Marshall L. Stoller, Maxwell V. Meng-Urinary Stone Disease
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Chapter 13 / Medical Evaluation of Stone Disease 259
259
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
13
Medical Evaluation of Stone Disease
Clarita V. Odvina, MD and Charles Y. C. Pak, MD
CONTENTS
INTRODUCTION
EVALUATION OF SINGLE STONE-FORMERS
EVALUATION OF RECURRENT STONE-FORMERS
MISCELLANEOUS CONSIDERATIONS
CONCLUSION
REFERENCES
Key Words: Nephrolithiasis; metabolic evaluation; etiology; urine collection.
INTRODUCTION
Medical management entails identification of causes of stone formation based largely
on detection of abnormal urinary biochemistry (risk factors) (1), and application of
dietary modification and pharmacological treatment designed to correct underlying dis-
turbances (2). The importance of medical management is based on two important find-
ings. Urolithiasis is characterized by a high recurrence rate (3–6). It is estimated that
approx 60–80% of patients will form another stone within 10 yr of the first episode.
Removal of existing stone does not prevent further stone formation (7).
It is now well recognized that a wide variety of biochemical derangements contribute
to the formation of kidney stones. These abnormalities are “metabolic” (such as in
cystinuria and primary hyperoxaluria) (8,9) or environmental (such as low urinary vol-
ume and high urinary sodium) (10–13) in origin, or combination of the two. The goals
of clinical and laboratory evaluation of patients with history of nephrolithiasis should be
directed toward obtaining sufficient information to guide the management and preven-
tion of further stone formation. With proper evaluation and identification of risk factors,
a treatment program can be developed that can alleviate further stone formation and
avoid expensive urologic procedures (2,13).
In this chapter, we shall review diagnostic approaches to the medical evaluation of
patients after the first stone episode (“single stone-formers”), as well as those with
260 Odvina and Pak
recurrent stone formation (“recurrent stone-formers”). Both simplified and detailed
protocols will be described.
EVALUATION OF SINGLE STONE-FORMERS
The question of whether patients should be evaluated after a first stone episode has
been a topic of considerable debate. Noting a relatively low morbidity associated with
a first stone episode and somewhat high occurrence of side-effects with pharmacological
therapy, some investigators have recommended that single stone-formers should not
undergo elaborate or detailed evaluation (14). However, patients with a single stone
episode were shown to suffer from the same metabolic abnormalities as those with
recurrent or multiple stones (15). Single stone-formers are therefore at risk for recurrent
stone formation, justifying a more detailed evaluation. In 1988, the National Institutes
of Health (NIH) Consensus Conference recommended that all patients should at least
have a serum chemistry panel checked for metabolic conditions (such as hyperparathy-
roidism) associated with nephrolithiasis (16). Regardless, the decision to pursue a simple
or comprehensive work-up should be made jointly by the patient and the physician,
taking into consideration the estimated risk for new stone formation judged from medical
history and laboratory tests.
Medical History
Complete medical history must be obtained for both single and recurrent stone-form-
ers, whether a simple or detailed evaluation is contemplated (Fig. 1). A detailed medical
history may provide clues to the underlying cause(s) of kidney stone. It should be focused
on stone episodes, other medical illnesses, dietary habits, and information on current and
previous medications (Table 1). Because some stone-forming conditions have a genetic
predisposition, a careful family history of stones should also be obtained (17).
The history should address other medical conditions associated with specific abnor-
malities, which could potentially cause or contribute to kidney stone formation. For
instance, chronic diarrhea caused by inflammatory bowel disease or laxative abuse can
Fig. 1. Simplified approach to evaluation of urolithiasis.
Chapter 13 / Medical Evaluation of Stone Disease 261
lead to hypocitraturia from bicarbonate loss in the feces (18). In addition, excessive fluid
loss usually results in low urinary volume. Patients with malabsorption (secondary to
pancreatic insufficiency, celiac sprue) are at risk of developing hyperoxaluria (19).
History of chronic or recurrent urinary tract infections may lead one to suspect infection
lithiasis, which would warrant identification and eradication of the offending organism
(20). Prolonged bed rest or immobilization also increases the propensity for kidney
stones, primarily through increased urinary calcium excretion (21). History of peptic
ulcer disease and skeletal involvement (nontraumatic appendicular fractures) may lead
one to consider hyperparathyroidism (22).
There is little doubt that diet plays a role in the development of kidney stones. Predis-
posing factors include high animal protein diet, which can produce hyperuricosuria,
hypocitraturia, and hypercalciuria (23). Two of the most common abnormalities found
among stone-formers are low urine volume (10,11)
and high urinary sodium (12). Low
urine volume results from inappropriately low fluid intake, excessive sweating, or intes-
tinal fluid loss. High sodium intake can exaggerate stone disease by increasing urinary
calcium, decreasing urinary citrate, and provoking sodium urate-induced calcium
oxalate crystallization (12). Diet high in oxalate and low in potassium-containing citrus
fruit products (24) could also enhance the propensity to stone formation, by increasing
urinary oxalate and lowering citrate.
A number of medications could either cause or increase the risk for stone formation.
Carbonic anhydrase inhibitors such as acetazolamide can produce systemic acidosis,
hypocitraturia and increased urinary pH (25). A high dose of vitamin C increases urinary
oxalate, without lowering urinary pH (26). Other agents that can potentially promote
stone formation include triamterene, vitamin D, calcium supplements, and protease
inhibitors, particularly indinavir (27,28).
Laboratory Tests
In addition to detailed medical history, patients presenting with kidney stones for the
first time should have (1) urinalysis to rule out infection, (2) spot qualitative urine test
Table 1
Recommended Work-Up of First Time Stone-Former
at the First International Consultation on Stone Disease (Paris, France)
Medical history
• Stone history
• Other medical illness
• Family history
• Diet history
• Medications
Laboratory tests
• Imaging study (KUB or CT scan or ultrasound)
• Urinalysis ± culture
• Stone analysis
• Spot urine for cystine
• Serum chemistry (electrolytes, calcium, uric acid, ± PTH if indicated)
• 24-h urine for stone risk while on random (or usual diet)
262 Odvina and Pak
for cystine, (3) serum electrolytes, calcium and uric acid to identify metabolic causes of
stone formation such as renal tubular acidosis, primary hyperparathyroidism, and gout,
(4) appropriate imaging study [plain X-ray of kidneys, ureter, and bladder (KUB; CT
scan or ultrasound)] to identify the presence of residual stone and detect anatomical
abnormalities, and (5) stone analysis (if available), which may provide clues to the
medical diagnosis (Fig.1).
Although the 1988 NIH Consensus Conference did not recommend it for single stone-
formers except those at risk (Fig. 1) (16), the First International Consultation on Stone
Disease in 2001 suggested that a 24-h urine sample be analyzed for calcium, citrate,
oxalate, uric acid, total volume, sodium and potassium in all single stone-formers (29)
(Table 1). This recommendation was justified, because metabolic risk factors (such as
hypercalciuria, hypocitraturia, hyperuricosuria, and low urinary pH) are frequently
observed among single stone-formers (15). In addition, the stone risk profile in a 24-h
urine may help identify important dietary risk factors (1,11).
EVALUATION OF RECURRENT STONE-FORMERS
Recurrence of stone formation suggests that underlying disturbances persist or are
more severe than in single stone-formers. Thus, recurrent stone-formers merit a more
thorough evaluation than single stone-formers. However, there is considerable disagree-
ment as to what constitutes adequate work-up. In part, this controversy reflects consid-
erable diversity in severity of recurrent stone disease, difficulty in conducting a
comprehensive work-up in the setting of urologists in private practice, and cost-effec-
tiveness of a detailed evaluation. For this reason, both simple and detailed approaches
were recommended at the 2001 First International Consultation on Stone Disease (29).
Simplified Approach
A simplified, step-by-step work-up for nephrolithiasis has been described previously
(30,31). This approach, applicable to routine uncomplicated cases of recurrent stone
disease, is summarized in Table 2.
Table 2
Simplified Approach for Evaluating Patients With Recurrent Kidney Stones
First step
• Medical history
• Imaging study (KUB or CT scan or ultrasound)
• Spot urine sample for urinary sediments
• Serum chemistry (electrolytes, calcium, uric acid)
• 24-h Urine for stone risk while on random diet
Second step
• Short-term dietary modification based on the result of 24-h urine
Third step
• Repeat 24-h urine
• Identify metabolic risk factors and consider medical therapy
Chapter 13 / Medical Evaluation of Stone Disease 263
STEP 1
The initial evaluation should include detailed medical history as previously described,
imaging study (KUB; CT scan or ultrasound), serum chemistry panel (electrolytes,
calcium and uric acid), spot urine for urinary sediments and 24-h urine for calcium,
oxalate, uric acid, citrate and pH to identify metabolic risk factors. Measurement of total
volume, sodium, potassium, sulfate, phosphorous and magnesium will help define the
environmental risk factors. A single 24-h urine sample on a random diet is felt to be
adequate because abnormalities in stone risk factors had previously been shown to
be remarkably reproducible (32).
S
TEP 2
The second step involves placing the patient on a short-term dietary modification. For
instance, if the urinary volume is less than 2 L/d, the patient should be instructed to
increase fluid intake. If urinary sodium is greater than 200 meq/d, salt intake should be
restricted. Usually, this modification can be achieved by advising patients to avoid using
salt shakers during meals and limiting ingestion of salty and processed foods. If urinary
oxalate is more than 45 mg/d, patients should be advised to avoid intake of high oxalate-
containing food products such as tea, spinach, dark roughages, nuts, and chocolate. If
urinary calcium is >250 mg/d, moderate calcium restriction should be advised especially
if calcium intake is high. If urinary uric acid is >700 mg/d and sulfate is >30 mmol/d,
intake of animal protein (beef, poultry, fish, and pork) should be limited to 6–8 oz/d.
Lastly, if urinary pH, citrate and potassium are low, patients should be advised to in-
crease intake of fruits, particularly with potassium-rich citrus products such as orange
(24) and grapefruit.
S
TEP 3
In the third step, another 24-h urine sample is collected for stone risk profile, while
subjects are maintained on a diet restricted in calcium, sodium, and oxalate for 1 wk. The
results are compared with those obtained while on the usual (random) diet. Correction
of abnormal risk factors on the restricted diet suggests that the abnormalities are envi-
ronmental in origin. When environmental risk factors such as urine volume or urinary
sodium remain abnormal after dietary intervention, the finding implies either poor com-
pliance or inadequate dietary modification. Persistent abnormalities in metabolic factors
(urinary calcium, citrate, pH, uric acid, and oxalate) despite dietary modification suggest
the need for pharmacological intervention such as potassium citrate for persistently low
pH and citrate, and thiazide for hypercalciuria. In even simpler version (32), Step 3 is
omitted.
Comprehensive Evaluation
A number of protocols are now available and are being used by different centers in the
evaluation of kidney stone disease. These protocols may be applicable for use in centers
specializing in the medical management of kidney stones and for evaluation of patients
with severe or complicated stone disease.
T
HE UNIVERSITY OF CHICAGO PROTOCOL
In this protocol, three 24-h urine samples are collected while patients are on their usual
diet, with corresponding blood samples (5). Blood samples are drawn between 7
AM and
264 Odvina and Pak
9 AM after a 12-h fast. Urine samples are analyzed for calcium, magnesium, phosphorous,
uric acid, oxalate, citrate, sulfate, ammonium, total volume, and pH. Concentrations of
calcium, magnesium, phosphorous, uric acid and creatinine (plus sodium and potassium
in one sample) are measured in the serum samples. Cystine screening is done on all
patients using the nitroprusside reaction.
U
NIVERSITY OF TEXAS SOUTHWESTERN PROTOCOL
The Stone Clinic at the Southwestern Medical Center uses an updated version of the
1978 ambulatory protocol (33). This protocol requires three outpatient visits (Table 3).
Before the initial evaluation, patients are instructed to discontinue all medications that
could affect the metabolism of calcium, uric acid and oxalate. Examples of such medi-
cations are thiazide, orthophosphate, allopurinol, vitamin C, acetazolamide, calcium,
and vitamin D supplements.
On the first visit, a detailed history is obtained as described previously. Radiologic
study (KUB; tomogram or intravenous pyelogram) is obtained to determine the presence
of residual stone or any structural abnormality. Fresh spot urine is collected to rule out
infection and for cystine screening. If not previously done and if the specimen is avail-
able, the stone is sent for analysis.
Three urine samples are collected. Two samples are obtained while the patient is on
his or her customary diet and fluid intake. The third 24-h urine sample is collected after
at least 7 d on a diet restricted in calcium (400 mg/d), sodium (100 meq/d), and oxalate
(avoidance of chocolate, tea, nuts, and dark roughages). Urine samples are analyzed for
calcium, magnesium, sodium, potassium, ammonium, uric acid, oxalate, citrate, phos-
phorus, sulfate, chloride, creatinine, pH, and total volume. Fasting venous blood sample
is drawn during the random diet for chemistry panel (electrolytes, BUN, creatinine,
calcium, phosphorous, magnesium, total protein, albumin, and uric acid).
Comparison of the results of urine analysis during random and restricted diets allows
for the assessment of the role of certain environmental factors in the development of
stones, as well as permit definition of certain abnormal risk factors. One week of the
restricted diet also provides the necessary preparation for the “fast and load” test (34),
which is performed to detect the presence of renal calcium leak and of intestinal
hyperabsorption of calcium.
Table 3
Comprehensive Work-Up (UT Southwestern Protocol [33])
• Medical history
• Imaging study (KUB or CT scan or ultrasound)
• Urinalysis ± culture
• Three 24-h urine collections, 2 on random diet and one after dietary restriction
of calcium, sodium & oxalate for 7 d
• Stone analysis
• Spot urine for cystine
• Serum chemistries corresponding to the urine collection, plus PTH in one
sample
• “Fast and Ca load test”
Chapter 13 / Medical Evaluation of Stone Disease 265
“Fast and load” testing involves collection of a fasting 2-h urine sample following an
overnight fast, a fasting venous blood sample, and a 4-h urine sample after oral ingestion
of 1-g calcium with a synthetic meal. Serum sample is analyzed for calcium, creatinine,
and PTH; urine samples during fasting and following calcium load are measured for
calcium and creatinine. The fasting urinary calcium, expressed as mg/dL glomerular
filtrate, is a measure of renal calcium leak or skeletal calcium mobilization. The incre-
ment in 4-h urinary calcium over the fasting value, expressed as mg calcium/dL glom-
erular filtrate, provides an indirect assessment of intestinal calcium absorption.
When hypercalciuria is present, bone density is measured in the spine, hip and radius.
This procedure recognizes the association of low bone density with hypercalciuric neph-
rolithiasis (35).
MISCELLANEOUS CONSIDERATIONS
Centralized vs Institutional Laboratories
For physicians practicing in the community, it may be convenient to use the commer-
cially available tests of urine for stone risks factors. Several specialized laboratories can
now provide kits that allow standardized biochemical assays and physicochemical
measurements to identify the risk factors for stone formation.
T
HE MISSION PHARMACAL COMPANY (SAN ANTONIO, TX)
This kit contains a volume marker and appropriate preservatives (1). The patient is
instructed to collect a 24-h urine sample after which two small (30 mL) aliquots are sent
to a central laboratory. The laboratory calculates the total volume from the dilution of
the volume marker and analyzes urinary metabolic risk factors (calcium, oxalate, uric
acid, citrate, and pH) and environmental risk factors (total volume, sodium, sulfate,
phosphorous, and magnesium). From the analyzed values, physicochemical risk factors
are calculated. The laboratory provides a visual display of all available data in a single
report. Each risk factor is assigned a vertical line on a linear scale, and the risk factors
are grouped into metabolic, environmental, and physicochemical risks. A horizontal line
intersecting each vertical scale at an approximate midpoint represents upper or lower
normal limit. Values below the horizontal line represent normal values (or reduced risk)
and values above the line represent increased risk. For the physicochemical risks, values
above the horizontal dashed line represent supersaturation beyond the mean values in
normal subjects with respect to four stone-forming salts (calcium oxalate, brushite, or
calcium phosphate, monosodium urate, and uric acid). Although the profile provided by
the laboratory has diagnostic utility, additional information such as medical history,
serum chemistry, and appropriate X-rays are still necessary to come up with a more
definite diagnosis.
T
HE LITHOLINK (CHICAGO, ILLINOIS)
This kit contains a urine collection container, a green topped tube for urine aliquot and
a collection data sheet. Patients are instructed to record the start and stop times and the
urinary volume on the data collection sheet. At the completion of the urine collection,
urine aliquot is collected and is sent with the data sheet to the laboratory. The laboratory
also provides a full evaluation of stone risk factors (metabolic, environmental and physi-
cochemical). However, unlike the visual display provided by Mission, Litholink sends
the ordering physician a tabulated report. Bigger and bolder fonts indicate that a given
266 Odvina and Pak
measurement is closer to that of a stone-forming population (therefore, increased risk).
Litholink also provides time sequential data that allows the physician to evaluate the
progress of the patient during treatment.
Adequancy of Urine Collection
Accurate interpretation of the results of urinary biochemistry depends on complete-
ness of urinary collection. Correction of urinary creatinine by bodyweight can help
assess the adequacy of urine collection. The average urinary creatinine is 13–21 mg/kg
for women and 17–27 mg/kg for men. A value that is below the lower end would suggest
undercollection. On the other hand, a value that is at the upper end would be consistent
with overcollection.
Clues to Detecting Dietary Influences From Urinary Stone Risks
The effects of environmental risk factors can be assessed by comparing the urinary
chemistries while on usual (random diet) vs those obtained during the restricted diet.
Diet-induced hypercalciuria should be suspected if the urinary calcium is normalized by
dietary modification. This finding may indicate excessive calcium intake or high intake
of sodium or animal proteins.
Hyperuricosuria in a patient with normal serum uric acid concentration suggests
increased intake of purine-rich foods (meat products). Urinary oxalate >45 mg/d in a
patient without history of malabsorption indicates either high oxalate consumption or
intake of large doses of vitamin C. Normalization of urinary oxalate during dietary
restriction would confirm this impression. Low urinary volume usually indicates inad-
equate fluid intake or excessive fluid loss either from diarrhea or excessive sweating.
Interpretation of Response to “Fast and Load” Test
For accurate interpretation of the fasting urinary calcium, it is important to place the
patients on a diet limited in calcium and sodium before the test is preformed. Patients
with intestinal hyperabsorption of calcium (absorptive hypercalciuria) may have high
fasting urinary calcium if this precaution is not followed. Without this preparation,
fasting hypercalciuria may be present from the delayed clearance of absorbed calcium
and persistent PTH suppression (which reduces renal tubular reabsorption of calcium).
Fasting urinary calcium is expressed as mg/dl glomerular filtrate to reflect renal function
rather than muscle mass. This derivation is obtained by multiplying urinary calcium in
mg/mg creatinine by the corresponding serum creatinine in mg/dl. Normal value for
fasting urinary calcium is <0.11 mg/dL glomerular filtrate. Fasting hypercalciuria in the
setting of normal serum calcium and PTH is indicative of renal hypercalciuria.
The increase in urinary calcium excretion after 1 gram calcium load provides an
indirect assessment of intestinal calcium absorption. A “post-load” urinary calcium of
>0.2 mg/dL glomerular filtrate or mg/mg creatinine in a patient with normal values for
serum PTH and fasting urinary calcium indicates absorptive hypercalciuria (34).
CONCLUSION
This chapter describes the different protocols that one may use in evaluating patients
with nephrolithiasis. The extent of the work-up should be based on whether (a) the
patient is presenting with an acute stone episode for the first time or (b) the patient has