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Video Article: How Stones Form
With considerable trepidation, I unfurl my first and certainly very unpolished video offering. The good part of the articles on this site is their devotion to scientific accuracy and referencing from PubMed. The bad parts are their opacity, length, and difficulty. I have long been a public lecturer and decided that video offerings might be a valuable add on. There is more room, I think I speak better than I write, and it seems to me one video can summarize and complement a group of written articles, so I did this one. It covers crystal formation, how crystals are made, and where in the niches and crevasses of the kidney they actually form. Its message is my usual one: Prevent crystals and you prevent stone disease. This is a beta version. I know it has some errors in it. I also know it lacks refinements I need. But, refinements and corrections will come. Let me know.
IDIOPATHIC CALCIUM OXALATE STONE FORMERS (ICSF)
Here is the most common kind of stone former, described in such detail as one can muster up at this time. They are simple to diagnose: Stones containing a preponderance of calcium oxalate, no uric acid, struvite, cystine, brushite, drugs, or rare organic materials, and exclusion of any systemic disease as a cause of stones. More or less, these patients are stone disease as it is seen in primary care and most urology practices. Of the millions of stone formers most are like this. The trials for prevention of calcium stones have mainly used these patients as a majority of subjects. However common they may be, and easy to define, they are complex in the way that they make stones, and it appears that there may be not one but perhaps two kinds of idiopathic calcium oxalate stone former. Because of modern flexible ureteroscopy the types of idiopathic calcium oxalate stone former will soon be told apart during stone removal surgery, and patients and their physicians confronted with a variety they may not fully expect. This article sums up what is known, as best as I can manage.
PATTERNS OF TISSUE MINERALIZATION
Three Pathways for Kidney Stone Formation All kidney stones share similar presenting symptoms, and urine supersaturation with respect to the mineral phase of the stone is essential for stone formation. These clinical similarities have made it difficult for researchers...
IMCD and BD plugs: Do they have a role in stone formation?
Between stone attacks, one can forget about the importance of prevention. So much water, pills, and nothing happens. This new post shows very new research done over the past decade or so, mainly by us, which shows that the tiny tubules of the kidneys can become plugged with calcium phosphate crystals. Fortunately kidney function appears to remain intact, but there is cell injury and inflammation. No one knows right now if stone prevention treatments will also prevent these plugs, but since the plugs form at the very ends of the renal tubules, where the final urine exits into the renal pelvis, one would think that whatever reduces crystal formation in the urine will reduce plugging.
CALCIUM PHOSPHATE STONES: Causes and Prevention
The second in this series of stone forming phenotypes, the calcium phosphate stone formers are less numerous than the calcium oxalate stone formers, but perhaps more worrisome, and certainly more complex. There are two types, those whose stones contain any brushite – an unusual form of calcium phosphate in stones, and those whose phosphate is only hydroxyapatite – the mineral found in bones. This latter group is to a large extent composed of young women, for reasons we do not know. Phosphate stones are likely than the calcium oxalate variety to be numerous, and often produce nephrocalcinosis, a mixture of small stones and tissue calcium deposits. Nephrocalcinosis, in turn, is often labelled medullary sponge kidney simply on radiological grounds, even when the distinctive lesions of MSK are not necessarily present. Likewise, phosphate stone patients can appear to have renal tubular acidosis because of nephrocalcinosis and because RTA and phosphate stone patients both produce a more alkaline urine than do normals, or patients with calcium oxalate stones. All in all, this is a complex form of calcium stones, challenging for clinicians and often very trying and concerning for patients with it. The article is long and difficult, so you might want to watch this video by way of an introduction.
Video article: Supersaturation – The calcium crystals
As I see things, all of stone disease concerns the balance between the opposing forces of supersaturation and kinetic retardation of crystallization. The former is better understood and more tractable because easily measured and commercially produced for clinical care. The latter is not fully understood in term of the molecules responsible and not commercially available as a clinical test. So of the two primary forces that control whether crystals can form, we have only supersaturation to use. Being so central, this one measurement, for each of the stone crystals, has unusual importance. These three relatively short videos cover the main elements of supersaturation: What it is, how kidneys produce it, and how it is measured and used in stone prevention. They combine with ‘How Stones Form’ to make what I think is a fine story about stone disease and a fine basis for understanding how stones are best prevented. I have gathered together in the article links to all of the supersaturation articles on the site thus far.
Web Apps and Smart Bottles
This is an article that can be written only by the readers of this site. We are not product testers nor do we do market surveys. But given how many fluid and diet apps one can find on the web and also given how many people come to this site every month we should be able to get a good idea about which ones seem of value. The benefit of accumulating your experience in comments to this very brief article accrues to all of you who come here. Whether you use an app or not crowd sourcing of a kind can tell us all which ones seem really good, and we can all use that knowledge. There are almost no words in the article, but as the results come in – in other words if you will share – we will count up by app in a table or so, ongoing. As for smart bottles, there are only a few on the market, but we should be able to get an idea about them if you will share. So, here it is: A blank slate for everyone to write on so everyone can benefit. Please share.
Control of Urine Oxalate Excretion
There is no doubt that urine oxalate excretion is an important factor in calcium oxalate kidney stone production, and that excretion is a very complex outcome of transport in the gut and kidney tubules and, of course, diet calcium intake. We have devoted a lot of energy to refining food oxalate lists and making a reasonable diet plan for oxalate. Here, we have taken on the harder task of reviewing the complex movements of oxalate from food into urine. The intestines not only absorb oxalate from food into the blood, they can secrete oxalate back out from blood into the gut lumen from which it is removed in the stool. The kidneys remove the net of diet oxalate absorbed minus that secreted by a process of filtration and subsequent renal cell reabsorption and secretion of that filtered oxalate. It is as though evolution has handled oxalate like a real hot potato: keep control of how much oxalate the kidneys need to remove and keep control of the blood oxalate concentration. This seems prudent – if one dares to speak this way about evolution – as oxalate can crystallize in blood as it does in urine and both processes can be dangerous. The new work on oxalate transport does not now directly translate into new tests or treatments for patients, but surely will. So I and my brilliant colleague Dr Hatim Hassan – who is the real expert here – have written about the future in medicine. Because the article is very complex and may not get a lot of readers – scared off – I have made a tiny movie to introduce it by way of encouragement.
My Lab Report
This little goodie started with my partner Dr Anna Zisman who to wanted us to have a simpler format for patients to follow in looking at their 24 hour urine lab reports. Answer five easy questions and get back a list of what you have to do with fluids and diet. Try it. Let me know if it works. If not, can you help make it better?
PUTTING IT ALL TOGETHER
Well, here it is, the last pillar in the foundation. My goal is to enable patients to achieve successful stone prevention and I believe this requires a partnership with their physicians, a partnership in which they play a very active individual role. Patients after all are the ones who can manage diet, fluid intake, and life demands, only they can assure that 24 hour urine collections are representative of normal life, and, frankly, only they can decide on a life of long term prevention. Stones being rarely fatal and usually not a cause of progressive kidney disease, patients can elect prevention or not, and their physicians are in a role more like attorneys and accountants than authoritarian directors of events. But as in Eden, one can expect proper choices only if one has provided full knowledge, which I have set out to accomplish. By proper I mean most suitable to patients given full knowledge, for some may not care to exercise themselves so much as I think they must to be successful, whereas others may consider the work of prevention slight indeed compared to the consequences of continued stones. In any event, this article is the end of that cycle of enablement I can manage, and I put it here, as in all writings, as the chef puts out her best effort – to face the indifferent judgement of the gourmet.