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The history • 275
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common cause of nephrotic syndrome is diabetes mellitus. Patients may notice that the urine is frothy due to the proteinuria;
hyperlipidaemia, hypercoagulability, and an increased risk of
infection may also develop.
Ask about:
• Weight loss, altered bowel habit, cough, back pain or chronic
inflammatory conditions such as rheumatoid arthritis, inflammatory bowel disease or bronchiectasis (in particular if
undertreated). The latter cause nephrotic syndrome as a
result of renal AA amyloid deposition.
• Ankle swelling (pitting oedema): Younger patients may also
notice facial swelling and puffy eyelids, especially first thing in
the morning.
• Breathlessness (pleural effusions).
• Abdominal swelling (ascites).
Acute kidney injury
AKI (Box 12.1) covers a range of presentations from relatively
mild changes in kidney function to dialysis-requiring kidney failure. The typical presentation is with a recently identified rise in
serum creatinine. AKI may have prerenal, renal or postrenal
causes (Box 12.2); there is an increased risk in patients with preexisting CKD. The history should focus on differentiating between these.
Prerenal acute kidney injury
This is almost always due to volume depletion (hypovolaemia).
Ask about:
• Fluid losses, such as vomiting, diarrhoea or bleeding, and
inadequate oral intake due to nausea or delirium.
• Recent operations or investigations that may be associated
with increased fluid losses or reduced intake (fasting, bowel
preparation).
12.1 Definition of acute kidney injury
a
RIFLE
b
AKIN
Risk
AKIN stage 1
Injury
AKIN stage 2
Failure
AKIN stage 3
Loss Renal replacement therapy
End-stage
kidney disease
a
Risk, injury, failure, loss, end-stage kidney disease
b
Acute kidney injury network
Serum creatinine criteria
Increase>50% < 0.5 mL/kg/h for
Increase>100% <0.5 mL/kg/h for
Increase>200% or serum
creatinine >350 mmol/L
(3.96 mg/dL)
for >4 weeks
Renal replacement therapy
for >3 months
Urine output
criteria
6 hours
12 hours
0.3 mL/kg/h for
24 hours or anuria
for 12 hours
–
–
• Any features of infection, such as fever, sweats, productive
cough or dysuria.
Establish whether there is an underlying condition that may
predispose to a reduction in renal blood flow.
Ask about:
• History of heart failure or liver disease.
• Recent drug prescriptions, such as those that block the
renin–angiotensin-aldosterone system (e.g. angiotensinconverting enzyme inhibitors), other antihypertensive
agents, diuretics (such as furosemide or spironolactone) and
non-steroidal anti-inflammatory drugs (NSAIDs); NSAIDs can
also cause intrinsic renal disease, such as interstitial nephritis
and minimal change disease
12.2 Causes of acute kidney injury
Prerenal
• Hypovolaemia (e.g. blood loss, diarrhoea, vomiting, diuresis or inade-
quate oral intake)
• Relative hypovolaemia (e.g. heart failure or nephrotic syndrome)
• Sepsis
• Drugs (e.g. antihypertensives, diuretics or non-steroidal anti-
inflammatory drugs)
• Renal artery stenosis or occlusion
• Hepatorenal syndrome
Intrarenal
• Glomerular disease (e.g. immunoglobulin A nephropathy, systemic
vasculitis or systemic lupus erythematosus)
• Interstitial nephritis (drug-induced)
• Acute tubular necrosis/injury (may follow a prerenal cause)
• Multiple myeloma
• Rhabdomyolysis
• Intrarenal crystal deposition (e.g. urate nephropathy or ethylene glycol
poisoning)
• Thrombotic microangiopathy (e.g. haemolytic uraemic syndrome or
scleroderma renal crisis)
• Accelerated-phase hypertension
• Cholesterol emboli
Postrenal
• Renal stones (in papilla, ureter, or bladder)
• Papillary necrosis
• Ureteric or bladder transitional cell carcinoma
• Intraabdominal or pelvic malignancy (e.g. cervical carcinoma)
• Retroperitoneal fibrosis
• Blood clot
• Bladder outflow obstruction (e.g. prostatic enlargement)
• Neurogenic bladder
• Urethral stricture
• Posterior urethral valves
• Iatrogenic (e.g. ureteric damage at surgery, blocked urethral catheter)
12
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Intrinsic acute kidney injury
The most common cause in the hospital setting will be acute
tubular injury (ATI), which may lead to acute tubular necrosis
(ATN). This usually follows renal hypoperfusion when any of the
causes identified above results in ischaemia–reperfusion injury. A
less common cause is rhabdomyolysis, which is suggested by a
history of prolonged immobilisation, such as following a fall. ATI
normally recovers, but this can take days to weeks. AKI can also
be the first clinical presentation of a systemic disease that affects
the kidney (such as myeloma, infective endocarditis, vasculitis or
systemic lupus erythematosus).
Ask about:
• Recent illnesses or operations.
• Drug history and any recent changes in medications; several
commonly prescribed medications (such as antibiotics,
NSAIDs or proton pump inhibitors) are recognised as causing
an allergic interstitial nephritis, but almost any drug can be
implicated.
• Symptoms of systemic disease: weight loss, fever, night
sweats, tiredness, arthralgia, myalgia, bony pain, numbness,
weakness, rashes, cough and breathlessness.
Occasionally, AKI can be the result of a primary glomerulonephritis. IgA nephropathy is the most common cause in the
northern and western hemispheres. This classically presents with
visible haematuria following an upper respiratory tract infection–
so-called ‘synpharyngitic haematuria’.
Ask about:
• Prior episodes.
• Loin pain and haematuria.
• Previous sore throat; a similar clinical illness can occur in
postinfectious glomerulonephritis due to preceding betahaemolytic streptococcal infection of the throat or skin.
Postrenal acute kidney injury
This is usually due to any cause of obstruction from the renal
pelvis to the urethra. The most common cause is bladder outflow
obstruction; in men, this is often due to prostatic hypertrophy,
either benign or malignant.
Ask about:
• Urinary urgency, frequency, nocturia and incontinence.
• Poor urine stream and terminal dribbling.
• Previous prostatic assessments, including prostate exami-
nation and measurements of prostate-specific antigen.
• Suprapubic pain.
• Leg weakness, perineal numbness or faecal incontinence
(may indicate a spinal cord lesion).
In acute urinary retention there is usually a complete inability to
pass urine and associated suprapubic discomfort. Chronic urinary retention is usually painless.
For ureteric disease to cause AKI, both kidneys need to be
affected (or the patient has a single functioning kidney). Ureteric
obstruction is most commonly due to malignancy, such as that
of the bladder, cervix, ovary or uterus. These conditions are
usually painless. The history should explore any previous diagnosis and recent operations and treatment, including
radiotherapy.
Chronic kidney disease
CKD is defined by degree of renal dysfunction and/or the presence of proteinuria (Boxes 12.3 and 12.4); these need to be
present for at least 3 months. The diagnosis of CKD therefore
requires preceding biochemical data to enable its distinction from
AKI. Most patients with CKD have few symptoms until they have
kidney failure.
12.3 Definition of chronic kidney disease
CKD stage eGFR (mL/min/1.73 m2) Description Management
1 ≥ 90 Kidney damage with normal or ↑ GFR
2 60–89 Kidney damage with mild ↓ GFR
3A 45–59 Moderate ↓ GFR
3B 30–44
4 15–29 Severe ↓ GFR Prepare for kidney failure
5 < 15 Kidney failure Dialysis, transplantation or conservative care
p: the addition of p to a stage (e.g. 2p, 3Bp) means that there is significant proteinuria. Proteinuria is quantified on the basis of an
albumin :creatinine (ACR) or protein:creatinine (PCR; see Box 12.4).
T: the addition of T to a stage (e.g. 4T) indicates that the patient has a renal transplant.
D: the addition of D to stage 5 CKD (i.e. 5D) indicates that the patient is on dialysis.
(e)GFR, (estimated) glomerular filtration rate.
Observe; control blood pressure and risk factors
}
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12.4 Quantification of proteinuria using either urine
albumin:creatinine ratio or protein:creatinine ratio
ACR
(mg/mmol)
>2.5/3.5
30 >50 Use ACE inhibitor or angiotensin-
70 100 Requires tight blood pressure control
>250 >300 Nephrotic-range proteinuria
a
Values for males/females
ACE, Angiotensin-converting enzyme; CKD, chronic kidney disease.
The key in earlier stages is to ask about:
• Underlying conditions that may explain the aetiology of CKD,
including diabetes mellitus, vascular disease (evidence of
previous myocardial infarction, stroke or peripheral vascular
disease), hypertension, hyperlipidaemia, episodes of acute
glomerulonephritis (such as IgA nephropathy) or nephrotic
syndrome (such as membranous disease)
• Previous incidental urine abnormalities, such as proteinuria or
non-visible haematuria that may suggest a preceding
glomerular disease.
A number of genetic diseases can present with CKD, so a
detailed family history is required (see later).
PCR
(mg/mmol) Interpretation
a
>15 Abnormal; adequate to define CKD
stages 1 and 2; start ACE inhibitor or
angiotensin-receptor blocker if
diabetes is present
receptor blocker if blood pressure is
elevated; suffix ‘p’ on CKD stage
patients may be masked by immunosuppression. Lymphoma, in
particular, needs to be considered post-transplantation.
Ask about:
• Date of transplant operation; organ rejection is more common
in the first few weeks.
• Current and previous immunosuppression and any recent
changes in treatment that may increase the risk of rejection;
any intercurrent illness that may have contributed to AKI.
• Fever, weight loss, cough, breathlessness, dysuria and
tenderness over the graft.
The dialysis patient
There are two main forms of dialysis: haemodialysis and peritoneal
dialysis. Each group can have specific presentations. Haemodialysis is delivered via an arteriovenous fistula or tunnelled vascular
access catheter. A fistula has an obvious thrill (p. 278), and the
patient may complain that this has been lost. This is usually due to
thrombosis and needs urgent attention from a vascular surgeon.
The most common problem with vascular access catheters is
infection. Peritoneal dialysis involves a tunnelled catheter, and
infection is also a common presentation. Ask about fever and rigors
(and their relation to haemodialysis), abdominal pain and peritoneal
dialysate fluid appearance (Has it become ‘cloudy?’).
Other presenting symptoms
Finally, hypertension, anaemia and electrolyte disorders are other
common features of renal disease.
12
Kidney failure and uraemia
Occasionally, patients will present with symptoms of uraemia.
This is most common in patients with known end-stage kidney
disease once the estimated glomerular filtration rate (eGFR)
is <10 mL/min/1.73 m
Ask about:
• Anorexia, nausea and vomiting.
• Lethargy.
• Poor concentration.
• Pruritus
• Breathlessness, which may occur due to fluid overload,
worsening acidosis and/or anaemia.
• Peripheral oedema.
Less commonly, uraemia may present with features of peri-
carditis or peripheral neuropathy.
The patient with a renal transplant
Identifying the fact that a patient has had a kidney transplant is
important early in the history. The main presenting problems are
a decline in kidney function (usually identified by routine blood
tests), infection or malignancy. The risks of the latter two are
increased by immunosuppression. Infections in renal transplant
2
. The symptoms are often nonspecific.
Past medical history
Ask the patient about their past medical history, including hypertension, vascular disease, diabetes mellitus, inflammatory
diseases (such as rheumatoid arthritis, inflammatory bowel disease, chronic infections), urinary tract stones or surgery and
previous evidence of renal disease, which may include dialysis
and renal transplantation.
Drug history
Enquire about long-term medication, any recent changes in
treatment, recent courses of antibiotics and use of nonprescription medications, such as NSAIDs and herbal remedies.
Family history
Document any family history of renal disease, hypertension, stroke,
diabetes or deafness. If the parents are deceased, ask at what age
and if the cause of death is known. The most common inherited
renal conditions are autosomal dominant polycystic kidney disease
(ADPKD) and Alport syndrome (hereditary nephritis). ADPKD usually
affects members in each generation, and both males and females
are affected. However, around 10% of those affected have no
preceding family history, possibly because family members died
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before the diagnosis was made. There is an association with berry
aneurysms, so enquire about a history of subarachnoid haemorrhage in family members. Alport syndrome is caused by abnormalities in type IV collagen and can be associated with early-onset
deafness. It is genetically heterogeneous, but the X-linked form is
the most common. The typical presentation is with non-visible
haematuria in childhood or more significant renal disease in the
late teenage and early adult years.
Social history
Ask about smoking, alcohol intake and recreational drug use.
Ask about the patient’s social support (family, housing and social
work input) and occupation. Enquire as to how independent they
are in their activities of daily living and how their illness has
affected their work.
The physical examination
The renal system can affect many aspects of the physical examination, but this may also be relatively normal, even with significant disease.
General appearance
Fig. 12.6 Muehrcke’s lines. (From Short N, Shah C. Muehrcke’s lines. Am J
Med. 2010;123(11):991–992, Elsevier.)
Advanced CKD is most likely to alter the general appearance. The
patient may look unwell with pallor; the skin may have scratch
marks from pruritus, and in severe cases there may be drowsiness,
myoclonic twitching (p. 153) or asterixis (p. 118). In marked uraemia
the patient’s skin may appear yellow, but this is a late feature.
Hiccupping may occur. Breathlessness may represent fluid overload or hyperventilation due to metabolic acidosis.
Hands
Examine the hands, looking for pallor of the palmar creases
suggestive of anaemia. Inspect the nails, looking for Muehrcke’s
lines (Fig. 12.6), which may be a sign of hypoalbuminaemia
(nephrotic syndrome) or the half-and-half (Lindsay’s) nails of CKD
(proximal half white, distal half red or brown; Fig. 12.7).
Dialysis access
Examine the arms for an arteriovenous fistula. This will look like
prominent blood vessels on the forearm or upper arm (Fig. 12.8);
there may be scars from previous fistulae on either arm. A functioning fistula will have a readily palpable fluid thrill (a continuous
buzzing feel). A tunnelled venous access catheter may be seen
exiting the anterior chest wall; the line can be followed under the
skin before it enters the internal jugular vein (Fig. 12.9).
Face
Inspect the face for rashes, which may indicate underlying
connective tissue disease: the butterfly rash of systemic lupus
Fig. 12.7 Half-and-half (Lindsay’s) nails.
erythematosus, for example. Look for conjunctival pallor, as
anaemia is common in CKD. An inflamed eye, seen with scleritis
and/or uveitis, may occur in systemic vasculitis. Fundoscopy
may reveal changes of diabetic or hypertensive retinopathy (see
Figs 8.17 and 8.18). Most patients with CKD due to diabetes
mellitus will have evidence of retinal disease. The presence of
hypertensive retinopathy (such as arteriolar narrowing, arteriovenous nipping, cotton-wool exudates or blot haemorrhages)
indicates end-organ damage due to high blood pressure; more
severe fundoscopy signs, such as flame haemorrhages and
papilloedema, may indicate accelerated-phase hypertension,
which can cause AKI. Inspection of the mouth may reveal
gingival hyperplasia caused by calcineurin inhibitors (such as
ciclosporin or tacrolimus). Uraemic fetor may be present.
Skin
Inspect the skin more generally for rashes, bruising, scratch
marks and excoriations. A vasculitic rash will appear as purpura,
Fig. 12.10 Vasculitic rash.
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The physical examination • 279
12
Fig. 12.8 Haemodialysis fistula.
Fig. 12.9 Tunnelled venous access catheter.
most commonly on the legs (Fig. 12.10), and may be due to
systemic vasculitis, Henoch-Schönlein purpura or cryoglobulinaemia, all of which can cause AKI and CKD. A drug rash
increases the likelihood of an allergic interstitial nephritis. All these
rashes will be harder to identify on darker skin tones, so ask
about changes in skin appearance.
Assessment of fluid balance
Examination sequence (Video 1)
An accurate check on fluid balance is critical to assessing
renal disease and can be completed as a single sequenced
process.
General appearance
Does the patient look hypovolaemic or fluid-overloaded? In a
dehydrated patient, the eyes may appear sunken and the mucous membranes, dry. Pinch the skin over the anterior chest wall
(rather than forearms) to determine if there is reduced skin turgor
(elasticity). These features, although relatively insensitive, are
most common when there has been significant salt and water
loss, as occurs with vomiting or diarrhoea. A patient with fluid
overload may be breathless due to pulmonary oedema or pleural
effusions, and there may be obvious signs of peripheral oedema.
Pulse and blood pressure
Measure pulse and blood pressure (avoiding an arm with an arteriovenous fistula). Hypertension is common in renal disease. Is there
evidence of hypovolaemia (tachycardia or hypotension)? Ascertaining whether blood pressure falls when the patients stands or sits
upright is a sensitive indicator of hypovolaemia.
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Jugular venous pressure
Assess the jugular venous pressure (JVP; p. 57). The JVP may
be elevated due to fluid overload or, rarely, due to cardiac
tamponade from uraemic pericarditis.
Examination of the chest
Examine the chest for signs of pulmonary oedema and/or pleural
effusion (p. 98); both are features of fluid overload. Auscultate the
heart (p. 50), listening for a third heart sound, which provides
further evidence of fluid overload. A fourth heart sound may
indicate left ventricular stiffening due to hypertension. A flow
murmur may be present in anaemia of chronic renal disease.
Quiet heart sounds suggest a pericardial effusion. A pericardial
rub may occur in uraemia.
Fig. 12.11 Renal transplant scar in the right iliac fossa.
Peripheral oedema
Examine for pitting oedema a t the base of the spine (sacral
oedema, common in bed-bound patients) and in the legs,
starting at the ankles and noting the highest level at which
oedema can be identified (such as midcalf, knees, or midthigh). In severe cases, oedema can extend into the scrotum
or la bia. Significant oedema is a hallmark of nephr otic
syndrome.
Weight
Look for sequential measures of a patient’s weight, as this will
provide an accurate assessment of fluid loss or gain over the
short term.
Fluid balance charts
The physical examination should be complemented, where
possible, by measurement of fluid input (oral and intravenous)
and output (urine volumes and other losses).
Abdominal examination
Examination sequence (Video 6G)
Ask the patient to lie flat with their arms by their sides. Expose
the abdomen fully down to the level of the anterior iliac spine.
Inspection
• Look for abdominal distension in the flanks (which may indi-
cate ascites, a further marker of fluid overload, or large
polycystic kidneys). Look for operative scars, such as those
relating to a renal transplant in the left or right iliac fossa,
extending inferiorly to the midline (Fig. 12.11) and those of a
previous nephrectomy in the left or right flank. A nephrectomy
is often needed in patients with ADPKD to make space for a
subsequent renal transplant. In addition, look for the presence of a peritoneal dialysis catheter.
Palpation
• Kneel beside the bed and use your right hand, keeping the
palmar surface flat. Observe the patient’s face for signs of
discomfort throughout. Palpate each region in turn, beginning
with light palpation followed by deeper palpation (p. 106 and
Fig. 6.1C). Describe any masses you feel. Examine for
abdominal aortic aneurysm (p. 73).
• Significantly enlarged kidneys are palpable as masses in the
flanks. You should be able to ‘get above’ the mass. Identi-
fication of less obviously enlarged kidneys requires deeper
palpation and a ballotting technique. Starting on the right
side, your left hand should be placed under the patient’s
back, with your index finger against the 12th rib in the paramedian position; the right pushes firmly down on the anterior abdominal wall. Ask the patient to take a deep breath,
and push up by flexing the fingers of your left hand
(Fig. 12.12A). The kidney can be felt against the fingers of the
right hand. The same procedure is followed on the left side
with your left hand under the patient and your little fi nger
against the 12th rib (see Fig. 12.12B). The procedure is
otherwise identical. ADPKD is the most common cause of
palpable kidneys.
• A transplanted kidney may be palpated as a mass (usually
12–14 cm in length) in either iliac fossa, although the right is
more common. Any tenderness should be noted, as this may
indicate graft pyelonephritis or rejection.
• A palpable bladder may be felt as a soft, midline, suprapubic
mass that you cannot ‘get below’. In acute retention,
palpation will worsen discomfort.
• When pyelonephritis is suspected, tenderness in the renal
angle should be determined. If this is nontender on palpation,
you may sit the patient up and percuss with a closed fist over
both renal angles.
Percussion
• Ascites should be assessed using the standard technique for
shifting dullness or a fluid thrill (p. 124). Peritoneal dialysis fluid
is also evident as a fluid level determined by percussion. To
identify an enlarged bladder, you should percuss over the
midline from a resonant area at the umbilicus, moving
Fig. 12.12 Palpation of the kidney. A Right kidney. B Left kidney.
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Investigations • 281
12
inferiorly to identify where the percussion note becomes dull.
The percussion note should be resonant over enlarged
kidneys.
Auscultation
• Listen for abdominal bruits over the epigastrium and both
renal arteries (p. 272). This may be a sign of renovascular
disease or atheromatous disease in other arteries.
Targeted examination of other systems
The kidneys are involved in many multisystem diseases. Renal
impairment itself may also affect other systems. The history will
help direct the examination to these elements.
Joints
Examine for inflammation and swelling of joints, which can occur
in systemic vasculitis. The presence of a chronic arthritis, such as
rheumatoid disease, may lead to amyloid (a cause of nephrotic
syndrome), and medication used to treat arthritis, such as
NSAIDs, can cause AKI. Examine for areas of bony tenderness in
the spine; this may be a feature of myeloma.
Nervous system
Examine for a peripheral neuropathy (sensory and/or motor),
which can occur with a systemic vasculitis. In diabetes mellitus,
the presence of neuropathy is common in those with CKD.
Interpretation of the findings
Renal disorders may come to light because of patient symptoms
or abnormalities on biochemical investigation. Clinical assessment will be dictated by the scenario; focus on the relevant
positive and negative findings when describing the case.
In patients with an acute presentation, the key element is to
begin with a description of the patient’s general appearance and
fluid status. This should summarise whether they are clinically
euvolaemic, hypovolaemic or fluid-overloaded. Are there any
features of a multisystem disease (such as rash, joint swelling, or
eye inflammation) or any signs in the abdomen that suggest renal
disease (such as enlarged kidneys, renal transplant, renal bruits
or enlarged bladder) that may point to a diagnosis? Urinalysis
(see below) should be used to identify infection or intrinsic renal
diseases, such as glomerulonephritis or nephrotic syndrome.
In patients with CKD, fluid balance assessment should be
presented in the same way. The examination findings should
focus on whether there is evidence of an underlying disease that
may explain CKD: for example, diabetes mellitus (retinopathy,
neuropathy), hypertension (retinopathy), ADPKD (enlarged kidneys, previous surgery), renovascular disease (renal bruits) or
previous renal transplantation. In addition, include any features of
the adverse effects of CKD, such as anaemia, skin excoriations
from pruritus or weight loss, in your presentation.
Investigations
Prostate
Physical examination of the prostate is covered on pages 126
and 128.
Urinalysis
Urinalysis should be considered an essential part of the renal
examination. Urine should be obtained as a midstream specimen
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so it can be optimally used for subsequent investigations (see
later). Urine abnormalities may reflect:
• Abnormally high levels of a substance in the blood
exceeding the capacity for normal tubular reabsorption, such as
glucose, ketones, conjugated bilirubin and urobilinogen.
• Altered kidney function: for example, proteinuria or failure to
concentrate urine.
• Abnormal contents, such as blood arising at any point between the kidney and the urethra.
The urine dipstick test uses chemical reagents, which change
colour when they are immersed and then removed from urine, to
detect abnormalities. Urine test strips contain up to 10 of these
chemical pads; however, not all are used in the assessment of
renal disease. The key elements are described in Box 12.5.
Normal fresh urine is clear but varies in colour. Cloudy fresh
urine is usually due to the presence of leucocytes (pyuria).
Discoloration of the urine can occur due to drugs (e.g. rifampicin),
foods (e.g. beetroot) or metabolites (e.g. bilirubin). Strong odours
can be due to infections; some foods, like asparagus, impart a
characteristic smell to the urine.
Investigation of renal function
Functional studies may be useful in patients with voiding symptoms (Box 12.6). In addition to urinalysis, there are a number of
other blood and urine tests (Box 12.7), as well as imaging studies
(Box 12.8), that may help in the assessment of the patient with
renal disease.
12.5 Key elements of urine dipstick test
Investigation Comment
Specific gravity Reflects urine solute concentration; varies between 1.002 and 1.035; raised when kidneys actively reabsorb water (e.g. in fluid
pH Normally 4.5–8.0; in renal tubular acidosis, pH never falls to <5.3 despite acidaemia
Glucose Small amounts may be excreted by normal kidneys. Glycosuria may indicate poorly controlled diabetes mellitus. It may occur in
Ketones Test is specific for acetoacetate and does not detect other ketones (e.g. b-OH butyrate, acetone). Ketonuria occurs in diabetic
Protein Varies between trace and 4þ. The greater the degree of proteinuria, the more likely there is to be significant renal disease. Most
Blood 1þ is positive for non-visible haematuria. The test does not differentiate between haemoglobin and myoglobin. If you suspect
Bilirubin and
urobilinogen
Leucocyte esterase Indicates the presence of neutrophils in urine; seen in urinary tract infection or infl ammation, stone disease and urothelial cancers
Nitrite Most gram-negative bacteria convert urinary nitrate to nitrite. A positive result indicates bacteriuria, but a negative result does not
depletion or renal failure due to decreased perfusion) abnormally low values indicate failure to concentrate urine
intrinsic renal disease when tubular glucose reabsorption is impaired.
ketoacidosis, starvation, alcohol use and very-low-carbohydrate diets.
patients with nephrotic syndrome will have 4þ protein. The presence of both blood (2þ) and protein (2þ)dan ‘active
urinary sediment’doften indicates intrinsic renal disease. As urinalysis is semiquantitative, confirmatory laboratory quantification
should be undertaken using either a urine albumin:creatinine or protein:creatinine ratio (see Box 12.4)
rhabdomyolysis, measure myoglobin with a specific laboratory test.
Bilirubin is not normally present. Urobilinogen may be up to 33 mmol/L in health. Abnormalities of bilirubin and urobilinogen
require investigation for possible haemolysis or hepatobiliary disease.
exclude its presence.
12.6 Functional assessment of the lower urinary tract
Frequency/volume chart
• Chart is used to monitor micturition patterns, including nocturia, and fluid intake.
• The patient collects their urine, measures each void and charts it against time over 3–5 days.
Urine flow rate
• The patient voids into a special receptacle that measures the rate of urine passage.
• A low flow does not differentiate between poor detrusor contractility and bladder outlet obstruction.
Urodynamic tests
• Invasive tests necessitating the insertion of bladder and rectal catheters to measure total bladder pressure and abdominal pressure and to allow bladder
filling.
• Filling studies determine detrusor activity and compliance.
• Low detrusor pressures with low urine flow suggest detrusor function problems.
• High detrusor pressures with low flow suggest bladder outlet obstruction.
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12.7 Blood and urine investigations in renal and urological disease
Investigation Indication/comment
Serum urea/creatinine Levels generally [ as GFR Y, but values are affected by diet and muscle mass, and do not measure renal
eGFR Usually provided by the laboratory and is based on the serum creatinine
Creatinine clearance A good measurement of GFR but requires a 24-hour urine collection and blood sample
Plasma electrolytes [ Potassium (Y excretion) in AKI and advanced CKD
Plasma and urine osmolality A measure of renal concentrating ability in unexplained hyponatremia. If the plasma osmolality is low, the urine
Alkaline phosphatase and parathyroid
hormone
Antinuclear factor and ANCA Systemic lupus erythematosus and vasculitis may affect the kidney.
ADH, Antidiuretic hormone (vasopressin); AKI, acute kidney injury; ANCA, antineutrophil cytoplasmic antibody; CKD, chronic kidney
disease; (e)GFR, (estimated) glomerular filtration rate.
function accurately
Usually reported as ‘normal’ if 60 mL/min/1.73 m
CKD is classified on the basis of the eGFR (see Box 12.3)
Y Bicarbonate (Y H
Y Calcium (impaired renal vitamin D
[ Urate common in CKD (may be associated with gout)
osmolality should be lower still (<150 mosmol/kg); in the absence of hypovolaemia, any other finding is
consistent with syndrome of inappropriate ADH (vasopressin) secretion
In patients with unexplained polyuria, test the concentrating ability of the kidneys by an overnight fluid deprivation
test. In healthy people, urinary osmolality should rise to >600 mosmol/kg; any other finding suggests lack of
ADH or renal tubular unresponsiveness to ADH.
[ in secondary hyperparathyroidism related to Y calcium and [ phosphate levels
þ
excretion) common in AKI and CKD
activation) and [ phosphate (Y excretion) in CKD
3
2
12
12.8 Imaging for the investigation of renal and urological disease
Investigation Indication/comment
Ultrasound scan Assesses kidney size/shape/position; evidence of obstruction; renal cysts or solid lesions; stones;
Doppler ultrasound of renal vessels Assesses renovascular disease, renal vein thrombosis
Computed tomography of the kidney ureter
bladder (CT KUB)
CT urogram Frank haematuria; renal or bladder malignancy
Angiography/CT or magnetic resonance
angiography
Isotope scan Suspected renal scarring (e.g. reflux nephropathy) diagnosis of obstruction
Renal biopsy Used to diagnose parenchymal renal disease
ureteric urine flow; gross abnormality of bladder, postmicturition residual volume
Used to guide kidney biopsy
Arterial resistive index may indicate obstruction
Renal colic; renal, ureteric or bladder stones
Hypertension Æ renal failure, renal artery stenosis; angioplasty and/or stenting
Assessment of glomerular filtration rate (GFR) in each kidneydmeasures renal uptake and excretion of
radiolabelled chemicals
284 • THE RENAL SYSTEM
https://t.me/med1917
OSCE example 1: renal history
Ms Measham, 60 years old, is attending to discuss the results of her recent blood tests. She has presented with a 3-month history of tiredness, and you know
that her renal function was normal 1 year ago.
Investigations
Haemoglobin: 101 g/L (10.1 g/dL) (reference range: female
115–165 g/L (11.5–16.5 g/dL); male 130–180 g/L (13.0–18.0 g/dL))
White cell count: 8.9Â10
Platelet count: 510Â10
Potassium: 5.2 mmol/L (normal range: 3.5–5.0 mmol/L)
Urea: 14.5 mmol/L (40.6 mg/dL; normal range: 3.0–7.0 mmol/L
(8.4–19.6 mg/dL))
Creatinine: 163 mmol/L (1.84 mg/dL; normal range:
60–120 mmol/L (0.68–1.36 mg/dL))
Dipstick urinalysis: blood: 3þ, protein 3þ
Take a history from the patient
• Introduce yourself to the patient, and clean your hands.
• Obtain consent to take a history.
• Establish that the patient was well until 3 months ago and that the main symptoms are tiredness and breathlessness on exertion.
• Ask about:
• Weight loss, appetite and bowel motions
• Peripheral oedema
• Haemoptysis
• Urinary symptoms: dysuria, nocturia, urgency, hesitancy, incontinence, loin pain
• Back pain, fevers and rigors
• Confirm details of the past medical history.
• Document current medication and any relevant recent changes.
• Determine how symptoms are affecting the patient’s lifestyle: both work and leisure.
• Establish the family history.
• Thank the patient and clean your hands.
Summarise your findings
The patient has presented with 3 months of lethargy, and investigations reveal that he has anaemia in the context of renal impairment.
Suggest a differential diagnosis
The most likely diagnosis is an intrinsic renal disease, probably a glomerulonephritis, which may be part of a multisystem disorder. Infection is also possible.
Suggest additional investigations
Relevant further investigations might include erythrocyte sedimentation rate, C-reactive protein, vasculitis and myeloma screens, and iron stores. Renal
ultrasound, chest X-ray and midstream urine for microscopy and culture could be considered. The patient would benefit from a referral to a nephrologist. They
may require a renal biopsy.
9
/L (normal range: 4.0–11.0Â109/L)
9
/L (normal range: 150–400Â109/L)
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