Elaine M. Worcester, James Williams, James E LingemanAbstract:The precise mechanisms of kidney Stone formation and growth are not completely known, even though human Stone disease appears to be one of the oldest diseases known to medicine. With the advent of the new digital endoscope and detailed renal physiological studies performed on well phenotyped Stone formers, substantial advances have been made in our knowledge of the pathogenesis of the most common type of Stone former, the idiopathic Calcium Oxalate Stone former as well as nine other Stone forming groups. The observations from our group on human Stone formers and those of others on model systems have suggested four entirely different pathways for kidney Stone formation. Calcium Oxalate Stone growth over sites of Randall's plaque appear to be the primary mode of Stone formation for those patients with hypercalciuria. Overgrowths off the ends of Bellini duct plugs have been noted in most Stone phenotypes, do they result in a clinical Stone? Micro-lith formation does occur within the lumens of dilated inner medullary collecting ducts of cystinuric Stone formers and appear to be confined to this space. Lastly, cystinuric Stone formers also have numerous small, oval, smooth yellow appearing calyceal Stones suggestive of formation in free solution. The scientific basis for each of these four modes of Stone formation are reviewed and used to explore novel research opportunities
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Three pathways for human kidney Stone formation
Urological Research, 2010Co-Authors: Andrew P. Evan, Elaine M. Worcester, James E LingemanAbstract:No single theory of pathogenesis can properly account for human kidney Stones, they are too various and their formation is too complex for simple understanding. Using human tissue biopsies, intraoperative imaging and such physiology data from ten different Stone forming groups, we have identified at least three pathways that lead to Stones. The first pathway is overgrowth on interstitial apatite plaque as seen in idiopathic Calcium Oxalate Stone formers, as well as Stone formers with primary hyperparathyroidism, ileostomy, and small bowel resection, and in brushite Stone formers. In the second pathway, there are crystal deposits in renal tubules that were seen in all Stone forming groups except the idiopathic Calcium Oxalate Stone formers. The third pathway is free solution crystallization. Clear examples of this pathway are those patient groups with cystinuria or hyperoxaluria associated with bypass surgery for obesity. Although the final products may be very similar, the ways of creation are so different that in attempting to create animal and cell models of the processes one needs to be careful that the details of the human condition are included.
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in idiopathic Calcium Oxalate Stone formers unattached Stones show evidence of having originated as attached Stones on randall s plaque
BJUI, 2010Co-Authors: Nicole L Miller, Elaine M. Worcester, Andrew P. Evan, James C Williams, Fredric L Coe, Sharon B Bledsoe, Larry C Munch, Shelly E Handa, James E LingemanAbstract:Study Type – Diagnostic (exploratory cohort) Level of Evidence 2b OBJECTIVE To analyse the structure and composition of unattached Stones in idiopathic Calcium Oxalate (CaOx) Stone-formers (ICSF) and compare them to attached Stones from the same cohort, to investigate whether there is more than one pathogenic mechanism for Stone formation in ICSF. PATIENTS AND METHODS ICSF undergoing percutaneous nephrolithotomy or ureteroscopy for the treatment of nephrolithiasis gave consent to participate in this study. All accessible renal papillae were endoscopically imaged using a digital endoscope. All Stones were removed and determined by the operating surgeon to be attached or unattached to the underlying papilla. Micro-computed tomography (micro-CT), which provides three-dimensional analysis of entire Stones, was used to compare the structure and composition of attached and unattached Stones. RESULTS Of 115 Stones collected from nine patients (12 renal units), only 25 Stones were found not to be attached to renal papillae. Of these 25 Stones, four were lost and 12 showed definite morphological evidence of having been attached to tissue, probably having been displaced from papillae during access. For the remaining nine Stones, micro-CT analysis showed at least one internal region of Calcium phosphate within each of these unattached CaOx Stones, i.e. the internal structure of the unattached Stones is consistent with their having originated attached to Randall’s plaque, and then having become detached but retained in the kidney, with new layers of CaOx eventually covering the original attachment site. CONCLUSIONS Micro-CT analysis supports the hypothesis that in ICSF, both attached and unattached Stones occur as a result of a common pathogenic mechanism, i.e. in this type of Stone former, CaOx Stones, even those not showing morphology that betrays attachment, all originate attached to interstitial plaque on the renal papilla.
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renal intratubular crystals and hyaluronan staining occur in Stone formers with bypass surgery but not with idiopathic Calcium Oxalate Stones
Anatomical Record-advances in Integrative Anatomy and Evolutionary Biology, 2008Co-Authors: Andrew P. Evan, James E Lingeman, Fredric L Coe, Sharon B Bledsoe, Daniel L Gillen, Elaine M. WorcesterAbstract:Whether idiopathic Calcium Oxalate (CaOx) Stone formers form inner medullary collecting duct (IMCD) crystal deposits bears on pathogenetic mechanisms of Stone formation. In prior work, using light and transmission electron microscopy, we have found no IMCD crystal deposits. Here, we searched serial sections of papillary biopsies from a prior study of 15 idiopathic Calcium Oxalate Stone formers, 4 intestinal bypass patients with CaOx Stones, and 4 non-Stone-forming subjects, and biopsies from an additional hitherto unreported 15 idiopathic Calcium Oxalate Stone formers and 1 bypass patient using polarized light oil immersion optics, for deposits overlooked in our original study. We found no IMCD deposits in any of 1,500 serial sections from the 30 idiopathic Calcium Oxalate Stone formers, nor in 87 additional sections from a frozen idiopathic Calcium Oxalate Stone former biopsy sample processed without exposure to aqueous solutions. Among 4 of the 5 bypass patients but in none of the 30 idiopathic Calcium Oxalate Stone formers or 4 normal Stone formers, we found tiny birefringent thin crystalline overlays on scattered IMCD cell membranes. We also found IMCD lumen deposits in two bypass patients that contained mixed birefringent and nonbirefringent crystals, presumably CaOx and apatite. In the bypass patients, we observed focal apical IMCD cell hyaluronan staining, which was absent in idiopathic Calcium Oxalate Stone formers. The absence of any IMCD deposits in 1,500 serial sections of biopsies from 30 idiopathic Calcium Oxalate Stone formers allows us to place the upper limit on the probability of their occurrence at approximately 0.002 and place the lower limit of their size at the resolution of the optics (<0.2 mu). The tiny deposits in bypass patients may be the initial crystal lesion.
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role of interstitial apatite plaque in the pathogenesis of the common Calcium Oxalate Stone
Seminars in Nephrology, 2008Co-Authors: Andrew P. Evan, James E Lingeman, Fredric L Coe, Elaine M. WorcesterAbstract:By using intraoperative papillary biopsy material from kidneys of idiopathic Calcium Oxalate, intestinal bypass for obesity, brushite, cystine, and distal renal tubular acidosis Stone formers during percutaneous nephrolithotomy, we have determined that idiopathic Calcium Oxalate Stone formers appear to be the special case, although the most commonly encountered one, in which Stones form external to the kidney and by processes that do not involve the epithelial compartments. It is in this one group of patients that we find not only abundant interstitial plaque, but also strong evidence that the plaque is essential to Stone formation. The initial site of plaque formation is always in the papillary tip, and must be in the basement membrane of the thin loop of Henle. With time, plaque spreads throughout the papilla tip to the urothelium, which under conditions we do not understand is denuded and thereby exposes the apatite deposits to the urine. It is on this exposed apatite that a Stone forms as an overgrowth, first of amorphous apatite and then layers of Calcium Oxalate. This process generates an attached Stone fixed to the side of a papilla, allowing the ever-changing urine to dictate Stone growth and composition.
G.e. Von Unruh - One of the best experts on this subject based on the ideXlab platform.
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The role of Oxalobacter formigenes colonization in Calcium Oxalate Stone disease
Kidney international, 2013Co-Authors: Ursula Bangen, G.e. Von Unruh, Harmeet Sidhu, Ruth Hönow, Albrecht HesseAbstract:About 75% of urinary Stones contain Oxalate. As Oxalobacter formigenes is a Gram-negative anaerobic bacterium that degrades Oxalate in the intestinal tract, we assessed the role of O. formigenes in Oxalate metabolism by evaluating its intestinal absorption, plasma concentration, and urinary excretion. Of 37 Calcium Oxalate Stone formers, 26 tested negative for O. formigenes and were compared with the 11 patients who tested positive. Patients provided 24-h urine samples on both a self-selected and a standardized diet. Urinary Oxalate excretion did not differ significantly on the self-selected diet, but was significantly lower in O. formigenes -positive than in O. formigenes -negative patients under controlled, standardized conditions. Intestinal Oxalate absorption, measured using [ 13 C 2 ]Oxalate, was similar in the patients with or without O. formigenes . Plasma Oxalate concentrations were significantly higher in noncolonized (5.79μmol/l) than in colonized Stone formers (1.70μmol/l). Colonization with O. formigenes was significantly inversely associated with the number of Stone episodes. Our findings suggest that O. formigenes lowers the intestinal concentration of Oxalate available for absorption at constant rates, resulting in decreased urinary Oxalate excretion. Thus, dietary factors have an important role in urinary Oxalate excretion. The data indicate that O. formigenes colonization may reduce the risk of Stone recurrence.
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intestinal Oxalate absorption is higher in idiopathic Calcium Oxalate Stone formers than in healthy controls measurements with the 13c2 Oxalate absorption test
The Journal of Urology, 2006Co-Authors: Susanne Voss, A Hesse, Diana J Zimmermann, T Sauerbruch, G.e. Von UnruhAbstract:Purpose: We assessed the importance of Oxalate hyperabsorption for idiopathic Calcium Oxalate urolithiasis, Oxalate absorption in healthy volunteers and recurrent Calcium Oxalate Stone formers was compared.Materials and Methods: The [13C2]Oxalate absorption test, a standardized, radioactivity-free test, was performed. On 2 days 24-hour urine was collected and an identical standard diet containing 800 mg Ca daily was maintained. On the morning of day 2 a capsule containing 0.37 mmol sodium [13C2]Oxalate was ingested. A total of 120 healthy volunteers (60 women and 60 men) and 120 patients (30 women and 90 men) with idiopathic CaOx urolithiasis (60% or greater CaOx) were tested.Results: Mean intestinal Oxalate absorption in the volunteers was 8.0 ± 4.4%, and in the patients was 10.2 ± 5.2% (p <0.001). There was no significant difference in mean absorption values between men and women within both groups. A high overlap between the absorption values of volunteers and patients was found. Only in the patient gr...
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the efficacy of dietary intervention on urinary risk factors for Stone formation in recurrent Calcium Oxalate Stone patients
The Journal of Urology, 2005Co-Authors: Roswitha Siener, G.e. Von Unruh, Claudia Nicolay, Natalie Schade, A HesseAbstract:ABSTRACT 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.
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dependence of Oxalate absorption on the daily Calcium intake
Journal of The American Society of Nephrology, 2004Co-Authors: G.e. Von Unruh, Susanne Voss, T Sauerbruch, A HesseAbstract:Two to 20% of ingested Oxalate is absorbed in the gastrointestinal tract of healthy humans with a daily 800 mg Calcium intake. Calcium is the most potent modifier of the Oxalate absorption. Although this has been found repeatedly, the exact correlation between Calcium intake and Oxalate absorption has not been assessed to date. Investigated was Oxalate absorption in healthy volunteers applying 0.37 mmol of the soluble salt sodium [(13)C(2)]Oxalate in the Calcium intake range from 5 mmol (200 mg) Calcium to 45 mmol (1800 mg) Calcium. Within the range of 200 to 1200 mg Calcium per day, Oxalate absorption depended linearly on the Calcium intake. With 200 mg Calcium per day, the mean absorption (+/- SD) was 17% +/- 8.3%; with 1200 mg Calcium per day, the mean absorption was 2.6% +/- 1.5%. Within this range, reduction of the Calcium supply by 70 mg increased the Oxalate absorption by 1% and vice versa. Calcium addition beyond 1200 mg/d reduced the Oxalate absorption only one-tenth as effectively. With 1800 mg Calcium per day, the mean absorption was 1.7% +/- 0.9%. The findings may explain why a low-Calcium diet increases the risk of Calcium Oxalate Stone formation.
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intestinal hyperabsorption of Oxalate in Calcium Oxalate Stone formers application of a new test with 13c2 Oxalate
Journal of The American Society of Nephrology, 1999Co-Authors: A Hesse, W Schneeberger, G.e. Von Unruh, S Engfeld, T SauerbruchAbstract:In up to one-third of patients with Calcium Oxalate Stones, a hyperoxaluria can be detected. Hyperoxaluria can result from increased endogenous production, from excessive Oxalate content of the food, or from intestinal hyperabsorption. For a causal therapy, it is important to discriminate between metabolic and hyperabsorptive hyperoxaluria. Our new 13C-Oxalate test allows this differentiation. Under standardized conditions, 50 mg of disodium salt of [13C2]oxalic acid was applied. From the amount of labeled Oxalate excreted in urine as measured by a gas chromatographic-mass spectrometric assay, the intestinal absorption was calculated. Seventy patients with recurrent Calcium Oxalate urolithiasis who had no signs of inflammatory bowel disease were tested. Their mean intestinal Oxalate absorption was 9.2+/-5.1%. This was significantly higher than the mean absorption of 50 healthy volunteers (6.7+/-3.9%). There was no difference in Oxalate absorption between male (n = 25) and female volunteers. Oxalate absorption correlated with the Oxalate excretion in the 24-h urine (volunteers: r = 0.46, P < 0.01; patients: r = 0.62, P < 0.001). Oxalate hyperabsorption was defined as an absorption exceeding 10%. According to this definition, 34% of the patients had Oxalate hyperabsorption; 20% of the volunteers showed a hyperabsorption, too. The 13C-Oxalate absorption test allows reliable determination of intestinal Oxalate absorption. Because of the use of a stable isotope, this test may be repeated as often as required. It will allow the control of therapeutic regimens and also help to unravel genetic influences in Stone formation.
Roswitha Siener - One of the best experts on this subject based on the ideXlab platform.
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The role of Oxalobacter formigenes in Calcium Oxalate Stone disease
2017Co-Authors: Roswitha SienerAbstract:Calcium Oxalate is the major component of about 75% of all urinary Stones. Hyperoxaluria is a primary risk factor for Calcium Oxalate Stone formation. The bioavailability of ingested Oxalate and the extent of intestinal absorption of dietary Oxalate are considered to be important factors in hyperoxaluria. Oxalobacter formigenes is a Gram-negative anaerobic bacterium that colonizes the intestinal tract. It is unique in that it requires Oxalate both as an energy and carbon source. The only known factor which reduces colonization with O. formigenes is the treatment with antibiotics to which the bacterium has been reported to be sensitive. A deficiency of Oxalate degradation by O. formigenes may increase urinary Oxalate excretion, attributed to decreased intestinal Oxalate degradation, leaving more Oxalate available for absorption at a constant intestinal absorption rate. A lack of colonization with O. formigenes increases the risk of recurrent Calcium Oxalate Stone formation. While evidence is emerging that orally administered O. formigenes can reduce urinary and plasma Oxalate, the possible treatment with a probiotic still remains a challenge.
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effect of n 3 fatty acid supplementation on urinary risk factors for Calcium Oxalate Stone formation
The Journal of Urology, 2011Co-Authors: Roswitha Siener, Brigitte Jansen, Bernhard Watzer, A HesseAbstract:Purpose: Findings are inconsistent in a few studies of the effect of n-3 fatty acid supplementation on urinary Calcium and Oxalate excretion in Stone formers. We evaluated the physiological effects of supplementation with eicosapentaenoic acid and docosahexaenoic acid on urinary risk factors for Calcium Oxalate Stone formation under standardized conditions.Materials and Methods: We studied 15 healthy subjects initially while consuming a standardized diet for 5 days (control phase). During consecutive intervention phases 1—5-day standardized diet, 2—20-day free diet and 3—5-day standardized diet participants received 900 mg eicosapentaenoic acid and 600 mg docosahexaenoic acid daily. While ingesting the standardized diets, daily 24-hour urine samples were collected.Results: After short-term supplementation with eicosapentaenoic acid and docosahexaenoic acid in phase 1 we noted no changes in urinary parameters compared to the control phase. After 30-day supplementation with eicosapentaenoic acid and docosah...
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Oxalate contents of species of the Polygonaceae, Amaranthaceae and Chenopodiaceae families
Food Chemistry, 2006Co-Authors: Roswitha Siener, Ruth Hönow, Ana Seidler, Susanne Voss, Albrecht HesseAbstract:Abstract A high dietary Oxalate intake influences mineral and trace element absorption in humans and may lead to Calcium Oxalate Stone formation due to the ability of Oxalate to form insoluble complexes with divalent cations in the gastrointestinal tract. The soluble and total Oxalate contents of species in the Polygonaceae, Amaranthaceae and Chenopodiaceae families were measured using an HPLC-enzyme-reactor method. Polygonaceae, Amaranthaceae and Chenopodiaceae include most of the foods with excessively high Oxalate concentrations. Amaranth is a specie of the Amaranthaceae family, Polygonaceae include buckwheat, rhubarb, and sorrel, whereas beetroot, mangold, spinach, and quinoa are species of the Chenopodiaceae family. Obviously, Oxalate is accumulated in these plant families in each plant tissue, i.e., in leaves, stems, hypocotyl-root and nuts. The highest Oxalate content was found in leaves and stems of plants in these families. Soluble Oxalate ranged from 59 to 131 mg/100 g in roots and nuts, and from 258 to 1029 mg/100 g in leaves and stems. Total Oxalate ranged from 143 to 232 mg/100 g in roots and nuts, and from 874 to 1959 mg/100 g in leaves and stems. Patients with Calcium Oxalate Stone disease should be advised to avoid these Oxalate-rich foods.
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the efficacy of dietary intervention on urinary risk factors for Stone formation in recurrent Calcium Oxalate Stone patients
The Journal of Urology, 2005Co-Authors: Roswitha Siener, G.e. Von Unruh, Claudia Nicolay, Natalie Schade, A HesseAbstract:ABSTRACT 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.
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The role of overweight and obesity in Calcium Oxalate Stone formation.
Obesity Research, 2004Co-Authors: Roswitha Siener, Sara Glatz, Claudia Nicolay, A HesseAbstract:Objective: The aim of the study was to assess the influence of overweight and obesity on the risk of Calcium Oxalate Stone formation. Research Methods and Procedures: BMI, 24-hour urine, and serum parameters were evaluated in idiopathic Calcium Oxalate Stone formers (363 men and 164 women) without medical or dietetic pretreatment. Results: Overweight and obesity were present in 59.2% of the men and in 43.9% of the women in the study population. Multiple linear regression analysis revealed a significant positive relationship between BMI and urinary uric acid, sodium, ammonium, and phosphate excretion and an inverse correlation between BMI and urinary pH in both men and women, whereas BMI was associated with urinary Oxalate excretion only among women and with urinary Calcium excretion only among men. Serum uric acid and creatinine concentrations were correlated with BMI in both genders. Because no association was established between BMI and urinary volume, magnesium, and citrate excretion, inhibitors of Calcium Oxalate Stone formation, the risk of Stone formation increased significantly with increasing BMI among both men and women with urolithiasis (p = 0.015). The risk of Calcium Oxalate Stone formation, median number of Stone episodes, and frequency of diet-related diseases were highest in overweight and obese men. Discussion: Overweight and obesity are strongly associated with an elevated risk of Stone formation in both genders due to an increased urinary excretion of promoters but not inhibitors of Calcium Oxalate Stone formation. Overweight and obese men are more prone to Stone formation than overweight women.
