AIM To analyse current literature focusing on pathogenesis and therapeutic aspects of urolithiasis with inflammatory bowel disease(IBD) and following bariatric surgery. METHODS A systematic literature search was perfo...AIM To analyse current literature focusing on pathogenesis and therapeutic aspects of urolithiasis with inflammatory bowel disease(IBD) and following bariatric surgery. METHODS A systematic literature search was performed using PubMed, supplemented with additional references. Studies assessing the association of IBD or bariatric surgery with renal stones in both paediatric and adulthood were included. RESULTS Certain types of stones are seen more frequently with IBD. Hyperoxaluria and hypocitraturia are the main metabolic changes responsible for urolithiasis. The incidence of renal stones in malabsorptive types of bariatric surgery such as gastric bypass is high; this is not as common in modern restrictive surgical methods. Preventative methods and urine alkalinisation have been shown to be beneficial.CONCLUSION Both conditions are associated with renal stones. Patients' counselling and prevention strategies are the mainstay of urolithiasis management in these patients.展开更多
Idiopathic hypercalciuria （IH） is the leading metabolic risk factor for urolithiasis and affects all age groups without gender or race predominance. IH has a high morbidity with or without lithiasis and reduced bone...Idiopathic hypercalciuria （IH） is the leading metabolic risk factor for urolithiasis and affects all age groups without gender or race predominance. IH has a high morbidity with or without lithiasis and reduced bone mineral density （BMD）, as described previously in pe-diatric patients as well as in adults. The pathogenesis of IH is complex and not completely understood, given that urinary excretion of calcium is the end result of an interplay between three organs （gut, bone and kidney）, which is further orchestrated by hormones, such as 1,25 dihydroxyvitamin D, parathyroid hormone, calcitonin and fosfatonins （i.e., fbroblast growth-factor-23）. Usu-ally, a primary defect in one organ induces compensa-tory mechanisms in the remaining two organs, such as increased absorption of calcium in the gut secondary toa primary renal loss. Thus, IH is a systemic abnormality of calcium homeostasis with changes in cellular trans-port of this ion in intestines, kidneys and bones. Re-duced BMD has been demonstrated in pediatric patients diagnosed with IH. However, the precise mechanisms of bone loss or failure of adequate bone mass gain are still unknown. The largest accumulation of bone mass occurs during childhood and adolescence, peaking atthe end of the second decade of life. This accumulation should occur without interference to achieve the peak of optimal bone mass. Any interference may be a risk factor for the reduction of bone mass with increased risk of fractures in adulthood. This review will address the pathogenesis of IH and its consequence in bone mass.展开更多
文摘AIM To analyse current literature focusing on pathogenesis and therapeutic aspects of urolithiasis with inflammatory bowel disease(IBD) and following bariatric surgery. METHODS A systematic literature search was performed using PubMed, supplemented with additional references. Studies assessing the association of IBD or bariatric surgery with renal stones in both paediatric and adulthood were included. RESULTS Certain types of stones are seen more frequently with IBD. Hyperoxaluria and hypocitraturia are the main metabolic changes responsible for urolithiasis. The incidence of renal stones in malabsorptive types of bariatric surgery such as gastric bypass is high; this is not as common in modern restrictive surgical methods. Preventative methods and urine alkalinisation have been shown to be beneficial.CONCLUSION Both conditions are associated with renal stones. Patients' counselling and prevention strategies are the mainstay of urolithiasis management in these patients.
文摘Idiopathic hypercalciuria （IH） is the leading metabolic risk factor for urolithiasis and affects all age groups without gender or race predominance. IH has a high morbidity with or without lithiasis and reduced bone mineral density （BMD）, as described previously in pe-diatric patients as well as in adults. The pathogenesis of IH is complex and not completely understood, given that urinary excretion of calcium is the end result of an interplay between three organs （gut, bone and kidney）, which is further orchestrated by hormones, such as 1,25 dihydroxyvitamin D, parathyroid hormone, calcitonin and fosfatonins （i.e., fbroblast growth-factor-23）. Usu-ally, a primary defect in one organ induces compensa-tory mechanisms in the remaining two organs, such as increased absorption of calcium in the gut secondary toa primary renal loss. Thus, IH is a systemic abnormality of calcium homeostasis with changes in cellular trans-port of this ion in intestines, kidneys and bones. Re-duced BMD has been demonstrated in pediatric patients diagnosed with IH. However, the precise mechanisms of bone loss or failure of adequate bone mass gain are still unknown. The largest accumulation of bone mass occurs during childhood and adolescence, peaking atthe end of the second decade of life. This accumulation should occur without interference to achieve the peak of optimal bone mass. Any interference may be a risk factor for the reduction of bone mass with increased risk of fractures in adulthood. This review will address the pathogenesis of IH and its consequence in bone mass.
