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Acute Renal Colic

Acute Renal Colic

Article Author:
Laryssa Patti
Article Editor:
Stephen Leslie
6/24/2020 3:39:20 PM
For CME on this topic:
Acute Renal Colic CME
PubMed Link:
Acute Renal Colic


Nephrolithiasis, also known as kidney stones, is a common condition affecting 5% to 15% of the population at some point, with a yearly incidence of 0.5% in North America and Europe, and is caused by a crystal or crystalline aggregate traveling from the kidney through the genitourinary system. [1] [2] [3] [4] 


There are multiple predictors and risk factors for stone formation. The following are the most common:

  1. Inadequate urinary volume. Patients with low urine volumes (usually less than 1 L per day) increase the concentration of solutes (indicated by urine with an osmolarity greater than 600 mOsm/kg) and promote urinary stasis, which can cause supersaturation of solutes and lead to stone formation.
  2. Hypercalciuria. Most often, this is an idiopathic finding, although it can be secondary to increased intestinal absorption of calcium, increased circulating calcium, hypervitaminosis D, hyperparathyroidism, high protein load, or systemic acidosis. Hypercalciuria increases the saturation of calcium salts like oxalate and phosphate, causing the formation of crystals. Calcium containing stones form approximately 80% of all renal stones.  Hypercalciuria is usually defined as urinary calcium of 250 mg or more per 24 hours.
  3. Elevated urine levels of uric acid (uric acid stones account for 5% to 10% of all renal calculi), oxalate, sodium urate, or cystine. Often these can be secondary to a high protein diet, high oxalate diet, or a genetic defect causing increased excretion. Most pure uric acid stones are caused by high urinary total acid levels and not by elevated urinary uric acid.
  4. Infection stones. These are caused by urea-splitting organisms (Proteus or Klebsiella spp but not Escherichia coli) that break down urea in the urine, increasing concentrations of ammonia and pH, which promote stone formation and growth. Also called struvite or triple phosphate (Magnesium, Ammonium, Calcium) stones.
  5. Inadequate urinary citrate levels. Citrate is the urinary equivalent of serum bicarbonate. It increases urinary pH, but it also acts as a specific inhibitor of crystal aggregation and stone formation. Optimal levels are approximately 250 mg/L to 300 mg/L of urine.


Approximately 5% to 15% of the population will be affected by a kidney stone, and of those, 50% will have a recurrent stone within five to seven years of the initial presentation if preventive measures are not taken. Over 70% of stones occur in people 20 to 50 years old, and they are more common in men than women by a factor of about 2:1. Patients with obesity, hypertension, and/or diabetes are at increased risk for kidney stone formation.[5][6][7]


As a stone moves from the renal collecting system, it can significantly affect the genitourinary tract. A stone can cause obstruction and hydronephrosis of the ureter, decreasing the rate of ureteral peristalsis and causing urine to back up into the kidney. This can cause decreases in the glomerular filtration rate of the affected kidney and increase renal excretion of the unaffected kidney as well as very severe, excruciating pain. Complete obstruction of the ureter can lead to the eventual loss of renal function, with damage becoming irreversible in one to two weeks. Additionally, there is a risk of rupture of a renal calyx with the development of a urinoma. Of even more concern is the possibility that an obstructed renal unit might become infected, causing obstructive pyelonephritis or pyonephrosis. This condition can be life-threatening and requires immediate surgical drainage as antibiotics alone are ineffective

Renal calculi can become impacted, most commonly at the ureteropelvic junction, as the renal pelvis narrows abruptly to meet the ureter, near the pelvic brim, or at the ureterovesical junction.

History and Physical

Patients with renal colic typically present with sudden onset of flank pain radiating laterally to the abdomen and/or to the groin. Patients often report a dull constant level of pain with colicky episodes of increased pain. The constant pain is often due to stretching of the renal capsule due to obstruction, whereas colicky pain can be caused by peristalsis of the genitourinary tract smooth muscle against the obstruction. Many patients report associated nausea or vomiting, and some may report gross hematuria. As the stone migrates distally and approaches the bladder, the patient may experience dysuria, urinary frequency, urgency, or difficulty in urination.

Patients experiencing renal colic may present in very severe pain. Classically, these patients are unable to find a comfortable position and are often writhing on or pacing around the examination table. The exam may reveal flank pain more commonly than abdominal pain, and the skin may be cool or diaphoretic. There is often a prior personal or family history history of stones.


Diagnosis is made through a combination of history and physical exam, laboratory, and imaging studies. Urinalysis shows some degree of microscopic or gross hematuria in 85% of stone patients, but should also be evaluated for signs of infection (e.g., white blood cells, bacteria). Urinary pH greater than 7.5 may be suggestive of a urease producing bacterial infection, while pH less than 5.5 may indicate the presence of uric acid calculi.

Basic metabolic panel (BMP) should be obtained to assess for renal function, dehydration, acid-base status, and electrolyte balance. Serum calcium should be checked. Complete blood count (CBC) can be considered to evaluate for white blood cell count if there is a concern for infection. Mild elevation of WBCs is commonly secondary to white blood cell demargination.

Consider obtaining a parathyroid hormone (PTH) level if primary hyperparathyroidism is suspected as a cause of any hypercalcemia. If possible, urine should be strained to capture stones for analysis to help determine if there is a reversible or preventable cause of stone development. Further metabolic testing such as 24-hour urine collection for volume, pH, calcium, oxalate, uric acid, citrate, sodium, and potassium concentrations should be considered in high-risk first-time stone formers, pediatric patients or recurrent stone formers. It is highly recommended in kidney stone patients with solitary kidneys, renal failure, renal transplants, gastrointestinal (GI) bypass, and any patient with high or increased anesthesia risk.

Unenhanced (or helical) CT is the gold standard of initial diagnosis, with a sensitivity of 98%, specificity of 100%, and negative predictive value of 97%. This modality allows rapid identification of stone, provides information as to the location and size of the stone, and any associated hydroureter, hydronephrosis, or ureteral edema, and can give information regarding potential other etiologies of pain (e.g., abdominal aortic aneurysm, malignancy). In those patients with no previous history of nephrolithiasis, CT should be performed to guide management. CT scans may underestimate stone size in comparison with an intravenous pyelogram or abdominal x-ray. 

However, CT scan does expose patients to a radiation burden, and it can be costly. In some patients with a history of renal colic that present with pain similar to previous episodes of renal colic, it may be sufficient to perform ultrasonography (US). However, US is less sensitive (60% to 76%) than CT for detecting calculi less than 5 mm, but can reliably detect hydronephrosis and evidence of obstruction (increased resistive index in the affected kidney). It is also the modality of choice for evaluating a pregnant patient with concern for renal colic. Studies have shown that using ultrasonography as a primary imaging modality does not lead to an increase in complications in comparison to CT. Ultrasound is also a good way to follow a patient known to have uric acid stones.

An abdominal x-ray (KUB) can identify many stones, but 10% to 20% of renal stones are radiolucent and provide little information regarding hydronephrosis, obstruction, or the kidneys. Additionally, bowel gas, the bony pelvis, and abdominal organs may obstruct visualization of a stone.  The KUB is recommended in kidney stone cases when the CT scan is positive, and the exact location of the stone is known. This helps in clearly identifying those stones that can be tracted by follow-up KUB and those that might be amenable to lithotripsy.

Using both a KUB and the renal US is a reasonable alternative to a CT scan and far cheaper with less radiation exposure. Symptomatic stones are likely to produce hydronephrosis or obstruction (visible on ultrasound) or will be seen directly on the KUB or the ultrasound.

Treatment / Management

Treatment includes the following:

  1. Immediate intervention with analgesia and antiemetics. NSAIDs and opiates are first-line therapies for analgesia. NSAIDs work in two ways in renal colic. First, NSAIDs decrease the production of arachidonic acid metabolites, which mediate pain receptors, alleviating pain caused by distension of the renal capsule. Additionally, they cause contraction of the efferent arterioles to the glomerulus, causing a reduction in glomerular filtration, and reducing hydrostatic pressure across the glomerulus. Because patients are frequently unable to tolerate oral medications, parenteral NSAIDs such as ketorolac (15 mg to 30 mg intravenously (IV) or intramuscularly (IM)) or diclofenac (37.5 mg IV) are most commonly used. 
  2. Successful use of intravenous lidocaine for renal colic has been reported. The protocol is to inject lidocaine 120 mg in 100 mL normal saline intravenously over 10 minutes for pain management. It has been quite effective for intractable renal colic unresponsive to standard therapy and typically starts to work in 3-5 minutes. No adverse events have been reported.
  3. Opiate pain medication, such as morphine sulfate (0.1 mg/kg IV or IM) or hydromorphone (0.02 mg/kg IV or IM), can also be used effectively for analgesia, especially when other measures have failed. However, opiates are associated with respiratory depression and sedation, and there is a risk of dependence associated with prolonged opiate use. 
  4. Fluid hydration. Although there is no evidence to support that empiric fluid will help “flush out” a stone, many patients are dehydrated secondary to decreased oral intake or vomiting and can benefit from hydration.
  5. Medical expulsive therapy. Alpha 1 adrenergic receptors exist in increasing concentration in the distal ureter. The use of alpha blockade medications (for example, tamsulosin or nifedipine) is theorized to facilitate stone passage by decreasing intra-ureteral pressure and dilating the distal ureter. However, data from randomized control trials are somewhat mixed as to whether these medications improved stone passage. The consensus opinion is they may be helpful in smaller stones in the lower or distal ureter.  They are probably of little use in larger stones in the proximal ureter.
  6. Definitive management of impacted stones. There are several invasive methods to improve stone passage. These include shock wave lithotripsy, in which high energy shock waves are used to fragment stones, ureteroscopy with either laser or electrohydraulic stone fragmentation, or in rare cases, open surgery.  In the presence of infection, a double J stent or percutaneous nephrostomy may be used to help with urinary drainage of the affected renal unit and definitive stone therapy postponed until the patient is stable.
  7. Behavior modification and preventative management. Increase fluid intake to optimize urine output with a goal of 2 L to 2.5 L of urine daily. Patients with calcium stones and high urine calcium concentrations should limit sodium intake and have a goal of moderate calcium intake of 1000 mg to 1200 mg dietary calcium daily. Those with calcium stones and low urinary citrate or those with uric acid stones and high urinary uric acid should increase intake of fruits and vegetables and decrease non-dairy animal protein. They may benefit from potassium citrate supplementation. Uric Acid stone formers are usually best treated with potassium citrate (urinary alkalinizer) to a pH of 6.5.  Hyperuricosuric calcium stone formers can benefit from allopurinol. Thiazide diuretics are indicated in those with high urinary calcium and recurrent calcium stones to reduce the amount of urinary calcium. Patients with hyperoxaluria should be encouraged to lower their oxalate intake (spinach, nuts, chocolate, green leafy vegetables). [8][9][10]

Differential Diagnosis

  • Aortic aneurysms
  • Biliary colic
  • Iliac aneurysms
  • Endometriosis
  • Ovarian torsion
  • Peritonitis
  • Pyelonephritis
  • Renal cancer
  • Renovascular compromise

Pearls and Other Issues

Calculus size, location, and patient discomfort predict the likelihood of spontaneous stone passage. Approximately 90% of stones less than 5 mm pass within four weeks. Up to 95% of stones larger than 8 mm can become impacted, requiring intervention to pass.

Indications for admission include a renal stone in a solitary kidney, severe kidney injury, an infected renal stone, intractable pain or nausea, urinary extravasation, or hypercalcemic crisis.

Patients with infected stones (e.g., nephrolithiasis plus evidence of urinary tract infection) require special and more urgent treatment. The infected stone acts as a nidus for infection and leads to stasis, decreasing the ability to manage infections. Frequently, these stones need to be removed in their entirety operatively to prevent a repeat infection and new stone formations.

24-hour urine tests are the cornerstone of long-term preventive therapy, but they require very high levels of patient dedication and compliance to be successful.  Nevertheless, they should be offered to patients with recurrent stones and a high risk of new stone formation.

Enhancing Healthcare Team Outcomes

The management of renal stones is by an interprofessional team that consists of a nephrologist, emergency department physician, radiologist, urologist, and a primary care provider. The majority of renal stones pass within four weeks, but stones larger than 8 mm may require some intervention before they can pass. Healthcare workers, including nurse practitioners who see patients with kidney stones, should contact the urologist when large stones fail to pass. Urologic nurses are involved in treatment, monitor patients, and update the team on changes in patient status. Pharmacists review prescribed medications for appropriate dosages, interactions, and provide patient education. In some cases of infected stones, surgery may be required. Because the recurrence of kidney stones is common, the patient should be educated on fluid intake and avoidance of certain foods. The prognosis for most patients with kidney stones is good. [Level 5]


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