Stones which are non-obstructing sitting in the kidneys do not usually cause any symptoms.

While uncommon, obstructing stones may not cause any symptoms (‘silent obstruction’) and this is potentially serious since permanent loss of kidney function may occur without anyone’s knowledge.

One’s ability to urinate does not exclude infection since the other kidney will continue to produce urine even if the other kidney is completely obstructed.

Renal colic has the following characteristics:

• Flank pain: pain in the area to the side of the back between the ribs and pelvic bone. May migrate to the lower abdomen and sometimes the testicle. Often severe and debilitating.

• Nausea and vomiting.

• Urinary symptoms: blood in the urine. Sometimes, the blood in the urine (may be frankly red or tea colored). Urinary urgency and frequency if the stone has move the bottom of the ureter, just before the bladder. Women often describe it as similar to a bladder infection without the burning or foul smelling urine.

• Other: serious symptoms may arise in patients with kidney failure or obstructed infection (urosepsis). Fever is not a normal symptom of uncomplicated renal colic. Any patient with a history of fever and kidney stones should seek emergency medical attention without delay.

Examination usually shows flank or abdominal tenderness. Urine often leaks around the obstructed kidney or the tense renal pelvis is very sensitive to movement. Tapping the back of front of the abdomen will usually elicit pain.

Most patients presenting to emergency will have a basic panel of blood and urine tests including:

• Creatinine/eGFR: to assess kidney function. Often impaired from obstruction. Creatinine and eGFR move in opposite directions.

• Urine testing: most (90%) of symptomatic kidney stones are associated with blood in the urine (hematuria). The blood may not be visible to the naked eye. Absence of blood in the urine should give one pause about the diagnosis. White cells (pus) may be found in small amounts, even in uncomplicated stones. However, the presence of infection should always be considered.

Specialized testing may be of benefit to patients after their acute episode has been dealt with. Patients should postpone metabolic testing for at least a month after completion of treatment for their acute episode. Metabolic stone testing is typically comprised of:

1. Blood testing: Creatinine, electrolytes, PTH, Ca, Mg, PO4, uric acid.

2. 24 hour urine collection: volume, creatinine, uric acid, sodium, calcium, citrate.

The imaging test of choice in most patients is a CT KUB (Computerized Tomography Kidney Ureter Bladder) which images the entire urinary system.

CT KUB does not require intravenous contrast/dye so there is no risk to kidney function. The amount of radiation from the scan is minimal and similar to a plain X-ray of the abdomen. The actual scan itself takes less than 60 seconds on our 64 and 128 slice CT scanners. In some cases, ultrasound, plain X-ray films or a combination are used.

There are a few important things to note about imaging for stones.

1. CT KUB: this is the gold standard and virtually every type of stone will be detectable. It is very accurate with respect to size and location. There is, however, a low dose of radiation. More information on radiation safety can be found here. A CT KUB has about 3 mSv radiation exposure. This handout provides a good summary of risk.

2. Ultrasound: there is no radiation, so it is very safe - even in pregnant women. However, ultrasound has several disadvantages: it tends to overestimate the size of stones, may miss small stones, may mistake normal structures for stones, is not good at locating stones in the distal ureter. Often the presenence of a stone is inferred by the findings on ultrasound rather than direct visualization of the stone itself.

3. X-ray (KUB - Kidney Ureter Bladder): this can only detect stones which are large enough and block X-rays (are 'radiopaque'). It cannot visualize very small stones or those with little or no calcium (e.g. uric acid). It is, however, helpful in determining if a stone can easily be treated with ESWL since fluoroscopy (a special type of 'movie' X-ray) is used to direct sound waves to the stone during this type of procedure. It is very easy and quick to perform - an appointment is usually not necessary.

High serum calcium (hypercalcemia) can be an indicator of serious underlying conditions such as parathyroid tumors. If high a high serum calcium or high parathyroid hormone level is found, referral can be made to an endocrinologist for further evaluation.

Lab evaluation for hyperparathyroidism:

• Basics: CBC, electrolytes, creatinine, calcium, calcium ionized, phosphate

• Thyroid function: TSH, T4 free

• Pituitary function: FSH, LH, prolactin, IGF-1

• Adrenal function: AM cortisol

• Testosterone

• Bone markers: 25-hydroxyvitamin D, PTH, calcitonin

• BCCDC laboratories: gastrin

Acute management applies to those patients who present with renal colic or some other immediate complication of kidney stones (renal insufficiency or infection). Addressing these issues takes priority over long term considerations.

The management of stones which are obstructing (which may not always be symptomatic) is time dependent because obstruction lasting longer than 4-6 weeks may result in permanent loss of kidney function. In otherwise health patients, there is little harm is waiting aside from symptoms.

Confirmation of stone is essential. If a stone has not passed within 4-6 weeks, it should be treated. The absence of symptoms is not sufficient to exclude a persistent obstructing stone.

1. Symptom management: pain medications, anti-nauseants and medications to facilitate stone passage.

2. Relief of obstruction: this addresses the cause of the pain and removes the risk of kidney injury. This may be done 2 ways.

   1. Ureteral stent: internal drainage.

   2. Percutaneous nephrostomy tube): drainage through the skin and into a bag.

3. Removal of stone: this may be accomplished in a number of ways and may occur at the same time as drainage of the kidney. Options are reviewed below.

Stone ‘dissolution’ is not a management options here.

Relevant to patients who have had their obstructing stone treated or who have non-obstructing stones.

There is less urgency to treat these stones since there is little risk of loss of kidney function. There are 2 components:

1. Addressing any remaining stones: see management of asymptomatic, non-obstructing stones.

2. Prevention of stone growth or recurrence: metabolic testing, surveillance imaging, diet and medications, pre-emptive surgery are all tools which may be used.

Review the sections below on dietary prevention of stones.

Untreated obstruction combined with infection can progress to sepsis, shock and death.

Obstruction + stone is a true urological emergency as even health, young individuals may develop life-threatening urosepsis. Antibiotics on their own can only temporarily delay progression. Treatment is decompression (drainage) of the collecting system (via a stent or percutaneous nephrostomy tube), combined with antibiotics and supportive care. Admission to hospital is almost always required and some patients will require admission to the intensive care unit.

Development of renal failure may results in serious complications including life-threatening severe metabolic derangements.

There is minimal risk to long-term kidney health with the first 6 weeks after the onset of obstruction in most situations. After this, obstruction may result in permanent loss of kidney function and removal/decompression should be considered

Stone width, location and duration of obstruction are the primary predictors of stone passage. Larger stones, those higher nearer the kidney and stones which have been present for longer are less likely to pass spontaneously.

Stone passage calculator.

The severity of pain is independent of stone size but is proportional to the severity of obstruction. Patients may elect to have stones removed rather than suffer for several weeks with renal colic.

Stone width and chance of passage with medical expulsive therapy (approximate):

• <2 mm: 90-95%

• 2-4: 75%

• 5-6 mm: 50%

• >6 mm: 30%

  • >9 mm: 10%

Stone Location

• Proximal ureter: 48% (nearest the kidney).

• Mid ureter: 60%

• Distal Ureter: 75%

• Ureterovesical junction: 79% (nearest the bladder)

doi: /10.1007%2Fs00330-017-4852-6

doi: /10.2214/ajr.178.1.1780101

Pain management:

• NSAIDS: non-steroidal anti-inflammatories are the mainstay of pain relief. They are intended for short term use only. Ibuprofen (Advil), diclofenac (Voltaren) and celecoxib (Celebrex) are examples Stomach upset, ulcers and kidney failure may occur with prolonged use.

• Opioids: these are used for severe pain only and for short durations. More likely to cause nausea and they may be addictive. Codeine, tramadol, morphine are examples.

Management of other symptoms.

• Stool softeners. Opioid pain medications frequently cause constipation. Consider also taking an over the counter stool softener like Restoralax or Miralax.

• Antiemetics and antinauseants. Diphenhydrenate (Gravol) and metoclopramide (Maxeran) may be helpful.

If symptom control is inadequate patients should consider intervention with decompression and stone removal.

Medical expulsive therapy (MET) is an option in all patients who do not have infection or renal insufficiency. MET should not be utilized for more than 6 weeks. MET may not make the most sense if the stone has little chance of spontaneous passage.

Most renal stones are not soluble and obstructing ureteral stones are even less likely to respond to dissolution therapy. Having said that, combination of an alpha-blocker plus urinary alkinalization may be attempted. There is never any guarantee that a particular stone will pass on its own regardless of how small it is.

Medications only modestly increase the chances of stone passage. Stone size and location remain the best predictors of spontaneous stone passage.

1. Strain/filter the urine: this is critical to confirm passage. Best is a fine wire mesh sieve (e.g. tea strainer). Note that blood clot may appear similar to stone.

2. Alpha-blockers: are the mainstay of medical expulsive therapy. They are most effective for moderate sized stones (>5 mm) in the distal ureter. They increase the chances of passage by about 10%.

Review the section on BPH for use and side-effects of alpha-blockers.

Confirmation of stone passage is ALWAYS necessary for patients on medical expulsive therapy. The absence of symptoms CANNOT be relied upon to determine if the stone has passed. PERMANENT LOSS OF KIDNEY FUNCTION MAY RESULTS FROM CHRONIC OBSTRUCTION WHEN A STONE HAS BECOME IMPACTED IN THE URETER.

Silent Obstruction

Silent obstruction is the presence of an obstructed stone without any significant symptoms. This is more common than one might think - up to 10% of patients with large stones with little chance of spontaneous passage may not manifest any significant symptoms.

The bottom line is that confirmation of stone passage is always advised unless a stone has been been definitely identified and it’s characteristics are consistent with passage of all of the stone identified on imaging at the time of diagnosis.

https://doi.org/10.1038/s41598-023-29866-5

There are two related options to address kidney stones.

Drainage/decompression

Pain from stone and loss of kidney function are related to obstruction of urine. There are 2 options for drainage which are considered equally effective at drainage but ureteral stents are less invasive and associated with fewer risks.

1. Ureteral stent: this is more desirable when ever it is possible. A ureteral stent is a minor surgical procedure where a slim, long plastic tube (roughly 24 cm in length and about 3 mm in diameter) is placed within the ureter extending from the kidney to the bladder. Stents allow urine to pass along side of the stent. Stents are temporary and must always be removed or replaced after 3-6 months though are usually removed within days of stone removal. They are often placed on a temporary basis after a ureteral stone is removed. No external bag is necessary. Review more on ureteral stents here.

2. Percutaneous nephrostomy tube (‘perc’): collecting system may be drained externally by placing a stone through the skin and parenchyma of the kidney into the collecting system. An external drainage bag is necessary. These are placed by a radiologist.

There are 2 main options for removal of ureteral stones.

1. Nephroureteroscopy: a long scope with a camera is advanced ‘upstream’ from urethra, through the bladder and into the ureter. The stone is broken into fragments to facilitate removal. This is the primary method for dealing with most ureteral stones.

2. Shock wave lithotripsy (SWL): utilizes focused sound waves to fragment stones. Most commonly used for intra-renal stones but may be used for stones in the proximal ureter.

The goal is for 2-3 litres of urine OUTPUT for day.

Just about any fluid will be helpful, but ideally water with lemon juice (see CITRATE below). How much you drink is much more important that what you drink.

People commonly ask about sodas, tea and coffee. You do not need to worry about an increased risk of stone with these fluids (despite what you might read on the internet - because the oxate content is minimal). Cranberry juice, while helpful for urinary tract infections, it probably makes no difference for stones (might try to avoid more than 6 ounces per day in oxalate stones, but might be helpful for calcium phosphate stones). All fluids are good with one exception: the only type of fluid associated with an increased risk of stone is SODA WITH SUGAR - avoid this.

High salt (sodium chloride, NaCL) intake predisposes to stones. Not all salt comes from the 'salt shaker'. A significant amount is found in breads and cereals. Small portions through the day add up. Also note that excess calcium intake will counteract the intended effect of thiazide diuretics which are sometimes used to treat high urine calcium levels (see below).

Tips to limit sodium intake:

No more than 2 servings/day of breads, bages, muffins, rolls, baked goods

Protein alternatives to the traditional lunch sandwich with processed meats. e.g. big salad, veggie wrap, non-processed meats

1. Limit cheese intake.

2. Use oil and vinegar salad dressings instead of creamy ones.

3. Unsalted snacks.

4. Eat less processed or prepared foods (e.g. eat out less often, fewer frozen entrees).

5. CHECK THE LABELS OF WHAT YOUR ARE EATING - you might be surprised by how much salt is in processed and packaged foods.

Note: Reduce your salt intake and you will have less calcium in the urine to form stones. For every 100 mEq of urinary sodium, there will be a corresponding 50 mg increase in calcium in the urine by 50 mg.

Acid loads can contribute to some types of stones. Acid loads reduce urinary citrate which is an important inhibitor of stone (see below).

GOOD: nearly all fruits and vegetables decrease acid loads and offset the stone-forming effects of high acid loads.

BAD: excess meats, fish, poultry, cheese, grains are high in acid load.

Balanced intake of calcium (about 1000 mg/day) is good - too much or too little is bad.

Balanced calcium intake is critical. Too little or too much and the risk of stone is increased. Counter to conventional wisdom LOW CALCIUM INTAKE (<600 mg/day) is associated with a markedly increased risk of stones.

Note that the TOTAL recommended dietary calcium per day is 1000 mg. If you are taking a calcium supplement for 1000 mg per day, you will easily exceed the recommended amount and predispose to stones. Assess the total amount that you take based on supplements and in your diet.

Note that dietary citrate reduces complexation of calcium with oxalate and phosphate and will reduce the formation of stones.

High oxalate can be a major contributing factor to recurrent stone, but a reduced oxalate diet is not necessary in everyone. Only about 20% of patients with stones need to reduce their oxalate. In addition, many of the foods high in oxalate are very healthy (many of the vegetables high in oxalate are high in phytate and magnesium which are stone inhibitors; some hare high in lycopenes which reduce prostate cancer risk).

Moderation is the key to managing oxalate! You do not need to eliminate any food completely.

THE FIRST STEP TO TAKE WITH HIGH URINE OXALATE IS TO TAKE CALCIUM (either in food or supplement) BEFORE/WITH MEALS. E.g. 300 mg for a glass of milk or cup of yogurt at each meal.

Note that some foods may be either high or low in oxalate depending on how they are processed. For example, when soybeans and soy foods are processed with calcium (which is common), they are NOT high in oxalate. Another example is tea. The oxalate in tea varies with the type of tea, the soil conditions in which it is grown and how long it is steeped. In general, tea intake does not need to be restricted. In general, soda is not healthy, but the oxalate content is negligable and therefore soda does not need to specifically be restricted (it is unclear if the phorphoric acid in sodas is an issue).

Vitamin C in excess increases the liver's production of oxalate. "High dose" vitamin C therapy (1000's of mg per day) should be avoided.

Probiotic with at least 3 strains of bacteria can decrease oxalate absorption by metabolizing the oxalate. Kefir is a fermented milk drink which is full of probiotics. Fish oil may also decrease absoption of oxalate.

If you have inflammatory bowel disease, you will be predisposed to absorb oxalate and you will need to be even more cautious.

Most of the citrate in the urine is produced in the kidney itself. LOW urine citrate is a risk factor for stone formation. The most common cause for this a excess acid load (see above). Limit foods with high acid loads.

An easy way to get citrate is to try a glass of orange juice for breakfast and some water with lemon in the afternoon.

Ways to increase citrate:

• Eat more fruits and vegetables (at least 5 servings, about 2 cups).

• Drink beverages flavored with citric acid (low-sugar, low-calorie lemonades and sodas).

• Lemons, limes and oranges. There is no one specific type of citrus which is best and any citrate will be beneficial.

• Either in foods or in drinks.

• Lemon or lime juice 2 ounces diluted in water in morning and before bedtime (provides 6 g citric acid). This only increase citrate levels but will not increase urine pH.

• Orange juice is just as effective as lemonade in increasing urinary citrate but will also increase urine pH. The downside to OJ is the sugar.

• Grapefruit juice has very, very high citrate, but can affect the metabolism of some medications such as coumadin by increasing enzyme activity of CYP450. Also has some oxalate.

• Supplement magnesium. In some circumstances, citrate levels cannot be increased sufficiently without correcting low magnesium levels (the RDA for Mg is 350 mg/day). In general, the data on magnesium supplementation is limited.

• Some patients require Potassium Citrate supplementation since it is highly effective at increasing citrate levels, pH and is well tolerated (see below).

Less common causes of low citrate include renal tubular acidosis (RTA). RTA is more common in young women and associated with very, very low levels of urine citrate, high urine PTH, high serum chloride and low potassium. Calcium phosphate stones are most common and potassium citrate will often times correct the high urinary calcium and low citrate which predisposes to stones in these patients.

Uric acid stones are most common in acid urine environments combined with high urinary uric acid load. Vegetables do have uric acid, but the amount is small and you do not need to decrease intake of fruits and vegetables to reduce uric acid levels.

All animal tissue ('flesh'), including fish and seafood, contains uric acid. Same for non-'red meat'. Not all animal protein, however, is the same. Dairy, for example, has limited uric acid. 'Flesh' foods are particularly bad because they contain sulfur which is metabolized to sulfuric acid and can cause an issue with ACID LOAD (see above). Avoid excesses in any of 'flesh' foods.

Tips to reducing urine uric acid:

• Reduce portion size of meats, fish, poultry at meals.

• Reduce frequency of meats, fish and poultry. Try having a meat-free meal once a day or go meat-free a couple of days per week.

• Increase fruit and vegetable intake so that the urine is less acidic.

• Limit high intake of fructose and/or alcohol

Atkins Diet promotes stones for many reasons (high acid and uric acid load, low citrate). Probably not a good long-term choice, but if you have your heart set on this (and don't want to try the other ways to reduce weight which don't increase your risk of stones) you can push fluids, take some supplemental citrate (e.g. potassium citrate). Get off the diet once you have lost your weight.

South Beach Diet is basically a more liberal form of the Atkins.

DASH Diet. This is effective in decreasing hypertension and is a very good diet to reduce stone formation. The only modification should be limitation of nuts.

Dietary supplements. Be cautious that some concentrated plant or spice-derived extracts may be very high in oxalate.

Weight loss surgery. These patients often have low urine output (because the size of their stomach has been reduced). Often citrate supplementation, pushing fluids, probiotic therapy and calcium (often in high doses up to 1000 mg with each meal) are important to correct for the surgery-induced changes. The urine studies will dictate what needs to be done.

Obesity. This is a major risk for uric acid stones

Thiazides are a type of diuretic that reduces the secretion of calcium in the urine. They are frequently paired with potassium supplements.

Options

• HCTZ 25 mg twice daily

• Chlorthaladone up to a maximum of 50 mg once daily

• Indapamide 1.25 mg daily

Monitoring:

• Potassium: check within a month of starting the medication

• 24 hour urine calcium, sodium and citrate in 6-12 months after starting.

Potassium counteracts the tendency of thiazides to lower blood levels of potassium while the citrate can help prevent stones and reduce the effects of acid loads in causing stones.

Options

• See dietary advice above.

• K-Citra 20 mEq twice daily.

• High potassium foods: tomatoes, bananas, canteloupe

Comments:

• Avoid in: active peptic ulcer disease, reduced kidney function, potassium sparing diuretics.

• Side effects: usually none, occasionally stomach upset

Monitoring:

• Check 24 hour urine calcium, sodium and citrate within a month of starting the medication then 6-12 months after starting

Notes: no increased risk of calcium phosphate stones as a result of increased urine pH

See the section on ‘Moderation of Protein’ above.

• Weight loss and optimal management of diabetes.

• Reducing acid load.

• Reducing uric acid load.

• Reducing salt load.

• High fluid intake.

Uric acid stones are most common in acid urine environments when there is high urinary uric acids. Vegetables do have oxalate, but the amount is small and you do not need to decrease intake of fruits and vegetables to reduce uric acid levels.

All animal tissue ('flesh'), including fish and seafood, contains uric acid. Same for non-'red meat'. Flesh foods are a 'double whammy' - they not only contain uric acid but also acidify the urine which predisposes to crystallization. Not all animal protein, however, is the same. Dairy, for example, has limited uric acid. 'Flesh' foods are particularly bad because they contain sulfur which is metabolized to sulfuric acid and can cause an issue with ACID LOAD (see above). Avoid excesses in any of 'flesh' foods.

Tips to reducing urine uric acid:

• Reduce portion size of meats, fish, poultry at meals.

• Reduce frequency of meats, fish and poultry. Try having a meat-free meal once a day or go meat-free a couple of days per week.

• Increase fruit and vegetable intake so that the urine is less acidic.

• Limit high intake of fructose and/or alcohol

Increasing the pH of the urine is important to try and reduce crystalization of uric acid. How this is done is important: once uric acid dissolves it will combine with either sodium or potassium; when it combines with sodium (Na), it becomes less soluble and can predispose to calcium stone; when uric acid combines with potassium it remains soluble.

Fluid Choices:

• Orange juice is probably best for uric acid stones (because it comes as potassium citrate).

• Others: grapefruit juice is probably similar to orange juice; lemon juice has a higher acid load and may not be as good (but probably better than water); diet sodas with citrate only have limited amounts.

• Mineral water with high bicarbonate is likely to be good.

• AVOID FLUIDS HIGH IN SUGAR.

Medications: there are 2 primary options.e

• Potassium citrate (K-citra). The citrate is metabolized to carbon dioxide and then bicarbonate once the citrate enters the circulation. The bicarbonate is then excreted in he urine. Dose: 60-80 mEq per day. The tablets are 10 mEg so 2 tablets 2-3 times per day is effective. Slightly more effective than sodium bicarbonate because it also reduced calcium excretion. May cause stomach upset and may be avoided in renal failure or if there is a history of stomach ulcers.

• Sodium bicarbonate. This is baking soda and does not require a prescription. The desired dose is 3-4 grams per day. 650 mg tablets are available. 2 tablets 2-3 time per day will provide the recommended amount. The sodium does not seem to increase the urinary calcium levels but it does not reduce it either.

Highly motivated patients may choose to check their urine pH with dipsticks. The target urinary pH is 6.5-7.2

When is the best time to take these medications? Ideally, they are taken a couple of times through the day and just before bed time.

This medication has limited use and should be considered second line treatment and only in those with high urinary uric acid levels that persists after urinary alkalinization (note that the urine uric acid levels may be falsely low and often are unimpressive because the uric acid can precipitate out and sit at the bottom of the collection jug, thus not accounted for in the uric acid concentration). The only study looking at allopurinol found that is was effective for calcium oxalate stones in patients with hyperuricosuria (not for uric acid stones per se).

Needs to be used with caution in patients with kidney insufficiency.

Observation, often combined with some surveillance imagine, is the default course of action unless one decides to intervene. The imperative to intervene for stones that are asymptomatic is entirely elective - unlike stones that are causing pain.

Stones are very common - afflicting between 1 in 15 to 1 in 7 people. Patients who have a history of stones in the past are more likely to have a problem in the future. This risk is even more acute in patients who currently have a stone.

The risk that a stone may produce symptoms in the future is highly variable. The risk depends on multiple factors:

• Size: larger stones are more likely to require intervention if they become symptomatic.

• Number: increased number of stones pose increased risks.

• Laterality: is the stone on one side only (unilateral) vs. both sides (bilateral). Bilateral stones pose an increased risk.

• Location: lower pole stones need to fight against gravity to enter the ureter and are almost half as likely to become symptomatic then stones located elsewhere. This is the same reason why SWL is less effective for lower pole stones.

• Time horizon: the risk that a stone will become symptomatic increases with the duration of time.

• Other: patients with diabetes and metabolic abnormalities are more likely to have stone progression.

The result of so many variables is that risk of any event is also highly variable. Here are the risks if one simply watches and waits for an asymptomatic stone.

• Symptoms: development of renal colic: averages 1 in 2 (50%) over 5-10 years. The range is between 1 in 25 to 2 in 3.

• Obstruction without symptoms: about 1 in 30 over about 5 years. The risk is that there may be silent loss of renal function and in some cases the stone will grow to quite a large size.

• Chance of spontaneous passage (i.e. not requiring surgery): between 1 in 30 to 1 in 3. The average risk is about 1 in 2 (50%). Stones almost always will be symptomatic when this happens.

• Need for surgical intervention: this is what happens when stones become symptomatic and do not pass. 5 year risk is 1 in 15 to 1 in 4. Studies disagree significantly on this risk.

If one were to look at these risks as a whole and pretend that there actually is an ‘average patient’, about 1 in 2 stones will cause problems in the next 5 years and about half of these will require surgical intervention - about 1 in 4 patients who elect to observe.

In practice, some patients are at quite low risk of requiring surgery whereas others are at high risk.

Consider the following:

• Patients who have stone in only one kidney and those stones have been treated (and ostensibly been rendered ‘stone free’): the 10 year risk of requiring any repeat surgery is about 1 in 4. That is, they’ve made a new stone and require intervention. When repeat surgery was necessary, over 80% of surgery occurred on on the same side as the original surgery. This should be considered the lowest possible risk.

• Patients who have stones in both kidneys the risk of a future stone episode on either side is about 1 in 2 over 5-10 years. The risk is equally distributed between both kidneys. Studies seem to agree on this risk. The risk is actually higher than 50% in those patients who have additional risk factors (e.g. multiple stones, larger, in areas other than the lower pole).

It is on this last point where there remains considerable controversy on the impact of pre-emptive intervention. To what degree does surgery an asymptomatic stones reduce the risk of a future event (symptoms or surgery)? This is incredibly important since why would one intervene and assume the inherent risks of surgery if it made no difference in the ultimate outcome?

One large study showed no difference in the risk of requiring surgery in the future if pre-emptive surgery is done on the contralateral side (an exception being a reduced future risk if surgery was done for stones greater than 6 mm). This study had the benefit of using repeat surgery as the end point and reviewed the records of thousands of patients. The primary weakness is that the study was retrospective.

Another study show a substantial reduction in risk (well over 50% reduction) if surgery was done pre-emptively. This included surgery for stones smaller than 6 mm on the opposite side. Pre-emptive surgery reduced the risk of visits to the emergency department by 30% over 5 years (from about 1 in 2 to 1 in 10). The chances of needing surgery was reduced from about 50% (from 65% to about 15%) - this is a softer end point because many patients might reasonably have been observed longer (with ongoing pain) with some of these stones passing without needing intervention. Interestingly, the risk of new stone formation was not affected by whether a patient had pre-emptive surgery or not. While this study had fewer than 100 patients, it was prospective and very well designed.

The patients at the highest risk have multiple bilateral stones which are larger and located in the upper to and mid-poles, plus a history of diabetes. If that patient lived ‘off grid’ or traveled out of country frequently, they would be subject to additional financial risk and the potential issue of quality healthcare.

Take away messages:

• There is no ‘one correct’ course of action for patients with asymptomatic stones.

• Treatment is likely to reduce the risk of ending up in the emergency department because of symptoms and to a lesser degree of requiring repeat surgery. The risk of the former is likely to be about 50% and the latter will be lower.

• Prevention is important - ensure you review the information on dietary modifications.

• Follow-up imaging is likely to be helpful - especially in those who have stones that have not been treated.

References:

doi: 10.1056/NEJMoa2204253

doi: 10.1089/end.2018.0695

doi: /10.1007/s11934-018-0782-3

doi: 10.1007/s00240-021-01281-3

Preemptive surgery is operating on a stone in the absence of the stone being symptomatic or posing an imminent or serious threat.

Patients most likely to benefit are those who are increased risk of developing symptoms or a complication from stones. Characteristics for increased risk include the following:

• Bilateral stones.

• Multiple stones.

• Larger stones (> 6 mm).

• Stone location anywhere aside from the lower pole.

• Comorbidities: diabetes, metabolic syndrome, history of rapid stone growth.

• At increased risk of stone-related complications: reduced kidney function (including solitary kidney), prone to urinary tract infection.

• Social factors: reduced access to health care, frequent travel.

• a decision is made to proceed with pre-emptive surgery, one should consider what options are available to them. These are the same treatment options available to all patients with kidney/ureteral stones. Some of these options may be unavailable or inappropriate depending on the characteristics of the stone.

Shock Wave Lithotripsy

This approach uses focused sound waves to break up stones in the kidney. It tends to be well tolerated though there is a definite risk of bleeding around the kidney and it relies on the flow of urine to flush fragments out. Larger fragments may become fragments in the ureter.

The most favorable characteristics of stone responsive to ESWL include upper and midpole location (gravity helps with clearance of fragments), smaller stones, radiopaque stones to assist with targeting and stone compositions which are softer (NOT COM or CaP). SWL is not very good for larger stones (those greater than 8-10 mm).

In summary, most effective against smaller, radiopaque stones not located in the lower pole.

Read more about SWL here.

Nephroureteroscopy

This approach uses ureteroscope (long flexible or semi-rigid scopes with built-in camera, light source and working channel) combined with a laser to turn stones to dust. It is sometimes called retrograde intra-renal surgery (RIRS) or URS.

Nephroureteroscopy is applicable to radiopaque and radiolucent stones in any location in the kidney. Historically restricted to stones less than about 10 mm in size, it has been utilized with good success in even larger stones and as a viable alternative to stones which might previously have required PNL (see below).

The risks of the intervention include ureteral injury, bleeding, infection, postoperative discomfort. The risk of a serious ureteral injury which may require something more than temporary stenting is 1 in a few 100.

Read more about nephroureteroscopy here.

Percutaneous Nephrolithotomy

Percutaneous nephrolithotomy (PNL) is a technique that approaches the kidney though a temporary channel that is created through the skin and renal parenchyma to enter the kidney. It allows the introduction of larger instruments and is excellent for clearing large stones which might be untreatable or require multiple treatments with other approaches. It is the treatment of choice for staghorn stones.

While PNL is highly effective, it carries a not insignificant risk of bleeding, requires overnight hospitalization and there are other risks associated with the access.

Read more on percutaneous nephrolithotomy here.

Staghorn stones are large stones that fill the collecting system. They may be partial (filling only part of the collecting system) or complete (filling the entire collecting system). On imaging, they appear similar to the antlers of stags, hence the name.

The pose particular risks. While they may be asymptomatic, they can gradually injure the overlying kidney parenchyma resulting in scarring. There are long-term risks of loss of kidney function.

Staghorn stones may also be associated with infection and treatment is almost always recommended in these cases to minimize the risk of sepsis as well as kidney function.