A kidney stone is a solid piece of material that forms in the kidney from substances in the urine. It may be as small as a grain of sand or as large as a pearl. Most kidney stones pass out of the body without help from a doctor. But sometimes a stone will not go away. It may get stuck in the urinary tract, block the flow of urine and cause great pain.
The following may be signs of kidney stones that need a doctor's help:
- Extreme pain in your back or side that will not go away
- Blood in your urine
- Fever and chills
- Urine that smells bad or looks cloudy
- A burning feeling when you urinate
Your doctor will diagnose a kidney stone with urine, blood, and imaging tests.
If you have a stone that won't pass on its own, you may need treatment. It can be done with shock waves; with a scope inserted through the tube that carries urine out of the body, called the urethra; or with surgery.
NIH: National Institute of Diabetes and Digestive and Kidney Diseases
A Remarkable Concordance
From 1980 to now the US government has published diet recommendations for the American people. Gradually and over time these have become quantitative and specify amounts of critical nutrients such as calcium, sodium, refined sugar, protein, and potassium – as alkaline anions in mainly fruits and vegetables. The goals are reduction of osteoporosis, hypertension, obesity, and diabetes. I shall call this the Ideal US Diet.
Surprisingly, though aimed at stone prevention and management of bone disease from idiopathic hypercalciuria, decades of kidney stone research have identified precisely the same diet. Even more surprising, the Diet Against Systolic Hypertension (DASH) diet resembles the current Recommended US Diet, and stone researchers have found a reduced risk of stone disease in people who eat ‘DASH – Like’ diets.
Is it possible we have come upon the Ur diet?
Research on three different problems – kidney stones, systolic hypertension, and healthy eating all end up with the same basic diet plan; is that plan the solution to an ancient riddle?
Ur diet or not, experts advise all Americans, hypertensive or not to eat the ideal stone prevention diet. Any stone patient can be advised to eat it, after even a single stone. You do not even need a stone.
Here is the science that says any stone former is well off eating this remarkable diet.
The other articles on the diet and the article on treatment of idiopathic calcium stone formersare good additions.
‘Still Life with Cheeses’, Floris Claesz Van Dijck, 1610, shows how healthy diets are not so modern. Note the fruits. The painter was well known for banquet still life paintings in which he pioneered.
Shared Features of the Kidney Stone and Ideal US Diets
The Principle Components
In the table, under the middle heading ‘TREATMENT’, ‘high’ and ‘low’ refer to changesfrom what is common now in the US but considered ideal as a future norm.
For the general health of the US nation, high calcium diet helps maintain bone mineral; low sodium intake and high potassium intake reduce blood pressure; low refined sugar helps stave off obesity and diabetes. A reasonable range of protein intake maintains nitrogen balance without imposing unneeded calories. Apart from potassium, fruits and vegetables provide high nutrient value with modest calorie costs.
Because idiopathic hypercalciuria causes negative bone mineral balance at present calcium intakes, high calcium diet can protect against fractures.
High calcium diet reduces absorption of diet oxalate so restriction of intake can be less onerous.
Low sodium intake reduces urine calcium, and also aids in achieving bone mineral uptake.
Refined sugar causes spikes of high urine calcium excretion that are best avoided.
Excessive protein intake raises urine calcium.
Diet potassium from fruits and vegetables is mainly potassium with organic anions that can be metabolized to bicarbonate and therefore increase urine citrate.
Oxalate and Fluids
Oxalate is important only for kidney stones but the healthy diet helps because high calcium intake lowers oxalate absorption. Rather than begin with cumbersome food oxalate lists I suggest patients raise their calcium intakes and then get a new 24 hour urine collection. Often urine oxalate will no longer pose stone risk. If it does despite high calcium intake and timing of high calcium foods or calcium supplements with meals, then is time enough for the lists.
I am quite the opposite about fluids. Any stone former is wise to achieve 2.5 liters of urine volume daily, which usually means 3 liters of intake. Nothing can more precisely undo the urine supersaturation kidneys achieve by water conservation than fluids enough to obviate a need for them to do it.
Components Secondary to Stone Prevention
The US diet plan is rich in fruits and vegetables as a way of controlling calorie and fat intake, and offering alternatives to high sugar desserts. The diet also emphasizes reduced fat intake and especially saturated fat, limitations that are irrelevant to stone prevention.
But I advocate for using the intact diet as opposed to only those aspects of it related to stone prevention. It is a coherent plan of nutrition whose structure that may help people create and maintain desirable eating habits.
High Calcium Intake
Let me again emphasize: ‘High’ and ‘low’ in what follows compare the desired diet to what is the common pattern right now in the US.
IH Bone Disease
Stone formers fracture at abnormal rates. Among people living in Rochester, Minnesota, the cumulative incidence of vertebral fractures in people with stones (irregular line) exceeds the rate of fractures in the entire population (the smooth line) between 1950 and 1974. Hip and forearm did not fracture excessively.
One can find two reasons for such fractures. The first is idiopathic hypercalciuria.The second is self imposed or iatrogenic low calcium intake in hopes of stone prevention. The US health recommendations for 1000 to 1,200 mg of diet calcium daily arise from massive research showing such diets help prevent bone disease in large populations. It will help stone formers especially, because people with IH cannot maintain neutral bone calcium balance as well as average unselected people, at least in part because of inefficient renal calcium conservation.
On the graph to the right those with IH are in red, those with normal urine calcium are in blue. ‘IH’ here is the research criterion of the upper 90th or 95th percentile of normal, so the urine calcium of the IH cases would approximate 250 and 300 mg of urine calcium daily for women and men, respectively. Even at calcium intakes of 1,200 mg/day the average calcium retention (red line) of those with IH thus defined barely reaches 0 – stable bone mineral content.
The US recommendations will hardly suffice for the most marked hypercalciuria and the lower calcium intakes in present use have the potential to cause bone mineral loss and eventual fractures.
Reduction of Urine Oxalate
Urine oxalate can rise because of genetic defects or bowel disease, which each have their own special place in stone prevention. But most people with stones have urine oxalate excretions dominated by diet oxalate content and intestinal oxalate absorption.
This latter is dependent on diet calcium.In the graph to the left, diet calcium is on the x axis and urine oxalate on the y axis. Each point represents values from trial data in which diet calcium was altered and urine oxalate measured. Oxalate intake varied from 200 to 50 mg/d and the symbol size reflects it. The data for the trials are available from the main article I wrote about this topic. The names are those of the principal investigators.
As diet calcium increases, urine oxalate falls more or less independent of oxalate intake. At 1,200 mg, most points are between 25 and 35 mg/d.
This does not mean that we no longer need to be concerned with diet oxalate. But it does mean that the recommended US diet calcium intake of 1,200 mg/d lessens the needed stringency.
In the small inset box, Hess makes this point with considerable drama. He gave people 2,000 mg/d of oxalate, a shocking amount, with 1,200 mg/d of diet calcium. Despite the drastic diet oxalate excess, urine oxalate was only 80 mg/d – too high of course, but consider the intake. He raised the calcium intake to near 4,000 mg and brought the urine oxalate down to near 30 mg/d. This is a powerful demonstration of how diet calcium can more or less balance diet oxalate.
From the graph, we can say that at about 1,200 mg/d diet calcium, diet oxalate can be in the range of 100 to 200 mg/d which is not very restricted. The exact relationship between urine oxalate and diet oxalate on this 1,200 mg/d diet might well be quantified by another trial, which could be of moderate duration.
Low Sodium Diet
Lowers Urine Calcium
One would be correct in saying that high diet calcium will increase urine calcium but the lower sodium content of the kidney stone diet will lower urine calcium and permit high diet calcium that protects bone and lowers urine oxalate.
Urine calcium varies with urine sodium in normal people – the red circles and triangles on the graph to the right. But the variation is much more marked for people with IH (blue circles and triangles) as defined by 95th percentiles as mentioned above. Circles denote prospective trials in which diet sodium was deliberately varied, triangles observational data. The non parametric ellipses contain 66% of the data.
Because the difference between IH and normal is in the slope, as diet sodium falls and lowers urine sodium – more or less, urine sodium is diet sodium on average – the two curves come together. A formal analysis of the slope difference is in the detailed article that presents these data.
At the US diet upper boundary of 100 mEq/d (2,300 mg/d) diet sodium, urine calcium in IH begins to overlap in part with normals. At what has been called optimal (65 mEq/d or 1,500 mg/d) diet sodium, the overlap is even better.
A single but well done trial of 1,200 mg calcium and 50 meq/d sodium (they actually ate about 120 mEq/d on average) was much more effective in preventing stones than was a low calcium high sodium diet – 400 mg/d calcium and uncontrolled sodium which was about 200 mEq – a diet that many people may be eating in the US today. More to the point, the urine calcium excretion of those eating 400 mg calcium and 200 mEq of sodium was the same as those eating 1,200 mg of calcium and 120 mEq of sodium. All of the subjects were males with calcium oxalate stones and IH. This trial is detailed in another article.
Improves Bone Mineral Balance
To date no trial has tested treatment of IH bone disease, but this one trial concerned menopausal osteoporosis and used high calcium low sodium diet with successful outcomes.
Each of the subjects ate in random order each of high and low calcium and sodium diets, and total bone mineral balance was measured. The time on each diet was long enough to get reliable data.
Calcium absorbed (leftmost bar (blue) for each diet type) was highest on the two high calcium diets (diet types are along the horizontal axis). Loss of calcium in stool and urine (second and third bars from the left (red and gray, respectively) over each diet type) were lowered by low sodium diet (second group of bars from the left over the ‘CA HIGH NA LOW’ caption), and that was the only diet that produced positive balance – black bar above the horizontal dashed line.
Of interest, the high diet calcium was not achieved entirely with foods. Supplemental calcium was used, eaten during the course of the meals. This means for those who cannot get in enough calcium from food it is not unreasonable to use supplements, but they must be taken directly with the meals, not in between or fasting.
Also note that high calcium with high sodium (first block of four bars) did not achieve positive bone balance, so it is not enough to just add calcium. One needs the two diet factors together. This is what the US diet plan attempts to accomplish.
Low Refined Sugar
We have no trial, but we do have the striking effect of sugars to produce a transient but lofty spike in urine calcium.
Normal people given 100 gm of glucose or sucrose in water increased their urine calcium – the periods numbered below the horizontal line are 20 minutes each so the increase is rapid.
Patients with IH were higher before and higher after the sugar loads. Their family members were the same, because IH is hereditary.
To date no trial has focused on reduced refined sugar per se, nor will this happen. Trials tend toward monotony, the test of things one by one, and sugar is probably not by itself enough of a factor to alter stone formation. But is has its effects, and there is no reason to provoke spikes of urine calcium loss. They will cause a transient rise in supersaturation. Also, since there is no calcium in the sugar drinks the sudden calcium loss in the urine is probably from bone.
Moderate Protein Intake
The US protein intake recommendations appear to be at the lower end of the commonly mentioned 0.8 – 1 gm/kg/d. In the appendices that quantify intakes values plateau at 0.8 mg/kg/d.
For stone formers, high protein intakes will indeed increase urine calcium, a matter of no dispute.
The blue points on this graph are from selected balance experiments of considerable duration. The red points are from shorter experiments. They are detailed in the original article.
The main point is that as one increments diet protein the protein provokes an acid load via the oxidation of sulfur from methionine and cystine, and thence a change in net acid excretion (NAE). Correlative to that change is an increase in urine calcium.
Some authorities doubt that the acid load per se is essential for the effect. The paired pentagons are from a single but well done experiment in which protein was given with and without sufficient alkali to abolish the acid load yet both protein feedings equally raised urine calcium. Even so, urine calcium rises with protein loads and higher urine calcium can raise stone risk.
Some important authorities have maintained that the acid load from protein adversely affects bone, whereas others of equal calibre deny this. Rather than pursue the debate here, I refer those interested to the linked primary article on this site.
The US diet proposes large amounts of fruits and vegetables that provide more alkali than we presently get, and that alkali may well offset the acid load from protein. Likewise, the diet asks for moderation of diet protein, so the urine calcium effects will be correspondingly moderated.
Urine citrate responds to net acid base balance, and if the moderated protein intake is combined with high organic anion intake from fruits and vegetables urine citrate may well rise. The US proposed diet aims toward a potassium intake of about 112 mEq/d mainly from fruits and vegetables.
These food sources will provide the potassium mainly associated with organic anions that include citrate and, like citrate, are metabolized. Being metabolized in their acid forms,their metabolism produces alkali in the form of bicarbonate will signal the renal citrate transporter to permit more citrate to enter the urine. In other words, the foods will act exactly like potassium citrate given as a medication.
Since our current US potassium intake approximates 60 mEq/d the diet will add about 60 mEq more, or the equivalent of six 10 mEq potassium citrate pills. It is precisely this food phenomenon that is exploited in the common idea of drinking lemonade. But lemonade like all fruit juices can be a source of refined sugars depending on the brand, and lemons vary considerably in citrate content. Likewise lemonade becomes monotonous. An altered diet seems far better,
It is possible that the new US diet guidelines, if enacted, will greatly reduce the need for medicinal potassium citrate, with a corresponding fall in cost and unpleasantness of taking the large pills. Although a trial of such a diet for urine citrate increase, would be desirable, it may never take place there being no obvious financial incentives.
When Should Stone Formers Start the Diet?
The Diet is Recommended for Everyone
At the first stone, of course, as it has general health benefits as well as specific and well supported special kidney stone prevention benefits.
More Stones Predicts Poorer Treatment Response
Another reason is that fragmentary data I have gleaned from the many stone trials suggest that waiting may not be an ideal strategy.
On the vertical axis are the percent relapse rates for the treated arms of the trials, plotted against the average number of pre-treatment stones. The names of the trials correspond to references in the detailed article this figure arises in, which is linked below.
Treated ingle stone formers had an about 10 – 12% relapse rate, ‘Mulit’ refers to my published treatment data that used multiple treatments at once. At best my estimates of pretreatment stone averages are coarse because of limited information in the original studies, so the points may well distribute differently. But the general impression will not likely change with details: More stones seems related to higher relapse despite treatment. The other two ‘Multi’ points are accurate, as is the NaKCit point – details were in the paper.
How Should Stone Formers Pursue the Diet?
Like everyone else in the US, of course. The government website is rich in food portion data and advice about diet change. Our patients can enter it with other Americans and essentially swim with the current.
But stones are a disease we want to treat so it is up to us and those who work with us to help. Jill Harris has already written about this matter, and we hope many more stone experts will begin to consider the reality of how to use the diet effectively.