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BASIC SYSTEMS
Renal and urology system
Sajeda Youssouf
17
Introduction
Many patients with renal disease have few or nonspecific symptoms, whereas disease within the
urinary tract usually does have symptoms, many
of which are reasonably specific for the disease
processes involved. As the kidney and urinary tract
are clearly and closely linked, this chapter combines
kidney and urinary tract problems in a coherent
whole.
The diagnostic process in nephrology and
urology
The clinical syndromes associated with kidney
disease are more dependent than most on laboratory,
histopathology and imaging techniques to complete
the diagnostic process, but the basic principles of
clinical assessment often lead towards an area of
diagnosis and investigation. An understanding of the
anatomy and physiology of the renal tract underpins
the definition of nephrological ‘syndromes’ caused
by groups of conditions with different types
of pathological processes. These allow clinical
investigation and assessment to be focused more
clearly. Structural lesions tend to present in a more
straightforward way with a constellation of symptoms
and signs enabling a differential diagnosis that can be
pursued in a more linear fashion. There is overlap
between presentations and syndromes, particularly
at different stages of a disease. This chapter describes
symptoms and signs associated with renal and
urological disease, as well as delineating some of the
syndromes
The history
The history in nephro- urological disease can
delineate specific structural abnormalities, intrinsic
or systemic conditions causing renal disease, or the
consequences of renal impairment, in particular salt
and water overload and metabolic abnormalities. In
addition, patients may be asymptomatic, with the
presence of disease identified on screening, such
as urinalysis or blood pressure monitoring. This
can provide a way of dividing kidney disease into
clinically meaningful syndromes, to aid diagnostic
investigation.
Pain
Pain, which can occur throughout the urinary tract
(Table 17.1), tends to be caused by infection, tumour
or obstruction. Unilateral loin pain can be caused
by pyelonephritis, renal stones causing obstruction,
urinary retention and bleeding cysts. Pyelonephritis
can be of abrupt or insidious onset, associated with
fever, vomiting, lower urinary tract symptoms
and urinary abnormalities. Laboratory analyses
frequently show elevated markers of inflammation.
Occasionally, pain may 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.
Renal stones cause pain in the presence of infection
if they cause obstruction to urine flow. In ureteric
tract obstruction, classically unilateral pain radiates
from loin to groin, and may radiate to the testes or
labia. A history of similar symptoms or family history
of renal stone disease can be useful.
Kidney tumours classically cause a triad of pain,
episodic macroscopic haematuria and a palpable
mass, although this is rarely seen in practice. Attention should be paid to other systemic symptoms
that may alert to the presence of metastases, such as
weight loss, respiratory symptoms from lung metastases and back pain from tumour in the spine.
Polycystic kidney disease causes a spectrum from
no symptoms at all, to recurrent or persistent loin
pain caused by cyst infection, haemorrhage or local
obstruction.
Bladder outflow obstruction (BOO) causes severe
suprapubic pain when acute, and is most frequently
owing to prostatic obstruction. BOO can also be
caused by bladder or pelvic masses and prolapse
in women. Acute urinary retention, which can also
cause suprapubic pain, can be caused by medications
and infection, and in post- operative patients.
Suprapubic and perineal pain most commonly
arises from lower urinary tract infection owing
to cystitis or urethritis. Such pain is frequently
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Renal and urology system
accompanied by dysuria, frequency or strangury
(painful micturition). It is nearly always associated
with urinary abnormalities on urine stick testing
(protein, blood and leukocytes). In men prostatitis
should be suspected in cases of severe perineal or
rectal discomfort. In young children with urinary
tract infection and cystitis the symptoms may be less
obvious; cystitis should be suspected in any child
who cries on micturating.
Bladder tumours infrequently cause pain; they are
more commonly associated with painless haematuria
and lower urinary tract symptoms.
Haematuria
Haematuria can be caused by bleeding anywhere
in the genito- urinary tract. If visible to the naked
eye it is termed macroscopic or visible haematuria;
Table 17.1 Site of pain in the renal tract and causes
Site Cause
Loin pain Renal stone causing obstruction
Tumour
Pyelonephritis; abscess
Infected or bleeding renal cyst
Suprapubic pain Acute bladder outflow obstruction
Urinary retention
Lower urinary tract infection (cystitis,
urethritis, pyocystis)
Bladder tumour
Strangury (painful
micturition)
Perineal pain Prostatitis
Urinary tract infection (UTI)
Cystitis
if seen only detectable using urine dipstick tests or
microscopy it is termed non- visible, microscopic
or dipstick haematuria. It can be continuous or
intermittent, and painless or associated with pain
and/or fever. Table 17.2 summarizes the causes of
haematuria. Blood arising from renal parenchymal
disease (glomerular bleeding) is usually, but not
always painless, continuous and microscopic, but it
can be macroscopic.. Haematuria from renal tumours
is more frequently intermittent, macroscopic and
associated with pain. Bleeding from bladder tumours
is often intermittent, with associated local symptoms
suggesting cystitis.
Infections in the urinary tract may also result in
haematuria; the presence of microscopic haematuria
should always be followed by urine microscopy
and culture as part of the diagnostic process. It is
important to decide whether haematuria originates
from the kidneys or elsewhere in the urinary
tract. This decision affects the order in which
investigations should be conducted. Over the age of
40, bleeding should generally be assumed to be nonglomerular in the first instance, unless there is other
compelling evidence for a glomerular lesion. Under
the age of 40, the presence of associated proteinuria
is likely to signify parenchymal renal disease, such as
a glomerulonephritis.
Transient painless haematuria in the absence of
any other urine abnormalities in women is most
likely owing to contamination from menstrual blood.
Other causes include exercise, intercourse and viral
illnesses. Systemic conditions and medications can
also cause haematuria; inquiry into a history of
bleeding elsewhere may alert to this.
Discoloured urine with positive urine on dipstick
can be owing to other causes. Myoglobin (released
from muscle owing, for example, to rhabdomyolysis
Table 17.2 Causes of haematuria
Systemic Glomerular Non- glomerular
Sickle cell trait
Coagulation disorders
Anticoagulant
medications
IgA
Thin basement membrane
nephropathy (TBMN)
Alport’s
Post- infectious
glomerulonephritis
Membranous
glomerulonephritis
Rapidly progressive
glomerulonephritis (RPGN)
Vasculitis (e.g. SBE, SLE)
Stones
Tumours (kidney/ureter/bladder/prostate)
Wilms’ tumour (children)
UTI/pyelonephritis
Trauma
Infarction (e.g. renal cortical necrosis, papillary necrosis)
Ureteric stricture/hydronephrosis
Prostatitis/cystitis/urethritis
Benign prostatic hypertrophy
Post catheterization
Rare infections (e.g. Schistosoma, bilharzia)
Drugs (cyclophosphamide/radiation)
Renal TB
Cystic disorders: polycystic kidney disease, medullary sponge kidney
Radiation cystitis
Vascular: AV malformations
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371
or trauma) and the presence of free haem both result
in positive urine dipstick for blood in the absence of
true blood in the urine. Various drugs and certain
foods can also result in discoloured urine.
Oliguria/anuria
Oliguria is defined as the passage of less than 500
ml of urine per day, whilst anuria is the complete
absence of urine flow. Progressive oliguria can be
physiological, owing to inadequate intake, fluid
loss such as in burns or blood loss, with preserved
glomerular filtration rate (GFR). Here kidney
function is not impaired; it is retaining sodium and
water, resulting in concentrated urine; restoring
adequate renal perfusion will restore normal urine
output. However, if inadequate intake or excess loss
leads to a significant reduction in the extracellular
fluid compartment, the resulting decrease in renal
blood flow leads to oliguria and a reduction in
GFR. Oliguria owing to reduced renal blood flow
is termed pre- renal; it can also occur in the context
of cardiogenic or septic shock. Intrinsic renal disease
causes loss of glomerular filtration in the absence
of reduced blood flow to the kidneys; note that not
all causes of intrinsic renal disease cause oliguria.
Mechanical obstruction to urine flow, such as caused
by stones, tumours or prostatic hypertrophy, is
termed post- renal oliguria. When the lesion is at the
level of the bladder, it may result in complete anuria.
Polyuria
Polyuria implies no more than a high urinary flow rate.
It is caused by excessive intake, an osmotic diuresis,
or renal tubular dysfunction (Table 17.3). Recovery
from acute kidney injury, particularly following
obstruction, can be accompanied by polyuria; the
concentrating ability of the renal tubules recovers
later than glomerular function. The description
of polyuria should always be accompanied by a
query about nocturia and polydipsia. The latter, in
particular, is a presentation of diabetes. Medications,
such as diuretics, can result in polyuria, whilst longterm lithium use is a common cause of nephrogenic
Table 17.3 Causes of polyuria
Cause Example
Excessive water
intake
Osmotic diuresis Glucose in diabetes mellitus
Renal tubular
dysfunction
Pathogenic polydipsia, beer drinking,
caffeine
Urea in chronic kidney disease (CKD)
Sodium chloride in diuretic use
Cranial diabetes insipidus
Nephrogenic diabetes insipidus
Recovery following acute kidney injury
(AKI)
diabetes insipidus. A broader past medical history
and systems inquiry assists in differentiating among
causes.
Frequency of micturition
Increased frequency of micturition results from
polyuria, a reduction in functional bladder capacity,
or bladder/urethral irritation (Table 17.4). The most
common cause is polyuria and excessive fluid intake,
but it is also a feature of urinary tract infection (UTI).
Incomplete bladder outlet obstruction, particularly
when it is chronic, can result in frequency without
accompanying polyuria. Some patients with
neurological disease, in particular multiple sclerosis,
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
The term nocturia implies the need to empty the
bladder during the hours of sleep. In the presence
of a normal urinary tract and normal renal function,
there is diurnal variation in the urinary flow rate:
at night time there is a reduction in urine flow, and
micturition is unnecessary. Polyuria can result in
nocturia, along with a reduction in functional bladder
capacity, which can happen with age. Polydipsia at
night and the use of diuretics later in the day are
also a cause. In chronic kidney disease, even in the
early stages, the concentrating ability of the kidneys
is reduced, and nocturia can be an early symptom
of renal impairment. Sickle cell disease results in
similar loss of concentrating ability.
Dysuria
Dysuria is 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 and decreased functional bladder
capacity. Infection or inflammation in the bladder
or urethra are the most common causes. Malignancy
in the lower urinary tract can also cause dysuria.
Table17.4 Causes of frequency of micturition
Polyuria All causes
Reduced functional bladder
capacity
Bladder/urethral irritation Lower urinary tract infection
Prostatic hypertrophy
Bladder outlet obstruction
Low capacity bladder
Multiple sclerosis
Post- stroke
Urethritis
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An extreme form of dysuria, strangury, implies an
unpleasant and painful desire to void when the
bladder is empty or near empty.
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. Urgency may lead to
urge incontinence. Stress incontinence is leakage
of urine associated with straining or coughing,
often owing to weakened pelvic floor muscles after
vaginal childbirth. Enuresis is defined as involuntary
micturition after the age at which bladder control
begins, and usually refers to nocturnal enuresis. It
can be primary, when in the vast majority of cases
is a developmental delay, or secondary (nocturnal
enuresis after a period of dryness). Occasionally, it
can be a presentation of urinary tract infection or
type 1 diabetes mellitus.
Slow stream, hesitancy and terminal
dribbling
The triad of slow stream, hesitancy and terminal drib-
bling is most frequently seen in older men with prostatic hypertrophy. Here, the bladder outlet is partially
obstructed by the enlarging prostate gland, and the
maximum achievable urinary flow rate is reduced.
There is often difficulty in initiating micturition (hesitancy) and in completing micturition (terminal dribbling). The symptoms are nearly always associated
with frequency of micturition and nocturia. There is
progressive bladder enlargement, with eventual overflow incontinence and continuous or intermittent
dribbling of urine.
Urethral discharge
Urethral discharge is usually noticed only 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 Chapter 18).
Past medical history
A history of urinary problems as a child may be
suggestive of structural abnormalities such as
posterior urethral valves. Previous urinary symptoms,
specifically a history of UTI or recurrent dysuria,
stones and prostate problems, should also be sought.
Episodic macroscopic haematuria during upper
respiratory tract infection is a classic presentation of
IgA nephropathy. Haemoptysis is a feature of rare,
but important, pulmonary renal syndromes, such as
antineutrophil cytoplasmic autoantibody-associated
vasculitis and antiglomerular basement membrane
disease. Upper respiratory tract symptoms, such as
epistaxis, may also be present. Systemic illnesses, in
particular hypertension, diabetes and cardiovascular
disease (ischaemic heart disease, stroke and
peripheral vascular disease), are a risk factor for
chronic kidney disease, which, particularly in the
early stages, can present with few or no symptoms,
and only be identified on screening.
Medication history
Many drugs can cause renal injury, or be nephrotoxic
in the context of kidney disease. Table 17.5 summa-
rizes some of the more common drugs of which to
be aware.
Social history
Smoking increases the risk of cardiovascular disease
and chronic kidney disease (CKD), and also the risk
of many cancers, including urothelial cancer. Also
enquire about risk factors for HIV and hepatitis B
and C. Drug use, including ketamine, cocaine and
cannabis, is important. Ketamine can cause ‘ketamine
bladder’, a syndrome characterized by pain, microscopic haematuria and reduced functional bladder
Table 17.5 Common medications that can cause
nephrotoxicity
Medication Effect
Diuretics Polyuria, nocturia
Pre- renal acute kidney injury (AKI)
Lithium Polyuria, polydipsia, nocturia,
chronic kidney disease (CKD)
Nonsteroidal antiinflammatory drugs
(NSAIDs)
PPIs (chronic use) Tubulo- interstitial nephritis
Angiotensin converting
enzyme (ACE)
inhibitors/ARB
Metformin Lactic acidosis at low glomerular
Spironolactone Risk of hyperkalaemia in
Antibiotics
(vancomycin,
gentamicin, penicillins)
Chemotherapeutic
agents
Immunosuppressive
agents (ciclosporin,
tacrolimus)
Antivirals Crystal formation
Renal papillary necrosis
Tubulo- interstitial nephritis
Haemodynamically mediated
injury
Can exacerbate pre- renal AKI
Hyperkalaemia
filtration rate (GFR)
advanced CKD
Acute tubular necrosis
Tubulointerstitial nephritis
Thrombotic microangiopathy
Thrombotic microangiopathy
Haemodynamically mediated
injury
Acute tubular necrosis
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capacity, whilst cocaine is associated with several patterns of renal injury. Occupation has been implicated
in urothelial cancer (painters, dry cleaners, diesel
fumes, metal- workers).
Family history
A family history of diabetes, hypertension, cardiovascular disease and CKD, including dialysis and transplantation, is important for assessing the risk of advanced
kidney disease and identifying potential causes of
CKD. Inherited kidney disease is relatively rare, the
most common being autosomal- dominant polycystic
kidney disease (ADPKD). Certain other rare genetic
disorders may also have renal involvement, for example cysts and tumours in the kidney in von HippelLindau syndrome.
Systems enquiry
Systems enquiry may point to a cause of kidney
disease, or the consequences of CKD. Table 17.6
summarizes systemic conditions associated with
CKD and associated signs on clinical examination.
Renal and urological syndromes
Renal and urological syndromes are listed in
Table 17.7. Some are exclusively renal, others
exclusively urological and some fall into both areas.
Whilst there can be overlap between syndromes,
they are a useful guide in delineating the level of a
lesion, and a focus for further investigation.
Acute kidney injury
Acute kidney injury (AKI) is the onset of declining
renal function occurring over a period of hours or
days, usually but not always accompanied by oliguria.
There is a rapid decline in the GFR, leading to electrolyte dysregulation, and nitrogen retention. The
outlook depends on the cause, which can be divided
into pre- renal, intrinsic and post- renal (Table 17.8).
The most common cause of intrinsic AKI is acute
tubular necrosis (ATN)—loss of renal tubular epithelial cells, usually as a result of pre- renal ischaemia or
nephrotoxins. A variety of classification systems for
AKI use measurement of serum creatinine and urine
output to stratify it into mild, moderate or severe.
These are used as a guide to predict risk of mortality
and outcome in hospitalized patients. It may reverse
spontaneously (repair of ischaemic injury in tubular
necrosis) or as a result of therapy (removal of stone
or other cause of obstruction). Severe AKI can manifest with uraemic symptoms (see below). These are
pre- terminal, but reversible with dialysis to remove
the excess uraemic toxins. Failure to recover GFR
partially or fully can result in progression to CKD.
Chronic kidney disease
Chronic kidney disease is defined by a persistent
(>3 months) disorder of kidney function or structure.
It can be caused by chronic renal ischaemia from
renal parenchymal disease, failure of acute kidney
injury to recover or unrelieved urinary obstruction.
The most widely used classification for CKD divides
it into stages based on GFR measurement and the
presence or absence of albuminuria (Fig. 17.1),
which, whilst imperfect, enables stratification of risk
of progression to end stage kidney disease (ESKD).
If renal impairment is severe, there may be clinical
manifestations of uraemia. These are usually evident
when the GFR has fallen to <20 ml/min (CKD 4 or
5), and are most severe once GFR is <10 ml/min.
Lethargy, poor concentration, irritability and failure
of higher mental functions and ability to handle tasks
are all commonly reported, as are nausea, anorexia
and vomiting. In advanced renal insufficiency, there
Table 17.6 Systemic conditions associated with kidney disease
System Association Clinical signs
Liver disease Hepatorenal syndrome with cirrhosis
Auto- immune/
inflammatory
Infection Gastroenteritis (pre- renal acute kidney injury [AKI])
Malignancy Secondary membranous nephropathy with malignancy
Haematological Sickle nephropathy in sickle cell disease Sickle pain, polyuria
Glomerulonephritis with hepatitis B or C
Systemic lupus erythematosus (SLE) and other connective
tissue disorders can cause glomerulonephritis or vasculitis
Sarcoidosis causes an interstitial nephritis
TB (granulomatous interstitial nephritis)
HIV (HIV- associated kidney disease)
Endocarditis (vasculitis)
Lymphoma
Myeloma (cast nephropathy)
Jaundice, abdominal swelling (ascites),
gastrointestinal (GI) bleeding (portal
hypertension)
Rash, joint pain or swelling, myalgia, mouth
ulcers, Raynaud’s, eye symptoms, dry eyes
or mouth
Fever, sweats, weight loss, GI symptoms,
shortness of breath
Weight loss, localizing symptoms, back pain,
fractures (lytic lesions, bone metastases)
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Table 17.7 Renal and urological syndromes
Renal Renal and urological Urological
Chronic kidney disease
Acute nephritic syndrome
Nephrotic syndrome
Acute kidney injury
Asymptomatic urinary abnormality
Recurrent visible haematuria
Renal hypertension
Tubular syndromes
Table 17.8 Causes of acute kidney injury (AKI)
Pre- renal Renal Post- renal
Reduced renal blood flow
- hypovolaemia (e.g. blood loss, inadequate
intake, fluid losses from burns)
Effective decreased blood flow:
- cardiac failure, vasodilation in sepsis
- intrarenal vasomotor changes (drugs, such as
Acute tubular necrosis from any cause of renal
ischaemia or nephrotoxic injury
Vascular—vasculitis, thrombotic
microangiopathy, hypertensive emergency
Acute glomerulonephritis
Acute tubule- interstitial nephritis
nonsteroidal anti- inflammatory drugs [NSAIDs])
Urinary tract infection
Urinary tract obstruction
Renal and urinary tract stone
Obstruction (tumour, stone,
retroperitoneal fibrosis)
Bladder outflow obstruction
Bilateral ureteric obstruction
Prognosis of CKD by GFR
and Albuminuria Categories
Normal or high
G1
)
2
Description and range
GFR categories (ml/min/1.73 m
G2
G3a
G3b
G4
G5
Mildly
decreased
Mildly to
moderately
decreased
Moderately to
severely
decreased
Severely
decreased
Kidney failure
≥90
60–90
45–59
30–44
15–29
<15
A1
Normal to
mildly increased
<30 mg/g
<3 mg/mmol
Albuminuria categories
Description and range
A2
Moderately
increased
30–299 mg/g
3–29 mg/mmol
A3
Severely
increased
≥300 mg/g
≥30 mg/mmol
Green: low risk (if no other markers of kidney disease, no CKD); Ye llow: moderately increased risk; Orange: high risk;
Red, very high risk.
KDIGO 2012
Figure 17.1 Classification of chronic kidney disease. (Source: Kidney disease: Improving Global Outcomes (KDIGO) working group 2012.
Available at: https://kdigo.org/guidelines/)
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may be confusion, fits and stupor. The presence of
these symptoms indicates the need for dialysis to
remove uraemic toxins, or transplantation to restore
GFR. Even in the absence of uraemic symptoms, renal
replacement therapy (dialysis or transplantation)
may be indicated once GFR falls to <15ml/min.
The nephritic syndrome
The nephritic syndrome is historically described as
the constellation of oliguria, microscopic haematuria
and hypertension, and is usually accompanied by mild
proteinuria and impaired renal function. It usually has
a fairly brisk onset (days, weeks or months). It is caused
by injury to the glomerulus, which can be insidious
or acute. Many of the causes of acute nephritis are
associated with functional abnormalities of the
immune system that may be detected by laboratory
tests and which may also manifest with disease in
other organs, for example the skin, joints or eyes, as
in SLE, Henoch- Schönlein purpura (Fig. 17.2) and
systemic vasculitis, post- infectious glomerulonephritis
(GN), anti- GBM disease and membranoproliferative
glomerulonephritis (MPGN).
The nephrotic syndrome
Nephrotic syndrome is defined as the presence
of heavy proteinuria (usually >3 g/day, compared
with normal of <150 mg/day), hypoalbuminaemia,
hypercholesterolaemia and oedema. It is unusual for
nephrotic syndrome to occur when the proteinuria
is <2 g/day; conversely, some patients are able to
maintain a normal or near- normal serum albumin
concentration despite very heavy proteinuria in
excess of 6 g/day.
Proteinuria of this magnitude implies glomerular
pathology and may coexist with a significant
reduction in GFR. Thus, a number of the pathological
entities capable of causing nephrotic syndrome may
also present as acute nephritic syndrome, acute
kidney injury or the syndrome of CKD.
Asymptomatic urinary abnormality
Asymptomatic urinary abnormality usually presents
as part of a routine medical examination, often in the
context of an employment or life insurance health
check or at a screening visit to primary care. Urine
testing leads to the finding of proteinuria, haematuria
or pyuria in an otherwise healthy patient. Further
assessment may reveal the coexistence of other
renal syndromes. This syndrome may reflect disease
of the kidneys, or be a manifestation of malignancy
anywhere in the urinary tract, infection or stone.
An asymptomatic urinary abnormality can be the
first sign of one of the other syndromes (nephritic,
tubular, renal stones, malignancy) or can alert to
renal disease in and of itself. Table 17.9 summarizes
abnormalities seen. They should alert the clinician
to take a more complete history, perform a clinical
examination and check, as a minimum, blood pressure
and renal function, with a view to further investigation.
Recurrent visible haematuria
Recurrent visible haematuria implies intermittent or
in some cases continuous bleeding into the urinary
tract. The source of the bleeding may be anywhere in
the urinary tract, from the glomeruli to the urethra.
Urinary tract infection
Figure 17.2
Purpura in Henoch–Schönlein disease.
Infection in the urinary tract leads to a range of
symptoms and signs that reflect the location and
severity of the infection. By far the most frequent
site is the bladder, and local symptoms reflect bladder
irritation. The presence of urinary tract infection
is defined by the presence of a significant number
of infecting organisms in the urine. A working
definition of a proven urine infection would be the
detection of more than 105 colony- forming units/
millilitre urine in a mid- stream specimen of urine
(MSU). In some infections, for example tuberculosis
of the urinary tract, the number of organisms being
excreted may be extremely low, and identification
on the basis of urine culture is difficult. Sterile pyuria
can be caused by a treated infection, parasites such
as schistosomiasis, tuberculosis (TB), bladder stones,
inflammation or a tumour.
Urinary tract obstruction
Urinary tract obstruction may be divided into
lower and upper tract obstruction. Lower urinary
tract obstruction is defined by residual urine in the
bladder after micturition or an inability to empty
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Table 17.9 Asymptomatic urinary abnormalities
Protein Blood Glucose Leucocytes Causes
± +++ - - Nephritic syndrome, glomerulonephritis (GN), systemic
lupus erythematosus (SLE), endocarditis, pulmonary
renal syndromes, IgA nephropathy, renal stones
± ± - +++ Urinary tract infection (UTI)
+++ ± - - Nephrotic syndrome, DM, FSGS, amyloidosis, myeloma
± - + - Diabetes (with or without nephropathy)
Rare tubular defects, pregnancy
the bladder at all. The most common causes relate
to prostatic hypertrophy (benign hyperplasia
or carcinoma), and signs include frequency,
nocturia, poor stream, hesitancy and terminal
dribbling.
The presence of an upper urinary tract obstruction
is established in most cases by the demonstration
of a dilated renal collecting system (renal pelvis
and/or calyces), often seen to be proximal to a
specific obstructing lesion. These features may
be demonstrated by ultrasound and intravenous
urography (IVU) as well as computerized
tomography (CT) scanning. Upper and lower urinary
tract obstruction may coexist, most frequently when
the lower urinary tract obstruction is severe and/or
long standing, and leading to progressive dilatation
of the upper urinary tract with consequent renal
parenchymal damage and loss of GFR. Unilateral
renal obstruction should not result in a rise in
the serum creatinine; if the creatinine is elevated,
there is also dysfunction of the contralateral
kidney.
An infected and obstructed urinary system is
considered an emergency and is potentially lifethreatening.
Renal and urinary tract stones
The operational definition of renal and urinary tract
stones is largely observational, depending on the
demonstration of stones in any part of the urinary
tract. Resulting symptoms and signs depend on the
location of the stone(s) and on their size. Small
stones in the kidneys are frequently asymptomatic
or lead to subtle urinary abnormalities, presenting
initially with asymptomatic urinary abnormality.
Larger stones in the kidneys can lead to renal pain;
and stones in the ureter are particularly likely to
cause acute obstruction and severe ureteric and
renal pain. Remember that the pain of renal colic
is one of the worst that a patient may experience.
Bladder stones are usually associated with symptoms
suggestive of cystitis, with frequency, haematuria
and pain all common, and often associated with
urinary tract infection.
Renal hypertension
The most common cause of sustained blood pressure
elevation is essential hypertension. However,
hypertension can be a cause and a consequence of
renal disease. A minority of patients with raised
blood pressure will have an underlying renal (or
other) cause. Hypertension may be one of the
presenting features of virtually any disease of the
renal parenchyma, including GN, many forms of
tubulo- interstitial disease, renal vascular disease, renal
stone disease and obstruction. Thus, in any patient
with newly identified hypertension, the possibility
of underlying renal disease should be considered.
Conversely, the exclusion of renal disease as a
cause of hypertension is generally straightforward,
composed of the absence of symptoms and signs of
renal disease, the absence of urinary abnormalities
on simple stick testing and the presence of a normal
GFR and renal electrolytes.
Renal tubular syndromes
Most patients with parenchymal renal disease
or obstructive renal damage manifest disordered
tubular function. Much less common is the
patient in whom the tubular defect dominates the
clinical picture. These defects may be inherited or
acquired. They usually require careful laboratory
testing to characterize them fully. Proximal tubular
abnormalities include renal phosphate wasting,
aminoaciduria (of these, cystinuria with cystine
stone formation is the most important) and renal
tubular acidosis leading to chronic metabolic
acidosis. Distal tubular defects are also associated
with metabolic acidosis and with disturbances of
potassium metabolism, sodium- losing nephropathy
and nephrogenic diabetes insipidus, with resulting
failure, respectively, of salt and water conservation.
Physical signs in renal and urological
disease
These physical signs fall into four groups:
1. Local signs related to the specific pathology, such
as an enlarged palpable tender kidney in renal
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377
carcinoma or a palpably enlarged bladder in a
patient with acute or chronic retention
2. Symptoms of disturbance of renal salt and
water handling, with resulting clinical evidence
of extracellular fluid volume expansion or
contraction
3. Signs of failure of the kidney’s normal excretory
and metabolic functions
4. Signs caused by a systemic or underlying
condition
In many renal patients, particularly those with
advanced CDK and uraemia, signs from all of the
above categories may be present. The effects of renal
failure on other organ systems are summarized in
Box 17.1.
General features
Patients with chronic renal failure (loss of the
kidney’s normal excretory and metabolic functions)
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
owing to uraemic pruritus, and also an underlying
disorder of platelet function and capillary fragility.
The nails can appear pale and opaque (leukonychia)
in the nephrotic syndrome and 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 (see Fig. 17.2).
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. It is rare and only usually seen in patients
who have not been cared for and therefore not
washed, as it may take days to develop. The onset of
chronic renal failure in childhood is associated with
impaired growth, causing short stature. Severe bony
deformity (Fig. 17.3) may be evident in some cases,
particularly in children, who may develop rickets.
Advanced uraemia is also associated with metabolic
flap, a coarse tremor which is best seen at the wrists
when in the dorsiflexed position. The presence of
metabolic acidosis leads to increased ventilation
with an increased tidal volume, known as Kussmaul
respiration.
Box 17.1
Disturbances of water and electrolyte balance
Breathlessness caused by salt and water overload
Deep sighing breathing (Kussmaul respiration) owing to
acidosis
Weakness and postural fainting due to hypotension
caused by salt and water depletion
Lethargy and weakness from hypokalaemia
Disturbances of the haematological system
Lethargy and breathlessness associated with anaemia
owing to impaired production of erythropoietin by the
kidneys
Defective coagulation and excessive bruising (advanced
renal failure)
Haemorrhage from the gastrointestinal tract or lungs
Disturbances of the cardiovascular system
Cardiac failure or angina associated with fluid overload,
hypertension, anaemia and impaired ventricular function
(uraemic cardiomyopathy)
Precordial chest pain owing to pericarditis
Cardiac arrhythmias associated with left ventricular
hypertrophy and hyperkalaemia/hypokalaemia
Disturbances of the gastrointestinal system
Nausea and vomiting, especially in the morning, owing to
uraemia
Anorexia
Disturbances of the respiratory system
Breathlessness and haemoptysis from fluid overload
Chest pain owing to pleurisy
Disturbances of the musculoskeletal system
Muscular weakness and bone pain owing to impairment
of vitamin D activation and to excessive parathyroid
gland activity
Acute pain caused by gout
Muscle wasting
Disturbances of the nervous system
Hypertensive stroke and encephalopathy
Clouding of consciousness, fits and coma in advanced
renal failure
Impaired sensation or paraesthesia in the feet, caused by
peripheral neuropathy in long- standing uraemia
Impaired higher mental/intellectual function
Entrapment neuropathies
Disturbances of the eyes
Pain from conjunctivitis caused by local deposits of
calcium
Visual blurring from hypertensive retinal damage or
retinal vascular disease
Effects of renal failure on other organ systems
The circulation in the renal patient
Correct assessment of the patient’s fluid volume
status is crucial. It is important to define whether
the patient is euvolaemic, hypovolaemic or
hypervolaemic. Objective assessment of volume
status is made by assessing lying and standing
blood pressure, jugular venous pressure and pulse
pressure. Subjective signs include skin turgor,
mucous membranes and ‘sunken eyes’. Patients
who are hypervolaemic may be hypertensive, with
evidence of excess extracellular fluid (oedema,
ascites, basal crackles on lung auscultation). Oedema
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Renal and urology system
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.
In patients with nephrotic syndrome (see below),
oedema and salt and water retention are caused
by reduced plasma oncotic pressure. The presence
of oedema can coexist with intravascular volume
depletion, especially in patients with nephrotic
syndrome.
Abdominal palpation
The detection of the kidneys in the abdominal
examination is described in Chapter 14. 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. Bimanual
palpation of the bladder with rectal examination 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 an absence of the
central groove.
merges with the sclera. Retinal changes can be seen
in patients with diabetes or hypertension. Diabetic
nephropathy in type 1 diabetes is extremely rare in
the absence of diabetic retinopathy. 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 CKD
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.
Laboratory assessment and imaging of the
kidneys and urinary tract
The most important laboratory assessment in renal
and urological disease is analysis of the urine, and
measurement of renal GFR and electrolytes. Because
of the kidneys’ importance in other systems, including
production of erythropoietin and regulation of bone
metabolism, additional tests are frequently necessary
if there is evidence of renal insufficiency.
The urine
Urine should be tested as part of every general
medical examination and not just in patients with
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 extra- renal 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 long- standing hyperparathyroidism
with elevation of blood calcium and phosphorus
concentrations (see Chapter 19), seen medially
and laterally or circumferentially. 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 superior and inferior cornea and
Figure 17.3 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.
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