EAU 2018: Bone Metabolism and Stones

Copenhagen, Denmark (UroToday.com) Hypercalciuria is the most common metabolic abnormality that is found in patients presenting with calcium-containing kidney stones. In addition to excreting more calcium than can be absorbed, the source of this additional urine calcium likely originates from the skeleton as most patients also exhibit decreased bone mineral density. Despite the high risk associated with hypercalciuria, there has been limited experience in comparing the role of metabolic disorders versus behavioral modifications as prevention (and, subsequently, as treatment) for patients with recurrent stone disease.

Dr. JP Haymann from Sorbonne Universities Pierre et Marie Curie in Paris, France presented his work on bone metabolism and stone formation. He asserts that patients deemed to be hypercalciuric stone formers, in addition to abovementioned, also exhibit decreased bone mineral density and increase in urine calcium turnover. Even further, this decreased bone mineral density increases in markers of bone turnover and, therefore, increased risk of fractures. Of note, it is important to consider these morbidities before assessing treatment options.

Dr. Haymann begins the discussion by pointing to his recent work in genetic hypercalciuric stone-forming (GHS) rats developed from the most hypercalciuric Sprague-Dawley rates. In comparison to the controls, GHS rates excreted significantly more urinary calcium than similarly fed controls and all the GHS rats formed kidney stones while the control rats did not. Additionally, regardless of behavioral and diet modifications to include a calcium-rich diet, there was little difference in rates of stone formation.

In these animal models, it was concluded that the hypercalciuria is due to a systemic dysregulation of calcium homeostasis. Further, this dysregulation often also resulted in enhanced bone mineral resorption, decreased renal tubule calcium reabsorption, or an increased number of vitamin D receptors in the target tissues.

As such, Dr. Haymann’s concludes his presentation with questions on whether these results can be applied into the clinical setting, particularly in treatment of patients with recurrent calcium stones. Because the mechanism for stone formation in the rat models is similar to that in the human, Dr. Haymann believes that the conclusions from his work can be translated easily to the clinical setting. In other words, regardless of an ample calcium diet, there is little evidence to support the fact that a change in diet can influence kidney stone formations and further work on prevention and treatment for (recurrent) stone disease should be considered.


Presented by: JP Haymann, MD Sorbonne Universités, Université Pierre et Marie Curie Paris-6, Paris, France

Written by: Linda M. Huynh, BS, Department of Urology, University of California-Irvine at the 2018 European Association of Urology Meeting EAU18, 16-20 March, 2018 Copenhagen, Denmark