What Is a Kidney Stone: Types, Causes, Symptoms, and Treatment

This article is for informational purposes only. Consult a qualified healthcare professional for medical advice, diagnosis, or treatment.

What Is a Kidney Stone?

A kidney stone (nephrolithiasis) is a solid crystalline mass that forms within the kidneys when substances in the urine — minerals and salts — become so concentrated that they precipitate out of solution and crystallize. Stones range in size from microscopic crystals to several centimeters in diameter (staghorn calculi that fill the entire renal collecting system). Small stones often pass spontaneously, but larger stones can obstruct the urinary tract, causing excruciating pain, urinary tract infection, and, if untreated, kidney damage. Kidney stones are one of the most painful and common urological conditions: approximately 10–15% of adults in developed nations will develop at least one kidney stone during their lifetime. The condition affects approximately 600,000 Americans annually, and global prevalence has been increasing, likely due to dietary changes, obesity, and climate-related dehydration. Recurrence is high — without preventive measures, approximately 50% of patients will develop another stone within 5 years.

Types of Kidney Stones

How Kidney Stones Form

Stone formation begins when urine becomes supersaturated with crystal-forming solutes. The key determinants of supersaturation are:

• Volume: Inadequate fluid intake concentrates urine; daily urine output <1–1.5 liters significantly increases risk
• pH: Calcium oxalate forms across a wide pH range; uric acid crystallizes when urine pH <5.5; struvite requires alkaline pH >7.2; calcium phosphate forms at higher pH
• Ion concentrations: Elevated calcium, oxalate, uric acid, or phosphate increase ionic activity products above the solubility threshold
• Inhibitors: Urine contains natural stone inhibitors — citrate (binds calcium), magnesium, pyrophosphate, Tamm-Horsfall protein, and nephrocalcin — that raise the threshold for crystallization. Hypocitraturia (low urine citrate) is a major risk factor and important treatment target.

Once crystals nucleate (either de novo in urine or on calcified plaques called Randall's plaques on the renal papillae), they aggregate into stones and may attach to the urothelium or pass freely until they either grow large enough to obstruct the urinary tract or are passed spontaneously.

Symptoms

Small stones (<5 mm) may pass without symptoms. When a stone moves from the kidney into the ureter (the tube connecting kidney to bladder), it can obstruct urine flow, causing dramatic symptoms:

• Renal colic: Sudden, severe, cramping pain in the flank (costovertebral angle), typically radiating to the groin, inner thigh, or genitalia as the stone descends the ureter. Pain comes in waves as the ureter peristaltically contracts around the stone, is typically the worst pain many patients have experienced, and is not relieved by position change.
• Hematuria: Blood in the urine (microscopic or macroscopic) from mucosal irritation is present in up to 85% of cases
• Nausea and vomiting: Reflex nausea from visceral pain often accompanies colic
• Dysuria and urinary frequency: As the stone approaches the vesicoureteral junction (bladder entrance), it produces bladder irritation symptoms
• Fever and chills: Indicate concurrent urinary tract infection with obstruction — a urological emergency requiring urgent drainage

Diagnosis

Diagnosis combines clinical assessment with imaging:

• Non-contrast CT KUB (CT urography): Gold standard — detects virtually all stone types (including radiolucent uric acid stones visible as filling defects), determines stone size, location, and degree of obstruction. Fast and widely available. Radiation dose is a consideration in young patients with recurrent stones.
• Renal ultrasound: No radiation; good for detecting hydronephrosis and renal calculi but less sensitive than CT for ureteral stones. Preferred in pregnancy and children.
• Plain abdominal X-ray (KUB): Detects calcified (radio-opaque) stones; useful for monitoring known calcium stones
• Urinalysis: Hematuria, crystals, and pH; urine culture if infection suspected
• Metabolic evaluation: For recurrent stone formers — 24-hour urine collection for calcium, oxalate, uric acid, citrate, sodium, creatinine; serum calcium, PTH, uric acid

Treatment

Conservative Management

Stones ≤5 mm pass spontaneously in approximately 68–98% of cases within 4 weeks. Patients are advised to drink large volumes of fluid (target urine output 2–2.5 liters/day), take NSAIDs for pain, and use medical expulsive therapy. Alpha-1 blockers (tamsulosin) reduce ureteral smooth muscle tone and have been shown in multiple meta-analyses to increase spontaneous passage rates by 29% for stones 5–10 mm.

Procedural Interventions

Prevention

The cornerstone of prevention is high fluid intake (2.5–3 liters/day; target urine output 2 liters/day), applicable to all stone types. Additional targeted strategies include: dietary calcium restriction is counterintuitively NOT recommended for calcium oxalate stones — adequate dietary calcium (1,000–1,200 mg/day) binds oxalate in the gut, reducing oxalate absorption. For hyperoxaluria, reduce high-oxalate foods (spinach, nuts, rhubarb). For uric acid stones, alkalinize urine with potassium citrate (targets pH 6.5–7.0). Thiazide diuretics reduce urinary calcium excretion in hypercalciuria. Allopurinol reduces uric acid production.