The kidney stone guidebook now has links to everything on the site. When you open it from here or from its big tab on the home page, you will find ‘ARTICLES BY TOPIC’. The site is so big, you need a topic guide; here it is.
Ileostomy causes loss of sodium alkali the colon normally absorbs back into the blood. Kidneys compensate as best they can by producing a scanty acidic urine. The acid pH promotes uric acid stones. The low volumes raise calcium oxalate supersaturation and risk of calcium oxalate stones. Kidney tubules frequently plug with both calcium and urate crystals. Supplemental fluids and alkali can help reverse these problems and are the keys to prevention of more stones. Early treatment with alkali, perhaps even before stones begin, may possibly be of value.
Although bariatric surgery does a lot of good in general, and most patients do well, it raises risk of kidney injury. People with such surgeries often excrete more oxalate than normal, and challenges such as high oxalate diet, or factors that cause volume depletion like diuretics and laxatives, or drugs that reduce kidney function – any or all of these in concert – can eventuate in acute kidney injury. Here, I I use an actual case to review the science behind all this, and spell out the details patients need to know about to protect themselves.
Some weight loss surgeries raise kidney stone risk, others do not. Here is my first article on the problem of bowel disease and stones. These common surgeries, whether they cause stones or not, greatly alter physiology of calcium, oxalate, citrate, even urine volume, so anyone concerned about stone disease should want to know their effects. This article tells about the procedures themselves, how they work, and what one needs to do for kidney stone prevention. It is therefore a fundamental article on which many others will come to depend.
Animal protein does not increase kidney stone risk. I know many may think so. Meats just seem like culprits. But this fine science by two remarkable contributors, Drs. Gary Curhan and Eric Taylor simply disproves ‘what everyone knows is true’. Over the ranges of what large groups of women and men ate, over many years, they detected no effect of animal protein to increase the rate of new stone onset. At the highest ranges within their groups stone rates did edge up, so massive excess is not a good idea. But let us say that within the range of 0.8 to 1 gm of protein per day per kilogram of body weight, which is the present US ideal diet intake, we need not fear animal protein, and have no reason to limit intake.
On the other side, Curhan and Taylor have bolstered their older observations and now show definitively that higher food potassium intakes from plants – fruits and veggies – reduce risk of new stones remarkably. So the US recommendations of 4,000 mg of potassium from these sources should greatly benefit kidney stone patients. Rather than the old and improper advice to limit animal protein, we need to tell everyone that grandma was right: Eat your vegetables, and all will be well.
Lower is better – that is the main burden of the new US hypertension guidelines. This applies to all of us. But kidney stone formers have a special place because their diet and treatment needs for stones closely overlay with those for blood pressure. The good part is synergy: If careful, treatment for the one will do for the other. The alternative is a piling up of treatments that eventually tire patients and lead to dropout. In this article I detail how to do the better way. The article is long because it includes home blood pressure techniques, and the evidence for lower treatment goals. But it is worth the read. Lower blood pressure saves lives, prevents strokes. It is so important. Give it your time.
This uncommon condition arises from selective impairment of urine acidification. As one result, kidneys cannot remove daily acid load efficiently and acid accumulates in the body. Because the urine they produce is excessively alkaline, kidney tubules plug with calcium phosphate crystals, and patients produce often very large numbers of kidney stones. Potassium alkali is needed to counteract the acid retention and restore blood to its proper pH. But the alkali can raise urine pH even more, so stone prevention usually requires the same combination of high fluids, and low diet sodium – to lower urine calcium as much as possible – as we use for calcium stone formers in general. One cause of dRTA is inherited defects of acid transporters, so the condition can run in families. Another is a group of autoimmune and acquired immune diseases. A third is a mixture of drugs that cause a picture like dRTA. Since perhaps 1959, scientists have encountered patients with normal blood acidity who form calcium phosphate stones and, when challenged with an extra acid load fail to lower their urine pH to levels attained by similarly challenged normal people. The unfortunate name ‘incomplete’ dRTA, coined for this rather common situation has plagued the field for decades since. It implies something special by way of treatment or prognosis, and perhaps cause. But with time it appears less and less useful as a diagnostic category and probably is best forgotten. Patients with this diagnosis so much resemble idiopathic calcium phosphate stone formers, and are treated identically to them, the special name has no value.
If the kidney stone diet – nee the ideal US diet – offers real potential to protect against not only kidney stones but also a host of other major diseases, one must admit to a certain bafflement about how to get the diet into use. I presume that time will bring good diet into every home, but for now we need more than patience. In what is certainly the most modest experiment of my career, I and Jill Harris have deployed an online course for stone patients in hopes of promoting their use of the diet and here are the initial results. The work Jill did with her first set of patients produced about the same lowering of 24 hour urine stone risk as Professor Borghi achieved with a comparable diet in his notable prospective kidney stone prevention trial. We have no controls, so you might say everyone would have done as well without us. But patients say otherwise – not published here. The usual obeisance to convention includes a hope for new funded research to further explore this model. But we demur. Obviously, funded trials like those of Borghi will return results like his. This is, possibly, of value in confirmation. But innovation in this one tiny area of health care delivery now concerns cost and convenience, acceptance in the real world, and most of all scalability. Can one person scale up to lower risk for reasonable numbers of patients? If so, can that experience be replicated within the cost structures not of NIH funding but of individual enterprise? Do social media and the general web now permit inexpensive and effective dissemination of diet information. Can they drive effective, inexpensive, and large scale diet change?
We cannot ignore the excellent body of work that has disclosed undeniable associations between stone forming and significant bone, hypertensive, and kidney disease. Multiple investigators have found that having stones predicts higher risks we need to mitigate through treatment that can both reduce stone forming and protect against fractures, high blood pressure, and kidney disease. The main stay of such treatment is the kidney stone diet. It so much resembles the diet recommended for all Americans I cannot but say every stone formers should adopt it. While incomplete treatments like very high fluid intake, or perhaps rigorous low oxalate diet may stave off stones, they fail to address the range of diseases to which stone formers are more prone than otherwise normal people. There is no sense to such incomplete measures when proper diet can do so much more.