Chapter 8
Stone disease
Kidney stones: epidemiology 356
Kidney stones: types and predisposing factors 358 Kidney stones: mechanisms of formation 360 Factors predisposing to specific stone types 362 Evaluation of the stone former 366
Kidney stones: presentation and diagnosis 368 Kidney stone treatment options: watchful waiting 370
Stone fragmentation techniques: extracorporeal lithotripsy (ESWL) 372
Intracorporeal techniques of stone fragmentation (fragmentation within the body) 374
Kidney stone treatment: flexible ureteroscopy and laser treatment 378
Kidney stone treatment: percutaneous nephrolithotomy (PCNL) 380
Kidney stones: open stone surgery 383
Kidney stones: medical therapy (dissolution therapy) 384 Ureteric stones: presentation 386
Ureteric stones: diagnostic radiological imaging 388 Ureteric stones: acute management 390
Ureteric stones: indications for intervention to relieve obstruction and/or remove the stone 392
Ureteric stone treatment 394
Treatment options for ureteric stones 396 Prevention of calcium oxalate stone formation 398 Bladder stones 400
Management of ureteric stones in pregnancy 402
356 CHAPTER 8 Stone disease
Kidney stones: epidemiology
Approximately 10% of Caucasian men will develop a kidney stone by the age of 70. Within 1 year of a calcium oxalate stone, 10% of men will form another calcium oxalate stone, and 50% will have formed another stone within 10 years.
The prevalence of renal tract stone disease is determined by factors intrinsic to the individual and by extrinsic (environmental) factors. A combination of factors often contributes to the risk of stone formation.
Intrinsic factors
Age
Peak incidence of stones occurs between the ages of 20 and 50 years.
Sex
Males are affected 3 times as frequently as females. Testosterone may cause increased oxalate production in the liver (predisposing to calcium oxalate stones) and women have higher urinary citrate concentrations (citrate inhibits calcium oxalate stone formation).
Genetic
Kidney stones are relatively uncommon in Native Americans, Black Africans, and U.S. Blacks, and more common in Caucasians and Asians. About 25% of patients with kidney stones report a family history of stone disease (the relative risk of stone formation remaining high after adjusting for dietary calcium intake).
Familial renal tubular acidosis (predisposing to calcium phosphate stones) and cystinuria (predisposing to cystine stones) are inherited.1
Extrinsic (environmental) factors
Geographical location, climate, and season
The relationship between these factors and stone risk is complex. While renal stone disease is more common in hot climates, some endogenous populations of hot climates have a low incidence of stones (e.g., Black Africans, Aborigines), and many temperate areas have a high incidence of stones (e.g., Northern Europe and Scandinavia). This may relate to Western lifestyle—excess food, inadequate fluid intake, limited exercise— combined with a genetic predisposition to stone formation.
Ureteric stones become more prevalent during the summer
The highest incidence occurs a month or so after peak summertime temperatures, presumably because of higher urinary concentration in the summer (encourages crystallization). Concentrated urine has a lower pH, encouraging cystine and uric acid stone formation.
Exposure to sunlight may also increase endogenous vitamin D production, leading to hypercalciuria.
1 Curhan GC, Willett WC, Rimm EB, Stampfer MJ (1997). Family history and risk of kidney stones.
J Am Soc Nephrol, 8:1568–1573.
KIDNEY STONES: EPIDEMIOLOGY 357
Water intake
Low fluid intake (<1200 mL/day) predisposes to stone formation.2 Increasing water hardness (high calcium content) may reduce risk of stone formation, by decreasing urinary oxalate.
Diet
High animal protein intake increases risk of stone disease (high urinary oxalate, low pH, low urinary citrate).3,4 High salt intake causes hypercalciuria. Contrary to conventional teaching, low-calcium diets predispose to calcium stone disease, and high-calcium intake is protective.5
Occupation
Sedentary occupations predispose to stones more than manual work.
2 Borghi L, et al. (1996) Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study. J Urol 155:839–843.
3 Curhan GC, et al. (1997) Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med 126:497–504.
4 Borghi L, et al. (2002) Comparison of 2 diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med 346:77–84.
5 Curhan GC, et al. (1993) A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med 328:833–838.
358 CHAPTER 8 Stone disease
Kidney stones: types and predisposing factors
Stones may be classified according to composition (Table 8.1), X-ray appearance, or size and shape.
Other rare stone types (all radiolucent) include indinavir (a protease inhibitor for treatment of HIV), triamterene (a relatively insoluble potas- sium-sparing diuretic, most of which is excreted in urine), and xanthine.
Radiodensity on X-ray
Three broad categories of stones are described, based on their X-ray appearance. This gives some indication of the likely stone composition and helps to some extent to determine treatment options.
However, in only 40% of cases is stone composition correctly identified from visual estimation of radiodensity on plain X-ray.1
Radio-opaque
Opacity implies presence of substantial amounts of calcium within the stone. Calcium phosphate stones are the most radiodense stones, almost as dense as bone. Calcium oxalate stones are slightly less radiodense.
Relatively radiolucent
Cystine stones are relatively radiodense because they contain sulfur (Fig. 8.1). Magnesium ammonium phosphate (struvite) stones are less radiodense than calcium-containing stones.
Completely radiolucent
Uric acid, triamterene, xanthine, indinavir stones are in this category (cannot be seen even on CTU).
Table 8.1 Composition of kidney stones
Stone composition |
% of all renal calculi* |
Calcium oxalate |
85% |
Uric acid† |
5–10% |
Calcium phosphate + calcium oxalate |
10% |
Pure calcium phosphate |
Rare |
Struvite (infection stones) |
2–20% |
Cystine |
1% |
* The precise distribution of stone types will vary depending on the characteristics of the study population (geographical location, racial distribution, etc.). Hence, the quoted figures do not equate to 100.
†~80% of uric acid stones are pure uric acid; 20% contain some calcium oxalate.
1 Ramakumar S, Patterson DE, LeRoy AJ, et al. (1999) Prediction of stone composition from plain radiographs: a prospective study. J Endosc Urol 13:397–401.
KIDNEY STONES: TYPES AND PREDISPOSING FACTORS 359
Size and shape
Stones can be characterized by their size, in centimeters. Stones that grow to occupy the renal collecting system (the pelvis and one or more renal calyx) are known as staghorn calculi, since they resemble the horns of a stag (Fig. 8.2). They are most commonly composed of struvite—magne- sium ammonium phosphate (being caused by infection and forming under the alkaline conditions induced by urea-splitting bacteria), but may consist of uric acid, cystine, or calcium oxalate monohydrate.
Figure 8.1 A left cystine stone, barely visible just below the midpoint of the 12th rib.
Figure 8.2 A large, right staghorn calculus.