Maitrey Darrad Ameet Gupta, and Nick Rukin

Urology Department, New Cross Hospital, Wolverhampton, UK


Hydronephrosis is a common urological finding of which the causes are numerous and its investigation can put significant demand on healthcare resources. The importance of correct investigations and diagnosis is imperative to elucidate appropriate treatments. Causes range from congenital to acquired and symptomatic to asymptomatic. Knowledge of the pathophysiology, diagnostic imaging, and management of hydronephrosis is vital for all urological practitioners.

Hydronephrosis needs appropriate early investigation with prompt treatment to enable renal preservation and prevent irreversible renal damage. An understanding of the pathophysiology of acute obstruction is important to fully appreciate the complex nature of the kidney in homeostasis. This chapter discusses the pathophysiology, investigation, and common causes of hydronephrosis.

Keywords ureteric obstruction; hydronephrosis; pelviuretric junction obstruction; megaureter; postobstructive diuresis; ectopic ureter; ureterocele; retrocaval ureter; perinatal hydronephrosis

10.1 Definition

Hydronephrosis is the dilatation of the renal calyces and pelvis with urine. Hydroureter is defined as a dilatation of the ureter. Both phenomena can be unilateral or bilateral, acute or chronic, congenital or acquired, and physiological or pathological. Although these terminologies are used synonymously with obstruction, both can be present without it (i.e. vesicoureteric reflux [VUR]).

10.2 Incidence

Urinary tract obstruction is of significant clinical relevance and can be partial, progressively occluding, or complete. It is a common feature of patients with renal failure and accounts for approximately 10% of cases. Superseded infection needs immediate intervention to prevent morbidity and mortality. A series of 59 064 autopsies of patients of all ages identified a prevalence rate of hydronephrosis to be 3.1% [1]. Out of the 21 587 women, the most common aetiology for hydronephrosis was either pregnancy or gynaecological malignancies (mostly cervical or uterine cancer). This was found to be most prevalent between the ages of 20 and60 years [1]. In contrast, out of the 37 477 men, the most common aetiology for hydronephrosis was prostatic disease (either benign prostatic hypertrophy or prostate cancer) with a peak prevalence of over 60 years [1].

Congenital hydronephrosis occurs in approximately 2–2.5% of children. Antenatal screening has led to early diagnosis with most obstructive conditions being detected prior to birth. An autopsy series of stillbirths, infants, and children found a higher prevalence in boys with the majority being younger than one year [2]. Table 10.1 outlines the causes of hydronephrosis.

Table 10.1 Causes of obstructive nephropathy.

Congenital Congenital
Renal Renal
Pelviureteric Junction (PUJ) obstruction Polycystic kidney
Renal cyst Lower urinary tract
Parapelvic cyst Posterior urethral valve
Ureter Phimosis
Ureteric stricture Acquired
Ureterocele Ureter
Obstructing megaureter Retroperitoneal fibrosis
Retrocaval ureter Radiation therapy
Acquired Schistosomiasis
Renal Pregnancy
Renal cancer Pelvic lipomatosis
Sloughed papillae Procidentia
Renal artery aneurysm Lower urinary tract
Ureter Bladder cancer
Ureteric cancer Neurogenic bladder
Metastatic ureteric obstruction Benign prostatic hypertrophy
Calculi Prostate cancer
Clot Urethral cancer
Trauma Urethral stricture
Ureteric stricture Penile cancer
Ureteritis cystica

All causes of bilateral obstructive nephropathy can be unilateral in the early stages.

Some causes of unilateral obstructive nephropathy can cause bilateral.

10.3 Pathophysiology

10.3.1 Macroscopic Changes in Upper Urinary Tract Obstruction

A combination of urinary pooling and reduced ureteric contractility following obstruction gives rise to back pressure to the proximal kidney. This subsequently causes dilatation of the collecting system resulting in hydronephrosis. The kidney eventually swells and increases in weight because of the urinary pooling, causing flattening of the renal papilla and back filling of the collecting system with eventual parenchymal oedema seven days following the obstruction. The renal cortex is compressed, resulting in the characteristic cortical and medullary thinning seen with obstruction, usually by days 21–28 [3].

10.3.2 Microscopic Changes in Upper Urinary Tract Obstruction

With prolonged obstructive nephropathy, the tubular swelling extends to the more proximal aspect of the nephron. The primary histological derangements are localised to the tubulointerstitial compartment of the kidney. The mechanical changes cause massive tubular dilatation and are associated with renal tubular cell stress leading to eventual apoptotic cell death and progressive tubulointerstitial atrophy and fibrosis with resultant renal injury. This is mediated by an influx of proinflammatory mediators, such as macrophages and suppressor T‐lymphocytes, which trigger proinflammatory cytokines and growth factors (tumour necrosis factor‐α, transforming growth factor‐β1, interleukin‐18, monocyte chemotactic protein‐1, and macrophage inflammatory protein‐1 and 1β) that stimulate fibroblastic proliferation and activation of the extra cellular matrix. The tubular epithelial stress response also leads to oxidative stress by increase in superoxide radical production with a reduction in catalase enzymes, which metabolises hydrogen peroxide. These changes destabilise the mitochondria and promote the release of cytochrome C, which in turn activates Caspase (cysteine aspartate specific protease)‐mediated apoptosis.

In early onset urinary tract obstruction, the glomeruli are relatively preserved; however, long‐standing obstruction leads to extensive glomerulosclerosis.

10.3.3 Ureteric Function in Upper Urinary Tract Obstruction

Ureteric peristalsis enables a coordinated contraction of the renal pelvis and ureter to propel urine into the urinary bladder. The central control mechanism of this phenomenon is still poorly understood, but the primary oscillator of ureteric peristalsis is thought to be renal pelvis urine volume.

Studies of sheep and human ureters in an obstructed state found that stretch dramatically increased contraction amplitude in both renal pelvis and distal ureter, but only increased contraction frequency in the renal pelvis [4]. In canine studies, after prolonged complete obstruction of four weeks, both canine renal pelvis and ureter were aperistaltic [5]. However, with the same duration of partial obstruction, peristalsis continued with roughly half the frequency but up to fivefold increase in contraction amplitude. In eight weeks following relief of complete obstruction, the contraction amplitude, and frequency returned to baseline. In partial obstruction however, contractile amplitude remained elevated.

10.3.4 Renal Haemodynamics, Glomerular Filtration Rate and Intrarenal Pressure in Upper Urinary Tract Obstruction

The normal resting pressures of the renal pelvis and ureter are approximately 0–10 cm H2O. Normal pressure change during peristalsis varies between 20 and 60 cm H2O. As mentioned previously, there is a dramatic rise in both intrarenal and intra‐ureteric pressure in acute obstruction. The rise in pressure is transient and is followed by a prolonged gradual decline. This is secondary to an increasing renal pelvis dilatation in proportion to the compliance of the system, reduced renal blood flow and glomerular filtration rate (GFR), and pyelolymphatic and pyelovenous backflow [6].

Obstructive nephropathy leads to haemodynamic changes of the kidney with resultant alterations in the glomerular filtration rate. These changes differ between subjects with unilateral or bilateral ureteral obstruction.

Animal studies have identified that changes in renal blood flow and ureteral pressures occur in three separate phases in unilateral ureteral obstruction (Table 10.2) [7, 8].

  1. In the initial phase, which lasts 90 minutes, there is an increase in renal tubule pressures from 6 to 7 mm Hg up to 50–70 mm Hg leading to a decrease in GFR. This pressure change leads to a compensatory nitric oxide and prostaglandin E2‐mediated decrease in afferent arteriolar resistance, which raises glomerular capillary pressure and maintains GFR at 80% of normal despite the raised renal tubular pressure.
  2. The second phase, lasting 1.5–4 hours, exhibits a decline in renal blood flow with a persistently elevated ureteral pressure secondary to afferent and efferent arteriolar vasoconstriction in response to substances including thromboxane A2 and endothelin. GFR is therefore reduced to roughly 20% of normal.
  3. In the final phase, which is mediated by an increase in afferent arteriolar resistance, there is a decline in both ureteral pressure (though reduced, but 50% higher than normal pressure) and renal blood flow resulting in loss of kidney function.

Table 10.2 Phases of ureteric obstruction.

Phase Time Promotor Effect on intrarenal pressure Effect on eGFR
Unilateral Obstruction
1 Up to 90 min Increase NO and PGE2 causing afferent arteriole dilation Increase Increase
2 90 min–5 hours Thromboxane A2 and endothelin cause efferent arteriole vasoconstriction Increase Decrease
3 >5 hours ACE and angiotensin II cause afferent arteriole vasoconstriction Decrease Decrease
Bilateral Obstruction
1 Up to 90 min
Increase Increase
2 90 min–5 hours
Increase Decrease
3 >5 hours
Increase Decrease

ACE, angiotensin‐converting enzyme; NO, nitrous oxide; PGE2, prostaglandin E2.

Bilateral obstruction differs as ureteral pressures remain elevated for greater than 24 hours, and by causing only a small initial rise of renal blood flow, lasting 90 minutes, followed by a decline in renal blood flow in both kidneys (or solitary kidney) [9].

All these experiments were conducted on animals with unicalyceal renal system (i.e. dogs, rats) and have not been consistently reproduced in animals with multicalyceal systems similar to humans.

10.3.5 Effect on Tubular Function

Sodium and potassium handling via opposing active transport mechanisms at the basolateral membrane of the proximal tubules, the ascending loop of Henle, distal tubule, and the countercurrent mechanism is crucial for controlling the extracellular fluid volume. In unilateral obstruction, down‐regulation of apical sodium antiporters and catalytic units of the basolateral Na‐K‐ATPase has been demonstrated. The disruption in sodium reabsorption leads to failure of the countercurrent multiplier because of the interruption of the corticomedullary gradient. Evidence from rat‐based studies has shown some reduction in sodium expression in the contralateral kidney leading to early natriuresis [10, 11]. There is a similar down‐regulation of sodium transporters in bilateral ureteral obstruction. Potassium excretion is also reduced, but compensatory mechanisms for the contralateral kidney prevent hyperkalaemia.

Urinary tract obstruction causes an alkalization of urine in both animal and human studies. This is due to the dependence of hydrogen ions on sodium transporters, which is impaired in the context of obstruction, to be in the urinary filtrate. The main acidification defect is thought to be in the distal tubule [12].

10.3.6 Effects of Obstruction on the Kidney

Obstruction leads to atrophy of the renal parenchyma. The principal effect of this atrophy is borne by the papillae, relatively more tubules being destroyed than glomeruli. Because there are fewer tubules to render the urine concentrated, the hydronephrotic kidney makes a larger volume of dilute urine and the effect of any obstruction is exaggerated.

Ultimately, entire nephrons are lost, and there is a deterioration in the creatinine clearance from the obstructed kidney, but for a considerable time, the obstructed kidney or idiopathic hydronephrosis remains a useful dialyser, and even when very thin, is still capable of sustaining life.

If infection supervenes at any time, then the devastating effect of inflammatory scarring – reflux nephropathy – are added to the slow atrophy caused by obstruction. This means that the presence of infection lends a measure of urgency to the need to relieve the obstruction.

10.3.7 Postobstructive Renal Recovery and Diuresis

Following relief of the ureteral obstruction, functional renal recovery is significantly dependent on the degree and duration of obstruction. In rat models, return of GFR following obstruction has been found to have an inverse relationship to duration of obstruction [13].

In canine studies, in unilateral ureteral obstruction of less than seven days, full recovery of GFR was achieved. After 14 days of obstruction 70% of GFR returned, after three weeks only 30%, and after six weeks there was no GFR recovery at all. Despite renal function recovery, interstitial fibrosis and apoptosis persists [14].

Following relief of obstruction, the kidney produces hypotonic urine. This is only clinically significant in subjects with bilateral ureteral obstruction due to the compensatory mechanisms of the unobstructed contralateral kidney in unilateral cases. After 24 hours of bilateral obstruction, there is a significant reduction in aquaporin 2 expression in the kidney. This protein channel is the predominant vasopressin‐regulated water channel in the collecting tubules and ducts. This results in impaired ability of the kidney to reabsorb water. Studies have shown that aquaporin 2 expression returns to only at 50% after seven days following relief of obstruction and can remain down‐regulated long term, contributing to chronic polyuria in obstructive nephropathy [15].

Bilateral ureteral obstruction also causes a postobstructive diuresis secondary to accumulation and retention of water, sodium, urea, as well as increasedatrial natriuretic peptide (ANP) production. These factors lead to a diuresis, potassium excretion, and natriuresis, which does not occur to a significant extent in unilateral obstruction. The osmolality of urine has been shown to take up to 1 month to return to normal in rat models with only 24 hours of urinary tract obstruction [16].

In more than 90%, the diuresis is physiological (i.e. natural consequence to remove excess water, electrolytes, and metabolism by‐products). However, 10% is pathological, mainly because of the loss of the cortico‐medullary concentration gradient with excess ANP production, which lead to exaggerated loss of water and electrolytes.

10.3.8 General Clinical Features

There are five easily recognisable syndromes.

  1. Pain with diuresis. Young people, usually men, boasting of their prowess at drinking beer, give a characteristic history of pain in the loin, followed by vomiting, after drinking several pints of beer. It is all too easy to jump to the diagnosis of a duodenal ulcer.
  2. Loin pain and fever may be caused by an infection in the hydronephrotic sac. Curiously, this is often almost silent, even though the urine in the kidney may look like pea soup. Occasionally, the pyonephrosis makes the patient desperately ill with septicaemia, and its relief by percutaneous nephrostomy is an emergency.
  3. A mass. Many patients notice a lump in the loin, even though it may not be clinically palpable. The patient who feels a lump in the loin is often right, and it deserves investigating.
  4. Gastrointestinal symptoms. In later life, the patient may not associate the consumption of fluid with the onset of pain. Commonly, a hydronephrosis is detected by chance in the course of investigating other abdominal pains. If the hydronephrosis is on the right side, distension of tissues behind the duodenum may give rise to dyspepsia closely resembling the pain of a peptic ulcer, and patients have often undergone prolonged treatment for a nonexistent duodenal ulcer before their hydronephrosis is discovered. Similarly, a left‐sided hydronephrosis may cause disturbance of bowel function. Many of these unfortunate patients are labelled as having colonic dysfunction or are even dismissed as valetudinarians, especially when they get relief by inexplicable manoeuvres such as lying face down or bending over the side of the bed.
  5. Hypertension. The routine investigation of a young person with hypertension sometimes reveals hydronephrosis. The dilated cortical tissue is secreting renin.

10.4 Diagnostic Imaging

10.4.1 Ultrasound

The first‐line imaging modality in the majority of cases is renal tract ultrasonography. It is safe, lacks ionising radiation, low cost, and easily available. Ultrasonography can detect the foetal kidney by 15 weeks of gestation and can easily detect anomalies by 20 weeks; therefore, it is the investigation of choice in the antenatal period. It provides the anatomical finding of hydronephrosis but offers limited functional information and therefore cannot exclusively diagnosis urinary tract obstruction.

Conversely, 50% of patients with acute urinary tract obstruction have normal ultrasound appearances in the immediate setting [17]. An extrarenal pelvis or a parapelvic cysts can give a false‐positive impression of hydronephrosis.

10.4.2 Nuclear Medicine Isotopic Renograms

Diuretic renography can provide noninvasive information about dynamic renal function. Either a dynamic scan using mercaptoacetyl triglycine (MAG3) or a static scan dimercaptosuccinic acid (DMSA) scans. Both are readily labelled by 99 m technetium (99 mTc), which emits gamma radiation detectable by a gamma camera. MAG3 undergoes tubular (90%) and glomerular (10%) excretion, while DMSA binds to the proximal renal tubules. Therefore, MAG3 renograms play an important role in differentiating a nonobstructed dilated system from an obstructed system as well as providing an approximate split functionality of the kidneys. A DMSA scan provides a better deferential split functioning. The scans also provide details of cortical defects like scars and delineation of duplex kidney deferential function between upper and lower moieties.

Furosemide is given either 15 minutes before the isotopic injection (F‐15), at the time of injection (F0) or 20 minutes after the injection (F + 20).

MAG3 renograms have three phases:

  • A vascular phase (first 10 seconds): reflecting renal blood flow
  • Uptake phase (10 seconds to 5 minutes): the uptake of the radio‐tracer, this reflects the parenchymal function, and a ‘static’ image can be taken at this stage to estimate the differential function.
  • Excretory phase (after five minutes): excretion of the radio‐tracer

Images are taken and plotted to give resulting curves (Figure 10.1):

  • Type I curve: normal renal uptake and drainage
  • Type II curve: Obstruction, continues to rise, with no response to a diuretic
  • Type IIIa curve: normal drainage from a hypotonic (stretched/bagged) renal pelvis
  • Type IIIb curve: equivocal, the curve very slowly falls and does not rise
  • Type IV curve (Homsy sign): A short‐lived response to the diuretic is followed by a rise in the curve. It represents obstruction, a F‐15 eliminates the transient effect, showing a continual rising curve.
Image described by caption and surrounding text.

Figure 10.1 (a) MAG3 curves. (b) As the dilated renal pelvis bulges out between the two lower anterior segmental arteries, it carries the obstruction segment outside, giving the misleading impression that it is the lower pole artery which is causing the obstruction. (a) View from behind and (b) View from in front.

In all these renographic tests, infection may give false results because oedema of the kidney may reduce its blood flow. Hence, if the kidney is infected, the renograms should be repeated after a period of drainage and antibiotics.

10.4.3 Computer Tomography Urography (CTU)

CTU is the modality of choice for a complete evaluation of the urinary tract obstruction. It has by in large replaced intravenous urography (IVU). It offers greater anatomical definition as well as provides functional information to aid with the diagnosis of the underlying cause of obstruction.

10.4.4 Magnetic Resonance Urography (MRU)

MRU can integrate anatomical and functional information without the radiation; however, it is poor at detecting urinary tract stones with a sensitivity of 68.9–81% [18, 19].

10.4.5 Pyelography (Either Retrograde or Antegrade)

Pyelography can accurately define ureteral and collecting system anatomy and can aid in the locality of upper urinary tract obstruction. It is useful in subjects where other imaging modalities have not accurately defined the anatomy of the collecting system.

10.4.6 The Whitaker Test

An objective method of detecting obstruction is to measure the pressure inside the renal pelvis during diuresis. Pressure flow studies are applied using percutaneous nephrostomy and bladder catheter. It carries a slight risk of introducing infection into the closed obstructed system.

In practice, there are some cases where it is obvious that the kidney is reduced to nothing more than a thin bag of scarred tissue which ought to be removed, and others in which there is a substantial thickness of renal tissue worth saving. When dynamic diuresis renogram results are equivocal, and investigations do not give a clear picture of the clinical symptoms of obstruction, a Whitaker test might come in handy.

With the patient lying on the urodynamics bed, a mix of saline with contrast is infused through the nephrostomy at a rate of 10 ml min−1 and the pressure difference between the kidney and bladder is measure. Results

Results indicate whether there is an obstruction.

  • <15 cm H2O: unobstructed
  • 15–22 cm H2O: equivocal; might need repeating
  • >22 cm H2O: obstructed

10.5 Complications of Hydronephrosis

10.5.1 Infection

After the progressive diminution of renal function, infection is the most important complication. In the presence of obstruction, urine in the renal pelvis is leading freely into the renal lymphatics, and if the urine is infected, organisms readily enter the bloodstream. Septicaemia is an ever‐present risk. The curious thing is how often patients seem to remain well despite having a kidney full of purulent urine.

When pyonephrosis is encountered, the first step should be to drain it by means of a percutaneous nephrostomy. For the first few days, thick pus will drain away but will soon be followed by the production of a useful quantity of urine. The creatinine concentration in this urine should be measured from time to time until it becomes stable before making a decision as to whether to try to save the kidney or perform a nephrectomy.

10.5.2 Stones

Stones readily form in the pool of stagnant urine in hydronephrosis. They are multiple and rounded like pebbles from the seashore in contrast to those stones which arise within the kidney and give rise to secondary obstruction and hydronephrosis. The latter are not smooth, and they retain the shape of the renal pelvis and its calices. When it is not easy to be sure whether the obstruction or the stone came first, a version of the Whitaker test may be used at operation or after percutaneous nephrolithotomy to see if there is an idiopathic obstruction at the pelviureteric junction.

10.5.3 Trauma

It is easier to burst a balloon when it is blown up, and for the same reason, a distended hydronephrosis is apt to be ruptured by external injury. The urogram performed as an emergency soon after the patient is admitted with suspected closed renal injury may show the unexpected coexistence of a hydronephrosis and extravasation of urine, but more often the renal function is too poor to display the anatomy of the kidney. A CT scan will show the thinned out parenchyma. This sometimes raises a medicolegal question; did the injury cause the hydronephrosis? This may be easy to answer if the renal parenchyma is already severely atrophied at the time of injury. In other cases, it is impossible to be sure that the injury was not responsible for the obstruction.

10.5.4 Hypertension

Hypertension associated with a hydronephrosis may resolve with cure of the obstruction. In former days, the lower pole artery used to be divided because it was believed to be causing the obstruction (Figure 10.1b), and in these cases, hypertension was a common sequel to the infarction of the lower pole.

10.6 Management (General Principles)

The generic principles of managing a patient with urinary tract obstruction are twofold:

  • identification and prompt treatment of the causative factor.
  • preservation or removal of the affected kidney, depending on the degree of reversibility of its function.

If acute urinary obstruction is presenting with pain then administration of analgesia is important. Nonsteroidal anti‐inflammatory drugs (NSAIDs) are first‐line treatment and superior to opioids in the case of renal colic. NSDAIDs inhibit cyclo‐oxygenase (COX) enzyme, which regulates prostaglandin synthesis. Prostaglandins increase glomerular afferent arteriolar vasodilatation, which lead to increase in GFR. NSAIDs inhibit prostaglandin synthesis, thereby preventing glomerular afferent arteriolar vasodilatation. This reduces glomerular filtration by up to one‐third, therefore, reducing renal pelvic pressure and stimulation of stretch receptors and leading to alleviation of the pain. Prostaglandin inhibition also reduces ureteric inflammation.

Immediate drainage of the obstructed kidney, particularly if there is superseded infection or in the presence of a solitary kidney or bilateral ureteral obstruction, is essential. This is not only potentially lifesaving but will also prevent further functional decline.

If the obstruction were from the lower urinary tract, then urinary bladder catheterization would be the immediate treatment. In cases of upper urinary tract obstruction, interventional radiological techniques such as percutaneous nephrostomy, or endourological procedures such as ureteric stents, would allow temporary or permanent drainage depending on the situation. Both these techniques have been equally effective in relieving an obstructed collecting system with similar morbidity [20].

10.7 Perinatal Hydronephrosis

Routine screening foetal sonography, at approximately 18–20 weeks gestational age, has dramatically increased the detection of urinary anomalies over the last 25 years. It identifies antenatal hydronephrosis (ANH) in 1–3% of all pregnancies (Table 10.3) [21, 22]. In the past, only symptomatic patients with a palpable mass, haematuria, or urinary tract infections (UTIs) would mandate further investigations.

Table 10.3 Causes of antenatal hyronephrosis (ANH).

Aetiology Incidence (%) Comments
Phyiological/Transient 50–70
Pelviureteric junction (PUJ) obstruction 10–30
Vesicoureteric reflux (VUR) 10–40
Vesicoureteric junction 5–15 Megaureter
Multicystic dysplastic kidney diease (MDCK) 2–5
Posterior urethral valves 1–5
Others Rare Ectopic ureter
Duplex system
Polycystic kidney disease
Prune belly syndrome

There is a lack of correlation between the final urological diagnosis and prenatal and postnatal ultrasound findings. This dilemma has led to many different grading systems, for ANH, with no global consensus as to the most consistent method. However, a collaborative unified grading system was developed to guide the diagnosis and management of perinatal urinary tract dilatation with risk stratification and proposed a standardised protocol for follow up [22, 23].

The parameters used in this grading classification were antero‐posterior renal pelvis diameter (APRPD), calyceal dilatation, parenchymal thickness, parenchymal appearance, ureter, and bladder (Table 10.4). Management is determined by initial risk stratification and is split into pre‐ and postnatal presentation (Figures 10.2 and 10.3).

Table 10.4 Normal values for urinary tract dilation classification system.

Ultrasound findings Time at presentation
16–27 weeks >28 weeks Postnatal (>48 hrs)
Anterior–posterior renal pelvis diameter (APRPD) <4 mm <7 mm <10 mm
Calyceal dilation
 Central No No No
 Peripheral No No No
Paenchymal thickness Normal Normal Normal
Parenchymal appearence Normal Normal Normal
Ureters Normal Normal Normal
Bladder Normal Normal Normal
Unexplained oligohyramnios No No N/A
Diagram illustrating the prenatal diagnosis, risk stratification, and management of hydronephrosis.

Figure 10.2 Prenatal diagnosis, risk stratification, and management of hydronephrosis. [22].

Source: Adapted from Nguyen et al.

Diagram illustrating the postnatal diagnosis, risk stratification, and management of hydronephrosis.

Figure 10.3 Postnatal diagnosis, risk stratification, and management of hydronephrosis. [22].

Source: Adapted from Nguyen et al.

High‐grade obstruction that may warrant antenatal surgical intervention accounts for less than 5% of all detected urinary tract abnormalities. The rationale for treatment is to maximise the development of pulmonary and renal function. There has to be a thorough analysis of risk–benefit ratio prior to embarking on any form of invasive intervention. Unilateral hydronephrosis does not usually require in‐uretero intervention. The most common indication for intervention is evidence of bladder outflow obstruction (BOO) with dilated bladder and bilateral hydroureteronephrosis. By and large, the most common form of intervention is in‐utero vesicoamniotic shunt placement under ultrasound guidance.

10.8 Pelviureteric Junction Obstruction

Pelviureteric junction (PUJ) obstruction causes impedance to the flow of urine from the renal pelvis to the ureter. The exact aetiology is unknown but there are several plausible theories described (Table 10.5). There are many acquired causes of obstruction including renal calculi, traumatic stricture, urothelial neoplasm, postinflammatory scarring, and fibro‐epithelial polyps. This chapter will focus on congenital PUJ obstruction.

Table 10.5 Causes of extrinsic and intrinsic pelviureteric junction obstructing.

Type Congenital Acquired
Extrinsic obstruction Horseshoe kidney Iatrogenic (postinstrumentation)
Crossing vessels polyps
Duplex collecting system
Intrinsic obstruction Noncontractile segment Urothelial malignancy
Fibrosis of vales Renal collecting system calculi
Kinking of ureter Traumatic stricture formation

Congenital PUJ obstruction affects between 1 in every 1000–2000 live births. It has a gender ratio of 1 : 1 and can present at any age of life. Two‐thirds of the subjects have a left sided PUJ obstruction, but between 10 and 46% have bilateral disease [24, 25].

10.8.1 Pathogenesis

PUJ obstruction can be congenital or acquired. In congenital, the causes are more likely intrinsic; however, extrinsic crossing vessels may contribute. PUJ obstruction the common pathology is of intrinsic luminal disease. Under normal physiology, the pacemakers of urine propagation, which lie in the minor renal calices, contract to direct urine down to the renal pelvis and ureters. The proximal ureter is open and accommodates the urine by stretch, which subsequently stimulates downstream flow by peristalsis. In PUJ obstruction, the proximal ureter is not receptive to the urine load, thus raising the pressures required to allow urine delivery into the ureter to above normal. This leads to the contraction dissociation of both the distal renal pelvis from the proximal ureter, as well as the proximal renal pelvis from the distal pelvis. As a consequence, the renal pelvis becomes increasingly dilated as pacemaker‐induced contractions become more ineffective. This dilatation is accelerated by the inefficient urine transport secondary to the reduced peristaltic transmission as well as reduced urinary bolus volumes.

A frequently found defect is an aperistaltic ureteric segment with abnormal fibrous tissue and longitudinal muscle fibres replacing the normal spiral musculature. Less frequently, the subject can have a primary ureteric stricture, due to excessive collagen deposition, which can occur anywhere throughout the lumbar ureter but most frequently are situated at the PUJ (Figure 10.4).

Diagram displaying a kidney attached to a normal ureter (left) and a kidney attached to a ureter with long narrow segment (right).

Figure 10.4 Usually the obstructing segment is only a few millimetres long; occasionally it may extend over 4–5 cm.

Abnormal folds of ureteral mucosa and musculature, retained from foetal development, can lead to kinks or valves. In some, a complete adventitial bridge can be retained leading to ureteral bands and adhesions. These congenitally retained folds can occasionally produce an angle of entry of the ureter to the distal renal pelvis in such a manner that the pelvis dilates inferiorly and anteriorly, with a resultant proximal ureteric insertion. This leads to inadequate drainage of the most dependent part of the renal pelvis. Although commonly a secondary phenomenon, high ureteric insertion can rarely be a primary congenital pathology.

The role of aberrant crossing vessels in causing extrinsic PUJ obstruction is still debatable (Figure 10.1). Studies have shown that 63% of patients with PUJ obstruction have aberrant crossing vessels on cross‐sectional imaging [26]. However, many of these patients with evidence of crossing vessels also have intrinsic luminal pathology causing renal pelvis dilatation, which subsequently balloons and impinges on to the crossing vessels [27]. Nonetheless, studies have found improvement in obstruction with ligation of aberrant vessels alone, suggesting this is the primary cause [28].

Acquired causes are more commonly caused by intrinsic causes rather than extrinsic compression. Intrinsic causes include trauma from a stone or endoluminal procedures (ureteroscopy), and urothelial tumours at the PUJ (polyps or malignancy). Extrinsic causes include retroperitoneal fibrosis, malignancy, or iatrogenic injury.

10.8.2 Natural History and Presentation

PUJ obstruction most commonly is a congenital problem; however, it can present at any stage of life. It has a variable natural history. Due to the widespread use of antenatal sonography, there has been a dramatic rise in the diagnosis of asymptomatic hydronephrosis in newborns. Obstruction can resolve spontaneously in some cases, whereas with others it increases in severity with deterioration in renal function. It can also remain stable for years in many patients (Table 10.6). It can occasionally present in a previously normal or mildly dilated kidney. A study of conservatively managed children with an antenatal diagnosis of PUJ obstruction showed 17% required surgical intervention due to worsening obstruction, 27% had spontaneously resolved obstruction, and 56% had stable disease with no deterioration in obstruction or renal function [29].

Table 10.6 Presenting symptoms of pelviureteric junction (PUJ) obstruction.

Flank pain Not uncommon. Usually after the age of 4. Persists for several hours or days. Usually in the loin but can be epigastrium. Pain following ingestion of fluid due to renal pelvic distension (Dietl crisis).
Urinary tract infection Common before advent for prenatal screening. Presents with pyonephrosis with high fever and warrants immediate urinary drainage.
Haematuria May be spontaneous or following minor trauma (i.e. exercise).
Palpable flank mass Most common presentation of neonates prior to prenatal screening. In children, can mimic Wilms tumour but can be differentiated by radiological imaging.
Hypertension Rarely a primary presentation.
Incidental Incidental finding from imaging organised for other reasons is not uncommon.

10.8.3 Investigations

Radiological modalities should be targeted at determining the anatomical site and functional significance of the suspected obstruction. Usually the first‐line investigation in children is ultrasonography. This can visualise the dilated collecting system and can determine the level of obstruction. In adults, a CT scan is standard protocol for patients with loin pain, or contrast‐enhanced CT urogram for patients with haematuria. Both modalities will accurately give you anatomical information regarding site of obstruction with CT urogram giving you functional data as well (Figure 10.5).

Image described by caption.

Figure 10.5 Coronal and axial computed tomography imaging to demonstrate a dilated renal pelvis at the level of the pelviurteric junction (a and b) and a nondilated ureter below this level (c). P, renal pelvis, U, ureter.

Source: Photographs courtesy of Dr. Mark Robinson Aneurin Bevan UHB Hospital.

Diuretic renography, most commonly mercaptoacetyltriglycine‐3 (MAG3) dynamic renogram, is used in the evaluation of PUJ obstruction (Figure 10.6). It gives functional information as well as quantitative data regarding split renal function and is a valuable tool to assess the success of surgical treatments. DMSA scan is useful in patients with poor renal function in determining whether a reconstructive procedure or nephrectomy would be the most appropriate surgical intervention.

Image described by caption.

Figure 10.6 MAG 3 Renogram showing reduced clearance of radio‐isotope form right kidney (a) and then post pyeloplasty improved drainage (b).

10.8.4 Management

If patients with suspected PUJ obstruction do not fulfil the criteria for surgical intervention, then close monitoring with serial diuretic renography may be appropriate.

The indications for intervention are:

  • progressive decline in unilateral split function.
  • impairment in overall renal function.
  • obstruction associated symptoms (pain or haematuria).
  • infection episodes (pyonephrosis).
  • renal tract stone development.
  • secondary hypertension.

Different endourological and open, laparoscopic, and robotic procedures have been described to treat PUJ obstruction. Age and comorbidities play a major role in decision making because a patient who is elderly and comorbid may be suitable for conservative monitoring or long‐term ureteral stenting, whereas reconstructive surgery would be most appropriate for a paediatric patient to potentially reverse renal dysfunction.

10.8.5 Pyeloplasty

Laparoscopic or robotic pyeloplasty are the current gold standard of treating PUJ obstruction because they are associated with quicker recovery and discharge from hospital and less postoperative morbidity and a low risk of conversion [30]. Laparoscopy can be done either by the more common transperitoneal or retroperitoneal approach. Robotic pyeloplasty is usually done via a transperitoneal approach. The steps of the procedure are identical regardless of approach.

Though minimally invasive techniques have replaced open pyeloplasty, the techniques of the procedures are similar. Anderson and Hynes popularised their novel technique in the middle of the twentieth century. It can be used almost universally for different PUJ obstruction scenarios even when there is a high ureteric insertion into the renal pelvis as well as when it is already dependent. It is the sole procedure that completely excises the abnormal PUJ itself. Its use is more debatable in situations with a predominantly inaccessible intrarenal pelvis or long proximal ureteric stricture. Nonetheless, the key principle is the use of a wide, well‐vascularized flap of renal pelvis to enlarge the narrow part of the ureter. Essential to success is absence of any tension and free drainage. Procedure

The colon is reflected medially off the kidney and the dilated renal pelvis presents itself into view. Once the renal pelvis has been exposed, it is carefully freed from all its confusing coverings of connective tissue. When these have been swept aside, the relationship of the lower pole vessels if these are present becomes clear, and they are lifted up on a silicone sling (Figure 10.7).

Diagram displaying two kidneys with a sling placed around the lower pole segmental vessels.

Figure 10.7 (a and b) A sling is placed around the lower pole segmental vessels.

If the lower pole vessels are in the way, a dismembered pyeloplasty will be performed, and this can be modified if there is a long narrow upper segment of ureter (Figure 10.8).

Image described by caption and surrounding text.

Figure 10.8 Dismembered pyeloplasty. A U‐shaped flap is formed from the redundant renal pelvis.

It helps to fill the renal pelvis with 30–40 ml of saline with a syringe before marking out the flap with fine stay‐sutures (Figure 10.9). Unless this is performed while the pelvis is distended, it is easy to mark it wrongly. Cut through the ureter near the pelviureteric junction, and thread it behind the lower pole vessels, slit up, and spatulate in the lateral aspect. The redundant renal pelvis is excised. The apex of the spatulated ureter is brought to the inferior border of the renal pelvis (Figure 10.10). It is important to use only absorbable suture material for the anastomosis, but whether interrupted or continuous sutures are used is of little consequence. A ureteral stent inserted through the anastomosis.

Image described by caption and surrounding text.

Figure 10.9 The renal pelvis is distended.

Diagram illustrating the procedure in the formation of a long elliptical a long elliptical anastomosis between the flat of the pelvis and the spatulated ureter.

Figure 10.10 (a–d) A long elliptical anastomosis is formed between the flap of the pelvis and the spatulated ureter.

If there is a long narrow segment of ureter, the flap can be made longer by using the Culp manoeuvre, carrying the flap in a spiral fashion round the pelvis (Figure 10.11). If there is no lower pole vessel, there is no need to detach the ureter and either a simple flap or the Culp spiral modification can be adapted. Using either method, the anastomosis is made in a long ellipse to prevent subsequent contraction, and there must be no tension.

Image described by caption and surrounding text.

Figure 10.11 (a–f) When there is a long narrow segment of ureter, Culp’s spiral flap of renal pelvis is used.

Other pyeloplasty procedures include Foley Y‐V Plasty and Scardino‐Prince vertical flap. Results

Stones have been seen to form on the suture material used to sew the ureter to the renal pelvis; they are almost inevitable if nonabsorbable suture has been used for the anastomosis, but they can occur on absorbable sutures as well.

Hypertension is an important late sequel of even a successful pyeloplasty, and it is wise for the patient to be closely followed by the general practitioner.

In a few patients, despite an apparently successful operation – as judged by a free runoff down the anastomosis and no hold‐up of contrast or isotope in the renal pelvis – the patient continues to experience recurrent pain in the loin, sometimes accompanied by verified infection in the urine. To some extent this kind of result, which is fortunately rare, represents a failure of selection of candidates for an operation; in retrospect, it is easy to say that it would have been better to have advised a nephrectomy.

In the majority, the outcome is excellent in terms of the absence of symptoms, infection, stones, and deterioration of renal function, but when assessed by the appearance of the kidney in a urogram, the patient and the surgeon need to be warned that the kidney often continues to look disappointingly dilated. This does not mean that it is obstructed. An initial ultrasound or a MAG3 renogram can show whether there is worsening hydronephrosis. However, it does mean that once there has been a thinning of the renal parenchyma and a deterioration in the muscular capacity of the renal pelvis, then the pyelographic appearances are unlikely to return to normal. This need not matter; the important point is that the obstruction has been permanently overcome and things will not deteriorate any further.

10.8.6 Endopyelotomy

The basic principle of this technique is a full‐thickness postero‐lateral incision through the obstructed anatomy in the PUJ from lumen to periureteric and peripelvic fat with bridging ureteric stent placement to allow healing. Rarely offered as first‐line treatment for PUJ obstruction, however, can be in recurrence of PUJ obstruction post pyeloplasty rather than a repeated pyeloplasty. Can also be offered in the symptomatic frail elderly patient.

Ramsey first described the technique in 1984 [31]. Multiple adaptations have been made since. The incision can be done by either an endopyelotomy knife or laser through either percutaneous or ureteroscopic approaches. Success rates do not approach that of laparoscopic or robotic pyeloplasty but have been shown to be as high as 87.5% in well‐selected patients [32]. Antegrade (via percutaneous tract) and retrograde approaches have been described as well as retrograde cautery wire balloon endopyelotomy and balloon endodilatation. There is no convincing evidence that any of these methods have superior outcomes. The benefits include shorter operative time with reduced hospital stays and postoperative recovery.

10.8.7 Nephrectomy in Hydronephrosis

When the preoperative investigations show that the kidney has minimal function, or when at operation it is clear that the cortex is but a paperthin shell, nephrectomy is the correct operation.

10.9 Retrocaval Ureter

Retrocaval ureter results from the persistence of the posterior cardinal veins during embryologic development. This is a rare anomaly where the ureter surrounds the vein at the level of the third and fourth lumbar vertebra. It almost invariably affects the right ureter, and its presence should be suspected with a S‐shaped ureter on imaging. Incidence rate is approximately 1 in each 1000 births [33]. Type I is more common (90%) and results in hydronephrosis due to compression of the ureter between the inferior vena cava and the vertebra. Type II presents with no obstruction. Management of obstruction is surgical with either open or laparoscopic pyelo‐pyelostomy with transposition of the ureter anterior to the inferior vena cava.

10.10 Duplication Anomalies, Ectopic Ureter, and Ureteroceles

10.10.1 Definitions and Incidences

Duplication implies that there is an upper and a lower renal function moiety, each with its own pelvicalyceal system and ureter. The individual moeity’s ureter may join anywhere along its length. Nearly 1% of postmortem examinations have been found to show upper urinary tract duplication to varying degrees [34]. Roughly 40% of cases show bilateral abnormalities. Duplication anomalies show an incomplete penetrance and are an autosomal dominant trait affecting 8% of member of affected families. The majority of upper tract duplications unite above the ureteric orifice and usually have minimal clinical manifestations. On the contrary, complete duplications often cause symptoms and affect renal functionality. These are much rarer affecting less than 0.1% of individuals, with the majority being female. Twenty‐five percent of complete duplications present bilaterally.

In incomplete ureteric duplication, the ureteric bud arises normally from the mesonephric duct but then undergoes variable degrees of bifurcation. Complete duplication occurs when two separate ureteric buds arise separately from the mesonephric duct. In complete duplication systems, inevitably the accessory ureteric bud drains the upper pole moiety and enters the bladder in a distal location more medially placed location than the lower moiety ureter (the Meyer‐Weigart law). This can lead the upper moiety to ectopic insertion, which may the urethra or the urogenital sinus. The ectopic ureter is prone to obstruction because of its long intramural course through the bladder wall, which can cause severe hydronephrosis. Upper moiety ureters are usually associated with dysplastic nonfunctioning upper renal moiety. In contrast, due to the insertion into the bladder with a shorter submucosal tunnel, VUR occurs predominantly in the lower moiety ureteric orifice (Figures 10.1210.14).

Image described by caption.

Figure 10.12 Computed tomography (CT) axial and coronal images showing left duplex renal collecting system with dilated upper moiety. B, bladder; LM, lower moiety; UM, upper moiety.

Image described by caption.

Figure 10.13 Computer tomography showing left kidney atrophic upper moiety with hydronephrosis to the bladder.

Source: Photographs courtesy of Dr. Mark Robinson Aneurin Bevan UHB Hospital.

Image described by caption.

Figure 10.14 MAG3 renogram showing split function of left kidney with the obstructed upper moiety.

Ectopic ureter is any ureter, single or duplex, that does not enter the trigonal area of the bladder. In females, the ectopic ureter may be suprasphincteric, at the level of the striated sphincter, or distal either at distal vagina or introitus. In contrast, male ectopic ureters are always suprasphincteric, connecting to the seminal vesicles, ejaculatory ducts, or the vas deferens, causing pain and infection rather than urinary incontinence clinically.

Ureteroceles are cystic dilatations of the distal ureter that are located either within the bladder or involving the bladder neck and urethra (Figure 10.15). These can also be single or duplex systems (usually in the ureter draining the upper pole moiety). There are several classifications of ureteroceles with the most clinically useful being intravesical (entire ureterocele above bladder neck) or extravesical (some part of ureterocele permanently at bladder neck or urethra).

Image described by caption.

Figure 10.15 Ultrasound scan showing a ureterocoele.

10.10.2 Management

Treatment of ectopic ureter or ureterocele, whether of a single or duplex system, is based on anatomical and functional investigations.

Anatomical assessment involves an ultrasound. It will easily identify upper tract dilatation in both a single and duplex system, as well as help differentiate a dilated ectopic ureter from a ureterocele (Figure 10.15). A CTU or MRU can provide the most detailed imaging of an affected urinary tract.

Functional assessment of renal function can be made by DMSA scan or to investigate obstruction form upper moiety (Figure 10.14) and bladder assessment by voiding cystourethrogram (VCUG) (Figure 10.16). Endoscopic evaluation is essential. The goals of therapy are preservation of renal function, elimination of obstruction, infection and reflux, and maintenance of urinary continence.

Image described by caption.

Figure 10.16 Voiding cystourethrogram show reflux up a lower moiety duplex.

Uncomplicated, asymptomatic duplex does not need treatment. Obstructed upper moiety will need a ureteric reimplantation. However, if the renal moiety is poorly functioning, a hemi‐nephrectomy and ureterectomy would be the treatment choice.

10.11 VUR

As the name implies, VUR is retrograde flow of urine from the bladder back up the ureters with or without hydronephrosis. Normally a physiological sphincter is formed by the ureters passing obliquely through the bladder wall for about 2 cm. When the bladder contracts during micturition, the intramural ureter is compressed by the bladder wall and prevents urine from passing back up the ureters.

10.11.1 Aetiology

Primary anatomical VUR is a defect in the intramural ureteric length to ureteric diameter ratio (ILUD ratio), whereby the intramural ureteric length is too short to allow successfully complete compression to prevent reflux. Normal ratio is 5 : 1. See mainly in duplexed lower moiety ureters, but this can happen in single ureters.

Secondary VUR is due to disease or conditions not related to the intramural ureter:

  • Most common cause is iatrogenic: during TURP or TURBT whereby the ureteric orifice is resected, reducing the ILUD ratio. Other causes include ureteric reimplantation without antireflux techniques or incising a ureterocoele open.
  • High bladder pressure leading to significantly high bladder pressures, overcoming the physiological sphincter mechanism (e.g. bladder outflow obstruction [i.e. prostatic obstruction or urethral strictures] or poor bladder compliance (i.e. [neuropathic bladders]).

VUR is more commonly asymptomatic detected incidentally; however, patients can present with loin pain occurring with a full bladder or after micturition or recurrent UTIs.

Investigation of choice to demonstrate VUR is a voiding cystourethrogram. Voiding cystogram can establish the grade of VUR. which can help guide management (Table 10.7).

Table 10.7 International reflux classification and suggested management of vesicoureteral reflex (VUR).

Grade Definition Suggested management
I Contrast into a ureter only; no dilation Asymptomatic: conservative management
Symptomatic: Deflux; if fails ureteric reimplantation
II Contrast into the whole collecting system, ureter, renal pelvis, and calyces; no dilation Asymptomatic: conservative management
Symptomatic: Deflux; if fails ureteric reimplantation
III Mild dilation Asymptomatic: conservative management
Symptomatic: Deflux; if fails ureteric reimplantation
IV Dilated ureter is slightly tortuous; moderate dilation of pelvis and blunting of calyces Ureteric reimplantation
If nonfunctioning kidney: nephroureterectomy
V Severe ureteric dilation and tortuosity, gross dilation of pelvis and calyces Ureteric reimplantation
If nonfunctioning kidney: nephroureterectomy

Urodynamics can be done to assess bladder pressures. CTU can be useful to establish anatomy. DMSA scan can be done to assess renal function and demonstrate renal scarring.

10.11.2 Management

Generally, VUR is not a dangerous or harmful condition; however, in the presence of high bladder pressure or infection, VUR can slowly kill the kidney. Ergo, treatment is tailored around the symptoms, renal functionality, as well as degree of VUR. VUR grades I–II resolve spontaneously in 80–90% of patients, whereas grade III in 50% and in 20% of grades IV and 10% of grade V [35].

10.11.3 Primary VUR

Conservative measures: with increased hydration and bladder toilet training, with the use of prophylactic antibiotics if there is a history of recurrent UTIs.

Endoscopic management: Deflux bulking agents can be injected intramurally with the distal ureter and ureteric orifice with high success rates. However, repeated injections might be required. Deflux is a hyaluronic acid/dextranomer copolymer.

10.11.4 Surgery

Ureteric reimplantation is indicated in higher grade VUR, or lower grade VUR failed to respond to endoscopic injections in a duplex renal system, or renal ectopia.

Nephroureterectomy if the kidney is nonfunctioning, or VUR is persistant and causing significant symptoms.

Treatment of secondary VUR is managing of the underlying pathology; if it fails, measures are similar to primary VUR managements.

10.12 Megaureter

Megaureter is a dilatation of the ureter irrespective of cause with or without associated renal pelvis dilatation. The upper normal limit diameter of the ureter in children up to 16 years old is 0.50–0.65 cm and 0.7 cm in adults. Megaureter refers to a ureteric diameter of 7 mm or greater [36].

Smith classified megaureters into four categories: obstructed, refluxing, refluxing with obstruction, and non‐refluxing and non‐obstructing [37]. It can also be classified into primary and secondary. The challenge with this condition is to promptly treat obstructing ureters and preventing unnecessary intervention in dilated nonobstructing stable ureters. For the purpose of this chapter we will focus on primary obstructive megaureter (POM).

POM is thought to be caused by an aperistaltic nonfunctioning segment of the distal ureter near the vesico‐ureteric junction leading to obstruction and proximal dilatation. Approximately 10–23% of antenatally detected upper tract dilatation is thought to be caused by POM [38]. It more commonly affects the left ureter and is more common in young boys.

The vast majority of the children are asymptomatic. Symptoms due include UTIs, abdominal pain, and haematuria.

Nonobstructive megaureters can be safely observed with serial sonography and the majority resolve spontaneously within the first two years. Studies have shown that ureters greater than 10 mm prove more difficult to manage and only 17% resolve with 21% of cases requiring surgical intervention [39]. These patients require close monitoring with functional (MAG3 renogram) and anatomical imaging (ultrasound) (Figure 10.17).

Image described by caption.

Figure 10.17 Coronal computed tomography image with contrast showing delayed excretion showing right megaureter. U, ureter.

Surgery is indicated in cases of POM with recurrent UTIs, persistence of dilatation, differential renal function of less than 40% of affected renal unit, or deterioration of greater than 5% function on serial renograms [36].

The procedure of choice for babies older than one year old is ureteric reimplantation with or without ureteral tapering. In grossly dilated ureters in infantile bladders of babies younger than one, temporising methods such as ureteric stenting, endoscopic balloon dilatation, endouretostomy, cutaneous ureterostomy, and refluxing ureteral reimplantation is favoured.

10.13 Ureteral Strictures

Ureteral strictures can be either congenital (rare) or acquired. The acquired causes include ureteral calculi, traumatic surgical instrumentation, malignancy, radiation, ischaemia, infection, and periureteral fibrosis. More commonly, strictures are benign and iatrogenic, caused either by endoluminal surgery or during laparotomy for nonurological operations; these lead to ischæmic strictures.

10.13.1 Pathophysiology

Ischaemic strictures are usually caused by injury at time of operation (i.e. colorectal, vascular, or gynaecological) or postradiotherapy. Ureteroscopic damage to the ureter causes a flap or perforation or ureteric anastomoses (i.e. urinary diversion or in transplanted kidneys) leads to urine extravasation and fibrosis formation causes a stricture.

Cross‐sectional imaging with CT usually identifies a hydronephrotic kidney with hydroureter up to a transition point. For exclusion of malignancy, retrograde pyelography and ureteroscopy with or without biopsy is commonly necessary.

Endourological treatments include:

  • Conservative management if asymptomatic and malignancy ruled out.
  • Ureteral stent placement: indicated in the symptomatic frail elderly patient
  • Balloon dilatation or endoureterotomy

If these treatments are unsuccessful, or in carefully selected patients, ureteric reconstruction according to site and size of disease and patient factors can achieve good success rates. Nephrectomy is also an option if the renal function is poor (<15%)

Aug 6, 2020 | Posted by in UROLOGY | Comments Off on Hydronephrosis

Full access? Get Clinical Tree

Get Clinical Tree app for offline access