Idiopathic hypercalciuria may well be the most complex and important issue in all of medical management of calcium kidney stones. It arises within the elaborate systems that regulate calcium metabolism and produces both a risk of stone formation and of bone disease with fractures. IH is strongly familial, almost certainly genetic in origin, and present in children as well as adults. Treatments used include high calcium – moderate protein – reduced sodium diet, moderation of dietary sugar loads, and potassium citrate, and thiazide type diuretics, each of which act through different and reasonably well characterized pathways which cannot be understood without a knowledge of how IH works in the first place. Unlike stones themselves, supersaturation, or citrate, each a very large and important topic, IH cannot be presented well – at least by me – in separated linked articles but only in one article that carries its many intersecting physiologies along side by side and uninterrupted. Being a long and comprehensive article, foundational for this site and – to me at least – for comprehension of the whole topic of pathogenesis and treatment of nephrolithiasis, this article is not necessarily meant to be read all at once but rather used as a resource. I will cover the treatments of IH later on, in separate articles.