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Chapter 12 / Associated Systemic Diseases 237

237

From: Current Clinical Urology, Urinary Stone Disease:

A Practical Guide to Medical and Surgical Management

Edited by: M. L. Stoller and M. V. Meng © Humana Press Inc., Totowa, NJ

Associated Systemic Diseases

Bowel and Bones

Michael E. Moran, MD

CONTENTS

INTRODUCTION

INFLAMMATORY BOWEL DISEASE

JEJUNOILEAL BYPASS SURGERY

IMMOBILIZATION SYNDROMES

SARCOIDOSIS

VITAMIN D INTOXICATION

BONE DENSITY

CONCLUSIONS

REFERENCES

Key Words: Nephrolithiasis; intestine; bone metabolism; vitamin D.

INTRODUCTION

Stone diseases have had known affinities to other systemic diseases for a large portion

of written medical history. The first known stone to afflict a human was probably a

metabolic product of uric acid metabolism in a boy of the predynastic Egyptian period,

almost 7000 years ago. Galen (131–201

AD) proposed the concept that etiologic aspects

of stone formation include heredity, climatic, and nutritional factors. Van Helmont

(1577–1644) noted that kidney stones were products of undesirable minerals within the

urine. Thomas Sydenham (1624–1689) suffered from gout and recurrent urolithiasis. He

describes his own disease process with clarity and proposed three hypotheses for the

pathophysiology of stone disease and other systemic illnesses. On his disquisition into

gout he states:

“…the gout breeds the stone in the kidneys in many subjects, either (1) because the

patient is obliged to lie long on his back, or (2) because the secretory organs have

238 Moran

ceased performing their proper functions; else (3) because the stone is formed from a

part of the same morbific matter…” (1).

Urolithiasis induced by systemic diseases such as inflammatory bowel disease is

complicated and the management of these patients is difficult. The patients tend to be ill

from other comorbid problems and the stone(s) must be dealt with in addition to other

troubles. The long term risk for bone depletion comes from complex interactions by

stimulation of vitamin D, parathyroid hormone, and calcium regulation. Bone resorption

could be a final common pathway in these systemic diseases with calcium stone forma-

tion.

INFLAMMATORY BOWEL DISEASE

A correlation between stone formation with bowel disease, specifically chronic diar-

rheal syndromes has been known since Lindahl and Bargen published in 1941 (2).

Chronic diarrheal illnesses have been well investigated since the 1940s and the preva-

lence of stone disease has been reported. Each of the types of inflammatory bowel

disease has a relative impact on stone formation. Worcester, in an extensive review of

published series has tabulated the prevalence of stones for patients with Crohn’s disease,

ulcerative colitis, and in those patients requiring bowel and/or ileal resections (3). There

are many complicating issues in these patients including duration of disease, hydration,

use of medications such as steroids and sulfasalazine, and disease-specific problems that

directly impinge on the urinary tract (such as retroperitoneal abscess, ureteral obstruc-

tion, and vesicoenteric fistulae). Stone prevalence in Crohn’s disease is about 6.3%

(range 3–8%). In ulcerative colitis the rate is 4.4% (range 3–10%). Worcester found that

these high risk patients have a threefold increase in stone formation by having bowel

surgery (3–7). In a modern large review of Crohn’s disease patients, a survey of 7210

patients in Germany found a 19.6% return rate of questionnaires (1414 patients). Of

these, it was noted that 17.2% had a urinary calculus dwarfing previous expectations (4).

Stone Type

Most stones associated with inflammatory bowel disease are calcium oxalate. It has

been estimated that 69–90% of stones associated with chronic diarrheal syndromes are

calcium oxalate (7–12). The incidence of uric acid stones is significantly higher than

the normal population (5–10%), occurring in 20–30% of these patients. Surgery alters

the relative distribution, and the presence of an ileostomy adversely affects the stone

prevalence as well as the number of patients that form uric acid stones (as high as 50%).

Other stones can be manifest in these complex patients. Struvite (magnesium ammo-

nium phosphate hexahydrate) or infectious stones in the urinary tract, although infre-

quent, are associated with obstructive changes. Briefly highlighted previously has been

the predisposition in patients with inflammatory bowel disease toward hydronephrosis.

Multiple recurrent urinary tract infections in patients with known inflammatory bowel

disease should be suspect for not only fistulae but also struvite stone formation. Another

rare type of stone associated with chronic diarrhea, especially in patients with laxative

abuse, are ammonium urate stones (13). These stones are typically found as endemic

bladder stones in developing countries and in impoverished regions. They are more

common in patients with chronic diarrhea, especially accompanied by laxative abuse

and in those patients with ileocolonic resection. Ammonium urate stones are typically

lucent but can be mixed with calcium oxalate, calcium phosphate, and struvite. A final

Chapter 12 / Associated Systemic Diseases 239

rare stone type deserves mention—acetylsulfapyradine stones. Sulfasalazine is a sul-

fonamide that has rarely been reported to cause crystalluria, stone formation, and acute

renal failure (14). These stones are also lucent and typically present in patients that are

elderly, are under long-standing treatment with sulfasalazine, and have accompanying

dehydration. The stone is usually a yellowish-brown color with a fine granular surface

(15). Acetylsulfapyridine is a metabolite of the drug sulfasalazine, which is metabolized

by intestinal flora into sulfapyridine and 5-aminosalicylic acid. These are absorbed and

acetylated by the liver before excretion in the urine. Acetylsulfapyridine is less soluble

in acidic urine and can be treated by urinary alkalinization. The drug sulfasalazine should

be discontinued and/or replaced with mesalamine (5-aminosalicylic acid) if these stones

occur (14).

Pathogenesis

The etiology of stone formation in patients with chronic diarrheal syndromes is

multifactorial and complex. Numerous investigations have been conducted in patients

and animal models. Of the inflammatory bowel disease patients, Crohn’s disease and

ulcerative colitis have been rigorously investigated. Both have tendencies toward chronic

hypovolemia with subsequent low urinary volumes (<1.2 L/urine output/24 h). Both

groups of patients tend to have chronic acid urine (pH <5.5). Both groups also tend to

have lower urinary magnesium and citrate levels, which are thought to be important

inhibitors of calcium oxalate stone formation in comparison to control groups and even

compared to other stone forming patients.

A primary additional risk factor in these subgroups is ileal involvement by the

primary disease, more common in Crohn’s disease patients and in patients undergoing

surgical interventions with small and large bowel resections. Ileal involvement by

these disease processes promotes more diarrhea, greater loss of water and steatorrhea,

which can complicate further the physiologic malabsorption leading to hyperoxaluria

and hypocalciuria. All of these processes adversely alter the risk of urolithiasis in these

patients. Add to that ileal and colonic resection and loss of greater lengths of small

bowel and stone rates climb proportionally in these patients. In addition, the bowel

flora itself have been altered by chronic antibiotic exposure. A gram-negative anaer-

obe, Oxalobacter formigenes, has been isolated from the feces of several animals and

humans. This bacteria uses intestinal oxalate as a substrate for its metabolism and

therefore may be important for the regulation of intestinal absorption of oxalate (16).

An overview of the pathophysiology of the intestinal derangements enhancing the

lithogenic potential in these patients is necessary.

Ulcerative colitis was the initial inflammatory bowel disease (IBD) reported to have

an increased incidence of urolithiasis from the Mayo Clinic (17). Sixteen patients (eight

males and eight females) followed for a prolonged period developed clinically signifi-

cant urolithiasis (most requiring open surgical intervention). This same group followed-

up on their original observations with a separate series clearly indicating that ileostomy

diversion in these patients enhanced the risk of stone formation appreciably (2). The risk

factors in patients with chronic bowel disease are best evaluated by stone type.

As mentioned previously, uric acid stones are more common in patients with IBD than

in the general population. The urine of these patients is low volume secondary to the

gastrointestinal loss. Add an ileostomy and volume loss is even more pronounced. The

average loss from pooled investigations of patients with an ileostomy is between 500 and

700 mL/d (18,19). More than 90% of ileostomy fluid loss is water. Compared to the

240 Moran

normal adult loss in feces of less than 150 mL per day, this loss is significant (19). These

same studies indicate that urine output is typically below 1 L/d.

In more detailed investigations, Clarke and colleagues noted total body water was

depleted by 11% in patients with an ileostomy (20). Additionally, sodium is lost account-

ing for a 7% decrease as well as significantly lowered urinary sodium concentrations

(21). Despite evidence for sodium conservation in these patients, plasma aldosterone

concentrations have been controversial in most series (22,23). Kennedy and coworkers

noted in a group of 39 ileostomists with proctocolectomy and less than 10 cm of terminal

ileum resected plus an ileostomy showed a significant rise in mean plasma aldosterone.

Also, the plasma renin activity was increased, but not markedly so. They speculated that

ileum adaptation might explain differences between studies (18).

The second contributing factor increasing the risk of uric acid stone formation in

patients with IBD is acidic urine. Because uric acid is a weak acid with its first dissociable

hydrogen ion with a pKa of 5.35, the urine’s pH plays a significant role in stone risk. At

a urine pH of 5, only approx 100 mg/L of uric acid can be held in solution. Hydrogen ion

excretion is known to be increased in IBD patients and markedly so in those with an

ileostomy (23). Unlike most uric acid stone formers without IBD, these patients have

increased ammonium excretion in addition to titrateable acid. This is thought to be

secondary to intestinal loss of bicarbonate. This again is intensified in patients with

active ileal disease and with ileostomies because the pH of ileal fluid is 7.0 (18).

There has been extensive investigation indicating that purine metabolism is not gen-

erally affected by IBD. The net excretion of uric acid is therefore not markedly higher

than in normal patients. The water loss with subsequent lower urinary volume in addition

to the lower pH drives the solubility product of uric acid into the high risk range. Ileo-

stomy patients excrete significantly more urine supersaturated with uric acid than con-

trols and even more than most patients with uric acid stone formation without IBD (24).

The second and more common stone is calcium oxalate. In this association, far more

complex physical chemistry is associated with the heightened risk of urolithiasis. The

low urine volumes and fixed, acidic pH still apply and although extensively investigated

will not be reiterated. The average daily excretion of both calcium and oxalate do not

appear to be significantly enhanced in patients with IBD with or without an ileostomy.

There are occasional series that note a rise in oxaluria following an ileostomy. Bambach

and others have measured significant calcium oxalate and calcium phosphate supersatu-

rations in patients with ileostomies. Volume appears to be the overwhelming risk factor

according to these investigations. The exception to this observation is when larger seg-

ments of small bowel become involved and longer segments of bowel are removed. At

this point the association with steatorrhea and enteric hyperoxaluria become critical.

Figure 1 represents a case with this clinical scenario. After having undergone several

abdominal explorations the patient is left with only 20 cm of small bowel and suffers

from short gut syndrome. This is discussed in detail in the section on jejunoileal bypass.

Inhibitors might be the other significantly measurable abnormality promoting cal-

cium-stone formation in these patients. Citrate is a major urinary inhibitor known to

bind with calcium, decreasing urinary supersaturation (25). In one large study of 66

patients with IBD, citrate urinary excretion in both ulcerative colitis and Crohn’s dis-

ease were low before any bowel surgery was performed. Following any type of surgical

resection, the urinary citrate levels were decreased further (p < 0.0001) (26). Compared

to citrate levels in healthy controls (654.0 ± 297 mg/24 h), ulcerative colitis patients

before surgery have only 386.0 ± 207 mg citrate/d (p < 0.01). Following surgical resec-

Chapter 12 / Associated Systemic Diseases 241

tion this dropped further to 231.2 ± 161 mg citrate/d (p < 0.0001) (26). In Crohn’s

disease patients before surgery the urinary citrate was 338.0 ± 233 mg/d (p < 0.001) and

following surgery was noted to fall further to 215.0 ± 253 mg/d (p < 0.001). These

authors further quantified stone forming risk in these patients by measuring crystalluria.

In ulcerative colitis patients, crystalluria incidence was 30% with 93% being calcium

oxalate dihydrate and 7% uric acid following surgical intervention. In Crohn’s disease

patients, crystalluria was significantly present before any surgical intervention (30%)

and decreased marginally following surgery to 23.5% (26).

Magnesium is another urinary inhibitor of calcium oxalate precipitation. Magne-

sium losses accrue secondary to loss in diarrheal stool. Systemic acidosis can lead to

decreased urinary excretion and there may be some degree of gastrointestinal malab-

sorption of magnesium (27). Using the data from Caudarella, urinary magnesium in

healthy controls was 87.1 ± 35 mg/d compared to 82.6 ± 48 (p < 0.005) before surgery

and 46.5 ± 17 (p < 0.001) following surgery in patients with ulcerative colitis. The

Crohn’s disease patient’s urinary magnesium values were before surgery 54.4 ± 26 mg/

d (p < 0.005) and 35.2 ± 25.4 (p < 0.05) following bowel resection (26).

It has also been speculated that the increased risk of calcium oxalate stone formation

of inflammatory bowel disease patients might be attributed to the high uric acid super-

saturation. The model of heterogeneous nucleation would allow for the precipitation of

calcium oxalate crystals on the readily available lattice of the uric acid crystals. No

matter which mechanism is of greatest significance, these patients do represent a com-

plex therapeutic dilemma.

Treatment

Having just outlined the primary pathophysiologic mechanisms of stone formation,

a multifaceted method to medically treat these patients is now possible. As with prophy-

Fig. 1. A 45-yr-old white female presents with an incidentally found renal calculus at follow-up

of her Crohn’s disease. She has had numerous small bowel resections and currently has only

20 cm of small intestine remaining. (A) Scout film showing a 1.4 cm opaque midpole stone.

(B) Intravenous urogram demonstrating no obstruction of the upper tracts.

242 Moran

lactic therapy in patients with “idiopathic” calcium stone disease, there exists very little

data on the success of these therapies.

The most cost effective therapy is probably rehydration. These patients need to be

encouraged to consume more fluids. The goal of getting urinary volumes to 2 or 2.5 L

daily is critical. One effective method is encouraging these patients to consume small

volumes more often. Patients should be encouraged to drink enough fluids so as to arise

during sleep to urinate so that more fluid can be consumed during the sleep cycle when

maximal urinary concentration is likely to occur. Although water is the classic fluid-of-

choice, there are reports that lemonade and orange juice are excellent fluids for both uric

acid and calcium stone formers (28,29). Citrus fruits are outstanding sources of dietary

citrate and magnesium.

Chronic acidosis can likewise be treated. Sodium depletion can be corrected by the

administration of oral sodium bicarbonate (30). Excess sodium loading can be detrimen-

tal to both uric acid and calcium stone prevention. Potassium-containing oral alkalizing

agents have therefore assumed a greater role in the armamentarium for prophylaxis.

Potassium citrate at doses from 30 to 80 meq/24 h increased urine pH from 5.3 to 6.19

and reduced new stone formation rate from 1.2 to 0.01 stones per year in patients with

uric acid stone disease. Unfortunately, potassium citrate is associated with a large num-

ber of side effects, predominately gastrointestinal upset and the consequence to patients

with IBD is not known. Compliance in the general stone population is known to be poor

in long-term follow-up investigations. In one such study, Tiselius from Sweden noted

that 62% of patients responding to a questionnaire reported compliance with citrate

therapy (31). In an intermediate follow-up study, Lee reviewed 493 patients with a

34.2% stone recurrence rate and only 49.3% remained on medical prophylaxis longer

than 12 mo (32). An additional study on patients with surgically active uric acid stones

demonstrated that all patients were either partially or totally noncompliant with oral

alkaline therapy for a variety of reasons including lack of physician-related information,

concerns regarding possible side effects and medical neglect (33). Drop out rates might

also be augmented by the inconvenience of multiple, timed, daily dosings necessary with

potassium citrate (34).

Magnesium depletion remains the other identified parameter that can be treated in

patients with inflammatory bowel disease. Magnesium, like citrate has gastrointestinal

side effects ranging from 17 to 45% with exacerbation of diarrhea being foremost.

Dietary methods of delivering magnesium were mentioned earlier by citrus fruit inges-

tion (28). Another study confirms the dietary efficacy demonstrating that navel oranges,

Valencia oranges, and grapefruit all represent significant sources of magnesium and

vitamin B6 (35). Confirmatory data exist for vitamin B6-magnesium supplements in

recurrent stone formers both clinically and in experimental models (36,37). Vitamin B6

might augment the magnesium supplementation by acting in the liver to up-regulate

enzymatic oxalate metabolism. The most recent possible therapeutic agent of interest

in IBD is the combination of potassium-magnesium citrate (38). The ingestion of a meal

with concurrent ingestion of citrate appears to decrease the gastrointestinal side effects

without sacrifice of the physiologic or physicochemical actions (38). Potassium-mag-

nesium citrate is capable of effectively correcting the magnesium, citrate, and potas-

sium wasting effects of hydrochlorothiazide 50 mg/d in 242 investigational subjects

(39). In follow-up studies, this same group studied the effect of varying the dose of

potassium-magnesium citrate to correct hypokalemia and magnesium loss in thiazide-

treated patients (40). Three dosages of potassium-magnesium citrate were randomized

Chapter 12 / Associated Systemic Diseases 243

for 3 wk: four tablets (24 mEq K/12 mEq Mg/36 mEq citrate/d), 7 tablets (49 mEq K/

24.5 mEq Mg/73.5 mEq citrate/d), and 10 tablets ( 70 mEq K/35 meq Mg/105 mEq

citrate/d). All three doses resulted in increased potassium serum concentrations. Only

the two higher doses resulted in significant elevations in serum magnesium. All three

doses significantly increased urinary pH and citrate levels (40). Another interesting drug

used in the bowel preparation for radiologic evaluation is sodium picosulphate-magne-

sium citrate (Picolax). It has not been investigated as a supplement to reduce stone

forming risks (41).

Much clinical work remains to understand these complex patients with inflammatory

bowel disease and stone formation. Both uric acid and calcium stone formation is pos-

sible at rates that exceed some of the “idiopathic” stone formers. One particular method

of prophylaxis includes performing a total proctocolectomy in patients with ulcerative

colitis, a mucosectomy of the anus with a continent ileal pull through and formation of

a J-pouch reservoir. In one such nonrandomized comparative investigation, 13 patients

with ulcerative colitis and an ileostomy were compared to 15 patients with J-pouches.

The formation of the J-pouch requires more mobilization of the small bowel and as such,

the patients were noted to have higher urinary concentrations of oxalate than those with

ileostomy. Otherwise, the urinary physical chemistry appears to be quite similar to the

ileostomy patients. The patients in both groups have lower urinary volumes, and subse-

quently higher concentrations of calcium, oxalate, and uric acid compared to control

patients. Both groups likewise, had similarly lowered urinary pH (42). There are thus

few differences in the urinary physiology by modern methods of proctocolectomy and

continent fecal diversion, and the long-term stone rates might still be similar to those of

the ileostomy era (43). The thought here is to minimize fluid loss by making a reservoir

that will hold the ileal contents longer and eliminating the incontinent ileostomy. Studies

on stone reduction have demonstrated that stone risk is reduced but still higher than in

the nonoperated patients. Figure 2 is a case with a left-sided, asymptomatic calcium

oxalate stone currently stable metabolically on magnesium and vitamin B6 plus potas-

sium citrate therapy.

JEJUNOILEAL BYPASS SURGERY

Small bowel resection and bypass have long been associated with urolithiasis. The

most common and best investigated groups are obese patients undergoing jejunoileal

bypass (JIB) (9–11). Other disease entities must also be considered as the pathophysi-

ology is similar. Patients with Crohn’s disease can have extensive involvement of not

only the ileum, but other areas in the small bowel resulting in recurrent small-bowel

resections. Infants can lose large sections of their small bowel secondary to vascular

compromise and develop short gut syndromes (44). Celiac sprue can compromise

normal small-bowel function resulting in malabsorption syndromes, steathorrea, and

chronic diarrhea (45). Pancreatic and biliary obstruction or insufficiency can have

profound effects on small-bowel function and result in steatorrhea and malabsorption

syndromes. Other diseases can effect bowel function and lead to increased risk of

urolithiasis including Hirsch sprung’s disease. The mechanism from one review sug-

gests that chronic constipation and enteric resections might be important to the 1.32%

of stone patients seen in a group of 302 patients (46). JIB surgery has been virtually

reduced to a footnote in surgery, as other methods of bariatric surgery have come to

the forefront of surgical practice, particularly laparoscopic techniques (47–49). The

244 Moran

epilogue to JIB surgery remains of significant interest to students of stone disease

because of the complex interactions between the bowel’s absorptive and adaptive

capacity and the relationship to diet, bone physiology, and stone formation (50). These

patients generally have normal gastrointestinal function before these procedures and

the primary disruption and malabsorption that appears postoperatively has been exten-

sively investigated.

JIB became a popular bariatric therapy for two decades, the 1970s and 1980s. There

were two methods widely practiced, the Scott and the Payne anastomoses (51). These

Fig. 2. This is a 64-yr-old white male with longstanding ulcerative colitis. He is status post total

proctocolectomy with mucosectomy and a J-pouch. (A) Scout film showing small bilateral stones

in clusters, left full KUB and right close tomographic view. (B) Intravenous urogram showing

full details of unobstructed upper tracts (arrows pointing to the staple lines of his small bowel

reconfiguration.

Chapter 12 / Associated Systemic Diseases 245

procedures included a 30–40-cm portion of the proximal jejunum that was attached to

a 10–20-cm piece of distal ileum. A third operation was devised by Eriksson to minimize

the metabolic consequences of JIB, the biliointestinal bypass thought to help by main-

taining the enterohepatic circulation of bile and bile salts (52). Individuals who under-

went JIB have a high incidence of hyperoxaluria (60–88 %). The source of hyperoxaluria

comes from intestinal oxalate absorption. Normally, humans absorb less than 20% of an

administered dose of oxalate. If oxalate ingestion occurs with food, this absorption can

be further reduced to <10%. In patients with small bowel resection (<50 cm) or JIB,

absorption may range from 35% to <50%. Stone formation in JIB patients ranges from

8 to 40% (53). The most common stone type is calcium oxalate, as expected (80–100%).

Many patients begin to form stones quickly, within months after having the bypass

procedure, but as many as 50% will not form their first stone until 3 yr postoperatively

and there have been anecdotal reports of stones beginning 10 yr following JIB. The

identification of the relationship of calcium oxalate stone formation led to a substantial

number of investigations in these patients to better understand the complex interactions

occurring in these individuals. In one investigation, all three types of JIB produced

enteric hyperoxaluria; Paynes’ end-to-side resulted in 863 ± 58 µmol oxalate/24 h,

Scott’s end-to-end produced 869 ± 65, and Eriksson’s biliointestinal shunt was the worst

with 1178 ± 68 (Fig. 3). The mean urinary oxalate excretion was 986 ± 49 µmol/24 h,

all significantly greater than controls. There is no difference in oxalate excretion in stone

formers with JIB vs nonstone formers (54). Finally, numerous studies suggest that there

is no decrease in hyperoxaluria over time.

In both animal experimental studies and radioisotope [

]oxalate ingestion studies,

intestinal oxalate transport occurs in both the small and large bowel. There are both

active and passive transport capacities involved. In addition, the distal small bowel is

the site of absorption and reclamation of conjugated bile salts. In increasing quantity,

these salts produce an osmotic secretion and net loss of intestinal water leading to

increased diarrhea. After an ileal resection, it has been estimated that 13 mmol/L of bile

acids can be found in fecal fluid of patients (55). Finally, the stool normally contains

little free fatty acids. Patients with JIB have malabsorption of these fatty acids with

resultant steatorrhea. The effect of dietary fat consumption in individuals with fat

malabsorption indicates that increasing dietary fat intake from 40 to 100 g/d increased

fecal fat from 35 to 94 g/d. The fecal fat causes saponification with the calcium present

Fig. 3. Types of JIB and the amount of hyperoxaluria.