nephrolithiasis Flashcards
What are the clinical signs and symptoms of nephrolithiasis?
Flank pain: Severe, colicky pain that radiates to the groin or lower abdomen.
Hematuria: Microscopic or gross hematuria.
Nausea and vomiting: Often associated with the pain.
Urinary urgency/frequency: If the stone is located in the lower urinary tract.
Fever/chills: Suggests concurrent infection (e.g., pyelonephritis).
CVA tenderness: Pain upon percussion of the costovertebral angle (CVA).
Absent peritoneal signs: Unlike gastrointestinal pathology, there is no guarding or rebound tenderness.
What are the common medications that can cause kidney stones?
Loop Diuretics (e.g., furosemide): Promotes hypercalciuria, increasing the risk of calcium oxalate and calcium phosphate stones.
Acetazolamide: Causes alkaline urine, which can predispose to calcium phosphate stones.
Topiramate: Increases urinary pH and promotes calcium phosphate stone formation.
Protease Inhibitors (e.g., indinavir, atazanavir): Lead to formations poor solubility in urine.
Sulfa Drugs (e.g., sulfadiazine): Can precipitate as sulfa crystals in the urine, causing stones.
Uric Acid Increasing Agents: Medications that promote hyperuricemia (e.g., chemotherapy agents, thiazides) can cause uric acid stones.
Vitamin C (high doses): Metabolized to oxalate, contributing to calcium oxalate stone formation.
Vitamin D (excessive supplementation): Increases intestinal calcium absorption, leading to hypercalciuria.
What is the most common type of kidney stone and its associated risk factors?
Calcium oxalate stones are the most common, associated with hypercalciuria, hyperoxaluria, low citrate levels, vitamin C toxicity, ethylene glycol, and disorders like inflammatory bowel disease (fat malabsorption).
Acidic pH (<5.5)
How does Crohn’s disease increase the risk of nephrolithiasis?
Fat malabsorption in Crohn’s binds calcium, freeing oxalate for absorption, leading to hyperoxaluria and increased risk of calcium oxalate stones.
What dietary modifications are recommended for preventing calcium oxalate stones?
Increase fluid intake (>2 L/day), maintain moderate calcium intake, reduce sodium and oxalate-rich foods (e.g., spinach, nuts), and consider citrate supplementation.
Why should patients lower their sodium intake when suffering from kidney stones?
This will increase calcium reabsorption.
Why is it not advisable to limit calcium intake when experiencing calcium stones?
Less dietary intake would amplify the problem.
What dietary adjustment is advisable for kidney stones?
- More fluids (> 2 liters per day)
- Citrate to help dissolve calcium.
- More potassium to increase urinary citrate.
- Less animal protein to lower urinary calcium.
- Less sodium to increase the amount of calcium reabsorption.
What vegetable should be limited while trying to mitigate the occurrence of kidney stones?
Spinach.
What is the role of thiazide diuretics in preventing nephrolithiasis?
Thiazides reduce calcium excretion in the urine, helping prevent calcium-containing stones.
Recurrent calcium stones and elevated urinary calcium (ie, hypercalciuria), which greatly increases the risk for recurrent calcium (eg, calcium oxalate, calcium phosphate) stone formation. Most patients with recurrent calcium stones can be treated with increased fluid intake (eg, ≥2 L/day) and dietary measures. However, in some patients, such as this one, stones continue to form despite these measures, warranting the addition of pharmacotherapy. Thiazide diuretics are the first-line pharmacotherapy for patients with hypercalciuria and recurrent calcium stones. They can reduce urinary calcium concentrations by up to 50%, primarily by creating relative hypovolemia that increases the reabsorption of both sodium and calcium in the proximal tubule and loop of Henle. Because reabsorption of sodium and calcium is tightly coupled, a low-sodium diet is crucial so that the medication can work effectively.
What should be used to decrease the occurrence of stones secondary to elevated vitamin D in the setting of sarcoidosis?
In patients with granulomatous diseases (eg, sarcoidosis) and severe or symptomatic hypercalcemia/hypercalciuria, glucocorticoids may be used to decrease the extrarenal formation of 1,25-dihydroxycholecalciferol (calcitriol) by macrophages.
What is the underlying pathogenesis of cystinuria?
An inherited genetic disorder characterized by the accumulation of cystine in the kidneys and bladder due to a disruption of amino acid transporter function in the proximal convoluted tubule and intestine. impaired renal reabsorption of dibasic amino acids (cystine, ornithine, arginine, lysine) → accumulation of cystine in the urine → frequent formation of hexagonal cystine stones.
What is biochemically unique about cystine?
made of 2 cysteines connected by a disulfide bond.
What are the characteristic crystals seen in cystinuria?
Hexagonal crystals, which are indicative of cystine stones, commonly associated with an autosomal recessive genetic defect in amino acid reabsorption.
Highly acidic.
Treatment is surgical removal (staghorn calculi often require percutaneous nephrolithotomy).
What is the inheritance pattern for cystinuria?
Autosomal recessive
How common is cystinuria?
Common (1:7000).
What is classically used to diagnose cystine stones?
Due to lucent (weakly opaque), requires a non contrast CT for diagnosis.
U/S can be used in pregnant women and children.
Nitroprusside Test: A qualitative test for cystinuria.
Positive Test: Turns purple when excess cystine is present in the urine.
proton nuclear magnetic resonance spectroscopy of urine.
Urine microscopy can also reveal hexagonal stones.
How are cystine stones managed?
Hydration: Increase fluid intake to at least 2.5-3 liters per day to reduce cystine concentration and promote stone prevention.
Urinary Alkalinization: Increase urine pH to >7.0 to improve cystine solubility
(medications: Acetazolamide, potassium citrate or sodium bicarbonate)
Cystine-Binding Thiol Drugs (for recurrent or refractory cases): Penicillamine or Tiopronin.
Dietary Modifications: Reduce methionine intake. Limit high-protein foods.
Regular urinalysis and 24-hour urine testing to monitor cystine levels and assess treatment efficacy.
How are struvite stones formed, and what organisms are commonly implicated?
Struvite stones (magnesium ammonium phosphate) form in alkaline urine and are caused by urease-positive organisms, such as Proteus, Klebsiella, Serratia, Enterobacter, and Staphylococcus species.
Can develop into staghorn calculi.
Basic pH (>5.5)
What is the hallmark finding of struvite stones on imaging?
Staghorn calculi, which fill the renal pelvis and calyces.
What is the treatment approach for staghorn stones?
Staghorn stones: Managed with percutaneous nephrolithotomy.
What are the risk factors for calcium phosphate stones?
Alkaline urine, hyperparathyroidism, and distal renal tubular acidosis (RTA 1).
What are the risk factors for developing uric acid stones?
Hyperuricemia from gout, luquid tumors (leukemia), chemotherapy, low urine volume, acidic urine pH, dehydration (hot/arid climates).
What are the features of nephrolithiasis due to uric acid stones, and how are they treated?
Features: Radiolucent stones on X-ray; detected on ultrasound or CT.
Treatment: Urine alkalinization with potassium citrate or sodium bicarbonate and allopurinol for hyperuricemia.
What is the mechanism of action of potassium citrate in nephrolithiasis prevention?
Citrate binds calcium, reducing stone formation by preventing crystallization.
What are the dietary recommendations for preventing calcium oxalate stones?
Increase fluid intake: >2 liters/day.
Moderate calcium intake (not low).
Reduce sodium and oxalate-rich foods (e.g., spinach, nuts).
Consider citrate supplementation.
What is the initial imaging study for suspected nephrolithiasis?
Non-contrast CT scan of the abdomen and pelvis, as it has the highest sensitivity and specificity for detecting stones.
What is the preferred initial imaging modality for diagnosing nephrolithiasis in children or pregnant patients?
Ultrasound, as it avoids radiation exposure, making it safer for children and during pregnancy.
If the ultrasound is negative while evaluating a stone in a pregnant patient, but the clinical suspicion is high (flank pain that radiates to the labia), what is the next imaging modality?
Tranvaginal ultrasound
Renal and pelvic ultrasonography (US), which avoids fetal radiation exposure, is the first-line imaging modality for diagnosing nephrolithiasis during pregnancy. Even if US does not directly visualize a stone, the presence of hydronephrosis and/or hydroureter is consistent with ureteral obstruction due to nephrolithiasis. If renal/pelvic US is nondiagnostic, transvaginal US may be performed to search for stones in the very distal ureter; MRI (eg, MR urogram) or low-dose noncontrast CT (during the second and third trimesters only) may also be considered.
If the tranaginal ultrasound is negative while evaluating a stone in a pregnant patient, but the clinical suspicion is high (flank pain that radiates to the labia), what is the next imaging modality?
MRI or a low dose CT only if the patient is in the 2nd or 3rd trimester.
Renal and pelvic ultrasonography (US), which avoids fetal radiation exposure, is the first-line imaging modality for diagnosing nephrolithiasis during pregnancy. Even if US does not directly visualize a stone, the presence of hydronephrosis and/or hydroureter is consistent with ureteral obstruction due to nephrolithiasis. If renal/pelvic US is nondiagnostic, transvaginal US may be performed to search for stones in the very distal ureter; MRI (eg, MR urogram) or low-dose noncontrast CT (during the second and third trimesters only) may also be considered.
What is the first-line treatment for kidney stones ?
IV fluids.
Pain control: NSAIDs or opioids.
Why are IV fluids critical in acute nephrolithiasis with AKI?
They help restore renal perfusion, promote diuresis, and prevent progression of acute kidney injury.
What is the next step in management for nephrolithiasis with fever, leukocytosis, and AKI?
Aggressive IV hydration with isotonic solutions (e.g., lactated Ringer’s) and initiate antibiotics if infection is suspected.
What size of kidney stones generally passes spontaneously, and what is the medical management?
<5 mm stones: Likely to pass on their own.
Medical management includes hydration, NSAIDs, and alpha-blockers (e.g., tamsulosin) or CCBs (nifedipine).
Between 5 and 10 mm monitor for spontaneous passage.
What is the first-line pharmacologic treatment for facilitating passage of kidney stones <10 mm?
Alpha-blockers such as tamsulosin, which relax smooth muscle in the distal ureter.
Alternative medication is a CCB (nifedipine).
In what instances would you use invasive interventions for a kidney stone?
AKI (elevated creatinine).
Infections.
Stones > 10 mm.
What are the hallmark lab findings in acute nephrolithiasis complicated by infection?
Elevated WBC count (leukocytosis), fever, and possible AKI (elevated creatinine).
Urinalysis may show pyuria, hematuria, or bacteria.
What are the invasive interventions for stones ?
Shockwave lithotripsy: Effective for stones in the renal pelvis or upper ureter but less effective for large or dense stones.
Ureteroscopy with holmium laser lithotripsy: Used for stones in the distal ureter or when other techniques are contraindicated.
Percutaneous nephrolithotomy: Preferred for very large stones, staghorn calculi, or septic patients with obstruction (plus antibiotics).
What is the management of urinary stones >10 mm?
Stones >10 mm are unlikely to pass spontaneously, and early urological intervention is typically required. Alpha-blockers (e.g., tamsulosin) may be used to improve stone passage in selected cases before intervention but are mainly used as and adjunct. The patient will also obtain appropriate IV fluid and pain control, but the definitive treatment will be with an invasive intervention.
What are the contraindications for shock wave lithotripsy (SWL)?
Pregnancy.
Stones in certain locations (e.g., distal ureter).
What is the management for obstructive nephrolithiasis in a septic patient?
Emergency decompression with percutaneous nephrostomy or ureteral stent placement, along with IV antibiotics.
