The occurrence of stones within the urinary tract is a problem that has plagued humans since the beginning of recorded history. Archaeologists have uncovered urinary stones in the mummified remains of Egyptians estimated to be more than 7,000 years old. Many improved methods of deal;ing with stones have been developed in the past, but none have had as much impact as the development of endourology and extractorporeal shock wave lithotripsy (ESWL)in the last decade. These two innovations have eliminated the need for open surgical removel of urinary calculi in the vast majority of paients.I. Epidemiology of Stones
In the United States, stone disease accounts for more than 40,000 hospitalizations annually. The peak incidence is in the third of fifth decaded. Men are affected three times as commonly as women, and white four to five times as commonly as blacks. In a patient who has passes one stone, the likelihood of passing another stone is about 15% by 3 years and 30% by 15 years. Urolithiasis is alife long disease, with an average of 9 years intervening between episodes. 

II. Aetiology and Pathogenesis
The development of stones in the urinary tract is a complex, poorly understood,multifacttorial process. A number of chemical and physical factors are known to play a role.  

A. Supersaturation When there is an overbundance of solute in solution, supersaturation is said to be present. This state depends not only on the amount of solute presented to the kidney but also on urine pH and temperature. In the supersaaturated state, nucleation and aggregation of solute crystals amy occur, leading to stone formation. Supersaturation and crystallization account fairly well for uric acid and custine stone formation but do not completely explain calcium stone formation. Other  stones that mat form by supersaturation include xanthine stones. Epitaxy is the growth of one type of crystal on a different type of crystal. For example, calcium oxalate stones frequently contain a core of uric acid. 

B. Inhibitors are substances in the urine that can block crystallization. One theory of stone formation holds that persons who form stones differ from those who do bot in their lack of sufficient urinary inhibitors. Substances that are known to act as urinary inhibitors pyrophosphate, citrate,magnseium, zinc, and macromolecules.  

C. Matrix is a noncrystallline mucoprotein often associated with urinary calculi. In persons who do not form stones, urinary matrix may acts as a inhibitor; however, matrix may acts as an intiator in some formers and may even provide the framework on which crystal deposition occurs. Pure matrix calculi may be seen in association with Proteus infection.  

D. Exogenous substances may be ingested and become stone components. Indinavir is a protease inhibitor recently introduced for the treatment of human immunodeficiency virus (HIV). Renal colic has occasioally been reported to develop in patients taking this drug. Indinavir stones are soft and gelatinous. They are radiolucent on x-ray examination of the kidney, ureter, and bladder (KUB) as well as on computed axial tomography (CT). Triamterene, a component of Dyazide, may also produce radiolucent stones 

III Stones of the Upper Urinary Tract

Factors associated with incidence   

Conditions of increased incidence
Genetics/heredity Cystinuria – autosomal recessive  Rental tubular acidosis – type I  

Medullary sponge kidney 

Geography High temperature/himidity (Southern United States)
Diet Increased intake of calcium or oxalate
Occupation Sedentary jobs

A. Clinical presentation Rental calculi are usually silent until the stone moves within the urinary tract and produces either hematuria or some degree of urinary obstruction. This may be accompained by pain, urinaryInfection, generalized sepsis, nausea, or vomiting. A urinary calculus should be suspected in a patient who presents with the sudden onset of severely colicky flank or abdominal pain (ureteral colic). Pain may radiate to the groin, testes, or tip of the penis, depending on the location of obstruction. In 25% of cases, patients give a family history of stone disease. Hematuria, gross or microscopic, almost always accompanies an acute episode of stone colic. Careful inspection of the urinary sediment occasionally allows indentification of crystals that may suggest the type of stone present.  

B. Diagnosis Initial evaluation should include urinalysis, urine culture, and plain film of the abdomen. More than two-thirds of urinary calculi are radiopaque and can be seen on KUB. The initial radiologic investigation should be a renal ultrasonogram (US). This may demonstrate the  presence of a stone (US shadowing) in the kidney or ureter as well as any evidence of hydronephrosis. An axial or spiral CT will confirm the presence of calculus in the urinary tact and demonstrate the degree of obstruction. After injection of intravenous (IV) contrast, delayed visualization is not uncommon, and follow-up films up to 24 hours later may be necessary. This is especially true when radiolucent stone [ uric acid) are present or when stones overlie bony areas (vertebral transverse process). Oblique films may be required to and differentiate phleboliths from ureteral stones. Prone films may ne helpfil in some instances of Serve obstruction. Although still used occasionally, the instravenous urogram (IVU) has gradualy been replaced by the spiral CT as the primary imaging modality for acute renal colic. The spiral CT is rapid, does not require a bowel preparation, and avoids the use of IV contrast. It is very accurate at identifying stones in the collecting system and ureter. 

Type of stone 
Frequency (%)  
Effect of pH on solubility  
Radiographic density (bone = 1.0)  
Calcium stones 80
Oxalate 35 Little effect 0.50
(Monohydrate and dihydrate)
Phosphate 10 Increased at pH<5.5 1.0
Oxalate and phosphate
Struvite 10 Increased at pH <5.5 0.20
Uric acid 8 Increased at pH>6.8 0.05
Cystine 1 Increased at pH>7.5 0.15
Other types  Triamterene  




1 Increased at pH>6.8 0.05

 C. Treatment of the acute episode depends on the size and location of the stone, degree of obsrtuction, and the patient’s clinical status.  1. Indications for intervention Patients with infection or high-grade obstruction require prompt intervention. This ususlly requires passsage of a retrograde ureteral catheter or percutaneous  nephrostromy drainage. Patients with small stones and minimal hydronephrosis may be treated conservatively as outpatients with oral hydration and alalgesics. About 90% of ureteral calculi measuring less than 4 mm in diameter pass spontaneously, whereas only 20% of stones greater than 6 mm in diameter pass. Stones are most likely to obstruct the upper urinary tract at one of three  locations: (1) the ureteropelvic junction; (2) the pelvic brim, where the ureter acrossess the iliac vessels; and (3) the ureterovesical junction, which is the narrowest of the three Stones located in the proximal ureter are much less likely to pass than those located at the ureterovesical junction.  

2. Expectant treatment is indicated in the asymptomatic, nonobstructed, noninfected patient with a stone less than 4 mm in diameter in the lower third of the ureter. The patient is instructed to drink copious quantities of water. Plain films of the abdomen should be obtained every week to monitor the progress of the stone as it passes down the ureter. Four to six weeks should be allowed for  stone passage.  

3. Stone extraction is indicated for lower ureteral stones that do not pass spontaneously. The advent of rigid and more recently, flexible ureteroscopy has has eliminated the need for blind or radiologically guided basket extraction. After passage of a guide wire above the stone, the ureteral orifice seldom requires dilatation if one utilizes the smaller semerigid miniscopes, many of which have an outer diameter of less than 7F (French). Once the stone is visualized, several options are available, Small stones may be grasped directly or engaged in astone basket and extracted. Larger stones may be fragmented using US, eletrohydraulic, pneumatic, or laser lithotripsy. Success rates are approximately 95%.  

4. Shock wave lithotripsy Although its primary use is in the fragmentation of renal calculi, SWL is also advantageous for ureteral stones, especially those less than 8mm in diameter. SWL may be performed either with or without a sent in place, as long as the stone can be adequately visualized. Patients are often placed in a prone position for distal ureteral stones to focus the stone within the shock path and avoid the bony structures of the pelvis.  

5. Ureterolithotomy is rarely necessary, given the high success rate of nonoperative and minimally invasive techniques, such as SWL,  ureteroscopy, and laparoscopy. 

IV. Baldder Stones
In the western world, baldder stones are most often found in male patients and are caused by bladder outlet obstruction or foreign bodies (portions of catheters, sutures, or object inserted through the urethra.) Ureteral stones that reach the bladder can also act as nidus for bladder stone are composed of variable proportions of calcium oxalate, uric acid, and ammonium urate. If uric acid is a major component, bladder stones may be radiolucent. They vary from extermely hard to quite soft. Patients with long standing bladder stones are at risk for squamous metaplasia or carcinoma.  

A. Clinical Presentation included pain felt in the hypogastrium or referred the penis, intermittent stream, dysuria, and hematuria Patients may also present with recurrent urinary tract infections.  

B. Diagnosis includes plain films of the abdomen and bladder US. Cystocopy is usually performed in conjunction with treatment.  

C. Treatment  

1. Lithotrites are mechanical devices that permit crushing of large, hard baladder stones under direct vision (Hendrikson lithotrite). The lithotrite should be closed only with the badder partially filled to prevent bladder wall injury. The fragements are then washed out through a resectoscope sheath.  

2. Electrohydraulic lithotripsy Based on the principle of underwater spark generation, the electrohydraulic lithotripsy probe produces a hydraluic shock wave near the stone that usually produces fragmentation after delivery of several shocks. The electrohydraulic lithotripsy probe is flexible and can be passes through both fiberoptic and rigid probe.  

3. US lithotripsy is based on US energy delivered through a rigid probe passed through an endsocope. Small fragments are removed by continuous suction attached to the hollow US probe. Larger fragments can be extracted with grasping forceps baskets.  

4. Cystolithotomy can be performed through a small suprapublic incision or may be combined with open prostatectomy. Cystolithotomy has the advantage of removing the entire stone rather than leaving fragments in the bladder.  

V. Recurrent Stone Disease 
A. Diagnosis It is estimated that predisposing factors can be identified in 80% of resurrent stone formers. Passage of a single urinary stone is an indication for screening studies, including determination of serum calcium, phosphorus, anduric acid levels andmeasurement of calcium phosphorus, uricacid,and oxalatelevels. Patients found to have any abnormalities on screening studies should have a more extensive evaluation, described below. Patients with “metabolically active” stone disease should also have a matabolic evaluation. Such patients include any with a radiologic evidence of new stone formation, an increase in size of a preexisting stone, or passage of stone in the past year. Metabolic evaluation should be performed at a time far removed from the acute stone episode. 

B. Metabolic evaluation 
1. Baseline studies While on their regular diet, patients collect a 24-hour urine sample for creatinine, calcium, phorsphorus, uric acid, oxalate, and cirate . Screening for cystinuria is  performed by the nitroprusside test. The pH of the urine is recorded. Blood is drawn for creatine, calcium, phorsphorus, and uric acid.  

2. Dietary restriction The patient is placed on a diet limited to 400 mg of calcium and 100 mEq of sodium for 1 week. A 24-hour urine specimen is again obtained and serum studies as described previously are repeated.  

3. Calcium loading After an overnight fast during which only distilled water is permitted, the patient reports to the office or clinic at 7.00 a.m. After the first urine voided is discarded, a 2-hour pooled specimen is collected from 7:00 a.m. to 9:00 p.m. The patient receives 1g of calcium gluconate orally at 9:00 a.m. and collects a 4-hour urine specimen from 9:00 a.m. to 1:00 p.m  

C. Hypercalciuria may be caused by bone resorption (most commonly from hyperparathyroidism), renal leak, or incresed absorption from the gastrointestinal tract.  

1. Resorptive hypercalciuria is characterized by constant hypercalciuria regardless of dietary restriction.  

a) Etiology Hyperparathyroidism accounts for fewer than 5% of patients with calcium urolithiasis and is a common cause of the resorptive type of hypercalciuria. Stones occur in aproximately 50% of patients with hyperparathyrodism. In instances caused by hyperperparathyrodism, serum calcium levels are also frequently elecvated, but normocalcemic forms of the disease exist. Other causes od resorpative hypercalciuria are neoplams metastatic to bone, Multiple Myeloma, immobilization (e.g., spinal cord injury), Cushing’s disease, and hyperthyroidism.  

    Normal 24-hour urine values in millgrams  

Biochemical component
Male patients (mg)  Female patients (mg) 
Calcium  <300  <250 
Uric acid  <800  <750 
Oralate  <50  <50 
Citrate  450-600  650-800 

Classification of hypercalciuria  

Type Serum calcium  Urine Calcium Fasting Urine Calcium 
After loading
Resorptive Up Up Up
Absorptive NI NI Up
Renal leak NI Up Up

b. Treatment if resorptive hypercalciuria consists of treatment of the underlying disorder.  2. Absorptive hypercalciuria is the single most common cause of hypercalciuria and is found in more than 50% of patients with stones.  

a. Etiology These patients are felt to have an exaggerated intestinal response to vitamin D, leading to hyperabsorption of ingested calcium. This mechanism explains why the urinary calcium may normalize when oral calcium is restricted and will rise to the abnormal range under calcium loading.  

b. Treatment 
i. Diet and hydration are important in controlling absorptive hypercalciuria. Patients should be placed on diet restricted to 400 mg of calcium per day and 100 mEq of sodium per day.  The addition of bran to the diet is useful because brain binds calcium in the gastrointestinal tract. Patients should be required to drink 3 to 4 l of water daily to reduce urinary concentration of calcium.  

ii. Cellulose phosphate is a calcium-binding resin that excahnges sodium for calcium in the gastrointestinal tract. It must be used in conjunction with a calcium-restricted diet. The usual dose is 5 g three times daily with meals. Because cellulose phosphate lowers serum magnesium and elevates urinary oxalate levels, patients should receive oral magnesium supplementation and should restrict oral intake of oxalate.  

iii. Orthophosphates act by decreasing urinary excertion of calcium and increasing excretion of citrate stone formation. Usual dose is 3 to 6 g daily. The most frequent side effect is diarrhoea.  

3. Renal hypercalciuria accounts for approximately 10% of instances of hypercalciuria.  

a. Etiology The disorder is thought to be caused by the inability of the kidney to resorb calcium from the tubular fluid. Thus, placing the patient on a calcium-restricted diet will not reduce  the loss of calcium in the urine. Calcium loading may increase urinary calcium even further. 
b. Treatment  

1) Thiazide diuretics are the drugs of choice in renal hyper calciuria. The mechanism of action involves increased calcium resorption in the distal tubule and contraction of extracellular volume, thus stimulating calcium resorption in the proximal tubule . The usal dose hydrocholorthiazide is 50mg twice daily. 

2) Orthophosphates In patients unresponsive to thiazide diuretics alone, orthophosphates may be used in combination with clacium restrictions. 

D. Hyperuricosuria Pure uric acid stones account for approximately 10% of urinary calculi. The solubility of uric acid is highly pH-dependent; uric acid becomes insoluble in urine at a pH of less than 5.8.  

Etiology Approximately 25% of patients with uric acid calculi will be found to have gout. Most patients with uric acid calculi, however, have neither hyperuricemia nor hyperuricosuria. The calculi are probably caused by excretion of a constantly acid urine, dehydration, or both Hyperuricosuria is also found in 20% of patients with recurrent calcium stones. Some investigators feel that uric acid crystals may act as a nidus for calcium stone  formation. 

Treatment is based on hydration, alkalinization of the urine, and reduction of uric acid load presented to the kidney.  

Hydration is achieved by oral intake of atlease 3L of water daily.  

Alkalinization of the urine is usually achieved by giving 650 mg of sodium bicarbonate (two tablets) orally every 6 hours. Urinary pH sodium restriction, potassium bicarbonate or potassium citrate may be used instead. In patients unable to take oral medication, IV hydration with sodium bicarbonate may be used. Alkalinization is usually effective in dissolving even large uric acid stones over a period of weeks.  

Reduction of uric acid load may be achieved by dietary restriction and use of allopurinol. Such measures are indicated in patients who are unresponsive to hydration and alkalinization of urine, who have myeloproliferative disorders, or who are receiving cancer chemotheraphy. Dietary protein should be restricted to 90g daily. Allopurinol is a xanthine oxidase inhibitor that is effective in doses of 200 to 600 mg daily. Xanthine stones may form in patients undergoing long-term allopurinol therapy. 

Hyperoxaluria Oxalic acid is an extremely insoluble end product of metabolism. Although the diet may contain large amounts of oxalate, less than 10% of ingested oxalate is absorbed from the gastrointestinal tract and most is derived from metabolism. 

Primary hyperoxaluria

    is a rare autosomal recessive disorders characterized by early onset of nephrocalcinosis. There are two types, distinguished by their specific enzymatic defect, but the clinical picture is similar in both. Urinary levels of oxalate may exceed 100mg/d. Widespread deposition of oxalate in the kidneys and other soft tissues (oxalosis( eventually occurs. Medical treatment with 100 to 400 mg of pyridoxine daily has been reported to reduce oxalate excretion in some patients. General measures should also be employed, including adequate hydration and reduction of dietary oxalate.Enteric hyperoxaluria may occur in patients with malabsorption from any cause (inflammatory bowel disease, small-bowel bypass surgery). The increased amount of fatty acids in the bowel binds calcium, leaving increased oxalate for absorption. Treatment includes a low-oxalate, low-fat diet; oral fluid hydration; and calcium supplementation. Cholestyramine has been found to bind oxalate and may be useful in patients with malabsorption.

    Exogenous hyperoxaluria occurs when substances metabolized to oxalate are ingested in large quantities, such as ethylene glycol (a component of antifreeze), ascorbic acid in amounts greater than 5g/d, and the anesthetic methoxyflurane.

    Struvite stones are composed of magnesium ammonium phosphate and carbonate apatite (“triple-phosphate stones”). They may grow to fill the entire renal pelvis and collecting system (“staghorn calculus”). These stones form only when urinary pH is markedly elevated and increased concentrations of ammonia, bicarbonate, and carbonate are present in the urine. Such conditions may be caused by organisms that produce the enzyme urease, which splits urea into ammonia and carbon dioxide. Proteus species are the most common “urea-splitting” organisms and are identified in more than 75% of patients with struvite stones. Other organisms may produced urease also, including Klebsiella, Pseudomonas, Providencia, and StaphylococcusUreaplasma urealyticum has recently been shown to be a urea-splitting organism. Female patients are affected about twice as often as male patients. Approximately 10% of spinal cord-injured patients have struvite calculi. Other populations at risk are patients with indwelling catheters for many years and persons with ileal conduit or other supravesical diversions.

    Diagnosis Struvite stones should be suspected in any patient with high urinary pH caused by infection. The organism cultured from the urine may not correspond to the organisms within the stone itself. Plain film of the abdomen will usually demonstrate the stones, but they may be poorly mineralized and relatively radiolucent. IVU should be performed to determine whether obstruction is present and causing persistence of infection. Radionuclide studies should be performed to assess renal perfusion and function. Voiding cystourethrogram (VCUG) and urodynamic studies may be indicated if bladder dysfunction is suspected.

    Treatment Successful treatment depends on complete elimination of the stones, correction of any obstruction that may be present, and eradication of infection. Selection of the best treatment method is still controversial, and each instance presents unique problems. For example, patients with obstruction or areas of stasis in the upper urinary tract are poor candidates for treatment by ESWL alone. Another consideration is that percutaneous techniques often require multiple treatments.

    Surgical techniques Surgical nephrolithotomy – “anatrophic nephrolithotomy”-can render approximately 80% of patients permanently stone-free. Nephrectomy should be performed when there is little or no renal function. In instances of partial staghorn calculi with renal parenchylmal damage, partial nephrectomy should be considered.

    Percutaneous lithotripsy recently has replaced open surgery in many patients with dentritic or large staghorn calculi. When rigid and flexible nephroscopes and a variety of fragmenting tools are used, approximately 85% of patients can be rendered stone-free at 3 months; long-term results are comparable with those of open surgery, although many large stones will require staged procedures.

    ESWL As mentioned previously, ESWL along can be used in patients without obstruction or stasis; however, stone-free rates are in the range of 40% to 60%, and multiple treatments are usually required. One of the most effective techniques is the so-called sandwich technique, involving percutaneous lithotripsy followed by ESWL, followed by secondary percutaneous lithotripsy, extraction, or chemolysis.

    Chemolysis Chemolysis is generally ineffective in calcium stones but can be used very effectively to dissolve uric acid, cystine, strutive, and carbonate apatite stones.

    Uric acid and cystine stones occasionally require local irrigation through a urethral catheter, ureteral catherter, or nephrostomy tube. These are readily soluble in alkaline solutions. Uric acid stones can be treated with a solution of sodium bicarbonate in normal saline solution to bring the pH to 7.5. Oral alkalinizing agents such as potassium citrate may be better tolerated for long-term maintenance of an alkaline pH. Cystine stones may be treated with a solution of 60 mL of 20% acetylcysteine and 300mg of sodium bicarbonate per liter of normal saline solution. An alternative agent is tromethamine B, an organic buffer with a pH of 10.2.

    2) Struvite and carbonate apatite calculi are amenable to dissolution by acidic solutions with pH of less than 5.5. The most widely used solution if 10% hemiacidrin (Renacidin), which has a pH of 4.0. The solution is delivered to the stone via nephrostomy tube or ureteral catheter. Normal saline solution should be infused at 30mL/h initially to determine the response of the collecting system. The saline infusion rate is increased over 24 hours to the maximal rate tolerated without flank pain or rise in pressure above 30cm H2O. Hemeacidrin is then infused at half the maximal rate achieved with normal saline solution. When chemolysis is used, several important precautions must be observed: (1) Care must be taken to avoid excessive pressure in the collecting system. A manometer must be placed in the infusion line to monitor pressure and provide a blow-off valve in case of obstruction. Intrapelvic pressure must be below 30cm H2O. Treatment should be discontinued if the patient reports any flank pain. (2) The infusate must have adequate egress, which may be a problem when infusion is through a single ureteral catheter. (3) Chemolysis is contraindicated in the presence of active urinary tract infection. The urine must be cultured daily during chemolysis, and treatment should be stopped if urinary infection is found or the fever develops. (4) Hemiacidrin contains magnesium that can be absorbed to cause hypermagnesemia. Serum magnesium levels should be monitored three times weekly during treatment. Success rates of 85% have been reported for complete dissolution of struvite calculi. Hemiacidrin may be used as primary therapy given through a nephrostomy tube, or as an adjunct to percutaneous lithotripsy, surgical lithotomy, or ESWL.  

    Prevention of struvite calculi depends on elimination of infection with urea-splitting organisms. When chronic infection cannot be eradicated, urease inhibitors such as acetohydroxamic acid may be used to de-effective in preventing struvite calculi in spinal cord-injured patients, although it may be different to tolerate. 

    Renal tubular acidosis is characterized by metabolic acidosis caused by defects of the renal tubule. Although several types of renal tubular acidosis are recognized, urinary lithiasis occurs only in type I, a disorder in which the distal tubule is unable to maintain adequate hydrogen ion gradients. Renal tubular acidosis accounts for approximately 1% of calcium stone-forming pascium oxalate, or mixed stones. Treatment involves alkalinizing the urine with sodium bicarbonate or potassium citrate. 


    Dr.S.Duraisamy MS,Mch (Uro) 
    Consultant Urologist 
    Email: <drduraisamy>[email protected]