Investigations

An approach to investigation is shown in Box 7.1.

In an otherwise healthy woman with a single lower UTI and no indications of a complicated infection, urine culture prior to treatment is not mandatory. It is necessary, however, in patients with recurrent infection or after failure of initial treatment, during pregnancy, or in patients susceptible to serious infection (e.g. older people, those with diabetes, the immunocompromised or those with an indwelling catheter).

PERSISTENT OR RECURRENT UTI

Treatment failure, with persistence of organisms on repeat culture, suggests an underlying cause, which should be investigated (Box 7.1) and treated. Reinfection with a different organism, or with the same organism after an interval, may also occur. In women, recurrent infections are common and further investigation is only justified if infections are severe or frequent (>2/yr).

If the cause cannot be removed, suppressive antibiotic therapy can be used to prevent recurrence and reduce the risk of septicaemia and renal damage. Regular urine culture and a regimen of two or three antibiotics in sequence, rotating every 6 mths, are used to reduce the emergence of resistant organisms. Other simple measures may help to prevent recurrence (Box 7.2).

ASYMPTOMATIC BACTERIURIA

This is defined as >10⁵/ml organisms in the urine of apparently healthy asymptomatic patients. There is no evidence that this condition causes renal scarring in adults who are not pregnant and have a normal urinary tract, and in general, treatment is not indicated. Up to 30% of patients will develop symptomatic infection within 1 yr.

LOIN PAIN

Dull ache in the loin is rarely due to renal disease but may be caused by renal stone, renal tumour, acute pyelonephritis or obstruction of the renal pelvis.

Patients with a first renal stone should have a minimum set of investigations (Box 7.4); more detailed investigation is reserved for those with recurrent or multiple stones, or those with complicated or unexpected presentations. Since most stones pass spontaneously, urine should be sieved for a few days after an episode of colic to collect the calculus for chemical analysis.

7.4 INVESTIGATIONS FOR RENAL STONES

Management

• Bed rest and application of warmth to the site of pain.

• Powerful analgesia, e.g. morphine (10–20 mg), pethidine (100 mg) i.m. or diclofenac as a suppository (100 mg).

• Fluid intake of 2 litres/day.

Around 90% of stones <4 mm in diameter will pass spontaneously, but only 10% of stones of >6 mm will pass and these may require active intervention. Immediate action is required if there is anuria or if severe infection occurs in the stagnant urine proximal to the stone (pyonephrosis). Most stones can be fragmented by extracorporeal shock wave lithotripsy in which shock waves generated outside the body are focused on the stone, breaking it into small pieces which can pass easily down the ureter. This requires free drainage of the distal urinary tract.

Endoscopic surgery is often required for stones, but open surgery is now very rarely needed except for large bladder stones. All stones are potentially infected and surgery should be covered with appropriate antibiotics.

EXCESSIVE MICTURITION

NOCTURIA

Waking up at night to void urine may be a consequence of polyuria but may also result from fluid intake or diuretic use in the late evening. Nocturia also occurs in chronic kidney disease, and in prostatic enlargement where it is associated with poor stream, hesitancy, incomplete bladder emptying, terminal dribbling and urinary frequency.

FREQUENCY

Frequency describes micturition more often than a patient’s expectations. It may be a consequence of polyuria, often due to diuretic therapy, when volumes passed are normal or high. It is also a symptom of UTIs when urine volumes are low and associated with dysuria, urgency and a feeling of incomplete emptying.

URINARY INCONTINENCE

Urinary incontinence is defined as any involuntary leakage of urine. Urinary tract pathology causing incontinence is described below. It may also occur with a normal urinary tract, e.g. in association with poor cognition or poor mobility, or transiently during an acute illness or hospitalisation, especially in older people. Diuretics (medication, alcohol or caffeine) may worsen incontinence.

Clinical assessment and investigations

• A voiding diary is used to record the pattern of micturition, including the estimated volume voided, frequency of voiding, precipitating factors and associated features, e.g. urgency.

• Cognitive function and mobility are assessed.

• Neurological assessment reveals disorders such as MS that may affect the nervous supply of the bladder. Perineal sensation and anal sphincter tone should be examined since the same sacral nerve roots also supply the bladder and urethral sphincter.

• The lumbar spine should be inspected for features of spina bifida occulta.

• Rectal examination is needed to assess the prostate in men and to exclude faecal impaction.

• Urinalysis and culture should be performed in all patients.

• An assessment of post-micturition volume should be made, either by post-micturition USS or catheterisation. Urine flow rates and full urodynamic assessment may also be helpful in selected cases.

Incontinence syndromes

Stress incontinence: Leakage occurs because passive bladder pressure exceeds the urethral pressure, due to either poor pelvic floor support or a weak urethral sphincter, most often both. This is very common in women, especially following childbirth. It is rare in men, usually following prostate surgery. Urine leaks when abdominal pressure rises, e.g. when coughing or sneezing. In women, perineal inspection may reveal leakage of urine with coughs, and sometimes also a prolapse. Women often respond well to physiotherapy but if incontinence is persistent, surgical treatment is indicated.

Urge incontinence: Leakage usually occurs because of detrusor over-activity producing an increased bladder pressure which overcomes the urethral sphincter (motor urgency). Urgency with or without incontinence may also be driven by a hypersensitive bladder (sensory urgency) resulting from UTI or bladder stone. The incidence of urge incontinence increases with age, and is also seen in men with lower urinary tract obstruction; it most often remits after the obstruction is relieved. The diagnosis is made on the basis of symptoms after exclusion of urinary retention by bladder USS; confirmation requires urodynamic testing. Treatment is by bladder retraining, teaching patients to hold more urine voluntarily in their bladder, assisted by anticholinergic medication.

Overflow incontinence: This occurs when the bladder becomes chronically over-distended. It is most common in men with benign prostatic hyperplasia or bladder neck obstruction, but may occur in either sex as a result of detrusor muscle failure (atonic bladder). This may be idiopathic but more commonly results from pelvic nerve damage from surgery (e.g. hysterectomy or rectal excision), trauma or infection, or from compression of the cauda equina from disc prolapse, trauma or tumour. USS reveals a significant post-micturition volume (>100 ml). Obstructed bladders should be treated surgically. Unobstructed bladders need to be drained, preferably by intermittent self-catheterisation. Urodynamic testing helps clarify the aetiology.

Post-micturition dribble: This is very common in men, even in the relatively young. It is due to a small amount of urine becoming trapped in the U-bend of the bulbar urethra, which leaks out when the patient moves. It is more pronounced if associated with a urethral diverticulum or urethral stricture. It may occur in females with a urethral diverticulum and may mimic stress incontinence.

Neurological causes: Neurological disease resulting in abnormal bladder function is almost always associated with obvious neurological signs; these are described on page 646.

REDUCED MICTURITION

OLIGURIA/ANURIA

On a normal diet, between 300 and 500 ml/day of urine is required to excrete the solute load at maximum concentration. Volumes below this are termed oliguria. Anuria is the (almost) total absence of urine (<50 ml/day). A low measured urine volume is an important finding and is a consequence of reduced production, obstruction to urine flow or both.

HAEMATURIA

This indicates bleeding anywhere within the urinary tract, and may be visible (macroscopic) or only detectable on urinalysis (microscopic). Macroscopic haematuria is more likely to be caused by tumours, severe infections and renal infarction. Common causes are shown in Box 7.6.

7.6 CAUSES OF HAEMATURIA

Renal	Infection, infarction, interstitial disease, glomerular disease, vascular malformation, tumour, cysts, clotting disorders
Ureters	Stones, tumour
Bladder	Infection, tumour
Urethra	Trauma

Investigations and management of haematuria are outlined in Figure 7.2.

Fig. 7.2 Investigation and management of haematuria.

PROTEINURIA

Proteinuria is usually asymptomatic, although large amounts may make urine froth easily.

Moderate amounts of low molecular weight protein do pass through the glomerular basement membrane (GBM). These are normally reabsorbed by tubular cells so that <150 mg/day appears in urine. Minor leakage of albumin into the urine may occur transiently after vigorous exercise, during fever or UTI, and in heart failure. Quantities do not reach nephrotic levels and tests should be repeated once the stimulus is no longer present.

Proteinuria >2.5 g/day indicates that a glomerular source is likely. Over 3.5 g/day is the nephrotic range.

‘Orthostatic proteinuria’, with positive daytime samples and negative morning samples, is usually benign.

Low molecular weight proteins may also appear in the urine in larger quantities than 150 mg/day (although rarely exceeding 1.5–2 g/24 hrs), indicating failure of reabsorption by damaged tubular cells, i.e. ‘tubular proteinuria’.

Heavy proteinuria denotes an increased risk of progressive renal failure. Treatments that are effective at lowering proteinuria (e.g. ACE inhibitors) also lower this risk.

Investigation of proteinuria is shown in Figure 7.3.

Fig. 7.3 Investigation of proteinuria.

MICROALBUMINURIA

Microalbuminuria (0.03–0.3 g/day) is a clear sign of glomerular abnormality and can identify very early glomerular disease, e.g. in diabetic nephropathy (p. 412). Persistent microalbuminuria has also been associated with an increased risk of atherosclerosis and cardiovascular mortality.

NEPHROTIC SYNDROME

Nephrotic syndrome describes the clinical consequences that occur when substantial amounts of protein are lost in the urine. The diseases that cause nephrotic syndrome always affect the glomerulus and tend to be non-inflammatory, or subacute examples of inflammatory glomerulonephritis. Diabetes mellitus and amyloidosis can also cause nephrotic syndrome.

Management

• Includes diuretics, low-sodium diet, statins, anticoagulation and vaccination against infection.

OEDEMA

Causes of oedema are shown in Box 7.7.

7.7 CAUSES OF OEDEMA

Low plasma oncotic pressure	Hypoalbuminaemia as seen in nephrotic syndrome, liver failure, malabsorption
Increased capillary permeability	Infection, drug-related (calcium channel blockers)
Increased hydrostatic pressure	High venous pressure/obstruction (congestive heart failure, DVT, pelvic tumour), lymphatic obstruction (malignancy, radiation injury, congenital abnormality)

HYPERTENSION

Hypertension is a very common feature of renal parenchymal and vascular disease and is an early feature of glomerular disorders. As glomerular filtration rate (GFR) declines, hypertension becomes increasingly common, regardless of the renal diagnosis. Control of hypertension is very important in patients with renal impairment because of its close relationship with further decline of renal function (p. 183) and with the adverse cardiovascular risk in renal disease.

ACUTE RENAL FAILURE

Acute renal failure (ARF) refers to a sudden and usually reversible loss of renal function, which develops over a period of days or weeks and is usually accompanied by a reduction in urine volume. There are many possible causes (Box 7.8) and it is frequently multifactorial. If the cause cannot be rapidly corrected and renal function restored, temporary renal replacement therapy may be required (p. 185).

REVERSIBLE PRE-RENAL ARF

Because haemodynamic disturbances can initially produce acute renal dysfunction that has the potential to be rapidly reversed, prompt recognition and treatment are important.

Management and prognosis

• Establish and correct the underlying cause.

• If hypovolaemia is present, restore blood volume as rapidly as possible (with blood, plasma or isotonic saline (0.9%), depending on what has been lost).

• Optimise systemic haemodynamics. Monitoring of the central venous pressure or pulmonary wedge pressure as an adjunct to clinical examination may aid in determining the rate of administration of fluid. Critically ill patients may require invasive haemodynamic monitoring to assess cardiac output and systemic vascular resistance, and the use of inotropic drugs to restore an effective BP (p. 27).

• Correct metabolic acidosis. Restoration of blood volume will correct acidosis by restoring kidney function. Isotonic sodium bicarbonate (e.g. 500 ml of 1.26%) may be used.

• Recent trials do not support the use of low-dose dopamine in severely ill patients at risk of ARF.

• If treatment is given sufficiently early, renal function will usually improve rapidly; in such circumstances residual renal impairment is unlikely.

ESTABLISHED ARF

Established ARF with the histological pattern of acute tubular necrosis (ATN) may develop following severe or prolonged under-perfusion of the kidney (pre-renal ARF). In patients without an obvious cause of pre-renal ARF, alternative ‘renal’ and ‘post-renal’ causes must be considered (Boxes 7.8 and 7.9).

7.9 DIFFERENTIAL DIAGNOSIS OF ARF IN A HAEMODYNAMICALLY STABLE, NON-SEPTIC PATIENT

Vascular event

• Due to major vascular occlusion or small-vessel diseases (p. 609)

• May be precipitated by ACE inhibitors in critical renal artery stenosis (p. 190)

• Urine usually shows minimal abnormalities but there may be haematuria in renal infarction

Pre-renal	Systemic, e.g. heart failure, blood or fluid loss Local, e.g. renal artery occlusion/stenosis, disease affecting arterioles
Intrinsic renal disease	Acute tubular necrosis/toxic/septic renal failure (85%) Glomerular disease (5%) Interstitial disease (10%)
Post-renal	Obstruction, e.g. stones, tumour, prostatic enlargement

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Kidney and urinary tract disease

Rapidly progressive glomerulonephritis (RPGN) (p. 195)

Acute interstitial nephritis (p. 195)

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