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Re: Hyperoxaluria: A Gut-Kidney Axis?
UROLITHIASIS/ENDOUROLOGY
1299
TRPV5 calcium channel. The actions of the calcium sensing receptor (CaSr) are also profiled. While most of the focus on CaSr has been regarding its regulation of parathyroid hormone levels, it is also present in the nephron. Animal models have demonstrated that CaSr induces polyuria via inhibition of aquaporin 2 water channels and stimulates Hⴙ ATPase activity in the distal nephron. The latter response results in decreased urine pH. Both of these actions would theoretically limit the development of calcium phosphate stones. Dean Assimos, M.D.
Re: Hyperoxaluria: A Gut-Kidney Axis? S. Robijn, B. Hoppe, B. A. Vervaet, P. C. D’Haese and A. Verhulst Laboratory of Pathophysiology, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Antwerp, Belgium Kidney Int 2011; 80: 1146 –1158.
Hyperoxaluria leads to urinary calcium oxalate (CaOx) supersaturation, resulting in the formation and retention of CaOx crystals in renal tissue. CaOx crystals may contribute to the formation of diffuse renal calcifications (nephrocalcinosis) or stones (nephrolithiasis). When the innate renal defense mechanisms are suppressed, injury and progressive inflammation caused by these CaOx crystals, together with secondary complications such as tubular obstruction, may lead to decreased renal function and in severe cases to end-stage renal failure. For decades, research on nephrocalcinosis and nephrolithiasis mainly focused on both the physicochemistry of crystal formation and the cell biology of crystal retention. Although both have been characterized quite well, the mechanisms involved in establishing urinary supersaturation in vivo are insufficiently understood, particularly with respect to oxalate. Therefore, current therapeutic strategies often fail in their compliance or effectiveness, and CaOx stone recurrence is still common. As the etiology of hyperoxaluria is diverse, a good understanding of how oxalate is absorbed and transported throughout the body, together with a better insight in the regulatory mechanisms, is crucial in the setting of future treatment strategies of this disorder. In this review, the currently known mechanisms of oxalate handling in relevant organs will be discussed in relation to the different etiologies of hyperoxaluria. Furthermore, future directions in the treatment of hyperoxaluria will be covered. Editorial Comment: This is an excellent review of the intestinal, hepatic and renal handling of oxalate. Most of the evidence regarding these transporters has been generated from animal models, including knockouts, isolated gut experiments and cell culture. Oxalate is filtered, secreted and absorbed in the nephron, and absorbed and secreted in the gut. A number of the solute linked carrier 26 (SLC26) anion exchangers are thought to have a role in these processes. Dean Assimos, M.D.
Re: Ethylene Glycol Induces Calcium Oxalate Crystal Deposition in Malpighian Tubules: A Drosophila Model for Nephrolithiasis/Urolithiasis Y. H. Chen, H. P. Liu, H. Y. Chen, F. J. Tsai, C. H. Chang, Y. J. Lee, W. Y. Lin and W. C. Chen Graduate Institute of Integrated Medicine, Graduate Institute of Acupuncture Science, College of Chinese Medicine, China Medical University, Taichung, Taiwan Kidney Int 2011; 80: 369 –377.
Several animal species are used to study calcium oxalate urolithiasis; however, an ideal model has yet to be identified. We used Drosophila as a model organism and fed the flies lithogenic agents such as ethylene glycol, hydroxyl-L-proline, and sodium oxalate. At different times, the Malpighian tubules,
1299
TRPV5 calcium channel. The actions of the calcium sensing receptor (CaSr) are also profiled. While most of the focus on CaSr has been regarding its regulation of parathyroid hormone levels, it is also present in the nephron. Animal models have demonstrated that CaSr induces polyuria via inhibition of aquaporin 2 water channels and stimulates Hⴙ ATPase activity in the distal nephron. The latter response results in decreased urine pH. Both of these actions would theoretically limit the development of calcium phosphate stones. Dean Assimos, M.D.
Re: Hyperoxaluria: A Gut-Kidney Axis? S. Robijn, B. Hoppe, B. A. Vervaet, P. C. D’Haese and A. Verhulst Laboratory of Pathophysiology, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Antwerp, Belgium Kidney Int 2011; 80: 1146 –1158.
Hyperoxaluria leads to urinary calcium oxalate (CaOx) supersaturation, resulting in the formation and retention of CaOx crystals in renal tissue. CaOx crystals may contribute to the formation of diffuse renal calcifications (nephrocalcinosis) or stones (nephrolithiasis). When the innate renal defense mechanisms are suppressed, injury and progressive inflammation caused by these CaOx crystals, together with secondary complications such as tubular obstruction, may lead to decreased renal function and in severe cases to end-stage renal failure. For decades, research on nephrocalcinosis and nephrolithiasis mainly focused on both the physicochemistry of crystal formation and the cell biology of crystal retention. Although both have been characterized quite well, the mechanisms involved in establishing urinary supersaturation in vivo are insufficiently understood, particularly with respect to oxalate. Therefore, current therapeutic strategies often fail in their compliance or effectiveness, and CaOx stone recurrence is still common. As the etiology of hyperoxaluria is diverse, a good understanding of how oxalate is absorbed and transported throughout the body, together with a better insight in the regulatory mechanisms, is crucial in the setting of future treatment strategies of this disorder. In this review, the currently known mechanisms of oxalate handling in relevant organs will be discussed in relation to the different etiologies of hyperoxaluria. Furthermore, future directions in the treatment of hyperoxaluria will be covered. Editorial Comment: This is an excellent review of the intestinal, hepatic and renal handling of oxalate. Most of the evidence regarding these transporters has been generated from animal models, including knockouts, isolated gut experiments and cell culture. Oxalate is filtered, secreted and absorbed in the nephron, and absorbed and secreted in the gut. A number of the solute linked carrier 26 (SLC26) anion exchangers are thought to have a role in these processes. Dean Assimos, M.D.
Re: Ethylene Glycol Induces Calcium Oxalate Crystal Deposition in Malpighian Tubules: A Drosophila Model for Nephrolithiasis/Urolithiasis Y. H. Chen, H. P. Liu, H. Y. Chen, F. J. Tsai, C. H. Chang, Y. J. Lee, W. Y. Lin and W. C. Chen Graduate Institute of Integrated Medicine, Graduate Institute of Acupuncture Science, College of Chinese Medicine, China Medical University, Taichung, Taiwan Kidney Int 2011; 80: 369 –377.
Several animal species are used to study calcium oxalate urolithiasis; however, an ideal model has yet to be identified. We used Drosophila as a model organism and fed the flies lithogenic agents such as ethylene glycol, hydroxyl-L-proline, and sodium oxalate. At different times, the Malpighian tubules,