Pain

Pain arising from the urinary tract is a common symptom that is often due to obstruction, infection or tumour. Renal pain is usually felt in the flank or the loin. When renal pain arises from ureteric obstruction (e.g. a stone), discomfort may additionally radiate to the iliac fossa, the testicle or the labia, the pattern depending to a certain extent on the level of the obstruction. Patients with polycystic kidney disease may suffer chronic flank pain. Exacerbations occur with cyst infection and haemorrhage.

Acute bladder outflow obstruction presents with severe suprapubic pain. However, pain in the suprapubic region and perineum most commonly arises from lower urinary tract infection, due to cystitis or urethritis. Such pain is frequently accompanied by dysuria, frequency or strangury (painful micturition). These symptoms comprise the syndrome of cystitis. It is nearly always associated with urinary abnormalities on urine stick testing (protein, blood and leukocytes). In men, this pain may be associated with severe perineal or rectal discomfort, in which case prostatitis is suggested.

In young children with urinary tract infection and cystitis, the symptoms may be much less obvious, but cystitis should be suspected in any child who cries on micturating. Pain from the kidneys, if it results from acute infection or abscess, may occasionally reflect tracking of pus upwards to the diaphragm, causing diaphragmatic pain, or in the retroperitoneal space to the psoas muscle, leading to pain when the muscle is stretched on passive hip extension. Glomerulonephritis is usually painless. Kidney tumours may cause a dull persistent flank pain.

Haematuria

Blood in the urine can be present with or without pain and may be continuous or intermittent. If visible to the naked eye, it is termed macroscopic or gross haematuria; if detected only by stick tests or microscopy, it is called microscopic haematuria. Haematuria as a result of parenchymal renal disease is usually:

continuous

painless

microscopic (occasionally macroscopic).

Haematuria arising from renal tumours is likely to be:

intermittent

associated with renal pain

macroscopic.

Bleeding from bladder tumours is often intermittent, with associated local symptoms suggesting cystitis.

It is important to decide early in the diagnostic process whether the haematuria originates from the kidneys or elsewhere in the urinary tract (Box 18.1). This decision affects the order in which investigations should be conducted. For example, continuous painless microscopic haematuria with associated proteinuria in a young man or woman is most likely to be the result of glomerulonephritis or other renal pathology. However, haematuria in an older person with risk factors for urothelial malignancy (smoking) is more likely to be caused by a bladder or ureteric tumour and merits a cystoscopy early in the investigative process. It is important to remember that the commonest cause of dipstick haematuria in women is contamination from menstrual blood.

Oliguria/anuria

Oliguria is the passage of less than 500 ml of urine per day. Anuria is the complete absence of urine flow. A reduction in urinary flow rate to the point of oliguria may be physiological, as in a patient whose fluid intake is low. Physiological reduction of urinary flow rate implies that the glomerular filtration rate (GFR) remains normal, and that the kidney is avidly retaining sodium and water. If inadequate fluid intake leads to a significant reduction in the extracellular fluid compartment, the resulting decrease in renal blood flow leads to oliguria and reduction of the GFR. Oliguria arising in this fashion is termed prerenal and is clearly pathological. Renal oliguria implies the presence of intrinsic renal disease, whereas postrenal oliguria results from mechanical obstruction at any level, from the collecting system in the kidney to the urethra. Anuria and oliguria may be signs of renal failure.

Polyuria

Polyuria implies no more than a high urinary flow rate. There will always be an associated increase in the frequency of micturition (frequency), and often nocturia as well. Polyuria results from excessive water intake (psychogenic polydipsia or beer drinking, for example), from an osmotic diuresis (glucose, as in diabetes mellitus, urea as in chronic renal failure and sodium chloride as in diuretic use) and finally from abnormal renal tubular water handling, as seen in cranial diabetes insipidus (inadequate secretion of antidiuretic hormone) or nephrogenic diabetes insipidus (renal resistance to antidiuretic hormone).

Frequency of micturition

Increased frequency of micturition results from polyuria, a reduction in functional bladder capacity or bladder/urethral irritation. The commonest cause of polyuria is excessive fluid intake, whereas reduced functional bladder capacity is seen most frequently in patients with prostatic hypertrophy and bladder outlet obstruction. Lower urinary tract infection (cystitis) causes bladder irritation and an increase in urinary frequency. Some patients with neurological diseases, in particular multiple sclerosis, also have frequency of micturition. The detrusor muscle of the bladder contracts at an inappropriately low bladder volume, resulting in a low functional bladder capacity.

Nocturia

This term implies the need to empty the bladder during the hours of sleep. In health, there is a substantial diurnal variation in urinary flow rate: a night-time reduction in urine flow, together with adequate functional bladder capacity, serves to obviate the need for night-time micturition. Thus polyuria of any cause, or any cause of reduction of functional bladder capacity, may lead to nocturia. In addition, failure of the urine concentrating ability of the kidneys, as occurs in renal impairment and sickle cell disease, will also lead to nocturia. Obviously, diuretics taken in the evening and at night will lead to this symptom.

Dysuria

This is a specific form of discomfort arising from the urinary tract in which there is pain immediately before, during or after micturition. The urine is often described as ‘burning’ or ‘scalding’, and there is usually associated frequency of micturition and decreased functional bladder capacity. Infection and neoplasia in the bladder or urethra are the most important causes. An extreme form of dysuria, strangury, implies an unpleasant and painful desire to void when the bladder is empty or nearly so.

Urgency of micturition, incontinence and enuresis

Urgency is the loss of the normal ability to postpone micturition beyond the time when the desire to pass urine is initially perceived. Incontinence is the involuntary passage of urine. In extreme cases, urgency may lead to urge incontinence, in which the desire to void cannot be voluntarily inhibited. Stress incontinence, on the other hand, is leakage of urine associated with straining or coughing, often due to weakened pelvic floor muscles. The term enuresis is usually used to describe noctural enuresis, or bed wetting.

Slow stream, hesitancy and terminal dribbling

This triad of symptoms is most frequently seen in elderly men with prostatic hypertrophy. Here the bladder outlet is partially obstructed by the enlarging prostate gland, with the result that the maximum achievable urinary flow rate during micturition is reduced. There is often difficulty in initiating micturition (hesitancy) and in completing micturition in a ‘clean stop’ fashion (terminal dribbling). The symptoms are nearly always associated with frequency of micturition and nocturia, the result of a low functional bladder capacity. In more advanced cases, there may be progressive bladder enlargement, with eventual overflow incontinence and continuous or intermittent dribbling of urine.

Urethral discharge

This is usually only noticed by men and always requires further investigation. There may be associated symptoms of urethral irritation and the underlying pathology is likely to be urethritis, which is often infective and sexually transmitted (see Ch. 21).

General features

Patients with chronic renal failure look unwell. The skin is pallid, the complexion sallow and a slightly yellowish hue is often evident. The mucous membranes are pale, reflecting the associated normochromic, normocytic anaemia. There may be bruises, purpura and scratch marks due to uraemic pruritus, and also an underlying disorder of platelet function and capillary fragility. The nails often appear pale and opaque (leukonychia) in the nephrotic syndrome, and sometimes in chronic renal failure. Intercurrent episodes of severe illness in the past may have led to the appearance of Beau’s lines, which appear as transverse ridges across the nails. Splinter haemorrhages in the nail beds point to underlying vasculitis, which may be the cause of the renal failure or be indicative of endocarditis; there may be an associated purpuric rash (Fig. 18.1). When blood urea is very high, a uraemic frost may be seen on any part of the body and appears as a white powder; it is formed from crystalline urea deposited on the skin via the sweat. The onset of chronic renal failure in childhood is associated with impaired growth, causing short stature. Severe bony deformity may be evident in some cases, particularly in children, who may develop rickets (Fig. 18.2). Advanced uraemia is also associated with metabolic flap, a coarse tremor which is best seen at the wrists when in the dorsiflexed position. It is similar to the metabolic flap (asterixis) seen in patients with advanced liver disease or respiratory failure. The presence of metabolic acidosis leads to increased ventilation with an increased tidal volume, known as Kussmaul respiration.

Figure 18.1 Purpura in Henoch–Schönlein disease.

Figure 18.2 X-ray of the hands of a patient with chronic renal failure and secondary hyperparathyroidism, showing renal osteodystrophy. There is a loss of density of the tips of the digits (acro-osteolysis) with loss of density on either side of the interphalangeal joints and subperiosteal bone resorption. The latter is best seen in the middle phalanges of the index and middle fingers.

The circulation in the renal patient

Of crucial importance here is the correct assessment of the patient’s fluid volume status. It is important to define whether the patient is euvolaemic, hypovolaemic or hypervolaemic. This is a bedside assessment that, with practice, can usually be made correctly.

Hypervolaemia is associated with some or all of the following:

In patients with nephrotic syndrome (see below), oedema and salt and water retention are caused by reduced plasma oncotic pressure. Oedema with expansion of the extracellular fluid is often accompanied by hypertension and, particularly if the cardiac reserve is poor, may progress to pulmonary oedema and other manifestations of heart failure. The presence of oedema itself, however, can coexist with intravascular volume depletion, especially in patients with nephrotic syndrome.

The diagnosis of hypovolaemia requires the absence of any signs of hypervolaemia. The hypovolaemic patient may have the following:

Poor skin turgor, ‘sunken eyes’ and dry mucous membranes are often cited as signs of volume depletion, but these are generally unreliable features.

Abdominal palpation

The detection of the kidneys in the abdominal examination is described in Chapter 12. In slim people with relaxed abdominal muscles, it is sometimes possible to feel a normal right kidney (the right kidney is situated slightly lower than the left at the level of T12-L3). More often a palpable kidney can only be felt because it is enlarged, as in hydronephrosis, multiple cysts (polycystic kidney disease) or tumour (generally unilateral). A distended bladder is identified in the lower abdomen by a combination of palpation and percussion. Rectal examination is an important part of the clinical assessment of the renal patient: bimanual palpation of the bladder is a more reliable way of assessing bladder enlargement than is simple per abdominal examination. In men, rectal examination also allows evaluation of the prostate gland, both for benign enlargement and for the detection of malignant change suggested by hard irregularity of the gland and absence of the central groove.

Auscultation

Uraemic pericarditis and pleurisy may be suggested by pericardial and pleural friction rubs, respectively. Their presence points to either advanced uraemia or a multisystem inflammatory disorder such as systemic lupus erythematosus (SLE), which may have both renal and extrarenal manifestations. Added heart sounds (S3 and S4) suggest, respectively, volume expansion and incipient heart failure, and ventricular hypertrophy, often as a consequence of hypertension. The presence of vascular bruits and/or impairment of the major arterial pulses is an important finding, raising the possibility of renal vascular disease, which may underlie hypertension and/or renal failure if bilateral.

The eye in uraemia

Corneal calcification (limbic calcification) occurs in patients with longstanding hyperparathyroidism with elevation of blood calcium and phosphorus concentrations (see Ch. 16). The presence of limbic calcification should not be confused with a corneal arcus (arcus senilis), which is a broader band at the edge of the cornea and merges with the sclera. Corneal arcus is usually most marked in the superior and inferior positions, whereas limbic calcification is seen medially and laterally or circumferentially. Retinal changes are extremely important in uraemic patients, many of whom have hypertension and/or diabetes. Renal dysfunction in the absence of diabetic retinopathy cannot be attributed to diabetic nephropathy in patients with type 1 diabetes. In type 2 diabetes, however, diabetic nephropathy is present in many patients without any diabetic eye changes. Patients with renal disease as part of systemic vasculitis may have manifestations of the latter in the retinae, with haemorrhages and exudates. Patients with chronic renal failure are at greatly increased risk of a range of vascular complications affecting both the macrovasculature and the microvasculature. In the retinae, thrombosis of the central retinal artery or its branches, or of the central retinal vein and its branches, is an important manifestation of this. The presence of Kayser-Fleischer rings may help confirm a diagnosis of Wilson’s disease.

Acute renal failure

This is the abrupt onset of declining renal function occurring over a period of hours or days, usually (but not always) accompanied by a marked reduction or cessation of the urinary flow rate. Central to the diagnosis, however, is a rapid decline in the GFR, leading to nitrogen retention and usually to sodium and water retention as well. An exception is the patient in whom the decline of GFR is not accompanied by reduction of urine flow, so-called non-oliguric acute renal failure. The outlook depends on the cause. Many are reversible spontaneously (repair of ischaemic injury as in tubular necrosis) or as a result of therapy (removal of stone or other cause of obstruction).

Chronic renal failure

Chronic renal failure implies that the GFR has been reduced for a considerable period and that the reduction is largely or completely irreversible. It can result from almost any form of renal parenchymal disease, chronic renal ischaemia or unrelieved urinary obstruction. If renal impairment is severe, there may be clinical manifestations of uraemia. These are usually evident when the GFR has fallen to one-third of normal or less. The implication of the term chronic renal failure is that the timescale of onset and progression is rarely shorter than a few months, and often much longer. A further and crucial implication is an irreversible reduction in the number of functioning nephrons with no prospect of significant recovery. These patients manifest a number of symptoms that are not attributable to specific pathophysiological changes. Lethargy, poor concentration, irritability and failure of higher mental functions and ability to handle tasks are all commonly reported. In advanced cases, there may be confusion, fits and stupor. These are preterminal, but reversible if steps are taken to remove the excess uraemic toxins by dialysis. Nausea, vomiting and diarrhoea are also common in advanced uraemia, and likewise improve following restoration of normal kidney function or treatment with dialysis or transplantation.

The acute nephritic syndrome

As in acute renal failure, the acute nephritic syndrome implies a fairly brisk onset (days, weeks or months) of reduction in GFR and retention of nitrogenous waste, and usually salt and water also. Oliguria is, therefore, common. The underlying pathology is an acute glomerulonephritis which, as well as causing the functional abnormalities described above, also results in florid abnormalities of the urine. Haematuria (macroscopic or microscopic), proteinuria and tubular casts are often present. Many of the causes of acute nephritis are associated with functional abnormalities of the immune system which may be detected by laboratory tests and which may also manifest with disease in other organs, for example the skin, joints or eyes, as in SLE, Henoch-Schönlein purpura (see Fig. 18.1) and systemic vasculitis.

The nephrotic syndrome

This is defined somewhat imprecisely as the presence of heavy proteinuria (usually >3 g/day, compared with normal of <150 mg/day), hypoalbuminaemia, hypercholesterolaemia and oedema. It is not generally very helpful to attempt a more precise definition because the clinical response to a given level of proteinuria shows considerable variability from patient to patient. It is, however, unusual for nephrotic syndrome to occur when the proteinuria is <2 g/day, and conversely some patients are able to maintain a normal or near-normal serum albumin concentration despite very heavy proteinuria in excess of 6 g/day.

Proteinuria of this magnitude implies glomerular pathology and may coexist with a significant reduction in GFR. Thus, a number of the pathological entities capable of causing nephrotic syndrome may also present as acute nephritic syndrome or the syndrome of chronic renal failure in other patients.

Asymptomatic urinary abnormality

This is the presentation that arises in the patient who presents for a routine medical examination, often in the context of employment or life insurance or at a screening visit to a GP surgery. Urine testing leads to the unexpected finding of proteinuria, haematuria or pyuria in an otherwise healthy patient. Further assessment may reveal the coexistence of other renal syndromes, but nevertheless it is worth maintaining the operational definition ‘asymptomatic urinary abnormality’ because this is such a frequent presentation in clinical practice. It should not be forgotten that this syndrome may not only reflect disease of the kidneys, as it can also be a manifestation of malignancy anywhere in the urinary tract, infection or stone (if asymptomatic).

Recurrent gross haematuria

This implies intermittent, or in some cases continuous, bleeding into the urinary tract to a degree sufficient to alter the macroscopic appearance of the urine. Depending on the circumstances of the bleeding, the urine may be a rusty-brown colour, lightly tinged with red blood or more heavily bloodstained. The source of the bleeding may be anywhere in the urinary tract, from the glomeruli at the top to the urethra at the bottom. Important causes are certain types of glomerulonephritis, renal tumours and infections (particularly tuberculosis), and tumours of the urinary tract transitional cell epithelium (urothelium) anywhere from the renal pelves to the bladder and urethra.

Urinary tract infection

The normal urinary tract is sterile except at its extreme distal end. Infection in the urinary tract leads to a range of symptoms and signs that reflect the location and severity of the infection. By far the most frequent site is the bladder, and the local symptoms reflect bladder irritation, with frequency of micturition, low functional bladder capacity and dysuria. The presence of urinary tract infection is defined importantly by the presence of a significant number of infecting organisms in the urine. A working definition of a proven urine infection would be the detection of more than 10⁵ colony-forming units/ml urine in a carefully collected mid-stream specimen of urine (MSU). For less common infections, this definition may not be appropriate. For example, in tuberculosis of the urinary tract, the number of organisms being excreted may be extremely low, and formal identification on the basis of urine culture is sometimes difficult or impossible.

Urinary tract obstruction

This syndrome may conveniently be divided into lower and upper tract obstruction. Lower urinary tract obstruction is defined by residual urine in the bladder after micturition, or in more extreme forms by urinary retention with inability to empty the bladder at all. The most common causes relate to prostatic hypertrophy (benign hyperplasia or carcinoma), and a characteristic array of symptoms and signs arises (frequency, nocturia, poor stream, hesitancy, terminal dribbling). All of these are a consequence of a low functional bladder capacity, an inability to empty the bladder completely and impairment of the urinary flow rate.

The presence of upper urinary tract obstruction is established in most cases by the demonstration of a dilated renal collecting system (renal pelvis and/or calyces), often seen to be proximal to a specific obstructing lesion. These features may be demonstrated by a number of imaging techniques, including ultrasound and intravenous urography (IVU) as well as cross-sectional imaging techniques such as computed tomography (CT) scanning. Upper and lower urinary tract obstruction may coexist, most frequently when the lower urinary tract obstruction is severe and/or of long standing, and leading to progressive dilatation of the upper urinary tract with consequent renal damage. It is important to remember that unilateral renal obstruction should not result in a rise in the serum creatinine. Therefore, if the creatinine is elevated, there is also dysfunction of the contralateral kidney.

Renal and urinary tract stones

The operational definition is largely observational, depending on the demonstration of one or more stones in any part of the urinary tract. Resulting symptoms and signs depend much on the location of the stone(s) and on size. For example, small stones in the kidneys are frequently asymptomatic, or they may lead to subtle urinary abnormalities, presenting initially with asymptomatic urinary abnormality. Larger stones in the kidneys frequently lead to renal pain, whereas stones in the ureter are particularly likely to cause acute obstruction and very severe ureteric and renal pain. Bladder stones are usually associated with symptoms suggestive of cystitis with frequency, haematuria and pain all common, and often associated with urinary tract infection.

Renal hypertension

By far the most common cause of sustained blood pressure elevation is essential hypertension. However, in a minority of patients with raised blood pressure, renal disease will be found to be the cause, and the likelihood of this is greatly increased in patients with coexisting renal disease of any kind. Hypertension may be one of the presenting features of virtually any disease of the renal parenchyma, including all forms of glomerulonephritis, many forms of tubulointerstitial disease, renal vascular disease, renal stone disease and obstruction. Renal tumours and renal infections may occasionally present with hypertension, which in some cases can be the only presenting feature. Thus, in any patient with newly identified hypertension, the possibility of underlying renal disease should be considered. Conversely, the exclusion of renal disease as a cause of hypertension is generally straightforward, comprising the absence of symptoms and signs of renal disease, the absence of urinary abnormalities on simple stick testing and the presence of a normal GFR as judged by serum creatinine concentration or other surrogate measurement for GFR.

Renal tubular syndromes

The majority of patients with parenchymal renal disease or obstructive renal damage manifest disordered tubular function, although in only a few of these are the tubular defects responsible for specific clinical manifestations. Tubular syndromes arising in this context are generally unobtrusive and are certainly common. Much less common is the patient in whom the tubular defect dominates the clinical picture. These defects may be inherited or acquired, and are seen mainly in children. They usually require careful laboratory testing to characterize them fully. Proximal tubular abnormalities include renal phosphate wasting, aminoaciduria (of these, cystinuria with cystine stone formation is the most important) and renal tubular acidosis leading to chronic metabolic acidosis. Distal tubular defects are also associated with metabolic acidosis and with disturbances of potassium metabolism, sodium-losing nephropathy and nephrogenic diabetes insipidus, with resulting failure, respectively, of salt and water conservation.

The urine

The urine should be tested as part of every general medical examination and not just in patients with known renal or urinary tract disease. Not only may the testing lead to the discovery of hitherto unsuspected diseases, such as diabetes or renal disease, but also documentation of normal urine often provides a very useful historical reference point in the event of the later development of renal disease or urinary abnormalities. The urine specimen should be passed into a clean container without additives. Testing should normally be conducted as soon as possible, and if delayed more than 2 hours, the urine should be refrigerated (not frozen) and returned to room temperature before testing. For microbiological assessment, it is essential to minimize the chances of contamination. This is best done by placing a sterile container in the path of the urine stream once voiding has commenced (i.e. a mid-stream specimen).

Specific gravity and osmolality

These measurements yield similar information and, in the absence of significant glycosuria, are functions of the urinary concentrations of sodium, chloride and urea. The range of specific gravity is 1.001-1.035, which is equivalent to 50-1350 mOsmol/kg water (Fig. 18.3). The presence of renal insufficiency leads to a reduction in the range of osmolality that the kidneys can generate and, in advanced renal disease, the osmolality becomes relatively fixed at about 300 mOsmol/kg water, close to that of the glomerular filtrate (Fig. 18.4). This is termed isosthenuria, and because the urine concentration cannot be varied, predisposes the patient to sodium and water overload if intake is high, and to salt and water depletion if intake is low.

Figure 18.3 Relationship between specific gravity and osmolality.

Figure 18.4 Relationship between renal concentration and diluting capacity, and serum creatinine concentration. The serum creatinine is plotted on a logarithmic scale. This therefore represents linear changes in GFR, such as might occur in progressive renal failure. End-stage renal failure is shown on the left, and normal renal function on the right. Curve (a) represents maximum concentrating capacity, e.g. in water deprivation, when the normal kidney can maintain the serum creatinine in the normal range by increasing urine osmolality. In renal failure, the urine cannot be concentrated and the serum creatinine rises. Curve (b) represents the maximum diluting capacity, e.g. after the ingestion of large volumes of water. The normal kidney excretes urine of low osmolality. In end-stage renal failure, urine osmolality cannot be reduced and the water load is not adequately handled. There is also isosthenuria, i.e. the urine tends towards an iso-osmolar state (specific gravity 1.010).

Plain radiographs

In many people, one or both of the kidneys can be seen outlined by perirenal fat on plain abdominal films or nephrotomograms. The information gleaned is limited, although certain types of renal stone or other calcifications may be identified.

Ultrasound

Ultrasound provides good images of the renal parenchyma and collecting system, and in nearly all patients gives a reliable estimate of renal size as well as identifying discrete lesions within the parenchyma, hydronephrosis and stone. Doppler studies often permit assessment of blood flow in the main renal arteries and in the larger intrarenal branches. The resistive index, measured by Doppler ultrasound, indicates the degree of chronic intrarenal ischaemic injury. Although the upper ureter can be seen quite well in most patients, the lower ureter is not adequately visualized. Ultrasound examination of the bladder is also extremely useful, allowing calculation of the bladder capacity when full and also after micturition (emptying should be virtually complete), as well as visualization of the bladder wall and lesions projecting into the bladder itself (e.g. tumours). It can be combined with a measurement of urinary flow rate.

Intravenous urography

Intravenous urography (IVU) involves the intravenous injection of organic iodine compounds that are excreted and concentrated radiographically. It is an extremely good technique for examining the renal collecting system, the ureters and the bladder, but gives less information than ultrasound about the renal parenchyma (Fig. 18.10). Imaging by IVU depends on renal function. This is useful in that it gives a crude measure of the symmetry or otherwise of excretory capacity, but it also means that the image quality is poor in patients with renal insufficiency in whom the GFR is low (Fig. 18.11).

Figure 18.10 Normal excretion urogram. In this film, taken 15 minutes after intravenous injection of the iodine-based contrast medium, the calyces of both kidneys, the ureters and the bladder can be seen.

Figure 18.11 Excretion urogram. In this film, made 30 minutes after injection of contrast, the left kidney fails to excrete a detectable concentration of contrast (non-functioning left kidney) and the right kidney shows dilated, hydronephrotic calyces. The right ureter is partially obstructed at the level of the body of the fifth lumbar vertebra. The circular lucency in the bladder is the dilated balloon of a Foley catheter.

Antegrade and retrograde urography

Here, X-ray contrast material is instilled directly into the urinary tract via a percutaneous needle (antegrade) or a ureteric catheter inserted via a cystoscope (retrograde). These tests are invasive and are most often used in the evaluation of patients with clear obstruction of the urinary tract.

Cystography

In cystography, the bladder is filled with contrast medium via a urethral catheter and X-rays are taken before, during and after micturition. The test indicates the completeness of bladder emptying, and also whether or not urine refluxes up the ureters during micturition. This also is an invasive test, the principal risk being the introduction of infection. Urodynamics (the measurement of pressure and urine flow) may be included in more detailed studies of bladder function.

Radionuclide studies

Diethylenetriamine penta-acetic acid (⁹⁹Tc-DTPA) is used to investigate the excretory function of each kidney selectively (Fig. 18.12). The test is very useful for the assessment of symmetry of function, delayed onset of excretion (as may happen in renal artery stenosis) and retention of excreted isotope (as seen in the presence of obstruction). ⁹⁹Tc-DMSA (dimercaptosuccinic acid) is a similar technique used to show the gross renal morphology.

Figure 18.12 Radioisotope excretion (ordinate) during the 30 minutes after intravenous injection in a patient with right renal artery stenosis and hypertension. The left kidney achieves more rapid excretion of isotope. The malfunctioning right kidney was the cause of the patient’s hypertension.

Computed tomography and magnetic resonance imaging

Computed tomography scanning of the kidneys sometimes complements the information gained from ultrasound and certainly yields important information about the surrounding structures in the retroperitoneum (Fig. 18.13). It is particularly useful in patients with ureteric obstruction from, for example, retroperitoneal malignancy or retroperitoneal fibrosis. Spiral CT is becoming the investigation of choice for renal calculi as well. In some cases, more information is obtained using magnetic resonance imaging (MRI). Caution has to be exercised, however, if gadolinium is required, as its use has been associated with nephrogenic systemic fibrosis in patients with renal disease. Current data suggest an increased risk of this condition in patients with a GFR below 30 ml/min.

Figure 18.13 (A) CT scan with (B) drawing showing normal kidneys.

Arteriography and venography

These are both invasive and are used in selected patients in whom detailed evaluation of the renal blood supply (arterial or venous) is required. The commonest indication is the patient with hypertension and/or renal insufficiency in whom renal artery stenosis is suspected. In the context of renal insufficiency, contrast-induced deterioration of function is often seen, but can usually be minimized by adequate prehydration and the use of non-ionic contrast agents. MRI can be used to generate images of the major renal vasculature. Although the images are generally not as good as those from conventional arteriography, the technique has the advantage of avoiding contrast nephropathy and of being non-invasive. CT imaging may also be used in this way but still requires some contrast.