Urolithiasis: causes, symptoms, treatment

Urolithiasis is the formation of stones (calculi) in the upper urinary tract (kidneys and ureters) and sometimes in the lower urinary tract (bladder, urethra). Stones form when urine is oversaturated with salts and/or natural crystallization inhibitors are reduced, then grow under conditions of stagnant flow and local pH changes. Most stones consist of calcium salts (oxalate, phosphate), while uric acid, struvite (infection stones), and cystine are less common. Current guidelines emphasize that treatment choice depends on the composition, size, location, clinical presentation, and associated risk factors for recurrence. [1]

Clinically, urolithiasis presents with pain (renal colic), hematuria, dysuria, nausea, and sometimes fever. Acute obstruction with infection is an emergency requiring urgent decompression of the urinary tract. In stable adults, low-dose computed tomography without contrast is the first-line imaging method for suspected stones; in pregnant women and children, ultrasound is preferred, followed by staged examination. [2]

Urolithiasis is a chronic, recurring condition: after the initial episode, the risk of recurrence is approximately 30-50% within 5 years, and is higher in the presence of metabolic disorders, a family history, and early onset. A "high risk of recurrence" is considered separately, including children, multiple/bilateral stones, cystine, uric acid, and struvite stones, as well as significant abnormalities in urine and blood tests. [3]

Modern therapy combines rapid pain control, safe removal of the stone (independently or with the help of shock wave lithotripsy, ureteroscopy, percutaneous nephrolithotomy) and the second, no less important “half of the treatment” - metabolic prevention based on the composition of the stone, 24-hour urine tests and targeted diet therapy and pharmacoprophylaxis. [4]

Code according to ICD-10 and ICD-11

In the International Classification of Diseases, Tenth Revision (ICD-10), urolithiasis is coded in blocks N20-N23: N20 - kidney and ureteral stones, N21 - lower urinary tract stones, N22 - stones in other diseases, N23 - colic of renal origin, unspecified. To clarify the location, the following subcategories are used: N20.0 (kidney stone), N20.1 (ureteral stone), N20.2 (kidney stone with ureteral stone), N20.9 (unspecified urinary tract stone). Additionally, medical history codes can be used (for example, Z87.442 - personal history of urolithiasis). [5]

The International Classification of Diseases, Eleventh Revision (ICD-11) uses the block "Urolithiasis" (GB70-GB7Z). For the upper urinary tract: GB70.0 - "Kidney calculus", GB70.1 - "Ureteral calculus", GB70.Z - "Upper urinary tract calculus, unspecified". For the lower: GB71.0 - "Bladder calculus", etc.; there is also a generalized "Urolithiasis, unspecified" (GB7Z). ICD-11 supports post-coordination (e.g. adding lateralization and clinical qualifiers). [6]

Table 1. Examples of urolithiasis coding

System	Code	Name
ICD-10	N20.0	Kidney stone
ICD-10	N20.1	Ureteral stone
ICD-10	N20.2	Kidney stone with ureteral stone
ICD-10	N20.9	Urinary tract calculus, unspecified
ICD-11	GB70.0	Kidney stone
ICD-11	GB70.1	Ureteral stone
ICD-11	GB71.0	Bladder stone
ICD-11	GB7Z	Urolithiasis, unspecified

Epidemiology

The prevalence of urolithiasis is increasing worldwide. Current estimates indicate a lifetime prevalence of approximately 10-12% in men and 7-8% in women, with regional variations and an overall upward trend in recent decades. This trend is associated with dietary changes, obesity, metabolic syndrome, warm climates, and dehydration. [7]

The risk of recurrence is high: aggregate data and reviews from the EAU/Eur Urol show a recurrence rate of approximately 30-50% over 5 years and up to 80-90% with long-term follow-up in high-risk patients. This emphasizes the importance of metabolic assessment and prophylaxis after each episode. [8]

The distribution of stone composition is stable: 75-85% are calcium stones (mainly calcium oxalate, less commonly calcium phosphate), 8-10% are uric acid, 7-8% are struvite (infectious), and 1-2% are cystine. In children and in patients with rare hereditary disorders, the proportion of "non-calcium" stones is higher. [9]

Table 2. Epidemiological landmarks

Indicator	Meaning
Lifetime prevalence (males/females)	≈ 10-12% / 7-8%
Risk of relapse	30-50% over 5 years; higher in risk groups
Composition of stones (approximately)	Calcium 75-85%; uric acid 8-10%; struvite 7-8%; cystine 1-2%

Reasons

Stone formation begins with urine oversaturation with crystal-forming salts (oxalate, calcium, phosphate, uric acid, cystine) against a background of insufficient urine volume, high sodium load, hypercalciuria, hyperoxaluria, hyperuricosuria, or cystinuria. A decrease in crystallization inhibitors (citrate), acid-base balance, and the urinary tract microbiome play a key role in infectious stones. [10]

For urate stones, low urine pH and insulin resistance are important; for struvite stones, infection with urease-producing bacteria with alkalization of urine and the formation of coral-shaped stones; for cystine stones, hereditary cystinuria (an amino acid transport defect). Drug stones (e.g., individual sulfonamide salts) are less common. [11]

Risk factors

Non-modifiable factors: male gender (before menopause), family history of urolithiasis, early onset, urinary tract anomalies, some genetic syndromes (including cystinuria). Modifiable factors: low hydration (diuresis < 2.0-2.5 l/day), high intake of table salt and animal protein, obesity, metabolic syndrome, hypertension, type 2 diabetes mellitus. [12]

Iatrogenic and dietary factors include high doses of vitamin C, generous consumption of cola-type beverages, oxalate-rich foods with low calcium intake, prolonged immobilization, and certain medications (eg, loop diuretics - hypercalciuria).[13]

Pathogenesis

The physicochemical basis is exceeding the solubility threshold of salts in urine, resulting in the formation of a crystallization "nucleus" on the matrix, followed by crystal growth and aggregation. The microenvironment (pH, citrate and magnesium concentrations, urine flow) and contact with the epithelium influence crystal attachment and calculus formation. [14]

For urate stones, acidic urine (pH ≤ 5.5-5.8) plays a key role, so they can be dissolved by alkalization. For struvite stones, bacterial urease hydrolyzes urea, forming ammonia, an alkaline environment, and the precipitation of magnesium and ammonium phosphates. Cystine is poorly soluble in urine, especially acidic urine; high diuresis and alkalization are important for prevention. [15]

Symptoms

The classic symptom is renal colic: sudden, wave-like pain in the side radiating to the groin, accompanied by nausea/vomiting. Macro- or microscopic hematuria, dysuria, frequent urination, and anxiety are possible. Fever and weakness indicate infection and require immediate care. [16]

Small stones may pass asymptomatically. Ureteral obstruction manifests as a decreased urinary flow, a sensation of incomplete emptying, and an urgent urge to urinate; with complete obstruction and a solitary kidney, azotemia rapidly increases. In children, symptoms are often nonspecific (abdominal pain, crying, vomiting). [17]

Classification, forms and stages

Practical classification includes: by location (renal calyces/pelvis, upper/middle/lower ureter, bladder), by size (≤ 5 mm; 6-10 mm; 11-20 mm; > 20 mm), by composition (calcium, urate, struvite, cystine, medicinal), by radiodensity (X-ray positive/negative). This division determines the choice of treatment and prevention. [18]

Table 3. Classification of stones (applied)

Axis	Categories	Tactical significance
Localization	Kidney; proximal/middle/distal ureter; bladder	Access selection (URS/UVL/CHNL)
Size	≤ 5 mm; 6-10 mm; 11-20 mm; > 20 mm	Probability of independent departure, method
Compound	Calcium, urate, struvite, cystine, medicinal	Diet and metaphylaxis
Radio density	X-ray positive / "X-ray transparent"	Is a CT scan necessary and what type of lithotripsy?

Complications and consequences

Acute obstruction leads to hydronephrosis and, if prolonged, to decreased renal function. Infection secondary to obstruction (obstructive pyelonephritis/pyelitis) is a life-threatening condition requiring urgent decompression (nephrostomy or stent). Repeated attacks contribute to scarring and chronic pain. [19]

Long-term risk of chronic kidney disease increases in some patients, particularly with recurrences, infectious stones, and bilateral kidney stones. Struvite and staghorn stones, if left untreated, lead to recurrent infection, sepsis, and loss of function. [20]

Table 4. Frequent complications

Complication	Term	Meaning
Obstructive uropathy	Early	Decreased filtration, pain
Infection + obstruction	Early	Sepsis, urgent decompression
Chronic kidney disease	Late	Decline in organ function
Recurrence of stone formation	Late	Frequent interventions

When to see a doctor

Immediately - if you have severe pain in the side/groin, fever, chills, nausea and vomiting, inability to urinate, pain due to pregnancy or a solitary kidney. These signs may indicate obstruction due to infection and require urgent care. [21]

Planned - for recurring episodes of colic, blood in the urine, detection of a stone on ultrasound/CT, a history of stones, a family history of urolithiasis, gout, or metabolic syndrome. Early screening reduces the risk of complications and the need for major surgery. [22]

Diagnostics

Initial assessment: collection of complaints, measurement of temperature, pain, and hydration; analysis of “danger signs” (infection + obstruction). The initial set of laboratory tests includes a complete blood count, creatinine, electrolytes, C-reactive protein, urinalysis, and, if necessary, urine culture. [23]

Imaging. In adults with a moderate to high probability of stone formation, low-dose computed tomography without contrast is the standard (it determines the size, location, Hounsfield density, and degree of obstruction). In pregnant women and children, ultrasound is the initial imaging modality; if the diagnosis is unclear, limited CT is used for strict indications. Abdominal radiography is useful for monitoring radiodense stones. [24]

Determination of stone composition. All patients are recommended to have their extracted/passed stone analyzed. In cases of recurrence, staghorn, urate, cystine, or struvite stones, in children, and in the presence of a solitary kidney, an extended metabolic assessment is performed: at least two 24-hour urine collections (volume, calcium, oxalate, citrate, uric acid, sodium, and creatinine) plus a blood profile. [25]

Table 5. Diagnostic algorithm (simplified)

Step	Action	For what
1	Rule out "obstructive sepsis"	Determines the urgency of decompression
2	Laboratory tests	Inflammation, kidney function
3	Low-dose CT (adults) / Ultrasound (pregnancy/children)	Localization, size, density
4	Stone analysis	Base for metaphylaxis
5	24-hour urine (if at risk)	Personalization of prevention

Differential diagnosis

Renal colic must be differentiated from acute surgical and vascular conditions: acute appendicitis, acute abdomen of other etiologies, herpes zoster prodrome, osteochondrosis, renal artery/vein thrombosis, gynecological and urogynecological conditions (ectopic pregnancy, ovarian cyst torsion, acute pyelonephritis without a stone). CT and ultrasound play a key role. [26]

In painless microhematuria, glomerular sources (nephritis), urinary tract tumors, and physical activity are differentiated. A comprehensive examination includes cytology and cystoscopy, as indicated, in older patients. [27]

Table 6. "Looks like, but not a stone": landmarks

State	What is in favor?	What does "against" say?	The next step
Acute appendicitis	Pain in the right iliac region, fever	No irradiation to the groin, no microhematuria	CT/ultrasound of the abdominal cavity
Pyelonephritis without stone	Temperature, kidney pain, bacteriuria	There is no typical colic	Ultrasound, urine culture
Gynecological pathology	Cycle related/positive test	No stone on CT scan	Gynecological ultrasound

Treatment

Primary care is aimed at relieving pain and controlling nausea. Nonsteroidal anti-inflammatory drugs (NSAIDs) are first-line treatment for renal colic (they reduce prostaglandins and decrease intrarenal pressure); if contraindicated, opioids are used briefly and under supervision. If signs of infection are present, antibiotics are immediately initiated according to local protocols, with subsequent culture-based adjustments. [28]

A watchful waiting approach is possible in stable patients with small stones in favorable locations. The likelihood of spontaneous passage decreases with increasing diameter: for stones ≤ 5 mm, it is approximately 70-90%; for stones 5-10 mm, it is 50-70% (higher for the distal ureter, lower for the proximal ureter). Dynamic observation and monitoring of renal function/inflammation are essential. [29]

Medical expulsive therapy with alpha-blockers (eg, tamsulosin, silodosin) may be considered in adults with uncomplicated distal stones >5 mm to speed passage and reduce analgesic requirements. Several reviews and guidelines support this approach, but the evidence base is mixed and debated; inform the patient of the potential benefits and risks. [30]

Shock wave lithotripsy is a non-invasive method for stone fragmentation, effective for many stones up to 20 mm in size with favorable anatomy. The outcome depends on the stone's density (HU), skin-stone distance index, and location. Adjuvant alpha-blockers may be used during lithotripsy for ureteral stones <10 mm (NICE "consider"). Monitoring of residual fragments is mandatory. [31]

Ureteroscopy (rigid/flexible) is the first-line treatment for many ureteral stones, when expectant management fails, when infection occurs after decompression, and when stones are dense or have unfavorable anatomy. Contact lithotripsy (laser) is used. Advantages include a high probability of a "clear" outcome in a single session; risks include trauma, strictures, and the need for a stent. [32]

Percutaneous nephrolithotomy is the standard for large stones >20 mm, staghorn and dense stones, and when other methods are ineffective. Modern mini-approaches and vacuum-assisted evacuation reduce trauma and increase the likelihood of complete removal. [33]

Decompression in “infection + obstruction” is vital and precedes any “definitive” stone removal: a nephrostomy drain or stent is placed, antibacterial therapy is started, and after stabilization, removal of the stone is planned. [34]

Dissolution therapy. Urate stones often respond to oral alkalinization therapy (potassium citrate or bicarbonate) with a target urine pH of 6.5-7.0 (some data - 7.0-7.2) until complete dissolution or significant reduction; strict monitoring of urine pH, daily diuresis, and electrolytes is necessary. In case of hyperuricosuria, xanthine oxidase inhibitors (allopurinol, febuxostat if intolerant) are possible. Struvite stones require removal and debridement of infection. [35]

Medical prevention (metaphylaxis) is selected based on the results of stone analysis and 24-hour urine. Universal measures: drink so that the daily urine volume is ≥ 2.5 L; limit table salt to 5-6 g / day; maintain normal dietary calcium intake (not "zero"); moderate animal protein; increase the proportion of fruits / vegetables and diets with the DASH type. For hypercalciuria in patients with relapses - thiazide diuretics after sodium restriction (the evidence base is debated, but the recommendations remain); for hypocitraturia - potassium citrate; for urate - alkalinization ± allopurinol; for cystinuria - intensive hydration, alkalinization, if necessary - thiol drugs. [36]

Table 7. Probability of spontaneous passage of ureteral stones

Diameter	Forecast (average)	Notes
≤ 5 mm	≈ 70-90%	Maximum for distal stones
5-10 mm	≈ 50-70%	Depends on location and form
> 10 mm	Short	Intervention is often required

Table 8. Intervention selection (EAU/AUA/NICE guidelines)

Scenario	Preferred method	Alternatives/Notes
Distal ureter ≤ 10 mm, stable	Expectant ± alpha blocker	URS in case of failure/patient preference
Kidney stone ≤ 20 mm, low density	UVL	Flexible URS in unfavorable anatomy
Stone > 20 mm or coral-shaped	CHNL (first line)	Combined techniques
Infection + obstruction	Emergency decompression	Definitive removal after stabilization

Prevention

Basic recommendations are suitable for most patients: maintain a daily urine volume of ≥ 2.5 L (targeted by a light straw color), limit sodium to 5-6 g/day, maintain normal dietary calcium intake (≈ 1,000-1,200 mg/day), moderate animal protein, and increase vegetable and fruit intake (alkalizing effect). These steps reduce urinary supersaturation and the risk of relapse. [37]

Personalized prevention is based on stone analysis and 24-hour urine data: potassium citrate for hypocitraturia, oxalate restriction and its "binding" with dietary calcium for oxalate stones, thiazides for persistent hypercalciuria despite diet, and alkalization for urate and cystine stones. For struvite stones, the key is eradication of urease-producing bacteria and removal of the source of infection (the stone). [38]

Table 9. Metaphylaxis by stone type

Type of stone	Key measures
Calcium	Diuresis ≥ 2.5 L; salt restriction; normal dietary calcium; in case of hypercalciuria, consider thiazides
Uric acid	Alkalization (potassium citrate/bicarbonate), target pH 6.5-7.0; for hyperuricosuria, allopurinol
Struvite	Stone removal + infection treatment
Cystine	Intensive hydration (target diuresis ≥ 3.0 L/day), alkalization; thiol preparations as indicated

Forecast

With proper acute management and metaphylaxis, most patients achieve long-term disease control. Frequent recurrences, struvite and staghorn stones, bilateral lesions, late diagnosis of obstruction with infection, and lack of prophylaxis worsen the prognosis. Timely metabolic analysis reduces the frequency of repeat interventions. [39]

Table 10. Prognostic factors

Factor	Influence
Performing a stone analysis and 24-hour urine	Reduces relapses through targeted prevention
Monitoring diuresis and salt levels	Reduces urine supersaturation
Timely decompression in case of infection	Reduces the risk of sepsis and loss of function
Composition/size/density of the stone	Determines the treatment method and the chance of a "clean" outcome

FAQ

Is it true that "small" stones always pass on their own?
Not always, but often: for stones ≤ 5 mm, the chances are high (around 70-90%), while for stones 5-10 mm, they are lower. Location (distal vs. proximal ureter) and shape are also important. Symptom monitoring and repeat imaging are necessary. [40]

Should alpha-blockers be used to "pass" a stone?
They may be considered for distal stones >5 mm in stable adults. Recommendations exist, but the evidence base is mixed; the decision should be made in consultation with a urologist, taking into account side effects and preferences. [41]

Is it possible to dissolve a stone without surgery?
Urate stones often respond to oral alkalinization of the urine (potassium citrate/bicarbonate) to achieve a pH of 6.5-7.0. Other types require crushing or removal. Self-medication with acids/alkalis without medical supervision is dangerous. [42]

Does everyone need "stone pills"?
No. Hydration and dietary adjustments are universal. Pharmacoprophylaxis (thiazides, citrate, allopurinol) is indicated for documented metabolic disturbances or recurrences and is selected individually after examination. [43]