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Nephrolithiasis with unusual initial symptoms
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Journal of Manipulative and Physiological Therapeutics Volume 23 • Number 3 • March/April 2000 0161-4754/2000/$12.00 + 0 76/1/105113 © 2000 JMPT
CASEREPORT NephrolithiasisWith UnusualInitial Symptoms K e i t h A. Wells, D C ~
ABSTRACT Objective: To describe a less contmon initial symptom of nephrolithiasis, its diagnostic pitfalls, risk factors, and mimicry of other conditions. Intervention and long-term management of nephrolithiasis is also discussed. Clinical Features: A Caucasian man aged 25 years had sudden bilateral inguinal and occasional periumbilical pain. The initial symptol suggested an abdominal pathologic conditi however, costovertebral angle pain followed . . . . . . later with no radiation between the 2 anatomic sites. The initial urine dipstick result was negative for hematuria, but a kidney, ureter, and bladder radiograph revealed a smooth 2-ram x 3-ram stone lodged at the left vesico-ureteral junction. Intervention and Outcome: The patient was referred to a regional university medical center to receive extracorporeal shockwave lithotripsy several days after his initial visit. He was given pain medicine for the waiting period and received daily lumbar spine adjustments with a mild reduction in pain. He eventually
INTRODUCTION Nephrolithiasis is the development of a renal calculus. These stones form in the kidney and typically move through the urinary tract as a ureteral calculus to be excreted. Some stones never exit the kidney (ie, staghorn calculus) and others become impacted in the ureter at several different possible sites, including the vesico-ureteral junction, the ureteropelvic junction, and the crossing o f the ureter at the iliac artery, sites where the ureter narrows. ~ The movement and/or impaction of the stone usually causes sudden, severe back and/or flank pain as the primary symptom, with eventual radiation from the initial site to the groin and/or genitalia. Nephrolithiasis is a significant cause of morbidity in the United States. 1-3Accurate diagnosis of the problem is necessary to avoid treatment delays in the acute patient, to identify the underlying metabolic cause and true extent of the disease, and to identify treatment methods for reduction or prevention of recurrence.
"Diagnosis Department, Los Angeles College of Chiropractic, Whittier, Calif. Submit reprint requests to: Keith A. Wells, DC, Diagnosis Department, Los Angeles College of Chiropractic, 16200 E Amber Valley Dr, Whittier, CA 90604. Paper submitted January 26, 1999; in revised form February 10, 1999. doi:l 0.1067/mint.2000.105113
:ceived ureteroscopic laser lithotripsy because the shock-wave unit had malfunctioned before his appointment. The fragment analysis showed a calcium oxalate composition, and the patient was advised to lower his intake of oxalates. The patient had become a vegetarian approximately 3 months before this first stone episode. onclusion: Nephrolithiasis is a condition com~nly seen in chiropractic practice. Although it is ly easy to recognize, the diagnosis can be elusive if the typical historic factors and diagnostic results are absent or altered. The short-term management of nephrolithiasis is pain management, stone elimination, and the collection of a specimen to identify the composition and underlying metabolic abnormality. Long-term management is to prevent the recurrence of stones. Conservative comanagement by the chiropractic physician can be implemented through nutritional means. (J Manipulative Physiol Ther 2000;23:196-201) Key IndexingTerms: Kidney Calculi; Lithotripsy; Ureter
Because the passing stone often causes back pain at the costo-vertebral angle, some patients may initially visit a chiropractor. This case reviews a less common initial symptom of nephrolithiasis and the typical symptoms, diagnostic protocols, and treatment recommendations. Dietary f~ictors may be addressed by the chiropractic physician in a conservative, preventive management strategy.
CASEREPORT A 25-year-old Caucasian man had bilateral stabbing inguinal pain that began abruptly several hours before his visit with occasional periumbilical pain. He believed he had appendicitis because of the periumbilical pain but elected to see if the symptoms would pass after consulting briefly with a chiropractic clinician. Soon after, the patient returned with a different and sharper pain that began in the left costo-vertebral angle. There was no radiation of pain between the left costo-vertebral angle and the inguinal region. This was a potential source of diagnostic confusion; in most cases, patients who pass ureteral stones typically believe that the pain radiating to the flank and groin is "connected." The physical examination of the patient was unremarkable. A urine dipstick test result was grossly, normal and negative for hematuria. This was another potential source for diagnostic error because the great majority of passing stones cause at least microscopic hematuria. A kidney, ureter, and bladder (KUB) radiograph demonstrated a smooth 2- x 3-
Journal of lVlanipulativcand PhysiologicalTherapeutics Volume 23 • Number 3 • March/April 20(10
Nephrolithiasis Table
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• Wells
Remd stone./?.'mation inhihitors
Nephrocalcin Glycosaminoglycan Uroponlin Tamm-Horsfall protein Crystal matrix protcin
Lithostathinc Uronic acid-rich protein Citrate Magnesium pyroplmsphatc
Table 2. Selected diseases and conditirms associated with nephrolithiasi.~" Primary hyperparathyroidism Renal tubular acidosis Gout Recurrent urinary, tract infection Crohn's disease
Sarcoidosis Milk-alkali syndrome Prolonged immobilization Laxative abuse
millimeter stone lodged at the left vesico-ureteral junction (Fig 1). The patient had no family history of renal calculi, and this was a first episode of nephrolithiasis. The patient was refen'ed to a regional university medical center, where a follow-up urine dipstick analysis result was negative for hematuria at first evaluation. The day after his symptoms began, pain began radiating between the flank and the inguinal region and out to the testicles and penis. The patient was scheduled for extracorporeal shock-wave lithotripsy (ESWL) at one of the university outpatient surgical clinics 2 weeks after his initial visit and was given pain medicine (Vicodin) for the waiting period. The pain continued relentlessly while he waited for his appointment, with occasional episodes of nausea and vomiting, a common symptom of nephrolithiasis, presumably because of the intensity of the pain. Nausea and vomiting usually begin concurrently with the onset of the pain but began a day later in this case with the escalation of pain. In addition to taking pain medication, he received lumbar spine adjustments drily, sometimes twice a day, in the student clinic. The treating intern requested that he complete a visual analogue pain scale before and after each adjustment, but these records were not available for review. The patient reported that the adjustments helped control the pain for brief periods of time. The patient was unable to receive ESWL because of failure of the lithotripter and was then scheduled tbr ureteroscopic laser lithotripsy. The stone was eliminated, and the fragment analysis revealed a calcium oxalate composition. The patient was advised to reduce his intake of oxalates. At this point, he indicated that he had become a vegetarian 3 months before the episode. Vegetarians may "greatly increase their intake of oxalates through green, leafy vegetables; excess dietary oxalate may enhance stone formation. He complied with the recommendation to reduce oxalates and has also maintained the habit of drinking a minimum of 2 liters of water daily. He has not had a recurrence of stones to the date of this writing.
DISCUSSION The true incidence of nephrolithiasis is difficult to establish but has been estimated at 7% in men aged >30 years and
Fig I. Arrow indicates stone.
3% in women (age range not specified). 2 The incidence is greatest in the southeastern United States and in hot climates, j'2 A total of 0.2% of the US population has stones annually, with 5% to 15% of the population expected to have a kidney stone in their lifetime. 2-4 The incidence of stones in men is 4 times greater than the incidence in women. 2-3 Caucasian men have 3 times as many stone episodes as black men) Approximately 50% of patients will have recurrence, with the estimates varying based on renal stone clinic versus population-based studies.n4 The majority of stones (70% to 80%) are calcium-based, typically calcium oxalate, and often calcium phosphate or a mixture of both. The other major stone types are magnesium ammonium phosphate (struvite), uric acid, and the uncommon cystine stone.l-4 Struvite stones typically form staghorn calculi in the renal pelvis and calyces and are also called infection stones because they are associated with urea-splitting organisms (Klebsiella, Proteus, Pseudomonas) and chronic kidney infections. 1.4 Uric acid stones are associated with purine-rich diets and form in acid urine (hydrogen ion concentration [pH] <5.5). Cystine stones are associated with cystinuria, an unusual genetic disorder of the renal tubules. Persons aged <21 years that have a kidney stone may have this disorder, although stones may develop for other reasons. The pathogenesis of stone formation involves 3 factors, including supersaturation of the urine with the involved salt,
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nucleation of the salts with crystal fornaation, and a decrease or absence of stone inhibitors. The process of crystal formation on a nucleus is known as epitaxy. The resultant stones are not strictly inorganic crystals but have varying amounts of organic matrix included in them. Stone inhibitors are substances known to interfere with stone formation at several points along the stone growth process (Table 1).2.3 The majority of stone formers have an underlying metabolic predisposition or outright abnormality that leads to stone formation. II The 4 most common types of metabolic dysfunction are hypercalciuria (with 4 subtypes), hyperuricosuria, hypocitraturia, and hyperoxaluria (with 3 subtypes). These abnormalities are relatively complex, with extensive coverage in the literature. I-5,~,~2 In addition to these causative factors, many diseases and conditions are associated with stone formation (Table 2). In recurrent stone formers or patients with a family history of nephrolithiasis, a more extensive diagnostic process should be followed to determine the presence of predisposing disease (ie, primary hyperparathyroidism). These listed conditions account for <5% of patients with nephrolithiasis, but it is important to pursue the diagnosis in this minority because of the morbidity of the diseases involved. 2 Dietary habits can be both risk factors and therapeutic approaches, depending on the circumstances. At this point, excess protein and salt and excessive calcium and oxalate intake can contribute to stone formation and chronic dehydration. ]2-j6 Several medicines, vitamins, and minerals may predispose a person to stone formation, including calcium, vitamins C and D, acetazolamide, and catabolic steroids (ie, prednisone). 4
Clinical Presentation and Diagnosis The clinical presentation of a passing ureteral calculus typically begins with the sudden onset of excruciating costovertebral angle pain and/or flank pain. Nausea and vomiting often accompany the onset. There may be gross hematuria, sometimes with an occasional visible clot. The patient may also report frequent urination and/or dysuria. If there is frequency, dysuria, and/or urinary incontinence, a concomitant urinary tract infection should be considered. There may be radiation of pain from the costo-vertebral angle or flank across the lower abdomen and into the labia in women and into the testicles and penis in men. At times the pain may radiate to the inner thigh, a radiation that may be from the embryonic relation of the urinary tract to the genitalia. 1The patient typically cannot find a comfortable position and frequently paces. In contrast to the usual symptoms, the patient in the case report had pain that began in the bilateral inguinal region, which escalated in severity, and also appeared in the periumbilical region, atypical for a kidney stone. Back/flank pain was absent until several hours after the onset of symptoms, and nausea and vomiting appeared the next day. For patients who have stones for the first time, the sudden pain and other accompanying symptoms are frightening and will typically lead to a visit to the emergency department. Irritation and spasm of the ureter or obstruction of the renal calyces, pelvis, or ureter cause the pain.
In some patients, tile pain will be less severe, depending on the individual tolerance and whether there is actual obstruction. Some material that passes can be no larger than a grain of sand and may pass with relatively little pain. Some patients have had several incidences of stones and tend to recognize the symptoms. If the pain is not severe, the patient may not seek treatment but will ingest large volumes of water until the pain stops (the stone is then presumed to have passed) or until it is obvious that the stone is impacted. The physical findings in renal colic (the symptoms of passing the stone) are nonspecific. Hypertension and tachycardia may be present because of the pain; as always, hypertension should be investigated to exclude other causes. Fever is uncommon with renal colic. If it is present, a urinary tract infection must be considered. The abdominal exam may exhibit tenderness along the flank or lower quadrant of the affected side, but if there is rebound tenderness or involuntary muscular guarding, peritoneal irritation is suspected. If the patient is seen in a private office setting, this should prompt immediate referral to the emergency department. Bowel sounds may be normal or diminished but should not be absent. The male patient may have testicular tenderness during examination but the testicles should be otherwise normal. Pelvic and rectal examinations are unremarkable. Patients may exhibit nonspecific soft tissue tenderness and/or muscle spasms in the lower thoracic/upper lumbar regions. In less severe episodes, a musculoskeletal diagnosis may be rendered if an incomplete history is taken. Further investigation of nephrolithiasis in the acute patient begins with the urine dipstick to assess for hematuria. Microscopic hematuria is typical. With the usual history and physical examination, the finding lends greater diagnostic weight. Hematuria may be tess commonly absent, however, and may indicate complete ureteral obstruction. A complete urinalysis with culture and sensitivity should be performed to evaluate for infection in the urinary tract, particularly by urea-splitting organisms. Urine pH may be helpful in determining the stone composition analysis. The urine dipstick gives a general indication of the pH, but the specific pH is determined in the laboratory. A pH <5.5 favors uric acid stone formation, whereas a pH >7.5 indicates possible urea-splitting organisms and infection. Microscopic analysis of the urine may reveal crystals that often have characteristic identifying shapes depending on the stone composition. 3'5 For patients who have nephrolithiasis f6r the first time, routine blood testing for serum calcium, phosphorus, uric acid, electrolytes, blood urea nitrogen, and creatinine is sufficient to screen for evidence of underlying abnormalities, such as gout and renal tubular acidosis.l'4 The typical biochemistry panel will contain all these serum tests. Patients with clinical evidence of infection should also have a complete blood count with differential performed. The KUB radiograph is routinely used for diagnosis, although some diagnostic issues must be considered, including that the stone may be radiolucent (uric acid stones) or very small; overlying feces and gas may interfere with analysis; and other calcific densities (ie, phleboliths) can be
Journal of Manipulative and Physiological Therapeutics Volume 23 • Number 3 • March/April 2000 Nephrolithiasis * Wells
found in the abdomen and pelvis. Nevertheless, plain abdominal films can identify stones in 80% to 90% of patients. 3 The KUB radiograph can be taken in the office setting and used in addition to the urine dipstick. Some researchers believe that the KUB does not add useful information to the diagnostic process, that it is actually an unnecessary expense to the patient, and that the intravenous pyelogram (IVP) is the best first-line imaging tool. l The IVP, a hospital-based procedure used as the gold standard for diagnosis of nephrolithiasis or ureterolithiasis, is routinely performed after the KUB radiograph to identify stone position and kidney function.~ The procedure itself may actually cause the stone to pass, and the patient is given a urine strainer to retrieve the stone. The IVP will reveal whether there is an obstruction, and the course of treatment will be directed to the outcome. In addition, the use of ultrasonography and computed tomography scanning has been described for diagnostic use in nephrolithiasis under a variety of circumstances, including inability to tolerate the contrast media used in the I V P . 6 Retrieval of the stone or a fragment is important in the first-time episode to identify its composition, which helps to determine subsequent treatment plans. The patient is typically given a urine strainer (consisting of nothing more than a plastic funnel with a fine mesh placed at the neck) and is instructed to drink enough fluids (preferably water) to produce at least 2 L of urine per day. This requires the patient to ingest at least 2 to 3 L of water. Specific instructions about intake should be given, such as "drink a 10-oz glass of water every waking hour of the day." In addition, the patient should ingest water if he or she awakens at night. The patient should be taught what to look for in the urine strainer because the material that passes in the urine may be a well-formed, recognizable stone or it may appear literally like grains of sand. Hydration should be recommended regardless of obstruction. I t m a y take hours to days to see if a stone will pass. Nevertheless, whether a "watchful waiting" approach is adopted or a future appointment for lithotripsy or surgery is scheduled, compliance with hydration is essential. Once the stone or fragment is retrieved, a reference laboratory will perform crystallography by polarization microscopy, x-ray diffraction, or infrared spectroscopy. 3,5 Depending on stone composition, further diagnostic studies may be performed and treatment approaches can be planned. In certain patients, more extensive analysis should be performed, including patients with a family history of renal stones, persons aged <21 years, patients who form multiple stones in the first episode, and patients with recurring stones. For example, persons aged <21 years must be assessed for cystinuria by the nitroprusside test. Cystinuria is an inherited renal tubule defect in which there is impaired resorption of the amino acid cystine. 2 As a result, there is excessive excretion of cystine with formation of cystine calculi. Stone formation is relatively uncommon in black men and particularly women; therefore, these patients should also be investigated more extensively. ~t These analyses include specific tests for specific abnormalities (ie, serum parathormone for
hyperparathyroidism) and a 24-hour urinalysis for underlying disorders of calcium metabolism. The 24-hour urine sample is also tested for phosphorus, uric acid, magnesium, sodium, citrate, oxalate, and creatinine concentration. 4
Short- and Long.TermManagement The treatment of acute nephrolithiasis depends on the clinical findings. Typically, patients want pain relief, especially in a first episode. Pharmaceuticals include a variety of narcotics (eg, meperidine, morphine) given in the hospital setting or prescribed on an outpatient basis. There is growing use of parenteral or suppository nonsteroidal antiinflammatory drugs (NSAIDs), including indomethacin and ketorolac, for acute renal colic. Several European, Asian, and US studies have compared the use of NSAIDs with narcotics and have found the NSAIDs effective in alleviating the pain. 2 Medicinal outpatient management of renal colic can be accomplished with oral narcotics and/or oral NSAIDs. 3 Hydration is necessary to encourage passage of the stone for diagnosis and may be therapeutic as well. Again, specific instructions on water ingestion should be given. Stones that are smaller than 4 to 5 mm will pass spontaneously 75% to 80% of the time, especially with hydration. 1.3.5Stones larger than 5 mm have a decreasing chance of spontaneous passage, with approximately 10% of stones measuring 8 to i0 mm passing spontaneously. The treatment approach is guided in part by the type of stone and whether it is impacted. For example, a struvite stone or other large stone may require percutaneous nephrolithotomy or open surgery. ESWL is a well-known and common treatment for impacted stones. ~-6The treatment is noninvasive but painful and requires anesthesia. In patients without contraindications to anesthesia or ESWL, the success rate is approximately 70% to 90%. The use of ESWL for lower urinary tract stones is controversial and therefore is typically used for impactions in the upper tract. Cystine stones do not shatter well and radiolucent stones are difficult to locate; therefore ESWL is not generally used with these types of stones. Fracture of stones larger than 2 cm may cause renal colic from the resulting fragments and are not usually treated with ESWL. In the previous case, the treatment technique used was ureteroscopic laser lithotripsy, 1 of 3 available intracorporeal lithotripsy techniques. The use of laser lithotripsy has gained momentum over the last 12 years because of the introduction of the pulsed dye laser. 7 Different laser instruments (eg, the holmium-yellow argon and the alexandrite) exist with technology beyond the scope of this report. A technologic discussion of the physics and procedural application involved occurs in the literature. 7"9 Laser lithotripsy requires anesthesia and results in a success rate at least as high as ESWL; in some circumstances, the rates are superior. Success of both modalities again depends on stone size, type, and location. Other ureteroscopic lithotrites include intracorporeal ultrasound and electrohydraulic treatments. Long-term pharmaceutical treatment is directed at prevention of stone recurrence. At least one author has studied
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the financial effects of kidney stone prevention and suggests that treatment directed at prevention is worthwhile for health savings and the reduced risk of morbidity from procedures. 1° Several medicines can be used to inhibit stone formationf1.3.5-11 Potassium citrate is used for patients with hypocitraturia; allopurinol is used for hyperuricosuria and is helpful for calcium stones in hyperuricosuric patients and uric acid stones; and thiazide diuretics, indapamide, or cellulose phosphates may be used in certain types of hypercalciuria. Hyperoxaluria can usually be controlled by dietary measures but may be controlled by calcium citrate if the patient is not hypercalciuric. Penicillamine is used in cystinuria. Each aforementioned medicine has potential complications and side effects, and practitioners should familiarize themselves with these when treating patients who take medicines for stone prevention.
Dietary Habits as Risk Factorsand Preventative Methods Dietary habits and practices as both risk factors and stone prevention methods have been investigated and described. 2.5.~2-16 Dietary practice as a preventive measure against stone recurrence is within the realm of chiropractic practice in most states. 17 Compliance with dietary management can be difficult because patients are often asked to eliminate or reduce beloved foods from their diets. Each dietary factor will be addressed below. A general dietary plan should be constructed based on the individual case and the practitioner's knowledge of the underlying metabolic abnormality. Dehydrationandproperbydration. Fluid ingestion, preferably in the form of water, was discussed as a therapeutic measure in the treatment of acute renal colic. Dehydration presumably encourages supersaturation of the salts that form stones. After the first stone episode, the patient should be encouraged to ingest water as if he or she were still attempting to pass a stone. Urine output should continue to be a minimum of 2 L per day, a lifestyle change for most patients. To achieve this output, the patient should drink a minimum of 2 L of water per day and preferably more. The water itself may have high mineral content (ie, calcium), so bottled water that specifies mineral contents or even distilled water may be best. Specific instructions must be given because the vague instruction to "drink a lot of water" will not be followed. The patient may want to substitute other fluids but this should be discouraged. Coffee, beer, tea, and colas have high oxalate content, and milk has high calcium. Dietary protein, It is generally accepted that dietary animal protein plays a causative role in stone formation, but whether reduction in dietary animal protein is beneficial is controversial. 13.14 Economic affluence correlates with the occurrence of nephrolithiasis, presumably because persons with higher incomes can afford to purchase meat and therefort ingest greater amounts of dietary animal protein. 14.16In general, vegetarianism has been shown to protect against calcium stone formation in some studies. However, excessive oxalate intake from green, leafy vegetables can cause stones in patients with hyperoxaluria. Excessive protein
probably contributes to stone formation in 2 ways: by excess purines possibly leading to uric acid stones and by the observed hypercalciuric effect that develops from protein loads. 2 A global reduction of protein, particularly animal protein, is typically recommended, with the daily protein intake suggested at 60 g/dayfl $odium intake. Natriuresis has a calciuric effect that presumably enhances stone formation in an environment of pH >6.5. 5 One suggestion is to restrict sodium intake to 3 to 4 g/day, and certain patients with other conditions (ie, cardiovascular disease) will be restricted to less. 2 Calcium intake. It is tempting to conclude that excessive calcium would lead to calcium stone formation. This conclusion may be true in type II absorptive hypercalciuria, an autosoreal-dominant disorder in which absorption of intestinal calcium is increased. The type I disorder causes increased absorption, regardless of dietary calcium intake, whereas the milder type II disorder is related to high calcium intake. 3 The other types of metabolic hypercalciuria are more complex. Restricting calcium intake in general may actually increase the chance of stone formation, 1-5 perhaps because of stimulation of vitamin D3 activity, which stimulates bone resorption and calciuria. Restriction of calcium in patients with hyperoxaluria can lead to stone formation because of preferential gut absorption of oxalates. The resulting oxaluria can cause calcium oxalate stones. 2A4A6The recommendation for calcium intake is 1 to 1.5 g/day to protect the bone pool and avoid excess intake. 14 Fiber intake, Hiatt et a113 argues that a high-fiber diet protects against nephrolithiasis. Although there are many types of bran sources and no absolute conclusions on how bran may be effective, there is some evidence that 10 to 15 g/day of bran may decrease incidence of new stone formation in patients with hypercalciuria.'6 Citrate intake. Hypocitraturia contributes to stone formation because citrate chelates calcium and acts as a stone inhibitor. Potassium citrate is typically given for this condition because pharmacologic dosing achieves acceptable levels of urinary citrate. Some patients are noncompliant with the medicine as a result of indigestion, multiple dosing, and taste (all depending on the method of delivery). Some research indicates that the amount of fruits and vegetables necessary to achieve acceptable levels of citraturia would likely cause hyperoxaluria.16 However, Seltzer et a115 studied the use of lemonade to achieve increased citraturia. Lemong contain the highest citrate concentration of the citrus fruits. Twelve subjects consumed 2 L/day of 4 oz of reconstituted lemon juice mixed with water. This regimen produced pharmacologic levels of urinary citrate excretion, and the patients tolerated the treatment well. The authors concluded that lemonade might be effective in treating hypocitraturia and may supplement or even replace prescription citrate. This new method is inexpensive and may reduce new stone formation but needs further study. Oxalate intake. Hyperoxaluria is known to contribute to calcium oxalate stone formation. Dietary hyperoxaluria may result from excess consumption of green leafy vegetables, tea, coffee, chocolate, tomatoes, beans, beets, radishes, beer,
Journal of Manipulative and Physiological Therapeutics Volume 23 • Number 3 • March/April 2000
Nephrolithiasis and certain nuts. In some people, vitamin C intake contributes to hyperoxaluria because ascorbic acid is metabolized to oxalate. Vitamin B 6 deficiency may also contribute to hyperoxaluria because pyridoxine is a cofactor in the interconversion of glycine and glyoxalate. 2,~4.~6 Whether excess vitamin C or reduced pyridoxine intake actually causes oxalate stones is debatable, but restricting vitamin C in patients with hyperoxaluria and increasing pyridoxine for those with deficiency is recommended. Vitamin C should be limited to 1000 mg/day and pyridoxine is recommended at I00 mg/day. Vegetarians are presumably at risk for oxalate stones but the overall stone rate in this population is reduced significantly. The risk for oxalate stones is probably higher in patients with hyperoxaluria who consume large amounts o f green leafy vegetables and other foods that are high in oxalate concentration. Magnesiumintake. Although it is not known whether dietary magnesium is adequate to protect against stone formation, there is a clear protective effect of magnesium against calcium oxalate stones. M a g n e s i u m supplementation has been shown to decrease stone recurrence. 16
CONCLUSION This case had an unusual initial symptom because the first symptoms suggested abdominal pathology. The suddenness of the onset of pain indicates a renal stone, even in an atypical clinical picture. In addition, microscopic hematuria is usually present, and the absence of hematuria with the initial urine dipstick can be misleading. The acute patient with a lower pain level may come to the chiropractic office believing the origin of the pain is musculoskeletal. In-office diagnosis is usually possible with the urine dipstick and the KUB radi.ograph. Once the diagnosis is established, emergency or urologic referral is appropriate. Depending on the resulting stone analysis and identification of the underlying metabolic problem, a variety of dietary measures can be suggested that may be successful in preventing stone recurrence. These measures should be carefully implemented based on the actual metabolic abnormality to avoid, for example, too little calcium intake when the initial reaction is
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to reduce calcium. Typical cases of nephrolithiasis are usually easy to suspect by using thorough patient history. The chiropractic physician is in a position to initially diagnose and eventually comanage this disorder.
REFERENCES I. Stewart C. Nephrolithiasis. Emerg Med Clin N Am 1988; 6:617-30. 2. Saklayen MG. Medical management of nephrolithiasis. Med Clin N Am 1997;81:785-99. 3. Trivedi BK. Nephrolithiasis--how it happens and what to do about it. Post Grad Med 1996;100:63-78. 4. Kupin WL. A practical approach to nephrolithiasis. Hosp Pract 1995;30:57-66. 5. Klugman V, Favus MJ. Diagnosis and treatment of calcium kidney stones. Adv Endocrinol Metab 1995;6:117-42. 6. LeRoy AJ. Diagnosis and treatment of nephrolithiasis: current perspectives. Am J Roentgenol 1994; 163:1309-13. 7. Pearle MS, Sech SM, Cobb CG, et al. Safety and efficacy of the alexandrite laser for the treatment of renal and ureteral calculi. Urology 1998;51:33-8. 8. Gould DL. Retrograde flexible ureterorenoscopic holmiumYAG laser lithotripsy: the new gold standard. Tech Urol 1998;4:22-4. 9. Gould DL. Holmium-YAG laser and its use in the treatment Of urolithiasis: our first 160 cases. J Endourol 1998;12:23-6. I0. Parks JH, Coe FL. The financial effects of kidney stone prevention. Kidney Int 1996;50:1706-12. 11. Preminger GM. Is there a need for medical evaluation and treatment of nephrolithiasis in the "age of lithotripsy"? Semin Urol 1994;12:51-64. 12. Pak CYC. Southwestern internal medicine conference: medical management of nephrolithiasis--a new, simplified approach for general practice. Am J Med Sci 1997;313:215-9. 13. Hiatt RA, Ettinger B, Caan B, Quesenberry CP, Duncan D, Citron JT. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones. Am J Epidemiol 1996;144:25-33. 14. Goldfarb S. Diet and nephrolithiasis. Annu Rev Med 1994; 45:235-43. 15. Seltzer MA, Low RK, McDonald M, Shami GS, Stoller ML. Dietary manipulation with lemonade to treat hypocitraturic calcium nephrolithiasis. J Urol 1996;156:907-9. 16. Parivar F, Low RK, Stoller ML. The influence of diet on urinary stone disease. J Urol 1996; 155:432-40. 17. Lamm LC, Wegner E. Chiropractic scope of practice: what the law allows. Am J Chiropr Med 1989;2:155-9.
Journal of Manipulative and Physiological Therapeutics Volume 23 • Number 3 • March/April 2000 0161-4754/2000/$12.00 + 0 76/1/105113 © 2000 JMPT
CASEREPORT NephrolithiasisWith UnusualInitial Symptoms K e i t h A. Wells, D C ~
ABSTRACT Objective: To describe a less contmon initial symptom of nephrolithiasis, its diagnostic pitfalls, risk factors, and mimicry of other conditions. Intervention and long-term management of nephrolithiasis is also discussed. Clinical Features: A Caucasian man aged 25 years had sudden bilateral inguinal and occasional periumbilical pain. The initial symptol suggested an abdominal pathologic conditi however, costovertebral angle pain followed . . . . . . later with no radiation between the 2 anatomic sites. The initial urine dipstick result was negative for hematuria, but a kidney, ureter, and bladder radiograph revealed a smooth 2-ram x 3-ram stone lodged at the left vesico-ureteral junction. Intervention and Outcome: The patient was referred to a regional university medical center to receive extracorporeal shockwave lithotripsy several days after his initial visit. He was given pain medicine for the waiting period and received daily lumbar spine adjustments with a mild reduction in pain. He eventually
INTRODUCTION Nephrolithiasis is the development of a renal calculus. These stones form in the kidney and typically move through the urinary tract as a ureteral calculus to be excreted. Some stones never exit the kidney (ie, staghorn calculus) and others become impacted in the ureter at several different possible sites, including the vesico-ureteral junction, the ureteropelvic junction, and the crossing o f the ureter at the iliac artery, sites where the ureter narrows. ~ The movement and/or impaction of the stone usually causes sudden, severe back and/or flank pain as the primary symptom, with eventual radiation from the initial site to the groin and/or genitalia. Nephrolithiasis is a significant cause of morbidity in the United States. 1-3Accurate diagnosis of the problem is necessary to avoid treatment delays in the acute patient, to identify the underlying metabolic cause and true extent of the disease, and to identify treatment methods for reduction or prevention of recurrence.
"Diagnosis Department, Los Angeles College of Chiropractic, Whittier, Calif. Submit reprint requests to: Keith A. Wells, DC, Diagnosis Department, Los Angeles College of Chiropractic, 16200 E Amber Valley Dr, Whittier, CA 90604. Paper submitted January 26, 1999; in revised form February 10, 1999. doi:l 0.1067/mint.2000.105113
:ceived ureteroscopic laser lithotripsy because the shock-wave unit had malfunctioned before his appointment. The fragment analysis showed a calcium oxalate composition, and the patient was advised to lower his intake of oxalates. The patient had become a vegetarian approximately 3 months before this first stone episode. onclusion: Nephrolithiasis is a condition com~nly seen in chiropractic practice. Although it is ly easy to recognize, the diagnosis can be elusive if the typical historic factors and diagnostic results are absent or altered. The short-term management of nephrolithiasis is pain management, stone elimination, and the collection of a specimen to identify the composition and underlying metabolic abnormality. Long-term management is to prevent the recurrence of stones. Conservative comanagement by the chiropractic physician can be implemented through nutritional means. (J Manipulative Physiol Ther 2000;23:196-201) Key IndexingTerms: Kidney Calculi; Lithotripsy; Ureter
Because the passing stone often causes back pain at the costo-vertebral angle, some patients may initially visit a chiropractor. This case reviews a less common initial symptom of nephrolithiasis and the typical symptoms, diagnostic protocols, and treatment recommendations. Dietary f~ictors may be addressed by the chiropractic physician in a conservative, preventive management strategy.
CASEREPORT A 25-year-old Caucasian man had bilateral stabbing inguinal pain that began abruptly several hours before his visit with occasional periumbilical pain. He believed he had appendicitis because of the periumbilical pain but elected to see if the symptoms would pass after consulting briefly with a chiropractic clinician. Soon after, the patient returned with a different and sharper pain that began in the left costo-vertebral angle. There was no radiation of pain between the left costo-vertebral angle and the inguinal region. This was a potential source of diagnostic confusion; in most cases, patients who pass ureteral stones typically believe that the pain radiating to the flank and groin is "connected." The physical examination of the patient was unremarkable. A urine dipstick test result was grossly, normal and negative for hematuria. This was another potential source for diagnostic error because the great majority of passing stones cause at least microscopic hematuria. A kidney, ureter, and bladder (KUB) radiograph demonstrated a smooth 2- x 3-
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Nephrolithiasis Table
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Remd stone./?.'mation inhihitors
Nephrocalcin Glycosaminoglycan Uroponlin Tamm-Horsfall protein Crystal matrix protcin
Lithostathinc Uronic acid-rich protein Citrate Magnesium pyroplmsphatc
Table 2. Selected diseases and conditirms associated with nephrolithiasi.~" Primary hyperparathyroidism Renal tubular acidosis Gout Recurrent urinary, tract infection Crohn's disease
Sarcoidosis Milk-alkali syndrome Prolonged immobilization Laxative abuse
millimeter stone lodged at the left vesico-ureteral junction (Fig 1). The patient had no family history of renal calculi, and this was a first episode of nephrolithiasis. The patient was refen'ed to a regional university medical center, where a follow-up urine dipstick analysis result was negative for hematuria at first evaluation. The day after his symptoms began, pain began radiating between the flank and the inguinal region and out to the testicles and penis. The patient was scheduled for extracorporeal shock-wave lithotripsy (ESWL) at one of the university outpatient surgical clinics 2 weeks after his initial visit and was given pain medicine (Vicodin) for the waiting period. The pain continued relentlessly while he waited for his appointment, with occasional episodes of nausea and vomiting, a common symptom of nephrolithiasis, presumably because of the intensity of the pain. Nausea and vomiting usually begin concurrently with the onset of the pain but began a day later in this case with the escalation of pain. In addition to taking pain medication, he received lumbar spine adjustments drily, sometimes twice a day, in the student clinic. The treating intern requested that he complete a visual analogue pain scale before and after each adjustment, but these records were not available for review. The patient reported that the adjustments helped control the pain for brief periods of time. The patient was unable to receive ESWL because of failure of the lithotripter and was then scheduled tbr ureteroscopic laser lithotripsy. The stone was eliminated, and the fragment analysis revealed a calcium oxalate composition. The patient was advised to reduce his intake of oxalates. At this point, he indicated that he had become a vegetarian 3 months before the episode. Vegetarians may "greatly increase their intake of oxalates through green, leafy vegetables; excess dietary oxalate may enhance stone formation. He complied with the recommendation to reduce oxalates and has also maintained the habit of drinking a minimum of 2 liters of water daily. He has not had a recurrence of stones to the date of this writing.
DISCUSSION The true incidence of nephrolithiasis is difficult to establish but has been estimated at 7% in men aged >30 years and
Fig I. Arrow indicates stone.
3% in women (age range not specified). 2 The incidence is greatest in the southeastern United States and in hot climates, j'2 A total of 0.2% of the US population has stones annually, with 5% to 15% of the population expected to have a kidney stone in their lifetime. 2-4 The incidence of stones in men is 4 times greater than the incidence in women. 2-3 Caucasian men have 3 times as many stone episodes as black men) Approximately 50% of patients will have recurrence, with the estimates varying based on renal stone clinic versus population-based studies.n4 The majority of stones (70% to 80%) are calcium-based, typically calcium oxalate, and often calcium phosphate or a mixture of both. The other major stone types are magnesium ammonium phosphate (struvite), uric acid, and the uncommon cystine stone.l-4 Struvite stones typically form staghorn calculi in the renal pelvis and calyces and are also called infection stones because they are associated with urea-splitting organisms (Klebsiella, Proteus, Pseudomonas) and chronic kidney infections. 1.4 Uric acid stones are associated with purine-rich diets and form in acid urine (hydrogen ion concentration [pH] <5.5). Cystine stones are associated with cystinuria, an unusual genetic disorder of the renal tubules. Persons aged <21 years that have a kidney stone may have this disorder, although stones may develop for other reasons. The pathogenesis of stone formation involves 3 factors, including supersaturation of the urine with the involved salt,
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nucleation of the salts with crystal fornaation, and a decrease or absence of stone inhibitors. The process of crystal formation on a nucleus is known as epitaxy. The resultant stones are not strictly inorganic crystals but have varying amounts of organic matrix included in them. Stone inhibitors are substances known to interfere with stone formation at several points along the stone growth process (Table 1).2.3 The majority of stone formers have an underlying metabolic predisposition or outright abnormality that leads to stone formation. II The 4 most common types of metabolic dysfunction are hypercalciuria (with 4 subtypes), hyperuricosuria, hypocitraturia, and hyperoxaluria (with 3 subtypes). These abnormalities are relatively complex, with extensive coverage in the literature. I-5,~,~2 In addition to these causative factors, many diseases and conditions are associated with stone formation (Table 2). In recurrent stone formers or patients with a family history of nephrolithiasis, a more extensive diagnostic process should be followed to determine the presence of predisposing disease (ie, primary hyperparathyroidism). These listed conditions account for <5% of patients with nephrolithiasis, but it is important to pursue the diagnosis in this minority because of the morbidity of the diseases involved. 2 Dietary habits can be both risk factors and therapeutic approaches, depending on the circumstances. At this point, excess protein and salt and excessive calcium and oxalate intake can contribute to stone formation and chronic dehydration. ]2-j6 Several medicines, vitamins, and minerals may predispose a person to stone formation, including calcium, vitamins C and D, acetazolamide, and catabolic steroids (ie, prednisone). 4
Clinical Presentation and Diagnosis The clinical presentation of a passing ureteral calculus typically begins with the sudden onset of excruciating costovertebral angle pain and/or flank pain. Nausea and vomiting often accompany the onset. There may be gross hematuria, sometimes with an occasional visible clot. The patient may also report frequent urination and/or dysuria. If there is frequency, dysuria, and/or urinary incontinence, a concomitant urinary tract infection should be considered. There may be radiation of pain from the costo-vertebral angle or flank across the lower abdomen and into the labia in women and into the testicles and penis in men. At times the pain may radiate to the inner thigh, a radiation that may be from the embryonic relation of the urinary tract to the genitalia. 1The patient typically cannot find a comfortable position and frequently paces. In contrast to the usual symptoms, the patient in the case report had pain that began in the bilateral inguinal region, which escalated in severity, and also appeared in the periumbilical region, atypical for a kidney stone. Back/flank pain was absent until several hours after the onset of symptoms, and nausea and vomiting appeared the next day. For patients who have stones for the first time, the sudden pain and other accompanying symptoms are frightening and will typically lead to a visit to the emergency department. Irritation and spasm of the ureter or obstruction of the renal calyces, pelvis, or ureter cause the pain.
In some patients, tile pain will be less severe, depending on the individual tolerance and whether there is actual obstruction. Some material that passes can be no larger than a grain of sand and may pass with relatively little pain. Some patients have had several incidences of stones and tend to recognize the symptoms. If the pain is not severe, the patient may not seek treatment but will ingest large volumes of water until the pain stops (the stone is then presumed to have passed) or until it is obvious that the stone is impacted. The physical findings in renal colic (the symptoms of passing the stone) are nonspecific. Hypertension and tachycardia may be present because of the pain; as always, hypertension should be investigated to exclude other causes. Fever is uncommon with renal colic. If it is present, a urinary tract infection must be considered. The abdominal exam may exhibit tenderness along the flank or lower quadrant of the affected side, but if there is rebound tenderness or involuntary muscular guarding, peritoneal irritation is suspected. If the patient is seen in a private office setting, this should prompt immediate referral to the emergency department. Bowel sounds may be normal or diminished but should not be absent. The male patient may have testicular tenderness during examination but the testicles should be otherwise normal. Pelvic and rectal examinations are unremarkable. Patients may exhibit nonspecific soft tissue tenderness and/or muscle spasms in the lower thoracic/upper lumbar regions. In less severe episodes, a musculoskeletal diagnosis may be rendered if an incomplete history is taken. Further investigation of nephrolithiasis in the acute patient begins with the urine dipstick to assess for hematuria. Microscopic hematuria is typical. With the usual history and physical examination, the finding lends greater diagnostic weight. Hematuria may be tess commonly absent, however, and may indicate complete ureteral obstruction. A complete urinalysis with culture and sensitivity should be performed to evaluate for infection in the urinary tract, particularly by urea-splitting organisms. Urine pH may be helpful in determining the stone composition analysis. The urine dipstick gives a general indication of the pH, but the specific pH is determined in the laboratory. A pH <5.5 favors uric acid stone formation, whereas a pH >7.5 indicates possible urea-splitting organisms and infection. Microscopic analysis of the urine may reveal crystals that often have characteristic identifying shapes depending on the stone composition. 3'5 For patients who have nephrolithiasis f6r the first time, routine blood testing for serum calcium, phosphorus, uric acid, electrolytes, blood urea nitrogen, and creatinine is sufficient to screen for evidence of underlying abnormalities, such as gout and renal tubular acidosis.l'4 The typical biochemistry panel will contain all these serum tests. Patients with clinical evidence of infection should also have a complete blood count with differential performed. The KUB radiograph is routinely used for diagnosis, although some diagnostic issues must be considered, including that the stone may be radiolucent (uric acid stones) or very small; overlying feces and gas may interfere with analysis; and other calcific densities (ie, phleboliths) can be
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found in the abdomen and pelvis. Nevertheless, plain abdominal films can identify stones in 80% to 90% of patients. 3 The KUB radiograph can be taken in the office setting and used in addition to the urine dipstick. Some researchers believe that the KUB does not add useful information to the diagnostic process, that it is actually an unnecessary expense to the patient, and that the intravenous pyelogram (IVP) is the best first-line imaging tool. l The IVP, a hospital-based procedure used as the gold standard for diagnosis of nephrolithiasis or ureterolithiasis, is routinely performed after the KUB radiograph to identify stone position and kidney function.~ The procedure itself may actually cause the stone to pass, and the patient is given a urine strainer to retrieve the stone. The IVP will reveal whether there is an obstruction, and the course of treatment will be directed to the outcome. In addition, the use of ultrasonography and computed tomography scanning has been described for diagnostic use in nephrolithiasis under a variety of circumstances, including inability to tolerate the contrast media used in the I V P . 6 Retrieval of the stone or a fragment is important in the first-time episode to identify its composition, which helps to determine subsequent treatment plans. The patient is typically given a urine strainer (consisting of nothing more than a plastic funnel with a fine mesh placed at the neck) and is instructed to drink enough fluids (preferably water) to produce at least 2 L of urine per day. This requires the patient to ingest at least 2 to 3 L of water. Specific instructions about intake should be given, such as "drink a 10-oz glass of water every waking hour of the day." In addition, the patient should ingest water if he or she awakens at night. The patient should be taught what to look for in the urine strainer because the material that passes in the urine may be a well-formed, recognizable stone or it may appear literally like grains of sand. Hydration should be recommended regardless of obstruction. I t m a y take hours to days to see if a stone will pass. Nevertheless, whether a "watchful waiting" approach is adopted or a future appointment for lithotripsy or surgery is scheduled, compliance with hydration is essential. Once the stone or fragment is retrieved, a reference laboratory will perform crystallography by polarization microscopy, x-ray diffraction, or infrared spectroscopy. 3,5 Depending on stone composition, further diagnostic studies may be performed and treatment approaches can be planned. In certain patients, more extensive analysis should be performed, including patients with a family history of renal stones, persons aged <21 years, patients who form multiple stones in the first episode, and patients with recurring stones. For example, persons aged <21 years must be assessed for cystinuria by the nitroprusside test. Cystinuria is an inherited renal tubule defect in which there is impaired resorption of the amino acid cystine. 2 As a result, there is excessive excretion of cystine with formation of cystine calculi. Stone formation is relatively uncommon in black men and particularly women; therefore, these patients should also be investigated more extensively. ~t These analyses include specific tests for specific abnormalities (ie, serum parathormone for
hyperparathyroidism) and a 24-hour urinalysis for underlying disorders of calcium metabolism. The 24-hour urine sample is also tested for phosphorus, uric acid, magnesium, sodium, citrate, oxalate, and creatinine concentration. 4
Short- and Long.TermManagement The treatment of acute nephrolithiasis depends on the clinical findings. Typically, patients want pain relief, especially in a first episode. Pharmaceuticals include a variety of narcotics (eg, meperidine, morphine) given in the hospital setting or prescribed on an outpatient basis. There is growing use of parenteral or suppository nonsteroidal antiinflammatory drugs (NSAIDs), including indomethacin and ketorolac, for acute renal colic. Several European, Asian, and US studies have compared the use of NSAIDs with narcotics and have found the NSAIDs effective in alleviating the pain. 2 Medicinal outpatient management of renal colic can be accomplished with oral narcotics and/or oral NSAIDs. 3 Hydration is necessary to encourage passage of the stone for diagnosis and may be therapeutic as well. Again, specific instructions on water ingestion should be given. Stones that are smaller than 4 to 5 mm will pass spontaneously 75% to 80% of the time, especially with hydration. 1.3.5Stones larger than 5 mm have a decreasing chance of spontaneous passage, with approximately 10% of stones measuring 8 to i0 mm passing spontaneously. The treatment approach is guided in part by the type of stone and whether it is impacted. For example, a struvite stone or other large stone may require percutaneous nephrolithotomy or open surgery. ESWL is a well-known and common treatment for impacted stones. ~-6The treatment is noninvasive but painful and requires anesthesia. In patients without contraindications to anesthesia or ESWL, the success rate is approximately 70% to 90%. The use of ESWL for lower urinary tract stones is controversial and therefore is typically used for impactions in the upper tract. Cystine stones do not shatter well and radiolucent stones are difficult to locate; therefore ESWL is not generally used with these types of stones. Fracture of stones larger than 2 cm may cause renal colic from the resulting fragments and are not usually treated with ESWL. In the previous case, the treatment technique used was ureteroscopic laser lithotripsy, 1 of 3 available intracorporeal lithotripsy techniques. The use of laser lithotripsy has gained momentum over the last 12 years because of the introduction of the pulsed dye laser. 7 Different laser instruments (eg, the holmium-yellow argon and the alexandrite) exist with technology beyond the scope of this report. A technologic discussion of the physics and procedural application involved occurs in the literature. 7"9 Laser lithotripsy requires anesthesia and results in a success rate at least as high as ESWL; in some circumstances, the rates are superior. Success of both modalities again depends on stone size, type, and location. Other ureteroscopic lithotrites include intracorporeal ultrasound and electrohydraulic treatments. Long-term pharmaceutical treatment is directed at prevention of stone recurrence. At least one author has studied
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the financial effects of kidney stone prevention and suggests that treatment directed at prevention is worthwhile for health savings and the reduced risk of morbidity from procedures. 1° Several medicines can be used to inhibit stone formationf1.3.5-11 Potassium citrate is used for patients with hypocitraturia; allopurinol is used for hyperuricosuria and is helpful for calcium stones in hyperuricosuric patients and uric acid stones; and thiazide diuretics, indapamide, or cellulose phosphates may be used in certain types of hypercalciuria. Hyperoxaluria can usually be controlled by dietary measures but may be controlled by calcium citrate if the patient is not hypercalciuric. Penicillamine is used in cystinuria. Each aforementioned medicine has potential complications and side effects, and practitioners should familiarize themselves with these when treating patients who take medicines for stone prevention.
Dietary Habits as Risk Factorsand Preventative Methods Dietary habits and practices as both risk factors and stone prevention methods have been investigated and described. 2.5.~2-16 Dietary practice as a preventive measure against stone recurrence is within the realm of chiropractic practice in most states. 17 Compliance with dietary management can be difficult because patients are often asked to eliminate or reduce beloved foods from their diets. Each dietary factor will be addressed below. A general dietary plan should be constructed based on the individual case and the practitioner's knowledge of the underlying metabolic abnormality. Dehydrationandproperbydration. Fluid ingestion, preferably in the form of water, was discussed as a therapeutic measure in the treatment of acute renal colic. Dehydration presumably encourages supersaturation of the salts that form stones. After the first stone episode, the patient should be encouraged to ingest water as if he or she were still attempting to pass a stone. Urine output should continue to be a minimum of 2 L per day, a lifestyle change for most patients. To achieve this output, the patient should drink a minimum of 2 L of water per day and preferably more. The water itself may have high mineral content (ie, calcium), so bottled water that specifies mineral contents or even distilled water may be best. Specific instructions must be given because the vague instruction to "drink a lot of water" will not be followed. The patient may want to substitute other fluids but this should be discouraged. Coffee, beer, tea, and colas have high oxalate content, and milk has high calcium. Dietary protein, It is generally accepted that dietary animal protein plays a causative role in stone formation, but whether reduction in dietary animal protein is beneficial is controversial. 13.14 Economic affluence correlates with the occurrence of nephrolithiasis, presumably because persons with higher incomes can afford to purchase meat and therefort ingest greater amounts of dietary animal protein. 14.16In general, vegetarianism has been shown to protect against calcium stone formation in some studies. However, excessive oxalate intake from green, leafy vegetables can cause stones in patients with hyperoxaluria. Excessive protein
probably contributes to stone formation in 2 ways: by excess purines possibly leading to uric acid stones and by the observed hypercalciuric effect that develops from protein loads. 2 A global reduction of protein, particularly animal protein, is typically recommended, with the daily protein intake suggested at 60 g/dayfl $odium intake. Natriuresis has a calciuric effect that presumably enhances stone formation in an environment of pH >6.5. 5 One suggestion is to restrict sodium intake to 3 to 4 g/day, and certain patients with other conditions (ie, cardiovascular disease) will be restricted to less. 2 Calcium intake. It is tempting to conclude that excessive calcium would lead to calcium stone formation. This conclusion may be true in type II absorptive hypercalciuria, an autosoreal-dominant disorder in which absorption of intestinal calcium is increased. The type I disorder causes increased absorption, regardless of dietary calcium intake, whereas the milder type II disorder is related to high calcium intake. 3 The other types of metabolic hypercalciuria are more complex. Restricting calcium intake in general may actually increase the chance of stone formation, 1-5 perhaps because of stimulation of vitamin D3 activity, which stimulates bone resorption and calciuria. Restriction of calcium in patients with hyperoxaluria can lead to stone formation because of preferential gut absorption of oxalates. The resulting oxaluria can cause calcium oxalate stones. 2A4A6The recommendation for calcium intake is 1 to 1.5 g/day to protect the bone pool and avoid excess intake. 14 Fiber intake, Hiatt et a113 argues that a high-fiber diet protects against nephrolithiasis. Although there are many types of bran sources and no absolute conclusions on how bran may be effective, there is some evidence that 10 to 15 g/day of bran may decrease incidence of new stone formation in patients with hypercalciuria.'6 Citrate intake. Hypocitraturia contributes to stone formation because citrate chelates calcium and acts as a stone inhibitor. Potassium citrate is typically given for this condition because pharmacologic dosing achieves acceptable levels of urinary citrate. Some patients are noncompliant with the medicine as a result of indigestion, multiple dosing, and taste (all depending on the method of delivery). Some research indicates that the amount of fruits and vegetables necessary to achieve acceptable levels of citraturia would likely cause hyperoxaluria.16 However, Seltzer et a115 studied the use of lemonade to achieve increased citraturia. Lemong contain the highest citrate concentration of the citrus fruits. Twelve subjects consumed 2 L/day of 4 oz of reconstituted lemon juice mixed with water. This regimen produced pharmacologic levels of urinary citrate excretion, and the patients tolerated the treatment well. The authors concluded that lemonade might be effective in treating hypocitraturia and may supplement or even replace prescription citrate. This new method is inexpensive and may reduce new stone formation but needs further study. Oxalate intake. Hyperoxaluria is known to contribute to calcium oxalate stone formation. Dietary hyperoxaluria may result from excess consumption of green leafy vegetables, tea, coffee, chocolate, tomatoes, beans, beets, radishes, beer,
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Nephrolithiasis and certain nuts. In some people, vitamin C intake contributes to hyperoxaluria because ascorbic acid is metabolized to oxalate. Vitamin B 6 deficiency may also contribute to hyperoxaluria because pyridoxine is a cofactor in the interconversion of glycine and glyoxalate. 2,~4.~6 Whether excess vitamin C or reduced pyridoxine intake actually causes oxalate stones is debatable, but restricting vitamin C in patients with hyperoxaluria and increasing pyridoxine for those with deficiency is recommended. Vitamin C should be limited to 1000 mg/day and pyridoxine is recommended at I00 mg/day. Vegetarians are presumably at risk for oxalate stones but the overall stone rate in this population is reduced significantly. The risk for oxalate stones is probably higher in patients with hyperoxaluria who consume large amounts o f green leafy vegetables and other foods that are high in oxalate concentration. Magnesiumintake. Although it is not known whether dietary magnesium is adequate to protect against stone formation, there is a clear protective effect of magnesium against calcium oxalate stones. M a g n e s i u m supplementation has been shown to decrease stone recurrence. 16
CONCLUSION This case had an unusual initial symptom because the first symptoms suggested abdominal pathology. The suddenness of the onset of pain indicates a renal stone, even in an atypical clinical picture. In addition, microscopic hematuria is usually present, and the absence of hematuria with the initial urine dipstick can be misleading. The acute patient with a lower pain level may come to the chiropractic office believing the origin of the pain is musculoskeletal. In-office diagnosis is usually possible with the urine dipstick and the KUB radi.ograph. Once the diagnosis is established, emergency or urologic referral is appropriate. Depending on the resulting stone analysis and identification of the underlying metabolic problem, a variety of dietary measures can be suggested that may be successful in preventing stone recurrence. These measures should be carefully implemented based on the actual metabolic abnormality to avoid, for example, too little calcium intake when the initial reaction is
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to reduce calcium. Typical cases of nephrolithiasis are usually easy to suspect by using thorough patient history. The chiropractic physician is in a position to initially diagnose and eventually comanage this disorder.
REFERENCES I. Stewart C. Nephrolithiasis. Emerg Med Clin N Am 1988; 6:617-30. 2. Saklayen MG. Medical management of nephrolithiasis. Med Clin N Am 1997;81:785-99. 3. Trivedi BK. Nephrolithiasis--how it happens and what to do about it. Post Grad Med 1996;100:63-78. 4. Kupin WL. A practical approach to nephrolithiasis. Hosp Pract 1995;30:57-66. 5. Klugman V, Favus MJ. Diagnosis and treatment of calcium kidney stones. Adv Endocrinol Metab 1995;6:117-42. 6. LeRoy AJ. Diagnosis and treatment of nephrolithiasis: current perspectives. Am J Roentgenol 1994; 163:1309-13. 7. Pearle MS, Sech SM, Cobb CG, et al. Safety and efficacy of the alexandrite laser for the treatment of renal and ureteral calculi. Urology 1998;51:33-8. 8. Gould DL. Retrograde flexible ureterorenoscopic holmiumYAG laser lithotripsy: the new gold standard. Tech Urol 1998;4:22-4. 9. Gould DL. Holmium-YAG laser and its use in the treatment Of urolithiasis: our first 160 cases. J Endourol 1998;12:23-6. I0. Parks JH, Coe FL. The financial effects of kidney stone prevention. Kidney Int 1996;50:1706-12. 11. Preminger GM. Is there a need for medical evaluation and treatment of nephrolithiasis in the "age of lithotripsy"? Semin Urol 1994;12:51-64. 12. Pak CYC. Southwestern internal medicine conference: medical management of nephrolithiasis--a new, simplified approach for general practice. Am J Med Sci 1997;313:215-9. 13. Hiatt RA, Ettinger B, Caan B, Quesenberry CP, Duncan D, Citron JT. Randomized controlled trial of a low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones. Am J Epidemiol 1996;144:25-33. 14. Goldfarb S. Diet and nephrolithiasis. Annu Rev Med 1994; 45:235-43. 15. Seltzer MA, Low RK, McDonald M, Shami GS, Stoller ML. Dietary manipulation with lemonade to treat hypocitraturic calcium nephrolithiasis. J Urol 1996;156:907-9. 16. Parivar F, Low RK, Stoller ML. The influence of diet on urinary stone disease. J Urol 1996; 155:432-40. 17. Lamm LC, Wegner E. Chiropractic scope of practice: what the law allows. Am J Chiropr Med 1989;2:155-9.