Материал: Oxford American Handbook of Urology ( PDFDrive )
352 CHAPTER 7 Miscellaneous urological diseases of kidney
Renal duplications
Definitions
A duplex kidney has an upper pole and a lower pole, each with its own separate pelvicalyceal system and ureter. The two ureters may join to form a single ureter at the pelviureteric junction (bifid system) or more distally (bifid ureter) before entering the bladder through one ureteric orifice.
Alternatively, the two ureters may pass down individually to the bladder (complete duplication). In this case, the Weigert–Meyer rule states that the upper-pole ureter always opens onto the bladder medially and inferiorly to the ureter of the lower pole, thereby predisposing to ectopic placement of the ureteric orifice and obstruction (due to the longer intramural course of the ureter through the bladder wall).
The lower-pole ureter opens onto the bladder laterally and superiorly, reducing the intramural ureteric length, which predisposes to vesicoureteric reflux (in up to 85%).
Epidemiology
Ureteric duplication occurs in 1 in 125 individuals, with a female-to-male ratio of 2:1. Unilateral cases are more common than bilateral cases, with right and left sides affected equally.
Risk of other congenital malformations is increased.
Embryology
In duplication, two ureteric buds arise from the mesonephric duct (week 4 gestation). The ureteric bud situated more distally (lower-pole ureter) enters the bladder first and therefore migrates a longer distance, resulting in the superior and lateral position of the ureteric orifice.
The proximal bud (upper-pole ureter) has less time to migrate, and consequently the ureteric orifice is inferior and medial (ectopic). Interaction of each ureteric bud with the same metanephric tissue creates separate collecting systems within the same renal unit.
With bifid ureters, a single ureteric bud splits after it has emerged from the mesonephric duct.
Complications
Ectopic ureters are associated with both upper renal-pole hydronephrosis (secondary to obstruction) and hypoplasia or dysplasia (renal maldevelopment related to ectopic displacement of ureteric orifice).
Lower-pole ureters are prone to reflux, resulting in hydroureter and hydronephrosis.
Bifid ureters can get urine continuously passing from one collecting system to the other, causing urinary stasis (predisposing to infection).
Presentation
Patients have symptoms of UTI or flank pain, or an asymptomatic incidental finding.
RENAL DUPLICATIONS 353
Investigation
-Renal ultrasound scan demonstrates ureteric duplication ± dilatation and hydronephrosis.
-IVP decreased contrast excretion from renal upper pole ± hydronepFlankhrosis (which may displace the lower pole downward and outward, producing a “drooping lily” appearance).
-Micturating cystourethrography (MCUG) will determine whether reflux is present.
-CT and MRI reveal detailed anatomical information.
-Isotope renogram (99mTc-DMSA) assesses renal function.
Treatment
In symptomatic patients, the aim is to reduce obstruction and reflux and to improve function. Common sheath ureteric reimplantation (where a cuff of bladder tissue is taken that encompasses both duplicated ureters) can treat both conditions.
Where an ectopic ureter is associated with a poorly functioning renal upper pole, open or laparoscopic heminephrectomy with excision of the associated ureter may be considered.
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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.