• The RIFLE criteria (Fig. 6.2) are an evidence-based guide to aid classification of the degree of renal dysfunction, based on serum creatinine and urine output.

Fig. 6.2 The RIFLE criteria for classification of renal dysfunction.

(Adapted from Bellomo et al. (2004) Crit Care Med 8:R204-R212, with permission.)

The acronym RIFLE encompasses three levels of renal dysfunction (‘risk of renal dysfunction’, ‘injury to kidney’ and ‘failure of renal dysfunction’) and two outcomes of renal dysfunction (‘loss’ and ‘end-stage renal disease’). The inclusion of these two separate outcomes acknowledges the important adaptations that occur in end-stage renal disease (ESRD) that are not seen in persistent acute renal failure (ARF). Persistent ARF (loss) is defined as need for renal replacement therapy (RRT) for more than 4 weeks, whereas ESRD is defined by need for dialysis for longer than 3 months.

Acute renal failure

See Table 6.1 for causes.

Table 6.1 Causes and classifications of acute renal failure

Classification		Example of causes
‘Pre-renal’	Pre-renal failure causing renal hypoperfusion and acute tubular necrosis	Circulating volume depletion: dehydration, haemorrhage, etc Low cardiac output of any origin Sepsis Drugs causing reduction in renal perfusion (e.g. NSAIDs, ACE inhibitors)
‘Intrinsic renal’	Acute glomerulonephritis and vasculitis	ANCA-positive vasculitis (e.g. Wegener’s) Goodpasture’s disease Systemic lupus erythematosus Endocarditis
	Disruption of renal vasculature	Large vessel occlusion (renovascular disease) Small vessel occlusion (DIC, haemolytic-uraemic syndrome; thrombotic thrombocytopenic purpura; pre-eclampsia)
	Toxic acute tubular necrosis	Drugs (e.g. gentamicin) Contrast nephropathy Myoglobinuria from rhabdomyolysis
	Interstitial nephritis	Idiopathic/autoimmune Drug-induced hypersensitivity Infection
	Myeloma/tubular cast nephropathy
‘Post-renal’ or ‘obstructive’	Urinary tract obstruction	Prostatic disease; renal stones

Prerenal uraemia versus acute tubular necrosis

• Both caused by renal hypoperfusion and ischaemia.

• In prerenal uraemia, renal function is salvageable with restoration of perfusion; in ATN, disruption of physiological mechanisms such as the renin-angiotensin system necessitate renal replacement therapy.

Management principles

• Identification and management of underlying cause.

• Treatment of fluid overload, acidosis and hyperkalaemia, using renal replacement therapy if required.

Chronic renal failure

See Table 6.2 for causes.

Table 6.2 Causes of chronic renal failure

Intrinsic causes	Obstructive causes
Diabetic nephropathy	Post-obstructive nephropathy
Chronic glomerulonephritis	Nephrolithiasis
Renovascular disease	Multiple myeloma
Chronic reflux nephropathy
Polycystic kidney disease
Amyloidosis
Post-acute renal failure
Chronic interstitial nephritis
Analgesic nephropathy

Other causes of a raised creatinine, without a concomitant rise in urea

• Drugs: cimetidine, trimethroprim, aspirin.

• Other: liver failure, racial variations, rhabdomyolysis (before onset of associated renal failure).

Management principles

• Identification and treatment of underlying aetiology.

• Renal replacement therapy with dialysis or transplantation when end-stage renal failure reached.

Limitations and complications

There is considerable inter-individual variation in normal serum creatinine due to muscle mass, age and diet. Thus, only serial measurements will provide a useful indication of changes in renal function.

Test: Serum urea measurement

Indications

1. Investigation of renal function.

2. As part of routine preoperative assessment for certain patients/procedures (see NICE guidelines).

Data presented as

Numerical value: units mmol/L.

Management principles

See under ‘Serum creatinine’.

Assessment of renal function: urinalysis

Test: urine dipstick

Indications

1. Bedside investigation of renal function.

2. Screening for diabetes.

3. Screening for urinary tract infection.

How it is done

• A reagent stick is dipped into a urine sample.

• The various reagents change colour according to the presence of various constituents of the sample.

Data presented as

Reagent stick colour changes compared to standardized colour chart.

Abnormalities and management principles

A few causes of an abnormal urine dipstick are listed in Table 6.3.

Table 6.3 Causes of abnormal urine dipstick

Finding	Causes
Glycosuria	Diabetes mellitus
	Tubular dysfunction
	Pregnancy
Proteinuria	Glomerular dysfunction, e.g. pre-eclamptic toxaemia
	Orthostatic proteinuria (benign; occurs after prolonged standing)
	Fever
	Severe exercise
	Lower urinary tract infection
	Nephrotic syndrome
High pH	Distal renal tubular acidosis (renal bicarbonate losses)
Low specific gravity	Diabetes insipidus
Red cells	Rhabdomyolysis
	Urinary tract infection
	Glomerulonephritis
Leucocytes	Urinary tract infection
Nitrites	Gram-negative bacterial urinary tract infection
Bilirubin/increased urobilinogen	Conjugated bilirubin appears in presence of obstructive jaundice

Limitations and complications

Urine dipstick is a very nonspecific test and further investigation will always be required in the presence of an abnormal result.

Test: Urine microscopy

Indications

• Investigation of abnormal renal function.

• Suspected urinary tract infection.

How it is done

Microscopic laboratory analysis of a fresh urine sample.

Data presented as

Written report detailing presence or absence of cells, crystals and casts.

Interpretation

Physiological principles

Cells, crystals and casts are not usually found in the urine and their presence may indicate the presence of intrinsic renal pathology or infection.

Abnormalities and management principles

See Table 6.4 for explanation of various findings.

Table 6.4 Findings in the urine on microscopy

Finding	Causes
Red cells	Glomerular bleeding or dysfunction
	Infection
	Traumatic catheterization
White cells	Infection
	Some cases of glomerular disease
	Some cases of interstitial nephritis
Crystals	Renal calculi
	Gout (uric acid crystals)
Casts
Hyaline casts	Normal
Granular casts	Nonspecific
Tubular cell casts	Acute tubular necrosis or interstitial nephritis
Red cell casts	Glomerulonephritis or glomerular bleeding
Leucocyte casts	Acute tubular necrosis or pyelonephritis

Limitations and complications

Sample contamination may affect the result. This is a fairly nonspecific test, and further investigations will be required to make a diagnosis if an abnormal result is found.

Test: Laboratory assay of urine sodium, osmolality, urea, creatinine and specific gravity

Indications

Differentiation between prerenal oliguria and acute tubular necrosis.

Interpretation

Physiological principles

• In prerenal uraemia an acute hypoperfusion insult to the kidney has occurred, but there is preservation of physiological mechanisms within the kidney (such as stimulation of the renin-angiotensin-aldosterone system) which maintain normal sodium and water handling within the nephron.

• In the case of acute tubular necrosis, kidney damage has occurred, impairing normal solute and water handling; in the oliguric patient, urinalysis may differentiate between these two disorders and guide management.

Normal ranges

See Table 6.5.

Table 6.5 Normal ranges for urine laboratory findings

Investigation	Prerenal oliguria	Acute tubular necrosis
Urine sodium (mmol/L)	<20	>40
Specific gravity	>1.020	<1.010
Urine osmolality (mosmol/kg)	>500	<350
Urine: plasma osmolality ratio	>2	<1.1
Urine: plasma urea ratio	>20	<10
Urine: plasma creatinine ratio	>40	<20
Fractional sodium excretion^*	<<1%	>1%