Marshall L. Stoller, Maxwell V. Meng-Urinary Stone Disease

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246 Moran

from the diet. This complexation to the dietary calcium leaves the anion oxalate readily

available for absorption. Therefore, fatty acids compete with oxalate for intestinal cal-

cium complexation and this phenomenon is capable of being manipulated to decrease

the adverse sequelae of hyperoxaluria. It is known that dietary calcium supplementation

in patients with steatorrhea can reduce intestinal oxalate absorption. Finally, it has been

noted that substituting medium-chain triglycerides for some of the dietary fat can pro-

duce a significant decrease in urinary oxalate excretion (56).

One study suggests that the only measurable difference in stone forming patients with JIB

was higher urinary magnesium excretion. At the University of Minnesota, a primary com-

parison between JIB (n=205) and gastric bypass (n=106) operations between 1975 and 1979

was undertaken. Weight loss was equivalent in each group but 7.1% of those in the JIB group

developed urolithiasis whereas none from the gastric bypass group had a stone. In all, far

fewer serious long-term complications were noted in the gastric bypass group (57).

There are some final lessons important to mention before moving on to the bone

diseases that increase the risk of stone formation. Patients having had a JIB also run the

risk of chronic renal failure secondary to oxalate nephropathy (58). Some have described

this as a reversible phenomenon by conversion of the bypass back to small bowel con-

tinuity (59). Renal failure can also occur secondary to renal amyloidosis, to which long-

term JIB patients are prone (60). It has been described in several investigations that stone

disease occurring with the malabsorption of JIB can spontaneously disappear after

reanastomosis (61). One investigation quantified stone resolution in 86% of patients

having reversal of JIB (62).

IMMOBILIZATION SYNDROMES

Early in the clinical literature of urolithiasis it was documented that humans who are

incapacitated and bed ridden are prone to kidney stones. In 1922, Paul from Toronto

reported on 20 cases of nephrolithiasis occurring in men aged 22–37 (average 28.5) who

developed renal calculi following war wounds. The average time from the wound to the

first symptoms of stones was 17.7 mo. All patients had extensive injuries including

osteomyelitis. Most of these patients were bedridden for prolonged times (63). Pyrah

followed by Pulvertaft both indicated that recumbency appeared to be the critical prob-

lem associated with calcium stone formation, not the degree of trauma (64,65). The

primary event increasing the risk of nephrolithiasis appears to be an acute mobilization

of calcium from the skeletal reserves (66). In some patients, hypercalciuria may be

pronounced (67). In these patients, indwelling Foley catheterization is also common and

subsequent bladder infection makes upper tract seeding commonplace. Recurrent uri-

nary tract infection therefore changes the primary stone risk in these

patients with high urinary pH with the potential for ammonium production to form

struvite stones (68). In current practice with the emphasis on early mobilization and

vigorous rehabilitation, no patients except perhaps those with global trauma (i.e., mul-

tiple organ injured individuals) run this risk. One current investigation on immobiliza-

tion-related hypercalcemia studied five patients (69). In this immobilized group, the

hypercalcemia during 3 mo of observation could be reversed by administration of low-

dose pamidronate (10 mg). In a review by Gordon and Reinstein, a discussion of com-

mon secondary problems associated with the management of complex trauma victims

revealed that urolithiasis was a significant problem. In addition, the cost in managing this

secondary problem was significant (70). It would seem reasonable despite a paucity of

published data, that immobilized patients are at higher risk and maintenance of adequate

Chapter 12 / Associated Systemic Diseases 247

hydration would be a minimal recommendation. The use of bisphosphonates is more

uncertain but indicated if hypercalcemia or urolithiasis develops. A final area of consid-

eration is the effect of physical activity on calcium balance, calcium requirements, and

bone mineral mass. Because of the aging population and the increasing risk of osteoporo-

sis-induced risk of presbic fractures, a significant volume of research is becoming fo-

cused on these issues. In some studies, physical activity has been noted to have a more

profound role in affecting enhanced bone mineral density before puberty (71). The need

for greater research and the potential for physical activity to have an effect on calcium

balance are critical (72).

Space Exploration

A corollary to the immobilization-related hypercalcemia and stone formation sce-

nario is the possibility of placing humans in microgravity activity in outer space. With

the advent of cooperative international endeavors such as the Space Station, plans for a

manned mission to Mars, and the real probability that China might attempt a mission to

the moon, these considerations have assumed more vigorous scientific scrutiny. The

physiologic changes that occur to astronauts exposed to microgravity during space flight

have been increasingly investigated. Body fluid volumes, electrolyte levels, and bone

and muscle undergo significant changes as the body adapts to the weightless environ-

ment. There are both short-term space missions similar to those of Gemini, Apollo, and

Space Shuttle flights and long-term missions such as Shuttle-Mir or Skylab (73). In the

former short-term space missions, negative calcium balance with bone mineral loss and

associated hypercalciuria was noted during Gemini, Apollo, and Space Shuttle missions

(73). Additional alterations include elevated urinary phosphate, decreased fluid intake

secondary to early flight space sickness (associated nausea and vomiting) with resulting

decreased urinary volume and rising formation product (74). Citrate has been shown to

fall during space flight (75). Whitson and coworkers have demonstrated that astronauts

are at greater risk of forming calcium oxalate, calcium phosphate, and uric acid stones.

In follow-up investigations, this same group studied more carefully six male astronauts

with a mean age of 42.5 (range 36–49 yr old) flying Space Shuttle missions of 11–16 d

(75). Urine specimens were collected before, early in the mission (2–4 d), late in the

mission (10–13 d), landing day, and 7–10 d after landing. Nutrition recommendations

were rigorously controlled. Urine volume declined during the early flight but tended to

equilibrate by post flight measurements. Urine output declined by 22–52% during space-

flight. Urine pH had a tendency toward increased acidity (lower pH), which also normal-

ized by 7–10 d post flight. Urinary calcium levels increased for all members with

individual variation being large (38–253 mg/d). Calcium excretion continued to increase

during the flight. Urinary potassium was less during the early flight and urinary citrate

was lower during the flight but neither was statistically different. The relative supersatu-

ration of calcium oxalate, brushite, sodium urate, and uric acid all rose during early space

flight. The calcium oxalate and brushite supersaturations remained statistically elevated

throughout the entire space flight (75).

Whitson and colleagues further speculate that dietary factors of the astronauts also

play a role in risk for urolithiasis formation. Fluid restriction, protein, and calorie inges-

tion all increase urinary calcium and uric acid concentrations while decreasing urinary

citrate. Dietary sodium can also promote renal calculus disease. Diets high in potassium

and magnesium may have beneficial effects (75). Zerwekh reviewed this metabolic data

and generated specific nutritional recommendations for crew members on longer space

248 Moran

missions. Pharmacologic intervention can raise urinary volumes, diminish bone losses,

and prevent reductions in urine pH and citrate levels (76).

There exists one published article suggesting that some cosmonauts have in fact

formed stones during space missions (77,78). Another report from NASA’s Life Sci-

ences Division suggests this to be a real probability (79). In Pak’s earlier investigations

in stone formation by astronauts, he suggested that stone risk factors among applicants

for spaceflight programs were environmental in origin (80).

SARCOIDOSIS

Sarcoidosis is a systemic granulomatous disease of unknown etiology. Hypercalce-

mia varies from 2 to 63% of patients with sarcoidosis. This hypercalcemia has classically

been ascribed to vitamin D formation when it was initially noted in 6 of 11 patients with

this disease (81). Henneman and colleagues noted that the calcium disorder of sarcoido-

sis was similar to vitamin D intoxication (82). About 5 yr following this, the seasonal

influence on serum calcium levels in patients with sarcoidosis led investigators to specu-

late on sunlight’s influence and vitamin D consumption (83). Adams, in 1983, suggested

that alveolar macrophages synthesized 1,25- (OH)

-D

in patients with sarcoidosis show-

ing that the hormone is produced outside of the kidney (84).

In a large series from Italy, Rizzato and colleagues noted that in 618 cases of sarcoi-

dosis, calculi were the presenting symptom in only 1% (85). Stones have been noted to

occur in about 10% of these individuals. Hypercalciuria represents a primary risk for

stone formation (86). Hypercalciuria is three times more common in sarcoid patients

than is hypercalcemia. Current mechanisms proposed for this phenomenon include

absorption secondary to 1,25- (OH)

-D

in the bowel, resorption with sarcoid involve-

ment of the bones with resulting osteopenia, and finally osteoclast-activating factor

perhaps produced by activated inflammatory cells (lymphocytes and monocytes) caus-

ing further bone resorption (87).

Treatment of hypercalcemia in sarcoid patients is typically not necessary because

their serum calcium levels are not critically elevated (often <14 mg/dL). More often

therapy is indicated when hypercalciuria and urolithiasis ensue. Here the clinician should

reduce oral vitamin D, calcium supplements, and dietary calcium consumption. Pushing

oral fluids expands intravascular volume and promotes diuresis, lowering the formation

product of calcium oxalate. To reduce endogenous production of 1,25- (OH)

-D

, cor-

ticosteroids such as prednisone, 20–40 mg/d remains the treatment of choice. Steroid

therapy will reduce serum calcium levels in patients with sarcoidosis in 3–5 d (88). If this

does not occur, the clinician should seek an additional diagnosis that is not secondary to

systemic granulomatous disease. Once controlled, the prednisone dose is tapered over

4–6 wk while monitoring serum and urinary calcium levels. Chloroquine and

hydrochloroquine have also been used in patients refractory or intolerant to corticoster-

oids(89). Ketoconazole is an imidazole antimycotic drug that inhibits cytochrome P450-

dependent enzymes and can reduce 1,25- (OH)

-D

(90). Thiazide diuretics, phosphates,

calcitonin, indomethacin, bisphosphonates, and plicamycin should not be considered in

treating the hypercalcemia or hypercalciuria from sarcoidosis.

Before leaving this discussion mention must be made of granuloma-forming diseases

that mimic sarcoidosis. These include tuberculosis, silicone-induced granulomatosis,

berylliosis, disseminated candidiasis and leprosy. Berylliosis is an environmental chronic

inflammatory disorder typically involving the lung from inhaled insoluble beryllium

Chapter 12 / Associated Systemic Diseases 249

(91). The clinical similarity of these diseases to sarcoidosis is striking but the therapy is

different.

VITAMIN D INTOXICATION

Vitamin D was identified as a fat soluble “factor” found in the diet by Sir Edward

Mellanby in 1919. Ricketts was a recognizable clinical problem at the outset of the 18th

century. Ergosterol or vitamin D

was identified in the 1930s initially in plants, and

Windaus discovered Vitamin D

in the skin of animals in 1936. It seems appropriate to

discuss the clinical entity of vitamin D intoxication following sarcoidosis because the

two clinical pictures are similar. Vitamin D intoxication and sarcoidosis have, in fact,

been likened to the same clinical findings in patients with absorptive hypercalciuria, type

I (92). In health, serum 1,25- (OH)

-D concentrations average about 85 pmol/L. Varia-

tions in dietary calcium across the usual normal range do not normally appear to alter

1,25- (OH)

-D levels. Parathyroid hormone augments renal production as does dietary

phosphate (93). Sunlight exposure, particularly high-energy photons from the ultravio-

let B (UVB) wavelengths between 295 and 305 nm are responsible for vitamin D syn-

thesis in human skin. Most people rely on the cutaneous synthesis of vitamin D as the

principle source of this hormone. Substantial amounts of vitamin D are present in fish

and animal liver, egg yolks, and fish oils. The United States has had a longstanding policy

of fortifying milk with vitamin D

and D

supplements. In other countries breads, cere-

als, and margarine might also contain vitamin D additives (94). A particular concern with

this process in the United States has been outbreaks of vitamin D intoxication, calling

to question the methods used to evaluate the level of vitamin D in both infant formula

and milk (95). Thirteen brands of milk and five brands of infant formula purchased at

random from local supermarkets in five Eastern states were investigated and high-

performance liquid chromatography was used to measure vitamin D. Seven out of the 10

samples of infant formula contained 200% more of vitamin D than stated on the label.

The highest concentration contained 419% more than the label (96).

Vitamin D intoxication is a well known but increasingly rare clinical condition prob-

ably secondary to the use of histamine-2 blockers for the treatment of indigestion and

gastric peptic disease. Patients exposed to excess vitamin D consumption have hyper-

calcemia and, occasionally, metastatic calcification secondary to mobilization of skel-

etal calcium. In addition, patients suffering from this malady also can have significant

hypercalciuria, stone formation, nephrocalcinosis, and, occasionally, acute renal failure

(97). The incidence of this disease has been declining but the outbreaks have been

reported with continued regularity. In one long-term crossover trial of the vitamins D in

6 patients with hypoparathyroidism the relative potencies were as follows (assigning

vitamin D an arbitrary potency of 1): vitamin D

, 1; dihydrotachysterol (DHT), 3; cal-

cifediol, 10; alfacacidol, 750; and calcitriol, 1500 (98). This study points out the two fold

superiority of calcitriol over alfacacidol. In addition, an important subgroup of patients

who are managed with vitamin D therapy is at risk for the development of vitamin D

toxicity, namely those patients that have iatrogenic hypoparathyroidism. Several series

of such patients indicate the significant potential risk of being over-treated with either

alfacacidol or calcitriol and secondary development of toxicity. Several of these series

have patients presenting with stone disease (97,99,100). Figure 4 represents this type of

case in which a surgically hypoparathyroid woman presented with numerous calcium

phosphate renal calculi.

250 Moran

Vitamin D intoxication should be treated aggressively. Hydration and restriction of

dietary supplements is the first line therapy (101). In some cases, the offending vehicle

of vitamin D source is not found (102). In cases of the milk-alkali syndrome the offend-

Fig. 4. This is a 68-yr-old female who is hypoparathyroid treated with Vitamin D (calcitriol) and

calcium carbonate tablets for continued muscle cramps. She presents acutely after having passed

predominately calcium phosphate stones with acute right renal colic. (A) Shown is a 9-mm stone

wedged into her ureteropelvic junction. Behind this stone is literally a hundred smaller stones.

(B) Her intravenous urogram showing hydronephrosis. (C) Percutaneous antegrade coagulum

pyelolithotomy (blue arrow) and grasping lead stone (yellow arrow). (D) Stone analysis and

photograph (80% apatite, 20% whewhellite).

Chapter 12 / Associated Systemic Diseases 251

ing agents are readily identified during the history. In other cases, the offending agent

can be quite exotic as in “enteque seco” an indigenous Argentinian disease from inges-

tion of the leaves of a toxic plant (Solanum malacoxylon) (103). The use of steroids has

classically been the next therapeutic intervention (97,104). Prednisone has been reported

to restore both mean serum calcium levels and mean calcium excretion within days in

patients treated with vitamin D intoxication. Decrease in calcium mobilization from

bone best accounts for the glucocorticoid-mediated amelioration of hypercalcemia in

patients with toxicity (104). The bisphosphonates have also been used to treat hypercal-

cemia in vitamin D toxicity. Pamidronate disodium, a bone resorption inhibitor through

osteoclast mediation, has shown clinical effectiveness in lowering serum calcium levels

within 24 h (105). In a clinical investigation of six patients with hypervitaminosis D, two

were treated with corticosteroids and three were treated with pamidronate. Pamidronate

resulted in the most rapid decline in serum calcium levels with a more delayed response

in the steroid treated group. These authors conclude that the bisphosphonates have a role

in managing these patients (106). But in refractory cases and chronic toxemia, at least

one report suggests that the bisphosphonates can actually stimulate a rise in serum

1,25-(OH)

D. These investigators speculate that possible factors predicting failure are

body weight loss, hypoproteinemia, and phosphate depletion which can promote a

bisphosphonte to stimulate PTH-independent production of 1,25-(OH)

D (100).

BONE DENSITY

The previous discussions should lead the reader to understand the complexity of

categorizing patients with urolithiasis. In one paper, Pak and colleagues have identified

14 metabolic causes of calcium stone formation (107). In other series, many if not most

patients with calcium stones have more than one risk factor for stone formation. It should

therefore be no great surprise that the coexistence of bone loss with the presence of

calcium stone formation is controversial. The different causes of stone formation, par-

ticularly the hypercalciurias, not only vary widely from patient-to-patient, but signifi-

cant variability of hypercalciuria can also be noted within the same patient from

day-to-day. Fournier and colleagues point out that different densitometry methods

employed in various published series do not always use standardized parameters and

biochemical markers of bone remodeling.

Calcium is the most abundant mineral in the human body, accounting for 1.5–2% of

an adult’s body weight. Ninety nine percent of the body’s calcium is found in bones and

teeth complexed with phosphate as hydroxyapatite. The remaining calcium is used

throughout the body for the biochemical processes necessary for life. Bone is therefore

an important reservoir for calcium and constantly being turned over. Throughout the

human life-cycle, there are three phases of bone growth and development. From birth

to about age 20 the bones are in an active growth phase. Here bones are shaped and

molded. This phase is overlapped by a phase of peak bone mass development from ages

12 to 40. Between the ages of 30 and 40, bone resorption begins resulting in a net loss

of bone (108). Bone mass itself is influenced in turn by many factors including physical

activity, gonadal hormones and nutrition (109). People of all ages and with a wide

variety of co-morbid medical problems such as urolithiasis need dietary calcium to

maintain positive calcium balance. The Committee on Dietary Allowances of the Food

and Nutrition Board, National Academy of Sciences periodically evaluates research

data and furnishes guidelines called Recommended Dietary Allowances (RDAs). Pub-

lished RDAs for calcium are shown in evolution over time in Table 1. The 1994 Con-

252 Moran

sensus Development Conference resolved that contemporary calcium requirement by

both men and women are too low for optimal bone health (110).

Various bone densitometry methods have been employed to study bone loss in

patients with calcium urolithiasis. Fournier and colleagues tabulated the world’s litera-

ture to state that calcium stone formation adversely effects bone mineral density (111).

The exceptions are those patients with absorptive hypercalciuria type I. Patients with

dietary calcium-dependent hypercalciuria (type I) do not have more progressive bone

mineral loss than age-matched controls. The patients with absorptive hypercalciuria

and phosphate leak (type III) are the most likely to have bone mineral loss. The familial

aggregation of this particular type of stone former has prompted numerous genetic

investigations regarding the etiology of this disease. It appears that the heterozygous

mutations of NPT 2a gene, a sodium-phosphate cotransporter, are the culprit (112).

As evidence mounts as to the potential for long-term sequelae of bone mineral loss in

calcium stone formers and the potential for a protective effect by dietary calcium intake,

prudent recommendations suggest not limiting calcium intake (113,114,). In addition to

potential deleterious effects on the bone, dietary restriction of calcium can result in

increased oxalate absorption (113). Loss of bone mineral density is a significant consid-

eration because of the prevalence of osteoporosis, 25 million people in the United States,

and the fact that it is the major underlying cause of bone fractures in postmenopausal

women and the elderly. Surveys have revealed that 1.5 million fractures annually in the

United States produce a $10 billion expenditure for our healthcare system (110). Com-

pared to the 1986 fiscal impact of dealing with stone patients surgically, $2 billion, the

impact in the United States alone is staggering (115).

CONCLUSIONS

It is always nice to bring the discussion full circle. In the introduction, the systemic

nature of the diseases of the bowel and bone and their relationship to stone disease was

stated. These are generally thought of as complex clinical scenarios even as far as stone

disease goes. There is not a single best medical modality for every patient suffering from

any of the disorders of the bowel or bone presented. As is often the case, each patient is

unique and treatment should be individualized.

Table 1

Evolving Estimates of Calcium Intake (milligrams)

Age 1984 RDA 1989 RDA NIH 1994 1997 DRI

0–0.5 yr 360 400

0.5–1 yr 540 600

1–5 yr 800 800 800 500/800

6–10 yr 800 800 800–1200 800/1300

11–18 yr 1200 1200 1200–1500 1300/1000

19–24 yr 800 1200 1200–1500 1300/1000

25–65 yr 800 800 1000 1000/1200

>65 yr 800 800 1500 1200

Female over 50 not on estrogens 1500

Pregnant/ lactating 1600 1200 1200–1500 1000

Chapter 12 / Associated Systemic Diseases 253

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