15.1 Kidney stones
Kidney stone disease is common, with a risk of 10% to 15% occurring more commonly in men, but with an increasing incidence in women. Stone formation is recurrent in 50% of those with one stone. , In addition to causing the pain of renal colic, kidney stone disease also may lead to complicated interventions to remove stones, urosepsis, or an increased incidence of chronic kidney disease.
Types and predisposing causes of kidney stones.
15.1.1 Presenting symptoms and signs of kidney stones
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Flank pain, severe and colicky in nature
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Pain often accompanied by restlessness, nausea and vomiting
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Hematuria, gross or microscopic
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Stone passage: occurrence may/may not be recognized, so best to strain urine to catch stone
15.1.2 Detection of kidney stones ,
Noncontrast CT is best, preferably using a reduced radiation dose (virtually all stones are radiopaque by CT and can usually evaluate obstruction without radiocontrast). Ultrasound (US) is less sensitive but can evaluate obstruction, avoids radiation, and can be used in pregnancy. Abdominal X-ray (KUB) can only detect larger radioopaque calcium-containing and some cystine stones so is no longer an imaging of choice. Intravenous pyelography (IVP) is less sensitive than CT, uses radiation, and requires radiocontrast.
15.1.3 Initial workup of kidney stones ,
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History and exam for predisposing risk factors
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Serum electrolytes (HCO 3 ), calcium, phosphate, creatinine (r/o RTA, hypercalcemia, evaluate renal function)
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Urinalysis to look for pH, hematuria, infection, and crystals
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Stone analysis if stone is available
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Radiology: see Detection of Kidney Stones , but if medullary sponge kidney is to be detected because there are multiple small stones or nephrocalcinosis, either CT or IVP with radiocontrast will be needed
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Assess daily urine output (UO) volume (UO of less than 1 L/day is common, and often the only Rx for first stone is to increase to 2 L/day)
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Metabolic workup to include 24-hour urine studies: often undertaken after recurrent stone formation or severe first presentation of stone episode
15.1.4 General principles of therapy for stone disease
15.1.4.1 Acute therapy
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Pain relief: nonsteroidal antiinflammatory drugs (NSAIDs), narcotic analgesics
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Intravenous fluid in dehydrated patients, also increases urine flow
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80% of stones 7 mm or less will pass without intervention
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Medications that increase successful stone passage: alpha blockers (tamsulosin) and calcium channel blockers (CCBs; nifedipine most commonly) are most useful with stones measuring 5 to 10 mm ,
15.1.4.2 Indications for hospitalization/interventional procedure
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Intractable pain and vomiting
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Severe urinary tract infection (UTI) or sepsis
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Complete ureteral obstruction for >3 days
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Partial obstruction of a solitary kidney
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Obstruction or infection may indicate need for temporary ureteral stent placement or nephrostomy
15.1.4.3 Urological interventions
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Extracorporeal shock wave lithotripsy (ESWL) has better success with smaller stones
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Ureteroscopic lithotripsy (useful for ureteral stones)
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Percutaneous nephrolithotomy (successful for larger stones but with increased complication rate than lithotripsy, equal success to open surgical procedures)
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Laparoscopic or open surgical stone removal
15.1.4.4 General stone management
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Specific stone therapy as noted below when stone composition is known
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Fluid intake to increase urine output to >2 L/day
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Dietary considerations:
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Reduce fructose and sugar-containing beverage consumption which may increase calcium stone occurrence;
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Replace sweet and dairy fluids with coffee, tea, and water;
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Reduce high intake of vitamin D and calcium supplementation but maintain normal calcium diet; and
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Reduce intake of animal protein.
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15.1.4.5 Follow-up
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Reassess effects of specific therapy when indicated with urinary and plasma chemistries in 2 months and yearly.
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Consider radiological assessment for new stone formation at 1 year.
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Whenever recurrent stone disease is uncomplicated by infection, obstruction, or underlying disorders, the major risks for patients are the occurrence of painful episodes and the possibility of requiring urological interventions for stone passage. In general, renal function has been thought to be well preserved, but recent data suggest that those with one or more kidney stones have about double the risk of developing chronic kidney disease (CKD) or end-stage kidney disease (ESKD), with the added hazard appearing to be greater in women than in men. ,
15.1.5 Predisposing causes of stone formation
15.1.5.1 Hypercalciuria or idiopathic hypercalciuria ,
15.1.5.1.1 Defining the defect
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Urinary calcium:
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In men: >300 mg/day,
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In women: >250 mg/day, or
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>4 mg/kg/day in all.
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15.1.5.1.2 Mechanisms involved
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Absorptive: increased gastrointestinal (GI) absorption of calcium—can be assessed by urinary calcium to creatinine ratio of >0.2 mg/mg after an oral calcium load
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Resorptive: increased bone resorption—may have elevated parathyroid hormone (PTH) without hypercalcemia
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Renal “leak”: decrease in renal tubular calcium reabsorption—can be assessed by fasting urinary calcium >0.11 mg/100 mL/min of creatinine clearance (CrCl)
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Hypophosphatemia: renal phosphate wasting may stimulate increased 1,25-dihydroxy-vitamin D, enhancing GI absorption of calcium
15.1.5.1.3 Treatment of specific causes of recurrent stones
Bone density studies of hypercalciuric patients have generally shown decreased bone density in all of the four mechanistic categories listed above, making evaluation of mechanism clinically unnecessary, with treatment as follows:
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Reduce dietary Na to <2 g/day to increase renal tubular reabsorption of calcium.
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Maintain a normal, rather than a low, calcium diet to bind dietary oxalates and avoid osteopenia since decreased bone mineral density and increased bone fractures have been shown , but avoid added calcium and vitamin D products.
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Thiazide diuretics (e.g., hydrochlorothiazide, 25–50 mg twice daily) decrease urinary calcium excretion by up to 50% with a demonstrated reduction in stone incidence. ,
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Avoid hypokalemia, which reduces urinary citrate. Potassium citrate may be used to prevent thiazide-induced hypocitraturia.
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Amiloride can be used with a thiazide instead of potassium citrate to reduce urinary excretion of both potassium and calcium.
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An alternative therapy, neutral sodium phosphate (500 mg four times daily) corrects the low serum phosphate in the hypophosphatemic form of hypercalciuria, which may decrease calcium excretion. It also increases urinary pyrophosphate excretion to solubilize calcium, but has not been shown to decrease stone occurrence.
15.1.5.2 Hypocitraturia ,
15.1.5.2.1 Defining the defect
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Urinary citrate <320 mEq/day
15.1.5.2.2 Mechanisms involved
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Idiopathic or associated with renal tubular acidosis (RTA), cystic fibrosis, chronic metabolic acidosis (diarrhea, carbonic anhydrase inhibitors)
15.1.5.2.3 Treatment of specific causes of recurrent stones
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Potassium citrate has been demonstrated to decrease stone occurrence (10–20 mEq three times daily for urinary citrate <320 mEq/day, 20 mEq 3–4 times daily for urinary citrate <150 mEq/day).
15.1.5.3 Hyperuricosuria (may be associated with either uric acid or calcium oxalate stones) , ,
15.1.5.3.1 Defining the defect
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Urinary uric acid >750 to 800 mg/day
Note: Uric acid stones can occur with normal excretion of uric acid due to low urine pH in chronic diarrheal states.
15.1.5.3.2 Mechanisms involved
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Overproduction of uric acid may occur with or without gout, certain enzyme defects, high purine intake, myeloproliferative and hemolytic disorders, cytotoxic drugs, and alcoholism.
15.1.5.3.3 Treatment of specific causes of recurrent stones
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For hyperuricosuria, allopurinol has been shown to decrease both uric acid stone and hyperuricosuric calcium oxalate stone occurrence.
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For uric acid stones with normal uric acid excretion or with intolerance to allopurinol or febuxostat, alkalinize the urine to pH >6.5 to increase urate solubility (NaHCO 3 or sodium or potassium citrate, 1–3 mEq/kg/day, usually given in 4 doses).
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Avoid purine-rich foods.
15.1.5.4 Cystinuria , ,
15.1.5.4.1 Defining the defect
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Urinary cystine >400 mg/day or cystine crystals in urinary sediment
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Cystine stone formation
15.1.5.4.2 Mechanisms involved
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Several genetic defects in cystine and dibasic amino acid transport decreasing renal tubular cystine reabsorption
15.1.5.4.3 Treatment of specific causes of recurrent stones
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Dietary protein and sodium restriction decreases urinary cystine
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Alkalinization of urine to pH >7.0 to 7.5 with potassium citrate
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Bedtime dose of acetazolamide or potassium citrate to maintain alkaline urine at night
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Fluid intake to very high urine output >3 to 4 L/day
If those measures fail:
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Thiol drug treatment with tiopronin (preferable), penicillamine, or perhaps captopril to decrease cystine by forming cysteine-drug disulfide bonds has been shown to decrease cystine stone occurrence.
15.1.5.5 Hyperoxaluria ,
15.1.5.5.1 Defining the defect
Urinary oxalate >45 mg/day
15.1.5.5.2 Mechanisms involved
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Primary hyperoxaluria (three types of genetic defects: rare, but overproduction may be as much as >>100 mg/day)
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May be associated with idiopathic hypercalciuria
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Secondary: intestinal hyperabsorption in malabsorption syndromes, postbypass surgery, inflammatory bowel disease, pancreatic insufficiency, and cystic fibrosis
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High-dose vitamin C intake increases endogenous oxalate production
15.1.5.5.3 Treatment of specific causes of recurrent stones
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Low-oxalate diet (restrict dietary intake of spinach and other leafy vegetables, cranberries, tea, cocoa, and nuts)
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Avoid high-dose vitamin C intake
To decrease intestinal absorption of oxalate:
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Low-fat diet helps reduce free oxalate in the intestine
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Calcium carbonate or citrate, 1 to 4 g/day with meals, binds oxalate in the intestine with a greater proportional decrease in urinary oxalate than increase in urinary calcium
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Cholestyramine, an oxalate-binding resin, at a dose of 8 to 16 g/day may help
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Restoration of small bowel continuity, if possible (if prior bypass surgery)
For primary hyperoxaluria:
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Pyridoxine at high dose (100–800 mg/day) for hereditary deficiency type 1
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Neutral sodium phosphate and potassium citrate as above may help decrease urinary supersaturation of calcium oxalate
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Segmental liver transplant, to correct the enzyme defect, combined with a kidney transplant for renal failure, has been successfully utilized in patients with hereditary hyperoxaluria
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A new treatment for primary hyperoxaluria type 1 (PH1) with an RNA interference agent that targets glycolate oxidase, lumasiran injected subcutaneously, has been shown to reduce hepatic oxalate overproduction, decreasing plasma and urinary oxalate.
15.1.5.6 Struvite stone crystalluria (magnesium ammonium phosphate “triple phosphate”) ,
15.1.5.6.1 Defining the defect
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Chronic urinary infection with a urea-splitting organism, urine pH > 7.0, struvite stone, or staghorn
15.1.5.6.2 Mechanisms involved
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Urease-producing bacteria break down urea to ammonia, leading to alkaline urine and struvite crystallization with ammonium, magnesium, calcium carbonate, and phosphate
15.1.5.6.3 Treatment of specific causes of recurrent stones
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Eradication of infection, if possible, with long-term antimicrobial therapy
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Urease inhibitor therapy (acetohydroxamic acid decreases stone formation but often causes side effects)
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Removal of stones with lithotripsy, percutaneous nephrolithotomy, or open surgery
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Evaluate for an underlying additional stone-forming disorder (e.g., hypercalciuria)
15.1.6 Nephrocalcinosis
Nephrocalcinosis is the deposition of calcium phosphate and/or calcium oxalate (the latter often described as oxalosis) in the kidney parenchyma, usually in the renal medulla and less commonly in the renal cortex. Nephrocalcinosis may be associated with hypercalcemia, hypercalciuria, hyperphosphatemia, hyphosphaturia, or hyperoxaluria. When severe, nephrocalcinosis can result in ESKD.
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