This chapter begins with a brief overview of the anatomy and physiology of the urinary system and of the male reproductive organs. With respect to the latter, this chapter complements the anatomy and physiology described in Chapter 7. Common disorders of the kidneys and the rest of the urinary tract and their treatment and nursing care are then described, including infections, significant renal disorders, obstructive disorders and disorders of the bladder. With regard to the male urinary system and reproductive organs, only prostatic disorders and conditions primarily affecting the urethra are considered here. Conditions more directly affecting reproductive and sexual function, such as erectile dysfunction (ED) and testicular cancer, are discussed in Chapter 7.

Anatomy and physiology

The urinary system comprises the kidneys, the ureters, the urinary bladder and the urethra. Its function is to excrete the waste products of metabolism in the form of urine.

The urinary tract

The kidneys – structure

The kidneys are paired organs which lie on the posterior abdominal wall, extending from the twelfth thoracic vertebra to the third lumbar vertebra. Because of the position of the liver, the right kidney is normally slightly lower than the left. Three layers of supportive tissue surround each kidney: an inner fibrous capsule, a middle fatty layer and an outer fascia. This fatty encasement is necessary for maintaining the kidneys in their normal position. Beneath this, a dark outer cortex surrounds a paler medulla, which consists of pale conical striations called the renal pyramids (Figure 8.1).

Figure 8.1 Longitudinal section of the right kidney.

At the hilus, i.e. the concave medial border of the kidney, blood vessels, lymph vessels and nerves enter and leave the organ. Medial to the hilus is the flat, funnel-shaped renal pelvis, which is continuous with the ureter leaving the hilus. Extending from the pelvis into the medulla are the cup-shaped calyces; these receive from the renal papillae the urine that has been formed in the nephrons and has passed through the collecting tubules. From the calyces the urine passes into the renal pelvis, which acts as a reservoir.

Each kidney receives approximately 625 mL of blood per minute from branches of the renal artery (the two kidneys receive around 25% of cardiac output) and are a key organ in maintaining homeostasis with the functions of:

• production of urine by glomerular filtration, reabsorption (selective) of substances needed by the body such as glucose, and tubular secretion of waste products and other substances in order to maintain fluid, electrolyte and acid–base balance

• control and maintenance of fluid balance (see Ch. 20)

• maintenance of acid–base balance (see Ch. 20)

• control and maintenance of electrolyte balance (see Ch. 20)

• renin production – initiates the renin–angiotensin–aldosterone system concerned in the control of blood pressure (see Ch. 20)

• erythropoietin production, a hormone that stimulates red blood cell production in the bone marrow (erythropoiesis)

• control of calcium reabsorption and vitamin D hydroxylation.

The nephron

The functioning units of the kidneys are the nephrons, of which there are two types: cortical and juxtamedullary. The cortical nephrons have their glomeruli in the cortex and have short loops of Henlé, and the juxtamedullary nephrons, with long loops of Henlé, are located in the medulla. Eighty-five per cent of the nephrons are cortical.

A nephron comprises a convoluted tubular system and a tuft of capillaries known as the glomerulus (Figure 8.2). The glomerulus is enclosed in the cup-shaped upper end of the tubule (glomerular or Bowman’s capsule). The tubule has three sections: the proximal convoluted tubule (PCT), the loop of Henlé, and the distal convoluted tubule (DCT). The DCTs merge to form straight collecting tubules; these ultimately terminate at the renal papillae.

Figure 8.2 Nephron with long loop of Henlé (deep nephron).

Blood supply

The renal arteries (see above) branch into smaller and smaller vessels, ultimately becoming wide-bore afferent arterioles which lead into the glomeruli. These capillaries then merge again to form a narrower-bore efferent arteriole which leaves the capsule and subdivides into a second network of peritubular capillaries which supply the renal tubule, and a specialised capillary network (the vasa recta) associated with the loop of Henlé. The capillaries merge into venules and then veins, eventually joining the renal vein, which in turn flows into the vena cava.

Formation of urine

The first process in the production of urine is filtration. Arterial blood arriving in the wide-bore afferent arteriole enters the glomerulus within the Bowman’s capsule, where substances that are between 3 and 7 nanometres can pass through holes in the capsule endothelium called fenestrations. Note that in health, blood cells and large molecules such as proteins with a molecular weight of 69 000 or above do not pass through the glomerular filtration barrier into the tubule. Once inside the body of Bowman’s capsule, the material that has been filtered, which is called filtrate, enters the first section of the PCT, which is the main site of reabsorption in the nephron. To maintain a flow of blood into the glomerulus, and therefore to maintain filtration, blood must enter at a constant pressure and constant volume. This is achieved by two structures that line the afferent arteriole, the macula densa and the juxtaglomerular apparatus (JGA). When the blood volume and pressure falls, perhaps as a result of blood loss during surgery, the diameter of the arteriole is reduced, thereby maintaining perfusion pressure. This situation cannot last, i.e. the arteriole cannot continue to get smaller because this would limit the kidney’s ability to remove waste products and maintain fluid balance. The constriction of the arteriole is achieved by release of renin. Renin combines with angiotensinogen to form angiotensin I, which is converted by angiotensin-converting enzyme (ACE) into angiotensin II, which is a strong vasoconstrictor. In addition, it stimulates the release of aldosterone (a hormone from the adrenal cortex), which promotes sodium reabsorption, which therefore enhances water reabsorption (see Ch. 20). This, in conjunction with antidiuretic hormone (ADH; also known as arginine vasopressin [AVP] or vasopressin), helps to increase water reabsorption and water intake, and accounts for the fact that urine would normally be expected to be concentrated, i.e. have a specific gravity towards 1.035, in states where fluid loss and dehydration had occurred (see Ch. 20).

Further material covering kidney function – glomerular filtration, selective reabsorption and tubular secretion – is available on the companion website.

See website for further content

The functions occurring in the nephron have been summarised in Table 8.1.

Table 8.1 Summary of processes occurring in the nephron

Location in the Nephron	Processes
Proximal convoluted tubule (PCT)	The PCT is the site of most selective reabsorption – the vast majority of filtrate is reabsorbed in the PCT. Specifically specialised cells that line the PCT reabsorb water (H₂O), electrolytes including bicarbonate (HCO₃^–), glucose and other substances, returning them to the circulation via the vasa recta. Substances such as the waste products urea and creatinine are not reabsorbed as they need to be excreted. At the end of the PCT the filtrate contains water, waste and some electrolytes
Loop of Henlé	The cells change their structure in the loop of Henlé, allowing selective reabsorption of water and sodium (Na⁺)
Distal tubule (DCT)	Sodium and chloride (Cl^–) can be reabsorbed here. The hormone aldosterone facilitates the reabsorption of sodium (and with it water) and chloride, but the hormone ADH is required for any reabsorption of water. The cells of the DCT are also concerned with the reabsorption and/or secretion of hydrogen (H⁺) and potassium (K⁺) ions into the filtrate. This last process, known as tubular secretion, is vital in the maintenance of acid–base balance
Collecting duct	Once the filtered fluid gets to the collecting ducts only in exceptional circumstances can water and sodium chloride (NaCl) be reabsorbed. ADH is required to make the collecting ducts more permeable to water in order to produce concentrated urine

The ureters

Urine is conveyed from the pelvis of each kidney to the bladder via the ureters (Figure 8.3). The ureters are tubular structures approximately 25–30 cm long, ranging in diameter from 2 to 8 mm at various points along their length.

Figure 8.3 The ureters and their relationship to the kidneys and the bladder.

Each ureter descends behind the peritoneum from the kidney to the bladder and comes obliquely through the bladder wall before opening into the bladder cavity on its posterior inner surface. This arrangement is such that, when the bladder fills or empties, it is compressed, closing the distal ends of the ureters; in this way, there is no back-flow into the ureters.

Each ureter is composed of three layers of tissue:

• an outer fibrous layer

• a middle layer of smooth muscle; contraction of the muscle layer produces peristaltic movement of urine along the ureter into the bladder

• an inner mucosa of transitional epithelium (urothelium).

The accessory glands

The seminal vesicles

secrete a thick, nutritive alkaline fluid that mixes with sperm on ejaculation. This fluid accounts for 30% of the volume of the seminal fluid and contains fructose and protein, which are essential to sperm motility and metabolism.

The prostate gland

is a lobulated structure which lies in the pelvic cavity in front of the rectum and behind the symphysis pubis, surrounding the uppermost part of the urethra. It is palpable on rectal examination. The prostate gland secretes a thin, milky, alkaline fluid that makes up 60% of the seminal fluid; this fluid creates an environment more hospitable to sperm by giving protection from the normally acidic environment of the male urethra and female vagina. A neutral or slightly alkaline medium also increases sperm motility.

The prostate begins to enlarge after the age of 40 years, which, because the urethra passes through it, can lead to urinary symptoms, such as difficulty emptying the bladder (see p. 292).

The bulbourethral glands

are two pea-sized glands opening onto either side of the urethra. They produce a lubricating alkaline mucus that is expressed into the urethra during ejaculation, further reducing its typically acidic state, and contribute less than 5% to the volume of seminal fluid.

The supporting structures

The penis

is a pendulous, soft tissue structure with a root and a body. There is erectile tissue supported by fibrous tissue and covered with skin. The three elongated masses include the corpus spongiosum containing the urethra, and two parallel columns, the corpora cavernosa, which provide the organ’s main structural support.

The expanded distal end of the penis, the glans penis, surrounds the urethral meatus. The covering of skin folds upon itself at the glans penis to form a movable double layer called the prepuce.

The scrotum

is divided into two compartments and each contains one testis, one epididymis and the testicular end of the spermatic cord. The temperature of the testes is 2–3°C below body temperature, which helps to preserve sperm viability.

Spermatic cords

Leading from each testis is a spermatic cord consisting of a testicular artery, a testicular venous plexus, lymph vessels, a deferent duct (vas deferens) and nerves.

Disorders of the urinary system

This section covers a range of investigations and disorders of the kidney and other parts of the urinary system. The nursing management is discussed along with an outline of the medical and surgical treatment. Readers who require more detail about treatment are directed to Further reading suggestions, e.g. Colledge et al 2010, Garden et al 2007, Levy et al 2009, and Reynard et al 2008, 2009.

General investigations of the renal and urinary tract

Disorders of the renal and urinary system can be detected using various tests and investigations. Some pathologies, for example, prostate enlargement and prostate cancer, have similar signs and symptoms, and therefore in practice, multiple tests and investigations can be used to aid diagnosis. The common tests and investigations have been divided into those testing urine (Table 8.2), those testing blood (Table 8.3) and those that examine the structure of the urinary tract (Table 8.4). Other investigations used include computed tomography (CT) scan, magnetic resonance imaging (MRI) scan and radionuclide studies.

Table 8.2 Urine tests

Type of Test/Investigation	Indication/Associated Pathology	Significance of Findings
Urinalysis a. Specific gravity (SG) b. Glucose c. Blood d. Protein e. Nitrites and/or leucocytes f. Ketones	All	a. Range 1.001–1.035 indicates degree of hydration b. Glycosuria may indicate diabetes mellitus, use of corticosteroids. If positive result, need fasting blood glucose c. Haematuria indicates infection, calculi, renal damage, tumour. A positive result for blood warrants further (specific) investigation d. Proteinuria or albuminuria indicates infection or renal damage; further investigation, e.g. MSU, needed e. Indicates urinary tract infection (UTI) f. Ketonuria indicates breakdown of fats and suggests starvation or possibly uncontrolled diabetes mellitus; further (specific) investigations needed (Steggall 2007)
Midstream urine (MSU) or catheter specimen of urine (CSU)	UTI – cystitis, acute pyelonephritis and chronic pyelonephritis (reflux nephropathy) Prostatic enlargement Renal failure	Detects presence of infection; ensure aseptic technique to avoid contaminants and false-positive results. Microbiological examination of the specimen will indicate the presence of and the types of infective organism
24-hour urine analysis e.g. calcium, phosphate, oxalate	Urinary calculi	Measures the substances excreted in the urine in different types of urinary calculi
Urine cytology	Bladder cancer	Detects presence of tumour cells. Not diagnostic but used in combination with other tests
Urinary flow rate	Prostatic enlargement/cancer	Determines the speed of bladder emptying, volume voided and time taken to empty the bladder. Used to determine the extent of prostate/urethral compression
Post-void residual volume	Urinary retention/prostatic enlargement	Determines the volume of urine in the bladder

Table 8.3 Blood tests

Type of Test/Investigation	Indication/Associated Pathology	Significance of Findings
Urea and electrolytes (U/Es)	All	Elevations in urea and creatinine indicate decreased renal function
Full blood count (FBC)	All	Low haemoglobin may indicate blood loss; anaemia. Increase in white cell count may indicate infection
Serum creatinine clearance (used to estimate GFR) See website Figure 8.1	Renal failure and conditions affecting renal function, e.g. diabetic nephropathy	Estimate of renal function. Monitoring patients with reduced renal function
Erythrocyte sedimentation rate (ESR)	Nephritis	Non-specific test that detects inflammation/infection Erythrocytes sediment more quickly in individuals in whom disease is present
Prostate specific antigen (PSA) (a screening test, also used to monitor response to treatment of prostatic cancer)	Prostatic cancer	PSA result <4 ng/mL is within normal range; PSA result 4–10 ng/mL indicates an intermediate risk of prostate cancer; PSA >10 ng/mL indicates a high risk of prostate cancer

Table 8.4 Tests of urinary tract structure/function

Type of test/Investigation	Indication/Associated Pathology	Significance of Findings
Intravenous urogram/pyelogram (IVU/IVP)	Renal failure, calculi, recurrent UTI, trauma	Indication of structural abnormality or obstruction
Urethrogram; endoscopy: urethroscopy, cystoscopy, nephroscopy	Calculi, obstruction	Indication of presence of calculi or mass
X-ray or ultrasound (U/S, USS) of kidneys, ureter and bladder (KUB)	Prostate, calculi, UTI	Imaging of renal tract may indicate presence of calculi
Biopsy	Kidney, prostate, bladder	Diagnostic for pathology, e.g. cancers, causes of renal failure, types of glomerular disease, etc. Determines the stage of the disease

Urinary tract infections (UTIs)

Urinary tract infections are a common problem across the lifespan; they are more common in females than males, except in the neonatal period. For most patients with a normal urinary tract, UTIs are easily treated by antibiotic therapy, although early identification and treatment of patients with complicated infections are essential.

Urinary tract infections are defined as an inflammatory response of the urothelium (cells lining the urinary tract) to bacterial invasion that is usually associated with bacteriuria and pyuria (Steggall 2007).

Normally the urine does not contain bacteria; the presence of bacteria in the urine is termed bacteriuria. Bacteriuria can be symptomatic or asymptomatic. Pyuria is the presence of pus (white blood cells [WBCs]) in the urine, indicating an inflammatory response of the urothelium to bacterial invasion. Bacteriuria without pyuria suggests bacterial colonisation not infection. Pyuria without bacteriuria warrants evaluation for renal tuberculosis, stones or cancer. Infections are generally defined clinically by their presumed site of origin.

Most bacteria enter the urinary tract through the urethra into the bladder. This is enhanced in individuals with significant soilage of the perineum with faeces and patients with intermittent or indwelling catheters. Depending on the location of the infection, there are further classifications of UTI (Table 8.5).

Table 8.5 Classification of common urinary tract infections by site

Site	Type of Infection	Causes/Signs
Kidney	a. Acute pyelonephritis	a. Chills, fever, flank pain; accompanied by bacteriuria and pyuria
	b. Chronic pyelonephritis (reflux nephropathy)	b. Chronic bacterial infection of the kidney associated with vesicoureteric reflux (VUR) (reflux of infected urine from the bladder into the ureters); causes scarring on the kidney
Bladder	Cystitis	Dysuria (pain on passing urine), frequency, urgency, cloudy urine that may have a strong odour and sometimes haematuria, suprapubic or back pain. There is inflammation of the bladder which can be bacterial or non-bacterial
Urethra	Urethritis	As cystitis but it is inflammation of the urethra

Recurrent urinary tract infections are commonly due to reinfection or bacterial persistence; reinfection is especially common in women.

Pathogens

Most UTIs are caused by facultative anaerobes (bacteria that can grow in the presence or absence of oxygen) that generally come from bowel flora.

The most common cause of UTI is the bacterium Escherichia coli (E. coli), accounting for 85% of community-acquired and 50% of hospital-acquired infections. Other Gram-negative Enterobacteriaceae include Proteus mirabilis and Klebsiella, and Gram-positive Enterococcus faecalis and Staphylococcus epidermidis.

Hospital-acquired infections are frequently caused by E. coli and Enterococcus faecalis as well as by Enterobacter, Klebsiella and Pseudomonas aeruginosa.

In patients with diabetes mellitus, the most common infection is by Klebsiella spp; less common organisms such as Gardnerella vaginalis, Mycoplasma spp and Ureaplasma urealyticum may infect patients with intermittent or indwelling catheters.

Defences against UTI

The main defences against infection are the flow of urine and the acidity of urine. Normally urine is acidic, which inhibits bacterial growth. In addition, the urine contains urea and organic acids that make the conditions less favourable for bacterial survival. Other factors that protect against UTI include the antibacterial effects of bladder mucosa, as well as neutrophils and the cytokines interleukin IL-6 and IL-8.

For women, the vaginal flora is an important host defence against UTI since it is an acidic environment. Lactobacilli make up the majority of the vaginal flora in healthy, pre-menopausal women; sexual intercourse, use of antibiotics and intravaginal antimicrobials can reduce the normal Lactobacillus-dominant vaginal flora, increasing susceptibility to UTI. One way in which to reduce the likelihood of getting a UTI after sexual activity is to pass urine after intercourse.

Pyelonephritis

Pyelonephritis, or inflammation of the renal pelvis and renal tissue, may occur in one or both kidneys. Bacteria may enter the urinary tract, especially the kidneys, via the bloodstream or, more commonly, the bladder. Most organisms causing urinary tract infection – E. coli, Klebsiella spp, Proteus, Pseudomonas, E. faecalis and S. epidermidis (S. albus) – are found in the bowel and the perineum. There are two types of pyelonephritis, acute and chronic (often called reflux nephropathy as it can result from vesicoureteric reflux [VUR]), but the presenting features are different (Table 8.5).

Investigations for acute and chronic pyelonephritis (reflux nephropathy)

• Collection of a midstream specimen of urine (MSU) for microscopy examination, culture for evidence of a causative organism and antibiotic sensitivity.

• A full blood count and urea and electrolyte estimation. A raised white blood cell count and erythrocyte sedimentation rate (ESR) may be revealed in response to E. faecalis and S. epidermidis infection.

• An ultrasound scan (U/S, USS) or sometimes an intravenous urogram (IVU) is performed to locate any obstruction in the urinary tract (Box 8.1).

• Specific investigations to demonstrate the presence of VUR, for example a micturating cystogram.

Box 8.1 Information

Intravenous urogram or pyelogram (IVU/IVP)

This investigation, which involves the intravenous injection of an iodine-based contrast agent which is then excreted by the kidneys, allows a series of X-ray images of the kidneys, ureters and bladder to be taken.

The IVU radiograph may demonstrate a variety of pathologies:

• absence of kidney

• congenital abnormalities affecting the urinary tract, e.g. duplex ureter, horseshoe kidney

• renal trauma

• obstruction of the kidney, e.g. a large calculus in the renal pelvis, or scarring from repeated UTIs caused by VUR

• obstruction of the ureter – within the lumen, in the wall or arising from outside the ureter, such as late stage cervical cancer

• irregularities of the bladder wall – causes include bladder cancer, calculi, diverticulum (an abnormal pouch in the wall) or a foreign body.

Before, during and following an IVU

Where there are no contraindications the patient is given a laxative to clear the bowel and thus ensure a clear image of the contrast agent on the X-ray. The patient may be requested to abstain from food and fluids for a period of time before the start of the X-ray examination. The patient should void beforehand to make sure that the contrast agent remains concentrated as it is excreted into ureter and bladder, thus providing high quality images. Voiding just beforehand is also important for patient comfort as the examination can take 40–60 min. Prior to the intravenous injection of the contrast agent, a control X-ray of the kidneys, ureters and bladder (KUB) is taken. Patients should be informed that some people experience a warm feeling and some may be aware of a metallic taste in their mouth following the administration of contrast agent; they can be reassured that it is short-lived. Rarely patients have an allergic reaction to the iodine-based contrast agents; they should tell the radiographer at once if they have difficulty breathing or their skin feels itchy. Following the investigation, the patient is allowed to eat and drink again. The contrast medium will be passed when the patient voids urine, with no after-effects or change in the colour of the urine.

Note: in some situations such as an emergency (e.g. suspected kidney trauma), the examination can be undertaken without withholding fluid.

Treatment of acute pyelonephritis

The main aim of treatment is to eradicate the infection by means of antibiotic therapy (often i.v.). This may be commenced even before organism sensitivities are known. A more specific antibiotic can then be used following urine culture results. Analgesics, antiemetics and antipyretics may be prescribed. Oral fluids are recommended, up to 3 L/24 h.

Further investigations may be needed to identify the underlying cause of the condition. Where inflammation persists, renal impairment may progress to end-stage renal failure requiring treatment by dialysis (pp. 286–289).

Cystitis

Cystitis may be chronic or acute and is characterised by severe inflammation of the bladder walls. More commonly affecting women, cystitis may also result from predisposing factors such as the presence of foreign bodies or stones, obstruction, tuberculosis, carcinoma in situ, chronic urinary infection and schistosomiasis (disease caused by flukes). Features of cystitis include burning on micturition, urinary frequency and urgency, and possibly incontinence. The results of MSU may be needed to treat any infection, although there is no need to wait for the results before commencing antibiotic therapy. Persistent infections warrant further investigations, for example IVU, and may be treated with long-term antibiotic therapy. A key feature in treatment should be increased fluid intake to help flush the urinary system. In addition to increasing fluid intake there is a range of self-help measures available to women who suffer from recurrent cystitis, for example attention to personal hygiene, passing urine frequently during the day and not ‘holding on’, emptying their bladder just before going to bed, cranberry juice, etc. (Boxes 8.2, 8.3). Nurses providing information to patients should be aware that cranberry juice may possibly increase the action of coumarin anticoagulants, e.g. warfarin.

Box 8.2 Reflection

Obstructive disorders of the urinary tract

There are many disorders that cause obstruction to the flow of urine, for example prostate enlargement, calculi or tumours (Figure 8.6). Although the early stages may cause only mild symptoms which are easily ignored, the progressive damage caused by abnormal pressure, infection and stone formation can lead to renal failure. The importance of early detection and intervention cannot be overemphasised.

Figure 8.6 Conditions causing obstruction to the urinary tract.

Urinary stones (renal calculi)

The formation of stones or calculi in the urinary tract is common in Europe, North America and Japan; there are many aetiological factors involved in their formation. Renal stones are more common in men than in women (M:F = 3:1).

Pathophysiology

Urinary calculi are formed by the aggregation of mineral crystal deposits in the urine (Steggall & O’Mara 2008). The main types of stone are calcium oxalate, although other compositions of stone occur (Steggall & O’Mara 2008). The frequency of different types of stone varies between countries and is probably related to diet, environmental factors and possibly genetic factors (Goddard et al 2006). The risk factors for developing calculi are stasis of urine, chronic urinary infection and excess excretion of stone-forming substances. The most common presenting feature is pain and haematuria, caused by movement of the calculi, although this is not a universal symptom. Stones lodged in the renal pelvis (e.g. ‘staghorn’ calculus) tend to be immobile and so the presenting features are urinary tract infection and pyrexia.

See website Figure 8.2

Medical management and treatment

Stones less than 5 mm in diameter may pass unobstructed through the urinary tract and be excreted in the urine. In some cases an alpha-blocker (e.g. tamsulosin) can be used to aid the passing of a stone. Increasing fluid intake to increase fluid output is not recommended in the acute phase of management because it will result in further distension of the urinary system; a normal fluid intake should be encouraged. For further information see Further reading, e.g. Reynard et al 2008, 2009.

Management of acute renal colic

Information about investigations is provided in Tables 8.2, 8.3 and 8.4.

The patient with renal stones may be acutely ill, suffering from excruciating pain arising in the loin and radiating to the groin (and the testis or labium), which can last 5–6 h. Pain is caused by small calculi being moved along the ureter by peristaltic movements, by impaction and by obstruction of urine. Bed rest, warmth to the site of pain (Boon et al 2006) and analgesics are the first line of treatment.

Medications include the opioid morphine intramuscularly. Pethidine should be avoided as it is associated with a higher incidence of vomiting (Holdgate & Pollock 2004). Diclofenac sodium (per rectum, usually at night) is a prostaglandin synthetase inhibitor which reduces renal blood flow and urination. It has an antispasmodic and anti-inflammatory effect and is long acting. Nausea may be relieved by an antiemetic such as i.m. prochlorperazine.

Flush-back of calculi and stenting

(Box 8.4) This procedure affords temporary relief when a calculus causes obstruction and pain in the ureter. The stone is flushed back to the pelvis of the kidney. A small silicone tube called a stent is positioned in the ureter from the pelviureteric junction (PUJ) to the bladder. This stent is left in position to hold the stone in place. Further treatment to remove the stone can now be planned. The stent should not be left for more than 6 weeks. If the planned treatment cannot be carried out by the end of this period, the stent should be changed.

Box 8.4 Information

Stenting

The stents used by most surgeons are called ‘double-J’ or ‘pigtail’ stents and have small holes down most of the length of their tubing. These stents are self-retaining and must be removed endoscopically.

Some surgeons use an infant feeding tube as a stent following pyeloplasty (reconstructive surgery on the renal pelvis), pyelolithotomy or ureterolithotomy (removal of a stone from the renal pelvis and ureter respectively). Infant feeding tubes are self-retaining to a degree, but the patient will need a urethral catheter in situ to keep the tube in place.

When the catheter is removed the patient may pass the feeding tube without intervention. If this does not happen within 24 h, endoscopic removal will be required.

Insertion of a nephrostomy tube

is indicated when obstruction in the kidney or the ureter cannot be relieved by flush-back and stenting (Figure 8.7).This is carried out under X-ray control, usually with a local anaesthetic. A small silicone tube is placed percutaneously into the collecting system of the kidney. The tube is held in place by a suture and connected to a closed-system drainage bag.