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.
Counting new stones right is absolutely necessary. You can’t sail a ship, or fly an airplane, or drive to the shopping mall without keeping track of where you are, and the same for stone prevention. New stone counts tell us if a patient is an active stone former or not, and if our treatment is a success or a failure. New stones are those passed or removed, or seen on an image, and not present on a prior image – radiographic or ultrasound. To know new from old requires, therefore, we read our images correctly and correlate stone numbers in time with stone events. Physicians have ultimate responsibility for counting right, but patients can help immeasurably by keeping track. This is how I count new stones, and I believe it is a correct way.
Clearance has long supported the entire apparatus of renal function. We measure everything in terms of clearances, and should, because for anything kidneys remove clearance is the ratio of its removal rate to its plasma concentration: lower clearance, higher plasma concentration. But we compute clearance as if kidneys were isolated organs and removing materials at a constant plasma concentration. Neither is true. When we analyse kidney removal rates as things are in life, where we eat and drink, clearance emerges automatically but in an altered form. It still relates plasma concentration to removal rate, but also gauges how long it takes for something we eat or drink to get out in the urine – the mean dwell time in plasma. This is not generally appreciated, so far as I know. If what matters is the exposure of our cells to a molecule, toxin or food, that is the product of its average concentration and average dwell time. Since clearance gauges both, exposure varies with the inverse square of clearance. So even small losses of kidney function may matter a lot. Likewise, that our renal clearances are far higher than we need to stay alive, that apparent surplus, may not be. Rather, we may need all of it to keep exposure in range. These are new ideas, as far as I know. We need experiments to prove their worth. But even now they emphasize the crucial importance of preserving kidney function above all: As great an effort as possible to prevent stones, and extreme care about their surgical management.
Plaque matters a lot, because a common anchoring site calcium oxalate stones grow on. How it forms gives clues to how to stop or slow it. Right now we have two hypotheses – visions – of plaque formation. One of them, my view, is that kidney anatomy and function conspire to deliver excess calcium to the site where plaque forms – the thin limbs of Henle’s loop. Plaque forms because supersaturation rises. If true, then what we do for stone prevention should do for plaque. The other vision, of Dr Marshall Stoller, is that through a complex sequence of crystallizations in kidney tubules the cells in the renal papillum transform into bone – like cells, and promote plaque as bone cells would. How to stop such plaque from forming is not as yet clear. This article supports the first vision – mine – by reporting a critical test of it carried out in human kidney tissue. So far, local supersaturation seems a sound mechanism for plaque, and stone prevention measures suitable for plaque reduction. But the alternative, bone cell transformation, has yet to have its unique predictions tested. It may prove equally valid.
Recent epidemiology has linked forming stones to these dire conditions. Increase in risk is not large, but seems undeniable. The increase is most evident among younger women perhaps because their baseline risk of vascular disease is lower than that of men, but it can be seen in both sexes. These new facts add weight to the need for comprehensive care of all stone formers. As a group they have increased risks for bone disease with fracture, hypertension, kidney disease, and now we know for stroke and heart attack. We have no information about whether prevention of stones helps reduce these risks, but certainly it can do no harm.
New work has given us two major benefits. For the first time we can use supersaturation values to assess the risk of new stone onset. Up till now we could say supersaturation was high, or low based on clinical experience or perhaps comparisons to normal populations, but we could not assign to a given supersaturation some statement about risk that was based on real trial evidence. Now we can. Perhaps more important scientifically, the new work was a true and rigorous test of the longstanding hypothesis that supersaturation was the efficient cause of stones. Physical chemistry says it should be, all things considered, but the system of inhibitors and anatomical specializations in the kidneys puts a considerable screen between pure solution chemistry and stone formation. Had the trial been negative we would have had to abandon or at least question the hypothesis; given it was positive, we can use it with a higher confidence. I rank this among the more important papers on stone disease in the past year – or more.
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.
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.