History and exam

Key diagnostic factors

Classical renal colic is described as severe, acute flank pain that radiates to the ipsilateral groin. However, cases may have no radiation and some stones are asymptomatic.

Other diagnostic factors

More than 50% of patients with renal stones will have another episode within 10 years.[40][41]

Commonly associated with acute episode.

As stones pass and get lodged in the distal ureter or intramural tunnel, this can lead to bladder irritation manifested as urinary frequency or urgency.

Microscopic hematuria is present on urinalysis in up to 85% to 90% of cases of nephrolithiasis.[30] Rarely, macroscopic hematuria can be present.

As stones pass through the ureter, flank pain can radiate toward the groin and testicle, leading to testicular pain.

Increased incidence of renal stones is correlated with increased body mass index (BMI) for both sexes.

May be positive for nephrolithiasis in first-degree relatives. If so, this could suggest an underlying metabolic abnormality.

Potential medications that can play a role in formation of renal stones include antacids, carbonic anhydrase inhibitors, sodium- and calcium-containing medications, vitamins C and D, and protease inhibitors.[28]

As stones pass through the ureter, flank pain can radiate toward the groin.

If also associated with urinary obstruction, urgent decompression is needed. May be a sign of struvite stones, which most commonly occur in association with a urinary infection.

May indicate urosepsis.

May indicate urosepsis.

May be pronounced in acute renal colic.

Risk factors

A higher energy diet with more protein may be associated with a higher incidence of stones.[14] This is secondary to the increased prevalence of hyperuricosuria, hypocitraturia, and hypercalciuria associated with this diet.

Higher sodium intake is associated with higher urinary sodium and calcium levels, and decreased urinary citrate.[15] This promotes calcium salt crystallization due to urinary saturation of monosodium urate and calcium oxalate/calcium phosphate being increased. Salt excess can also lead to bone loss, thereby worsening hypercalciuria.

In US men, the highest prevalence of nephrolithiasis is found in white men, followed by Hispanic men, Asian men, and black men.[16] Among US women, the prevalence is highest among white women but lowest among Asian women.[17]

Nephrolithiasis typically affects adult men more commonly than adult women, with a male to female ratio of 2 or 3:1.[18][16][19] However, there is evidence that this difference in incidence between men and women is narrowing.[20]

Fluid intake is very important and should be at least 2-3 liters per day.[21][22] In two large observational studies, fluid intake was found to be inversely related to the risk of renal stone formation.[23][24] A low urine output can produce a higher concentration of urinary solutes, therefore leading to stone formation.

Two large prospective cohort studies of men and women found that the prevalence and incident risk of nephrolithiasis were directly correlated with higher weight and BMI in both genders, although the magnitude of the association was greater in women than in men.[23][24]

Evidence linking obesity with low urine pH and uric acid stones and an association with hypercalciuria could account for an increased risk of uric acid and/or calcium stones in obese patients.[1]

Stone formers (especially calcium oxalate stones) frequently excrete more calcium oxalate crystals in the urine. Increased urinary excretion of cystine, struvite, and uric acid crystals is also a risk factor for stone formation.[14]

Dehydration and heat exposure are risk factors for nephrolithiasis. Those exposed to high temperatures demonstrate lower urine volumes and pH, higher uric acid levels, and higher urine specific gravity, leading to higher urinary saturation of uric acid, as well as calcium oxalate. As a result, people exposed to dehydration and heat are at increased risk for forming stones.[3][25]

Seasonal variation in nephrolithiasis is likely related to temperature because of fluid losses through perspiration. It has been reported that the highest incidence of nephrolithiasis is in the summer months, with the peak occurring within 1-2 months of maximal mean temperatures.[3][25]

In the US, prevalence of nephrolithiasis in the southeastern states (“stone belt”) is nearly double that in other areas.[26]

A positive family history of nephrolithiasis is associated with an increased risk of forming stones. A stone former is twice as likely as a non-stone former to have a first-degree relative with a history of stones. Patients with family history have a higher incidence of multiple stones and early recurrence.[14] Studies into possible genetic mutations responsible for inherited forms of nephrolithiasis are ongoing.[27]

Medications that are associated with an increased risk of stone formation include calcium-containing antacids, carbonic anhydrase inhibitors, sodium and calcium-containing medications, vitamin C, and vitamin D. Most of these medications lead to higher urinary levels of calcium, uric acid, sodium, or oxalate, in turn promoting stone formation. Other medications are poorly soluble with high urinary excretion, favoring direct crystallization and stone formation in urine. These include protease inhibitors (e.g., indinavir, atazanavir), ephedrine, guaifenesin, triamterene, and sulfadiazine.[28] Antibiotic exposure (sulfas, cephalosporins, fluoroquinolones, nitrofurantoin, broad-spectrum penicillins) is associated with an increased likelihood for nephrolithiasis, with the greatest odds for recent exposure and exposure at younger age.[29]

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