With the patient relaxed, the kidney can be balloted; lifted with one hand placed behind the loin and compressed by the other hand pressing downwards (Fig. 23.1). The ureter cannot be palpated. An enlarged bladder rises centrally out of the pelvis, is dull to percussion and may even be visible. In men, the hernial orifices, cords, testes and epididymes are examined with the patient standing and lying. If the foreskin is uncircumcised, it must be confirmed that it retracts and that the glans and meatus are normal. In women, the vulva, urethra and vagina must also be examined. A speculum examination should be carried out if there is any suspicion of vaginal or cervical abnormality. A full pelvic bimanual examination, whether in males or females, is best carried out under general anaesthesia with a muscle relaxant. A rectal examination is mandatory, not only to examine the prostate but also to detect abnormalities of the anal margin (haemorrhoids, fissures) and lower rectum (carcinoma).

Fig. 23.1 Bimanual palpation of the right kidney.

Investigations

Ultrasonography

This is another means of first-line imaging (Fig. 23.3), tending to give superior information about the renal parenchyma but less about the collecting system. It also allows visualization of other related organs, such as the liver, spleen and gynaecological organs.

Fig. 23.3 Renal ultrasound.

A Normal kidney. B A simple cyst occupies the upper pole of an otherwise normal kidney. C The renal pelvis and calyces are dilated by a chronic obstruction to urinary outflow. The thinness of the remaining renal cortex indicates chronicity. D, E and F The diagrams beneath show the anatomical features.

CT Urogram

The IVU is largely becoming superceded by the ‘plain’ CT KUB, a non contrast enhanced CT, which has a higher specificity and sensitivity for the detection of renal and ureteric calculi. Furthermore, CT urography allows the ureters to be delineated by contrast, as in an IVU, but also allows other structures within the abdomen to be assessed.

Special radiological investigations

In certain circumstances a retrograde ureteropyelogram may be necessary. This involves retrograde injection of contrast material through a catheter placed in the lower ureter (Fig. 23.4). Abnormalities of the renal vessels can be demonstrated by renal angiography. Computed tomography (CT) is now the preferred method for imaging renal tumours. A micturating cystourethrogram (MCU) will outline the bladder, detect ureterovesical reflux and examine the bladder neck and urethra. The bladder is filled with contrast material (via a catheter) and emptying is then studied by X-ray screening. An ascending urethrogram, in which contrast medium is injected into the urethra, can be used to define strictures. When used in conjunction with a MCU, a descending urethrogram can also be obtained.

Fig. 23.4 Retrograde ureteropyelography.

A Cystoscope and ureteric catheterization. B The best views of the normal collecting system are shown by pyelography. A catheter has been passed into the left renal pelvis at cystoscopy. The anemone-like calyces are sharp-edged and normal.

Nuclear imaging

Radio-labelled substances are used for two main purposes:

1. Detecting bony metastases from carcinoma of the prostate (bone scan). ^99mTc-labelled methylene diphosphonate (MDP) is the most reliable method.

2. Measurement of renal function (scintigraphic renography). Occasionally ‘how a kidney looks’ does not correlate with ‘how it behaves’, e.g. hydronephrosis does not always mean the presence of obstruction. Renography allows assessment of obstruction to a kidney (e.g. from a pelviureteric obstruction), differential kidney function (i.e. how much each kidney is contributing to overall function), assess non-functioning areas of renal parenchyma (e.g. scarring) and allow accurate assessment of GFR. Radio-labelled mercaptuacetyltriglycine (MAG-3) has largely superseded technetium labeled diethylenetriamine pentaacetic acid (Tc-DTPA) for dynamic scanning. It is secreted from the renal tubules and is used in the identification of obstructed kidneys and to assess differential function. Dimercaptosuccinic acid (DMSA) is concentrated in the renal tubules and static imaging can be carried out some 2–3 hours after injection. Parenchymal defects such as scars, haematomas, lacerations or ischaemia may be demonstrated. Differential renal function can be quantified from measuring the DMSA concentration/density in each kidney.

Urodynamic studies

The maximum urinary flow rate during micturition can be measured using a flow meter when the voided volume is at least 150 ml or the values may be misleadingly low. The norm in males is 15–30 ml/s and in females 20–40 ml/s and a flow rate of less than 10 ml/s is abnormal. The flow rate pattern can help to determine the cause of obstruction (Fig. 23.5). Measurements of flow rate can be combined with cystometry to provide a measure of residual urine, bladder capacity, the capacity at which a desire to void occurs, and the detrusor pressures when the bladder is full and during maximum flow. Spontaneous detrusor contractions during bladder filling may indicate an unstable bladder, a cause of urgency and urge incontinence.

Fig. 23.5 Urinary flow rates.

The normal flow rate shows a rapid rise to maximum high-peak flow. In a typical bladder outflow obstruction due to benign prostatic hyperplasia, there is a slow rise to poor maximum flow rate and prolonged variable flow. In a typical urethral stricture, there is prolonged flow with little variability, giving a plateau- or box-shaped curve.

Semen analysis

Microscopic examination of the semen is a basic investigation in infertile males. The specimen is collected following a period of abstinence of at least 3 days and is examined within 2 hours. Normal semen has a volume of > 2 ml and a sperm concentration of > 20 × 10⁶/ml. More than 50% of the sperm should be motile at 2 hours. The morphology, biochemistry and viability of the sperm may also be studied. In selected cases, immunological tests may help to determine the cause of infertility.

Biochemical screening for stones

Recurrent urinary tract calculi should raise the suspicion of hyperparathyroidism, idiopathic hypercalciuria, hyperoxaluria or cystinuria. Serum calcium, phosphate, oxalate and uric acid should be measured. If more detailed investigation is required a 24-hour collection of urine for determination of calcium, phosphate, oxalate and uric acid excretion can be obtained. The composition of passed or removed stones should be analysed to determine their metabolic type.

Upper urinary tract (kidney and ureter)

Anatomy

The two kidneys lie retroperitoneally on the posterior abdominal wall. Each is approximately 12 cm long, 6 cm wide and 3 cm thick. The upper pole of the kidney lies on the diaphragm, which separates it from the pleura and the 11th and 12th ribs. Below this, it lies on the psoas, quadratus lumborum and transversus abdominis muscles from medial to lateral (Fig. 23.6). Anteriorly, the right kidney is covered by the liver, the second part of the duodenum and the ascending colon. The spleen, stomach, tail of pancreas, left colon and small bowel overlie the left kidney. The renal hilum lies medially and transmits from front to back the renal vein, renal artery and renal pelvis. The ureter begins at the renal pelvis and runs for 25 cm to the bladder. The abdominal ureter lies on the medial edge of the psoas muscle, which separates it from the tips of the transverse processes. It then crosses the bifurcation of the common iliac artery, which separates it from the sacroiliac joint, to enter the pelvis. The pelvic ureter runs on the lateral pelvic wall to just in front of the ischial spine, when it then turns medially and forward to enter the bladder. In the male, it is crossed by the vas deferens. In the female, it lies close to the lateral fornix of the vagina and is crossed by the uterine vessels, where it is vulnerable to damage during hysterectomy. The section of ureter that lies within the bladder wall functions as a flap valve to prevent reflux. Stones tend to impact at the three points where the ureter narrows: namely, the pelviureteric junction, the pelvic brim and the ureteric orifice.

Fig. 23.6 Anatomy of kidneys and ureters.

Physiology

The healthy kidney can produce between 0.3 and 17 ml of urine per minute, depending on the state of hydration, but on average produces 1 ml of urine per minute. This is transported down the ureter by 4–5 peristaltic waves per minute to reach the bladder, where it is stored without refluxing up the ureters.

Renal cysts

Simple cysts

These are usually single, almost always asymptomatic, and often found incidentally on ultrasound where they can usually be differentiated from carcinoma. Complex cysts containing multiple septa raise the suspicion of malignant change

Polycystic kidney disease

An autosomal dominant congenital anomaly affecting both kidneys that often leads to chronic renal failure in middle life. Despite their very large size, the cystic kidneys cause few symptoms. Infection or bleeding may occur in a cyst causing pain or haematuria.

Benign tumours

Renal adenomas are small and are usually an incidental finding. Haemangiomas are a rare cause of dramatic haematuria.

Nephroblastomas

Epidemiology

This tumour usually occurs in children under 4 years of age, and is the most common childhood urological malignancy, with an incidence of 7 per million children per year. Growth is rapid and there is early local spread, including invasion of the renal vein. Invasion of the renal pelvis occurs late, and so haematuria is seen in only 15% of cases. Distant metastases most commonly appear in the lungs, liver and bones. Tumours presenting in the first year of life have a better prognosis.

Clinical features

The cardinal sign is a large abdominal mass. Some of the unusual clinical features associated with a renal carcinoma in adults, such as fever or hypertension, may be present.

Investigations

CT of the abdomen and chest is essential for diagnosis and staging. The main differential diagnosis to consider is adrenal neuroblastoma, but other causes of a large kidney, such as hydronephrosis and cystic disease, must also be considered. The tumour is bilateral in 5–10% of cases.

Management

The diagnosis is confirmed by biopsy. Chemotherapy is followed by transabdominal nephrectomy with wide excision of the mass. Further chemotherapy ± radiotherapy is performed dependent upon the histopathological features of the removed tumour; the 5-year survival rate is in the region of 70–90%.

Renal adenocarcinoma

Epidemiology

This tumour arises from the renal tubules and is the most common malignant tumour of the kidney. The incidence is 16 cases per 100 000, being twice as common in males. It is uncommon before the age of 40 years and has a peak incidence between 65 and 75 years of age. There can be spread into the renal pelvis, causing haematuria. Invasion of the renal vein, often extending into the inferior vena cava, can also occur. Direct spread into perinephric tissues is common, so that the whole fascial envelope and kidney should be removed en bloc. Lymphatic spread occurs to para-aortic nodes, but blood-borne metastases (which may be solitary) may develop almost anywhere. In the lungs, these characteristically give the appearance of ‘cannon ball’ metastases.

Clinical features

The triad of pain, haematuria and a mass is an important, albeit late, feature occurring in only 15% of cases. Historically, 60% present with haematuria, 40% with loin pain and only 25% with a mass, but increasing access to ultrasonagraphy and CT has increased incidental diagnosis. Patients may present with pyrexia of unknown origin, raised ESR, polycythaemia, disorders of coagulation, and abnormalities of plasma proteins and liver function tests, or with neuromyopathy due to secretion of renin, erythropoietin, parathormone and gonadotrophins.

Investigations

The initial investigation is ultrasound, followed by a staging contrast CT of the abdomen and chest (Fig. 23.7).

Fig. 23.7 Contrast-enhanced CT of renal cancer.

The right kidney is expanded by a low-density cancer that fails to take up the contrast. Tumour is seen extending into the renal vein and inferior vena cava (arrow).

Management

Organ confined renal adenocarcinoma should be treated with curative intent, either by laparoscopic or open nephrectomy. Metastatic renal adenocarcinoma is relatively radio and chemoresistant. Immunotherapy, in the form of interferon, gives a modest survival benefit (3–5 months) but angiogenesis inhibiting drugs, such as tyrosine kinase inhibitors, are showing more promising results. A further modest survival benefit may be seen in metastatic disease by reducing the tumour burden if nephrectomy is performed prior to starting immunotherapy.

Summary Box 23.1 Renal carcinoma

• Renal adenocarcinoma is the most common malignant renal tumour and is twice as common in males

• The carcinoma arises in the renal tubules and spreads early to the renal pelvis, producing haematuria. Later spread involves the renal vein (with bloodstream dissemination), perinephric invasion and lymphatic spread

• The clinical presentation is very varied. The triad of pain, haematuria and a mass may be late features, and early systemic effects include fever, polycythaemia, disordered coagulation and pyrexia of unknown origin

• The key investigations are ultrasonography, chest X-ray and contrast CT

• Treatment consists of radical nephrectomy; the tumour is not radiosensitive. The natural history of renal carcinoma is very variable and excision of solitary metastases may be worthwhile.

Renal and ureteric calculi

Mechanism of stone formation

A solute dissolves in a solvent to form a solution but when the concentration of solute in solution reaches a certain level, termed the solubility product, the compound precipitates out to form crystals. This initial crystal formation (nucleation) may progress such that crystals clump together (aggregation) to form calculi. There are substances in urine that act to keep compounds in solution by inhibiting nucleation (inhibitors) but, above a certain concentration of solute, nucleation will occur despite their presence (formation product). Where the concentration of a compound lies between the solubility product and the formation product, being kept in solution solely by the action of inhibitors, it is described as being metastable. A solution with a concentration above the formation product is described as being supersaturated. The ability of urine to keep compounds in solution, and prevent calculus formation is a balance between forces keeping the solute in solution and those that promote nucleation. Therefore, stones form when the amount of solute increases (e.g. hypercalcuria), the amount of solvent decreases (e.g. dehydration) or the concentration of inhibitors falls (e.g. decreased citrate excretion). Foreign bodies, anatomical abnormalities, and calculi can all act as a nidus for nucleation and promote further stone formation.

Types and causes of stone formation

The commonest stone types are; calcium oxalate (85%), uric acid (10%), mixed calcium phosphate/calcium oxalate (10%), magnesium ammonium phosphate (5–15%) and cystine (1%). Calcium oxalate stones are commonly caused by hypercalciuria, hypercalcaemia, hyperoxaluria or hypocitraturia. Uric acid stones are formed due to increases in uric acid formation either through gout or myeloproliferative disorders. Approximately 50% of patients with urate stones have gout but only 20% of patients with gout develop urate stones. Calcium phosphate stones are generally secondary to renal tubular acidosis. Magnesium ammonium phosphate (struvite) stones are usually due to urinary tract infection by pathogens that can break urea down into CO₂ and ammonia, thereby alkalinizing the urine.

Clinical features

Renal pain, renal colic and ureteric colic are characteristically unilateral. Renal pain is dull and aching, whereas ureteric colic is acute and severe, occurring in waves. A stone may cause bleeding or there may be symptoms of urinary tract infection. However, a stone in the kidney may remain silent, even one large enough to fill the pelvis and calyces (‘staghorn’ calculus).

Investigations

IVU or CT KUB provides all the necessary information on the position of the stone (Fig. 23.8). Routine hematological and biochemical tests are needed to assess renal function and to exclude metabolic causes. A urine sample is cultured to determine whether there is infection. If obstruction is acute, its relief is the prime clinical need; if it is chronic and has caused renal damage, the surgical approach depends on the function of the affected kidney. This is best determined by radioisotope methods (renography).

Fig. 23.8 IVU showing ureteric stone.

A Eighty percent of stones are visible on a plain X-ray (arrow). B The contrast excreted by the kidney in an IVU clearly shows the obstruction caused by the stone in the ureter (arrow).

Management

Symptomatic treatment should be instituted as soon as the diagnosis is confirmed. Intramuscular diclofenac, a non-steroidal anti-inflammatory, is the most effective analgesic; pethidine is an alternative. The likelihood of spontaneous passage depends on the size of the stone and on its smoothness. A stone less than 0.5 cm in diameter should pass. Immediate treatment should be considered in cases of ongoing pain, renal obstruction or, more importantly, where there are signs of sepsis (infected obstructed kidney). Extracorporeal shock-wave lithotripsy (ESWL), the technique of focusing external shock waves to break up stones, has revolutionized the treatment of renal and ureteric stones. If a stone can be visualized on X-ray or ultrasound, then it can be treated by ESWL. Other stones can be visualized directly by passing a fine telescope up the ureter (ureteroscope) and the stones may be either broken up or removed intact. Some stones in the kidney that are unlikely to pass even if broken up are best treated by direct puncture of the kidney, insertion of a sheath and removal under vision with a nephroscope (percutaneous nephrolithotomy, PCNL). It is now very rare to remove stones from the renal tract at open operation. In cases of acute obstruction leading to sepsis (infected obstructed kidney) or renal impairment, decompression of the kidney either via insertion of a ureteric stent or percutaneous nephrostomy is required. Stones and infection within a kidney can be the cause of renal destruction and if the kidney contributes less than 10% of total renal function, then a nephrectomy is recommended.

Upper tract obstruction

Obstruction may be due to extrinsic, intrinsic or intraluminal causes (Table 23.1). In the kidney, stones within the pelvicalyceal system and a congenital abnormality of the pelviureteric junction (see below) are the main causes of obstruction leading to hydronephrosis. More rarely, a sloughed renal papilla, blood clot or tumour may be the cause.

Table 23.1 Causes of urinary tract obstruction

Extrinsic

• Retroperitoneal fibrosis

• External pressure (e.g. carcinoma of the cervix, prostate)

Intrinsic

• Transitional cell tumours

• Tuberculosis / schistosomiasis

• Ureterocoele

• Ectopic ureter

Intraluminal

• Calculi