HOW TO READ YOUR KIDNEY STONE LAB REPORT – Uric Acid Stones

HOW TO READ YOUR KIDNEY STONE LAB REPORT – Uric Acid Stones

These two articles cover the main stone types, and this new one on uric acid parallels the prior one on calcium stones. Like the calcium stone article it is meant for patients, although physicians might like some of the nuances. The purpose is not to make patients into their own physicians but to enable them to understand their own stone forming abnormalities. My ruling hypothesis is that patients want prevention, and will embrace and implement the changes needed with more enthusiasm and endurance if they fully understand the goals. LIkewise if they can themselves follow the effects of their efforts on stone risk factors they will believe that what they are doing has real meaning. I know that hypotheses are for disproving, and I know someone may well do a prospective double blind randomized trial, some day, to test mine. Right now, I believe in the idea because of Eden whose resident twosome were not just told about the tree but exactly why they should not eat of its fruit. I know it is an unfortunate comparison, given the outcome, but much effort was expended on education. My source for the details, apart from the Hebrew Bible, is Milton, J: Paradise Lost; Books V – Viii.

HOW TO BE A SUCCESSFUL KIDNEY STONE PATIENT

HOW TO BE A SUCCESSFUL KIDNEY STONE PATIENT

It has always seemed to me that medical practice is a dance. One leads, perhaps, but the other does, too. If physicians know more steps, patients can prepare their parts in advance and organize their large roles in long term treatments so the final result is graceful and ultimately elegant in obtaining the best results with the least extra effort and resources. After all, it is patients who know the past and will determine the future. Here are lists for you, ways to think about time with physicians, and especially a way to think about your treatment over the long years of stone prevention. For it is years, this being a chronic and recurrent disease, years of work by you with only a rare burst of medical guidance here and there. Yet so important as rare needs preparation and curating so what transpires is not lost. What is here is my own ideal of how things should happen, how the dance is conducted – so brief, so important.

IDIOPATHIC HYPERCALCIURIA (IH)

IDIOPATHIC HYPERCALCIURIA (IH)

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.

HYPERCALCIURIA

HYPERCALCIURIA

This is a foundational article for the site. High rates of urine calcium excretion (hypercalciuria) will raise calcium concentration at any given urine flow rate, and therefore raise supersaturation with the calcium stone forming salts. Genetic (‘idiopathic’) hypercalciuria, simply the upper end of the normal range, is greatly over-represented among stone formers, and idiopathic hypercalciuria (IH) is a main focus of treatment for stone prevention. As well, people with IH, stone formers or not, are at risk for bone disease. This article introduces hypercalciuria: IH itself and a few of the less uncommon named diseases that cause hypercalciuria like primary hyperparathyroidism, renal tubular acidosis, and sarcoidosis. It mentions confusing disorders such as normocalcemic primary hyperparathyroidism, secondary hyperparathyroidism, and familial hypocalciuric hypercalcemia. It also offers evidence linking specific levels of urine calcium excretion to risk of stones, a very important matter in deciding what needs to be treated.

THE LOW FLOWS

THE LOW FLOWS

Given that kidneys supersaturate the urine by conserving water, no treatment can be more immediate and direct than to drink more water than one needs so the kidneys can excrete it and in the process dilute the urine salts – which is to lower supersaturation. Alas, there are many patients who cannot or will not drink enough water, and it is these Joan Parks writes about in this article. Over our 40 years of collaboration very many patients with the problem of persistent low flow have come through our stone program at UC, but Joan and I never wrote a paper about them so much of what we found is buried in their charts. By way of redress, Joan has conjured up a lot of details that we think people will find valuable, even though they have not been shaped into the formal character of a scientific paper.

Scroll to Top