Renal, metabolic and endocrine systems

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TOPIC 6 Renal, metabolic and endocrine systems

Topic Contents

Assessment of renal function: Serological tests 97

Test: Serum creatinine 97
Test: Serum urea measurement 100
Assessment of renal function: urinalysis 101

Test: Urine dipstick 101
Test: Urine microscopy 101
Test: Laboratory assay of urine sodium, osmolality, urea, creatinine and specific gravity 102
Assessment of renal function: Measurement of glomerular filtration rate 104

Test: Radioisotope assay 104
Test: Inulin clearance 105
Test: Creatinine clearance 105
Assessment of renal function: Radiological 106

Test: Renal ultrasound 106
Serological measurement of electrolytes 107

Test: Serum sodium measurement 107
Test: Serum potassium measurement 109
Test: Serum magnesium 112
Test: Serum calcium 113
Test: Serum phosphate 115
Test: Serum chloride 117
Test: Serum lactate 117
Test: Serum bicarbonate 118
Investigation of salt and water disturbance 119

Test: Serum osmolality 119
Assessment of thyroid function 120

Test: Serum thyroid hormones measurement 120
Assessment of glycaemic control 121

Test: Serum glucose 121
Test: Glycosylated haemoglobin (HbA1C) 124
Investigation of the hypothalamic–pituitary axis 124

Test: Short synacthen test 124
Measurement of hormones: Phaeochromocytoma 125

Test: Plasma and urine catecholamines and their metabolites 125
Measurement of hormones: Carcinoid tumours 127

Test: Urinary 5-hydroxyindole acetic acid (5-HIAA) 127
Investigation of allergic reactions 127

Test: Serum mast cell tryptase measurement 127
Test: Serum and urine histamine assay 128

Assessment of renal function: Serological tests

Test: Serum creatinine

Indications

1. Assessment of renal function.
2. Suspected or proven rhabdomyolysis.
3. As part of routine preoperative assessment for certain patients/procedures (see NICE guidelines available at http://www.nice.org.uk/CG003).

Data presented as

Numerical value: units (μmol/L).

Interpretation

Physiological principles

• Creatinine is a basic compound that is formed mainly in skeletal muscle from phosphorylcreatine.
• Except in rhabdomyolysis, production of creatinine is fairly constant; thus creatinine levels in the serum are a useful reflection of renal function as its elimination is entirely renal.

Normal range

• 60–130 μmol/L. Normal values vary according to gender and ethnic origin.

Abnormalities and management principles

• Serum creatinine increases slowly with a reduction in glomerular filtration rate (GFR) down to 40 mL/min; thereafter, creatinine rises sharply with small reductions in GFR, reducing its usefulness as a measure of renal function at high values (Fig. 6.1).
image

Fig. 6.1 Serum creatinine versus renal function.

Renal failure/impairment

• Renal failure may be acute or chronic. Identification of the cause of renal failure can only be achieved using a combination of history taking and clinical evaluation, in conjunction with further investigations.
• 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.
image

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.

Interpretation

Physiological principles

• Urea (NH2CONH2) is a product of the hepatic metabolism of amino acids, produced from the hydrolysis of arginine in the urea cycle.
• It is freely filtered by the glomerulus; approximately 50% is subsequently reabsorbed in the proximal tubule and contributes to the counter-current exchange mechanism.
• The remainder is excreted in the urine, accounting for over 80% of the body’s daily nitrogen excretion.

Normal range

2.5–7.0 mmol/L.

Abnormalities

• In most cases, an elevated urea (>12 mmol/L) represents impairment of renal function and is accompanied by a concomitant increase in serum creatinine.
• In some situations, serum urea may rise out of proportion with serum creatinine:

1. Prerenal failure (e.g. due to dehydration, heart failure, renal artery stenosis)
2. Gastrointestinal bleeding (protein meal)
3. High dietary protein intake
4. Steroids
5. Old tetracycline ingestion
6. Addison’s disease

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.

Interpretation

Physiological principles

• If substances such as glucose, protein or red or white cells appear in the urine, this indicates either an abnormally high systemic generation of these substances, or an inability of the kidney to handle these substances normally, as may be the case with intrinsic renal disease.

Normal range

• pH <5.3.
• Specific gravity 1.002–1.005.
• Trace protein and white cells.
• Absence of glucose, ketones and red cells.
• No bilirubin; minimal urobilinogen; no nitrites.

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%

* Percentage of sodium filtered at the glomerulus (normally 1000 mmol/hour), which actually appears in the urine (normally 6 mmol/hour; i.e. 0.6%).

Abnormalities and management principles

Patients with prerenal oliguria may have their renal function salvaged by aggressive haemodynamic and fluid resuscitation. In patients with established ATN, renal replacement therapy is likely to be required.

Limitations and complications

These values will be affected by the use of diuretics. In clinical practice, it would be unusual for clinical decision making to be based on urinalysis alone.

Assessment of renal function: Measurement of glomerular filtration rate

Test: Radioisotope assay

Indications

‘Gold standard’ laboratory assessment of renal function.

How it is done

A precalculated dose of a radiolabelled isotope such as 51chromium-EDTA or 99technetium-DTPA is injected intravenously into the patient. The clearance of the isotope is calculated using the formula:

image

Data presented as

Numerical value: units mL/min.

Interpretation

Physiological principles

Glomerular filtration rate (GFR) is the volume of fluid (in mL) filtered from the renal glomerular capillaries into the Bowman’s capsule per unit time (minutes). This is a measure of renal function.

The radioisotope is cleared entirely renally, thus its clearance will correlate with GFR.

Normal range

Male: 97–137 mL/minute
Female: 88–128 mL/minute

Abnormalities and management principles

Glomerular filtration rate is reduced by:

1. Any cause of renal impairment
2. Age: GFR reduces by approximately 1 mL/minute/year over the age of 30.

Glomerular filtration rate may be increased by:

1. Pregnancy
2. Exercise

Limitations and complications

• Not accurate in patients with significant oedema, as the expanded extracellular volume will influence the disappearance of the plasma tracer.
• Isotope assay is a relatively time-consuming and invasive technique. In clinical practice, creatinine clearance is usually preferred to isotope assay in the assessment of renal dysfunction.

Test: Inulin clearance

Indications

Laboratory assessment of renal function.

How it is done

Inulin, a chemically inert substance, is administered to the patient by a constant infusion and the plasma and urine concentrations measured. GFR is calculated using a variation on the clearance formula.

Physiological principles

• Measurement of glomerular filtration rate is possible by measuring the clearance of a substance that is metabolically inert, does not interfere with renal function, is neither bound nor excreted by an extrarenal route and is freely filtered by the glomerulus without being secreted or reabsorbed elsewhere in the nephron.
• Inulin fulfils all the above criteria. Prior to the development of radioisotope assays, it was used as the ‘gold standard’ for measuring glomerular filtration rate.

Limitations and complications

Inulin clearance is rarely used now as it has been superseded by isotope assays. It is a relatively invasive and complicated investigation, and in the bedside assessment of GFR, measurement or calculation of creatinine clearance (see below) is preferred as a simpler, less time-consuming and more practical method.

Test: Creatinine clearance

Indications

Bedside assessment of renal function.

How it is done

Creatinine clearance can be estimated using a variety of methods; three of the commonest are listed below.

1. 24-hour creatinine clearance

Laboratory assays of serum and urinary creatinine are required (see before). The creatinine clearance is then calculated using a modification of the generic equation to calculate clearance:

image

(1440 = number of minutes in 24 hours.)

2. Cockroft-Gault formula

Laboratory measurement of serum creatinine and the patient’s age, sex and weight are required.

image

image

3. Abbreviated MDRD Study equation

MDRD is the acronym for the Modification of Diet in Renal Disease Study equation:

image

Adjustments:

• Female: multiply GFR by 0.742
• Afro-Caribbean: multiply GFR by 1.210.

Data presented as

Numerical value.

Units: mL/minute for 24 hours creatinine clearance and Cockroft-Gault and mL/minute/1.73 m2 for abbreviated MDRD Study equation.

Interpretation

Physiological principles

• Creatinine is the naturally occurring molecule that most closely fits the above criteria.
• 24-hour creatinine clearance thus measures GFR; the Cockroft-Gault and abbreviated MDRD equations estimate creatinine clearance and thus GFR.

Normal range

1. 24-hour creatinine clearance and Cockroft-Gault formula:

• Male: 97–137 mL/minute
• Female: 88–128 mL/minute.

2. Abbreviated MDRD equation 75–116 mL/minute/1.73 m2 depending on age.

Limitations and complications

• Creatinine secretion in the tubule may be a cause of a small error; not generally clinically relevant.
• Drugs that reduce tubular creatinine secretion may cause inaccuracies, e.g. cimetidine, certain antibiotics and quinidine.

Assessment of renal function: Radiological

Test: Renal ultrasound

Indications

1. Investigation of renal impairment/failure.
2. Preoperative assessment for live related kidney donors.

How it is done

Abdominal ultrasound examination.

Data presented as

Radiological imaging, with measurement of kidney size.

Interpretation

Physiological principles

• Renal size:

– Renal length will be normal bilaterally in most causes of acute renal failure
– The kidneys will be small bilaterally in many causes of chronic renal failure (<8 cm)
– Asymmetrical renal size may reflect renovascular disease.

• Structural abnormalities:

– Mass lesions such as tumours, simple cysts or polycystic kidney disease can be identified
– Causes of postrenal obstruction such as prostatic enlargement may also be revealed
– Calculi may be visible within the kidney or urological tract
– Cortical scarring caused by reflux nephropathy or following segmental ischaemia will be visible.

Normal range

Bipolar renal length: 9–13 cm in adults.

Limitations and complications

• Operator dependent.
• Difficult in patients with large body habitus.

Serological measurement of electrolytes

Test: Serum sodium measurement

Indications

1. Preoperative biochemistry profile according to NICE guidelines.
2. Critical illness, renal or hepatic failure.
3. Disordered water homeostasis of any cause including suspected diabetes insipidus or syndrome of inappropriate ADH secretion (SIADH).
4. Adrenal disorders.

How it is done

Radioimmunoassay.

Interpretation

Physiological principles

• Sodium is the predominant extracellular cation and principal osmotically active solute in plasma and interstitial fluid; it is vital for membrane potentials and action potentials.
• It is actively absorbed from the small intestine and colon under the influence of aldosterone; freely filtered at the glomerulus and then actively reabsorbed in the proximal convoluted tubule, utilizing Na,K-ATPase.
• Lost predominantly in urine (150 mmol/day); some loss from sweat, faeces and saliva (10 mmol/day each).
• Sodium balance is regulated via:

– osmoreceptors, which monitor extracellular sodium concentration then influence the renin-angiotensin-aldosterone system
– Baroreceptors, which monitor changes in extracellular volume so influencing antidiuretic hormone and atrial natriuretic hormone secretion as well as the renin-angiotensin-aldosterone system.

Normal range

135–145 mmol/L.

Abnormalities and management principles

Hyponatraemia

Causes

Hyponatraemia may be divided into three categories:

1. ‘Real’ hyponatraemia (hypo-osmolar plasma)
2. Pseudo-hyponatraemia (i.e. presence of high levels of triglycerides or proteins with a normal serum osmolality)
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