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.