Nephrolithiasis & Cysts

Presentation and imaging

Renal colic. A stone moving down the ureter causes sudden, severe, colicky flank pain that radiates to the groin, with nausea and hematuria in 85–90% of patients. The patient writhes and cannot find a comfortable position, unlike the patient with peritonitis, who lies still because movement hurts. Pain migrates with the stone, and a stone at the ureterovesical junction adds urgency and frequency.

Because 10–15% of stones cause no hematuria, a negative dipstick does not exclude one. Check a pregnancy test in women of reproductive age, and in an older patient with a first episode of "renal colic" think of a leaking abdominal aortic aneurysm.

Imaging. Noncontrast helical CT is the gold standard: it detects nearly all stones and shows their size, location, and any hydronephrosis. Ultrasound is first-line in pregnancy and in children because it avoids radiation. A plain KUB film misses radiolucent (uric acid) stones and is mainly used to follow known radiopaque stones.

"Radiolucent" refers to plain x-ray only: uric acid stones are invisible on KUB but still visible on noncontrast CT.

Stone types: chemistry, urine pH, and radiography

Calcium oxalate is the most common stone. It is radiopaque, forms at any urine pH, and shows envelope (dihydrate) or dumbbell (monohydrate) crystals. The drivers are hypercalciuria (e.g., primary hyperparathyroidism), hyperoxaluria, and hypocitraturia; citrate normally chelates urinary calcium. Enteric hyperoxaluria occurs in fat malabsorption (Crohn disease, ileal resection, gastric bypass): unabsorbed fat binds gut calcium, leaving oxalate free to be absorbed. Calcium phosphate stones favor alkaline urine, classically in distal (type 1) renal tubular acidosis and with carbonic anhydrase inhibitors such as acetazolamide.

Struvite (magnesium ammonium phosphate) stones form when urease-producing organisms (Proteus, Klebsiella, Staphylococcus saprophyticus) split urea into ammonia and alkalinize the urine. They grow into staghorn calculi with coffin-lid crystals. Bacteria live inside the stone, so antibiotics alone cannot sterilize it and complete surgical stone removal is required to clear the infection.

Uric acid stones are radiolucent on plain film, form in acidic urine, and show rhomboid crystals. Risk factors are gout, high purine intake, tumor lysis, and low urine volume. They are the stones that can be dissolved medically, by alkalinizing the urine with potassium citrate.

Cystine stones come from cystinuria, an autosomal recessive defect in renal (and intestinal) transport of cystine and the dibasic amino acids ornithine, lysine, and arginine. Cystine precipitates in acidic urine, causing recurrent stones from childhood with hexagonal crystals and a positive urinary cyanide-nitroprusside test. Manage with hydration, urine alkalinization, and tiopronin or penicillamine, which bind cystine into a more soluble complex.

Acute management and when to intervene

Analgesia. NSAIDs such as IV ketorolac are first-line for renal colic and outperform opioids because they reduce prostaglandin-mediated pain and ureteral tone. Add antiemetics and hydration, and reserve opioids for breakthrough pain or when NSAIDs are contraindicated (e.g., AKI).

Trial of passage. Most stones under 5 mm pass spontaneously. The patient strains the urine and the stone is sent for analysis, because composition directs prevention. Medical expulsive therapy with an α1-blocker (tamsulosin) relaxes distal ureteral smooth muscle and aids passage of distal ureteral stones roughly 5–10 mm. Larger or non-passing stones need urologic intervention.

Indications to intervene. Stone >10 mm, failure to pass, intractable pain or vomiting, obstruction of a solitary kidney, AKI, or obstruction with infection.

• Ureteroscopy with laser fragmentation and basket extraction suits most ureteral stones.
• Shockwave lithotripsy is noninvasive for smaller renal and proximal ureteral stones; avoid it in pregnancy and uncorrected coagulopathy. When anticoagulation or antiplatelet therapy cannot be stopped, ureteroscopy is preferred.
• Percutaneous nephrolithotomy is first line for symptomatic renal stones over 20 mm and staghorn stones.

The infected, obstructed kidney

A urologic emergency. An obstructing stone plus infection (fever, pyuria, or sepsis) carries a high risk of sepsis: infected urine is trapped under pressure, and antibiotics cannot sterilize an undrained system. Perform urgent decompression with a retrograde ureteral stent or a percutaneous nephrostomy and give IV antibiotics after blood and urine cultures. Do not delay drainage for definitive stone removal, which is done once the infection has cleared.

A febrile patient with an obstructing stone, especially one who is diabetic or hypotensive, needs emergent drainage, not a trial of passage, outpatient oral antibiotics, or elective lithotripsy.

Prevention

Universal measures. The single most effective prevention for every stone type is high fluid intake to make >2.5 L of urine daily. Recurrent stone formers need a 24-hour urine study (volume, calcium, oxalate, citrate, uric acid, sodium) and analysis of any passed stone. Advise moderating sodium (it increases urinary calcium) and animal protein (it raises urinary calcium and uric acid and lowers citrate).

Do NOT restrict dietary calcium. Normal dietary calcium binds oxalate in the gut; restricting it frees oxalate to be absorbed and excreted in the urine, raising stone risk.

Match the drug to the stone.

• Hypercalciuria → thiazide, which increases distal calcium reabsorption; loop diuretics raise urinary calcium and worsen stones.
• Hypocitraturia → potassium citrate.
• Uric acid stones → potassium citrate to alkalinize; allopurinol for hyperuricosuria.
• Hyperoxaluria → lower dietary oxalate while keeping normal calcium intake.
• Cystine → hydration, potassium citrate, tiopronin or penicillamine.

Renal cysts and polycystic kidney disease

Simple cysts are common, increase with age, and are benign (Bosniak I). On ultrasound they are anechoic and round with a thin smooth wall and posterior acoustic enhancement, and they need no follow-up. The Bosniak system stratifies complex cysts for malignancy risk: categories I–II are benign, IIF gets surveillance imaging, and III–IV (thick or enhancing walls, septa, or solid components) are suspicious for cystic renal cell carcinoma and go to urology.

Autosomal dominant polycystic kidney disease (PKD1 or PKD2) causes bilateral cysts that progressively enlarge the kidneys, with hypertension, hematuria, flank pain, and progressive CKD in adulthood. Extrarenal features are berry aneurysms (subarachnoid hemorrhage), hepatic cysts, and mitral valve prolapse. Treat hypertension, typically with an ACE inhibitor or ARB; tolvaptan, a vasopressin V2-receptor antagonist, slows cyst growth in rapidly progressive disease.

In ADPKD, screen with noncontrast MR angiography for berry aneurysms when there is a family history of intracranial aneurysm or subarachnoid hemorrhage, a prior rupture, or a high-risk occupation (for example, pilots).