A large but fit man in his fifties has had kidney stones, for the first time 7 – 8 years ago and the last time 4 months ago. In between he had 6 SWL and one URS procedure as well as perhaps over a hundred stone passage events. Looking back, he may have had a first attack as long as 12 year ago, but that is uncertain. At the onset 7 -8 years ago he was told his CT showed ‘staghorn’ stones bilaterally. Four of his 6 SWL procedures were for these staghorn stones. His stones were said to contain a mixture of uric acid and calcium but I had no analysis reports. He was given potassium citrate 10 mEq three times a day but for how long was unclear – perhaps several years. He did not believe the treatment had improved things. No images were available when I saw him.
His brother has had kidney stones, but not his father, mother, two sisters, or four young adult children. Apart from an ACE for hypertension he has no significant medical history.
His occupation for the prior 37 years, though complex, did not generally lead to dehydration. But there was a period of 10 years during which he did skilled construction work instead, ending 20 years ago before his stones were discovered. This was very dehydrating work, in his opinion.
His breakfast is a veggie omelette; he used to use considerable spinach but stopped it 5 -6 years ago. Lunch is salad and a sandwich, and supper a commonplace US cuisine except very high in meats. He avoids dairy products because of stones. He used to eat a lot of chocolate but moderated this habit a few years ago.
His blood pressure was 155/83. His labs were collected while taking the potassium citrate.
Three serums collected fasting between 7 and 9 am were normal in our laboratory for calcium, phosphate, creatinine, uric acid, magnesium, sodium, potassium, chloride, and total CO2. Dates were 0, 7, and 11 days apart. Three corresponding 24 hour urines were collected and analysed in our laboratory.
All values apart from SS are mg/24hr, mEq/24hr Na, SO4 and NH4, or l/24 hr, VOL.
I have proposed what I have called the fundamental premise of stone prevention, and here is an actual person. How does it work in real life?
The premise is this: The urine supersaturations of an active stone former are too high in relation to the crystals in stones forming. Lower them.
Application to This Patient
Is my patient an active stone former?
He would say so. He came for prevention of stones because he has had many procedures and continuous passage of fragments that are disturbing his very life. They number – as I quoted from him – in the hundreds.
I would say I am not sure. He began with the discovery of bilateral large stones, perhaps staghorn shaped stones, which were treated with shock wave lithotripsy four times, then two more times presumably because of retained fragments. Are his many events newly forming stones or merely passage of the many fragments one might get from 6 SWL attempts at disrupting staghorn stones? I could not tell unless I had his CT scans in hand and could trace the stone burden over time along with his passage events, and I told him that. So whether or not he has active stones is unknown.
Do we know the crystals in stones forming?
Hardly. I do not know the crystals in any of the materials thus far, but in fact I tend to trust his comments that he had been told that they contain uric acid and calcium – he is very smart and well organized. Even if I do, these elements may not be in stones forming but in stones formed long ago, perhaps when he was in a very dehydrating occupation.
Do we know his urine supersaturations?
We do and we do not. We have the numbers, they are in the table above – SS values. But what do they mean? They are recent – near when I saw him, but his stones may have remote or recent origins, and I cannot know right now which is which. Likewise, the urines were collected while he was taking potassium citrate, and the drug was begun after the discovery of his stones. So he formed the large stones while not on this drug. His continued passage events have been despite the drug – which he says has not been of material benefit – and this could be because supersaturations remain too high or because he is passing old fragments for which the drug would be irrelevant.
I do know the urine samples were not collected on weekends but during his working week – I know the real dates which I cannot share with you, and have a calendar. So they probably represent life as lived for him. He also says they do. If indeed he has been forming recent stones then his supersaturations as measured are indeed too high in relation to the crystals in those recent stones, but do we have recent stones to assay?
Although I was paralysed for lack of proper information, his labs were and are interpretable, and lead somewhere if not exactly to where we want to go.
The supersaturations themselves are not interpretable, as any given value above 1 could support crystallization. For uric acid and CaP this statement is very accurate in that the upper limits of metastability – the supersaturation at which crystallization begins – tend to be close to the supersaturation and supersaturation itself, in normals, below 1. For CaOx the upper limits of metastability run to at least 3 or 4, tend to be proportional to supersaturation, and supersaturations themselves are usually far above 1. We need to know the stone crystals and whether stones are active before we can really interpret the supersaturations.
This case then highlights an important point of practice. It is futile to look for ‘normal ranges’ for supersaturations, as normal and stone forming patients have overlapping values – or can. Unfortunately in his brilliant studies of urine stone risk, Curhan did not publish supersaturations, so we cannot link them stone stone risk in general.
Judging consistency of collection from the urine creatinine values the first of the three urine collections is under collected, so we must allow for that in going further.
The urine volumes are just adequate to reduce risk – 2.25 – 2.5 l/d would be better.
Urine calcium is eye catching, being far above the risk limit of 200 – 299 mg/d. Almost certainly it is idiopathic hypercalciuria (IH), and his brother may well have the same. Some of his four children, likewise. We know at least four ways to increase urine calcium in this condition – sodium, protein, calcium, and sugar loads. Of these, he has the first two, does not favor sweets, and eats a barren low calcium diet.
High sodium intake drives urine calcium upward at a higher slope in IH than in normal people, and his sodium intakes as judged by what is in his urine are immense. He is large – 159 kg, and not all fat – urine creatinine per kg body weight is 15, but his urine volume is not remarkably scaled to his weight.
So lots of sodium and therefore calcium in his urine translate into considerable urine calcium concentrations – 3.7 – 6 mmol/l. Large people are at a peculiar disadvantage, are they not? Being large means diet is scaled up but does not mean urine volume is scaled the same way because non renal water losses can be larger in large people and desire for water is not at all scaled to size.
He has high blood pressure and is being treated with an ACE. Even so my measurement shows poor control. He does not do home blood pressures. Reducing sodium intake is recognized as way of lowering blood pressure.
His diet is low in calcium – no dairy products. IH easily produces negative bone balances when diet calcium is low, and therefore he is at risk for bone mineral loss and later in life fractures.
His diet is and is not high in protein. His urine sulfate (SO4) is very high and sulfate arises from oxidation of sulfur on methionine and cystine from diet protein, but his PCR – protein catabolic rate – is only 0.9 – 1.2 gm/kg body weight. For him it is not so much protein intake on a body size basis. Protein will increase urine calcium, but the body of opinion is that it does not deplete bone mineral stones – no links to the site because I have not written a proper article on this topic yet. There are no low protein diet trials for prevention. The one major diet trial was of a 93 gm protein diet, but altered to 40% was of plant and dairy origin. So I said nothing about his diet protein.
His urine oxalate varied from above the risk limit to rather high but I had no interest in it because I planned to increase his diet calcium by a large margin and know that low calcium diet will often raise urine oxalate excretion. Low oxalate diet may ultimately be useful but only when high diet calcium has been in place.
His urine uric acid excretion is very high no doubt because of his high intake of purines in the large portions of meat. High urine uric acid was proposed as a possible cause of calcium oxalate stones but epidemiological data do not support that idea. Urine uric acid excretion has little role in uric acid stones, which are controlled by urine pH. It is for this reason that his potassium citrate would be ideal treatment for that part of his stone disease – assuming analyses confirm his history. Allopurinol is effective in preventing calcium oxalate stones but given his uncertainties and far better treatment alternatives I gave the drug no thought.
His urine ammonium excretion is very low, despite his high urine sulfate. This is because of his alkali therapy. Acid loads promote ammonia production and excretion, and their neutralization by potassium citrate will reverse this and lower ammonia excretion.
CLINICAL SUMMARY AND TREATMENT
This first visit was not unusual in my practice. Although he was referred and has very serious problems with all of his stone events he did not know – was not told – what he needed to bring. Our one person who speaks with every patient before coming is ‘programmed’ to mention what we need, and we have handouts, but even so missing information is commonplace. I have written pretty good instructions for patients, and maybe we need to use them instead of what we do now.
The main things that were obvious from the visit were his idiopathic hypercalciuria complicated by low calcium diet, and massive sodium and protein intakes, the latter not inappropriate to his size. Lore has it that stone formers are larger on average than those without stones and he points to one reason why – urine volume does not scale to size, diet does. Since potassium citrate can lower urine calcium, the magnitude of the losses may have been greater when he made his stones. The combination of low calcium and high sodium diet bode poorly for long term bone health and the sodium loading surely hampers blood pressure control. Although his urine pH was not in the usual low range of uric acid stone formers, he was nevertheless supersaturated with that phase because of his combination of modest volume and high urine uric acid excretion.
Treatment and Follow up
For all of these reasons, and in the absence of a proper basis for stone prevention, I strongly suggested an extreme moderation of his diet sodium intake – to below 2000 mg. Presently the CDC and AHA guidelines call 1,500 mg of diet sodium optimal for the US population. Likewise, I suggested a high calcium intake – from foods – of 1,000 mg. I left his potassium citrate in place because I did not know what were his stone crystals. Even with the drug he has a considerable uric acid supersaturation which I hoped more fluids would reverse. I did not increase the dose of the agent, pending those results. Finally, I suggested an increase of fluids to achieve another half liter of daily urine volume.
I will see him again, and when I do I will add to this case report.