Case 2 A 74-year-old man with acute
renal failure
Mr James Jones is a 74-year-old man who is referred
urgently by h is GP who saw him this morning and did some
blood tests. The results of these tests have been called
through to the GP surgery and show:
Na 145 mmol/L, K 6.9 mmol/L, Urea 29.3 mmol/L, Creat inine
686 mol/L
The GP letter tells you that Mr Jones has had benign
prostatic hypertrophy previously but is otherwise usually very
fit and uncomplaining. He attended the surgery because
he’d been feeling lethargic and under the weather for the
past week. Given the blood results, Mr Jones is called by his
GP and asked to urgently attend the Medical Admissions
Unit. He arrives at 5pm, and his initial observations are
unremarkable.
What is your first concern on being
asked by the nursing staff to see him?
The morning bloods done at the GP surgery show
sig- nificant hyperkalaemia. This may be spurious,
due to haemolysis of a sample in which there has
been delay in processing (potassium is found
predominantly within cells, therefore when red
blood cells haemolyse, their potassium load is
released into the blood). Box 2.1 shows the causes of
pseudohyperkalaemia.
However, this degree of hyperkalaemia could be
life- threatening, so it should be considered a genuine
result until proven otherwise, particularly given the
severity of renal impairment present on his blood
results. Hyperka- laemia can occur in both acute and
chronic renal failure and should be treated as a
matter of urgency because it can lead to serious
cardiac arrhythmias and even cardiac arrest.
Therefore your main concern is: does he have ECG
changes associated with hyperkalaemia? If he does
have hyperkalaemia, he is at risk of having an
arrhythmia and of cardiac arrest.
Nephrology: Clinical Cases Uncovered. By M.
In view of the risk of cardiac
arrhythmias associated with
hyperkalaemia, what immediate
measures would you undertake?
• Establish intravenous access.
• Move the patient to a monitored bed so that
any cardiac arrhythmia will be immediately
detected.
• Perform an urgent repeat potassium. This is
often most quickly achieved by running a venous
PART 2: CASES
sample through the arterial blood gas machine (most
emergency departments have one).
• Perform a 12-lead ECG looking for signs of
hyperka- laemia (Box 2.2).
• If the ECG has significant hyperkalaemia-
associated changes, then treat the hyperkalaemia
before waiting for the result of the urgent potassium
measurement.
The patient’s ECG is shown in Figure 2.1.
What does it show and what treatment
would you give after viewing it?
The ECG shows broadening of the QRS and early
‘sine’ waves consistent with hyperkalaemia. Mr Jones
is at risk of developing a cardiac arrest. He should be
given 10 mL 10% calcium gluconate as soon as
possible in order to protect the heart from the
development of arrhythmias. He should then be
commenced on an insulin-dextrose infusion
(preferably through a 18 G+ needle inserted into a
large vein; 50% dextrose can be irritant to veins, so
it is best to avoid putting into small veins).
Why does insulin-dextrose
lower serum potassium?
If 50 mL of 50% dextrose is administered
intravenously to a young person with functioning
islets of Langerhans, they will rapidly secrete
significant quantities of insulin from their  cells. The
dextrose infusion is usually given
with 10 units of a short-acting insulin, e.g. Actrapid, in
Clatworthy. Published 2010 by Blackwell Publishing.
case of underlying islet caemia. Insulin stimulates the uptake of potassium
dysfunction, to prevent hypergly- from

37
 Case 2 38

the blood into cells via cell surface sodium-
potassium pumps. Thus both the exogenous and
endogenous insulin will cause a temporary
redistribution of potas- sium. Patients may need
repeated treatments if the underlying cause of the
hyperkalaemia is not dealt with. It should be
emphasised that insulin-dextrose is only a holding
measure because the total body potassium does not
fall following its administration, it is merely
redistributed.
Box 2.1 Causes of pseudohyperkalaemia
Prolonged tourniquet time
Test tube haemolysis due to delayed processing of the
sample
Marked leucocytosis and thrombocytosis: measure plasma
(liquid component of unclotted blood)
PART 2: CASES
In Mr Jones’ case, the cause of hyperkalaemia
is likely to be renal failure given his elevated urea
and creatinine.
What other causes of hyperkalaemia
do you know?
The causes of hyperkalaemia are summarised in Box
2.3. As mentioned above, 95% of the body’s
potassium is found within cells. Thus, if there is
massive cell lysis (as seen in rhabdomyloysis when
muscle is damaged or in tumour lysis syndrome when
cancer cells are lysed fol- lowing the administration of
chemotherapeutic agents), potassium will be
released into the blood. K+ can also exit cells in
exchange for H+ if there is acidosis, in an attempt
to buffer the elevated H+ ions in blood. K+
excretion occurs in the kidney and acidosis will lead
to a reduced renal excretion of K+ as H+ is

not serum (liquid component of clotted blood) concentration preferentially excreted instead.
in these disease states
Renal failure can cause hyperkalaemia because a
Sample taken from a limb infused with IV fluids containing
reduction in GFR will lead to a reduced delivery of
potassium
Na+ to the distal nephron. This results in reduced
Na+ resorp- tion and therefore a lower K+ excretion
by the distal convoluted tubule Na/K-ATPase (see
Box 2.2 ECG changes associated with hyperkalaemia Part 1, Figure D). An isolated reduction in function
of the Na/K-ATPase pump can also lead to
Tenting of T waves hyperkalaemia, e.g., as seen in Addisons disease,
Prolonged P-R interval
where there is aldosterone deficiency, or following the
Widening of QRS complex
use of drugs which indirectly block aldo- sterone
‘Sine’ waves
production by inhibiting the synthesis or action of
angiotensin II, e.g. ACEI or ARB.
In practice, hyperkalaemia is often caused by a
combi- nation of factors, e.g. renal failure plus an
ACEI.

I aV V1 V4
R

II aV V2 V5
L

II aV V3 V6
I F

II

Figure 2.1 An ECG with tented T waves and wide QRS complexes (3 small squares, i.e. 0.12 seconds).
Box 2.3 Causes of hyperkalaemia What questions would you ask?
Mr Jones’ bloods show significant renal
Movement of K+ out of cells
impairment. The history, examination and
Acidosis: H+ transported into cells at the expense of K+ efflux
investigations should aim to answer three main
Cell death causes release of K+, e.g. rhabdomyolysis, tumour
questions.
lysis syndrome
• Is this acute or chronic renal failure?
Failure of K+ excretion by kidney (distal convoluted tubules)
Renal failure • Why does he have renal failure? A pre-renal
Aldosterone deficiency (hypoten- sion/hypovolaemia), renal or post-renal
Potassium-sparing diuretics, e.g. spironolactone (obstruction) cause?
ACEI, ARB • Does he have any symptoms as a result of his
Excess intake of K+ from gut renal impairment?

Is this acute or chronic renal failure, or perhaps

Box 2.4 Treatment of hyperkalaemia
acute-on-chronic renal failure?
This is important to establish because many cases
of acute renal failure are reversible, if the
precipitating/ aetiological factors are rapidly
remedied. If the patient has no past medical history
of renal disease or of diseases which commonly cause

PART 2: CASES
10 mL 10% calcium gluconate (cardioprotectant)
chronic kidney disease (e.g. dia- betes mellitus,
intravenously
50 mL 50% dextrose + 10 u Actrapid hypertension, prostatic disease), then an acute
Consider salbutamol nebulisers if IV access difficult pathology is more likely. Unfortunately, symptoms
In chronic hyperkalaemia, give advice on low-potassium diet such as lethary or vomiting can be associated with
and consider calcium resonium to prevent GI absorption both acute and chronic renal impairment. If a patient
Stop any drugs associated with hyperkalaemia, e.g. ACEI, gives a short history of rapid-onset oligoanuria over a
ARB, postassium-sparing diuretics such as spironolactone or period of days, then an acute cause is more likely.
amiloride Ultimately, the only definitive demonstration of the
acute nature of renal failure is the availability of
previous blood test results showing a recent
normal creatinine. Chronic kidney disease also
tends to be associated with small kidneys on US
scan.
you are able to get some more history from the patient.
In the unlikely scenario that IV access
cannot be immediately established,
what alternative therapy could you use
to bring down his potassium?
Salbutamol acts on 2-adrenoreceptors and has the
same effect as insulin, in that it stimulates potassium
uptake by cells. However, it is only effective if used
at relatively high doses, e.g. 2  5 mg salbutamol
nebulisers given almost back to back. Patients
tend to become rather tremulous and tachycardic
and tolerate such high doses poorly.
The treatment of hyperkalaemia is shown in Box
2.4.

Mr Jones’ venous blood gas sample showed a potassium of

7.7 mmol/L. Following the calcium gluconate and insulin-
dextrose, a repeat measurement shows that his K+ is now
5.9 mmol/L. His ECG changes have resolved. Now that you
have tackled the immediate urgent issue of his potassium,
Why does he have renal failure?
The GP letter stated that he had a
previous history of prostatic disease so a
post-renal cause, i.e. obstructive uropathy,
is high on the list of possible causes of his
renal impairment. Overall, obstruction is the
underlying cause in around 5–10% of
patients with ARF. In elderly males, up to
30% of cases of ARF may be due to
urethral obstruction. It is therefore
important to ask about urinary symptoms
such as frequency, nocturia, terminal drib-
bling, hesitancy or poor stream. ‘Can you
still hit the wall in a public toilet?’ is a
useful question to assess urinary stream.
• Pre-renal cause? Has he had any recent
illnesses which might cause volume
depletion or hypotension, e.g. vomiting,
diarrhoea?
• Renal cause? Is there a history of recent
pharyngitis or infection which might
precipitate a postinfectious GN? Does he
have any symptoms suggestive of a systemic
inflammatory/autoimmune disease? A past
medical
 history of MI/CVA/PVD increases the probability of
atherosclerotic renovascular disease.
• Family history. There are a number of inherited
causes of CKD, for example autosomal dominant
polycystic kidney disease, Alport’s syndrome and
familial FSGS, although these are less likely to present
for the first time in a patient of this age.
• Drug history. Some medications can be
associated with CKD including NSAID, ciclosporin,
lithium; others can cause ARF due to interstitial
nephritis, e.g. PPI and antibiotics.
• Smoking history. Smoker? (associated with atheroscle-
rosis and therefore renovascular disease) Alcohol?
(chronic liver disease and liver failure can be
associated with renal impairment).
Does he have any symptoms associated with
the complications of renal failure?
PART 2: CASES
• Symptomatic uraemia: nausea, loss of appetite,
symp- toms associated with uraemic pericarditis
(sharp chest pain, worse on lying down,
breathlessness) or uraemic encephalopathy
(confusion, drowsiness, fitting).
• Acidosis: patients may hyperventilate in an attempt
to blow off CO2 and compensate for their metabolic
acidosis.
• Volume overload: ankle swelling, pulmonary oedema
causing shortness of breath.
• Anaemia: can be associated with shortness of
breath, angina and tiredness.
• Hyperphosphataemia: secondary to hyperparathyroid-
ism can cause very troublesome itchiness.
What features of the examination
might indicate that Mr Jones needs
urgent dialysis?
Dialysis provides a means by which water, K+, urea
and H+ can be removed. Whether renal failure is
acute or chronic, there are certain features which
suggest that urgent dialysis is likely to be
required.
• Pulmonary oedema: as evidenced by hypoxia,
elevated respiratory rate and bibasal coarse inspiratory
crackles in the chest.
• Severe acidosis: the kidneys are responsible for
the excretion of acid. Therefore, in renal failure
there is a metabolic acidosis. In an attempt to
reduce the H+ ions in the blood, there will be
respiratory compensation, i.e. the patient will
hyperventilate to blow off CO2 (which is an acidic
gas; Box 2.5) and may have a respiratory rate of 30–
40 rpm.
Box 2.5 The Henderson – Hasselbach equation
demonstrates why CO2 is an acidic gas
CO2  H2O  H2O2  H  HCO
3

• Symptomatic uraemia: evidenced by pericarditis
(char- acterised by a pericardial rub, which classically
sounds like feet crunching in the snow, coinciding
with each systole). Uraemia can also cause
encephalopathy which may cause the patient to be
confused (assess this with a mini mental test) or
have asterixis (flap).
• In addition, hyperkalaemia refractory to medical
treatment should also be treated with dialysis.
On examination, Mr Jones is clinically euvolaemic with a
pulse of 90 bpm and a BP of 160/90 mmHg. On auscultation
of his chest, there is no pericard ial rub but he does have
bibasal crackles posteriorly. On examination of his abdomen,
his bladder is palpable at 2 cm below the umbilicus. A rectal
examination reveals a smooth, significantly enlarged
prostate. He has mild peripheral oedema in his ankles.
His admission blood tests show:
Na 145 mmol/L, K 7.7 mmol/L, Urea 34 mmol/L, Creatinine
729 mol/L, CRP 8 mg/L
Hb 12.7 g/dL, WBC 6.5  109/L, Platelets 438  109/L.
He has an ultrasound scan
performed urgently (Figure
2.2). What does this show?
The ultrasound scan shows a kidney of normal size
(10– 12 cm) with some preservation of
corticomedullary dif- ferentiation but gross
hydronephrosis (Figure 2.2a) and a full bladder post
attempted micturition (Figure 2.2b). The other kidney
is also hydronephrotic on US, and both ureters are
dilated. This is suggestive of distal obstruction (i.e. at
the level of the urethra or beyond). Other causes of
obstruction with their typical US patterns are shown
in Figure 2.3.
What would you do next
for Mr Jones?
Mr Jones has an ultrasound scan which suggests that
the most likely cause of ARF is urethral outflow
obstruction. Therefore a urinary catheter should be
inserted. Given his history of prostatic disease, this
may not be easy and may require urology input
(Figure 2.4). If a catheter cannot be placed per-
urethrally due to the size of the
(a)
Figure 2.2 Ultrasound scan of the renal tract showing (a) pelvicaliceal dilatation of the kidney (dark space centrally in the kidney) and
(b) a full bladder.
prostate, then a suprapubic catheter is placed directly
into the bladder through the skin.
He will also need repeated U+E measurements to
ensure resolution of hyperkalaemia with treatment.
What is the main problem which
can develop following resolution
of obstruction by insertion of
a urinary catheter?
Following treatment of urinary obstruction by
insertion of a catheter, patients frequently become
polyuric due to temporary tubular dysfunction.
In the 8 hours following catheterisation, Mr
Jones passes 6 litres of urine and unless he is
placed on an adequate fluid replacement regimen, he
will be at risk of developing pre-renal failure due to
intravascular volume depletion. Thus his fluid
balance should be carefully monitored and he is
likely to require intravenous fluids in addition to
encouraging increased oral intake.
With the diuresis post catheterisation and adequate fluid
replacement, Mr Jones’ renal function tests improved
rapidly over the next 48 hours. His creatinine plateaus
at 150 mol/L. He is reviewed by the urologists and
commenced on tamsulosin (a selective 1a-blocker used in
the treatment of BPH). His PSA level is unchanged from the
last measurement a year previously. He undergoes a
successful trial without catheter in the community
2 weeks later.
Two years later Mr Jones is readmitted when he notices
a reduction in his urine output and the development of
(b)
PART 2: CASES
similar symptoms of lethargy and nausea. His blood tests
show Na 135 mmol/L, K 5.8 mmol/L, Urea 36 mmol/L,
Creatinine 460 mol/L. He is clinically euvolaemic and his
bladder is not palpable but he does have inguinal
lymphadenopathy. His ultrasound does not demonstrate
significant hydronephrosis.
What is the most likely cause
of his renal failure?
Obstruction is still the most likely cause of his
renal failure, given his previous history. Patients with
advanced pelvic malignancy may develop functional
obstruction in the absence of hydronephrosis because
the urinary tract becomes encased in an
inflammatory infiltrate or with metastases, thus
preventing the development of hydro- nephrosis.
Functional obstruction can be demonstrated using a
nuclear medicine scan such as a MAG3 showing
delayed tracer excretion to the bladder or
encasement of the ureters or other retroperitoneal
disease can be visualised on a CT scan.
A MAG3 scan shows obstruction.
How should he be treated?
Mr Jones should be treated by insertion of
percutaneous nephrostomies. This may lead to a
similar polyuric period and thus his fluid balance
should be carefully monitored. A nephrostomy will
temporarily relieve obstruction but a long-term
solution is achieved through the insertion of stents
into the ureters, either in an anterograde fashion
via the nephrostomy or in a retro- grade manner
via cystoscopy.
 Causes within the lumen:
• calculus
• blood clot
• tumour (bladder, ureter, renal pelvis)

Causes within the wall:

• pinhole urethral meatus
• urethral stricture
• neurogenic bladder
• ureteric stricture
• pelviureteric neuromuscular dysfunction

Ureters
Causes outside the wall:
• pelvic tumours, e.g. cervical Ca2+
PART 2: CASES

Bladder • prostatic enlargement

• Crohn’s diseases
Prostate • retroperitoneal fibrosis
• aortic aneurysms
Urethra • abdominal malignancy
e.g. colonic Ca2+ or
(a) Normal
lymphoma

(b) Obstruction at or below the

(c) Obstruction at the level of (d) Obstruction at the level of
level of the urethra
the bladder or lower ureter the upper ureter

Figure 2.3 Causes of obstruction (which occur at different sites in the upper and lower urinary tract) and patterns of dilation observed
depending on the level of obstruction (b–d).
 Insert water to
inflate balloon

Urine
flow

Catheter tip

(a)

PART 2: CASES
Insert water to Irrigation
inflate balloon fluid
Urine
(b) flow

Figure 2.4 Urinary catheter insertion. (a) 14 ch urinary catheter.

(b) 18 ch three-way (irrigation) catheter. (c) Catheter tips with
balloon inflated in a three-way (irrigation) catheter (left) and a
standard catheter (right). The balloon is inflated following the
introduction of the catheter into the bladder and prevents it from
falling out. (c)

CASE REVIEW

A 74-year-old man with a history of benign prostatic

improves. He is started on an -blocker (tamsulosin)
hypertrophy is admitted with acute renal failure.
and the catheter is successfully removed a week or so
Admission blood tests show significant
later. Two years later, he again presents with ARF. US
hyperkalaemia, with ECG changes. This is treated
shows no hydronephrosis but a MAG3 demonstrates
with calcium gluconate and an insulin-dextrose
functional obstruction. He is therefore treated by
infusion. A renal US shows hydronephrosis and a full
nephrostomy placement.
bladder post micturition. He is catheterised and has an
excellent diuresis and his renal function rapidly
 KEY POINTS

• Acute renal failure can be complicated by

• Obstruction causes around 5–10% of all ARF and is
hyperkalaemia. This is a medical emergency because it
usually due to prostatic disease. It is usually visible on
can cause significant cardiac arrhythmias and even
an US of the renal tract as hydronephrosis. Obstruction
cardiac arrest.
should be treated as quickly as possible to prevent
• The signs of hyperkalaemia seen on ECG are tenting long-term damage to the kidneys. In most cases,
of T waves, prolongation of the QRS complex and the
insertion of a catheter will do the trick. Following relief of
development of sine waves.
the obstruction, patients may develop polyuria and are
• Hyperkalaemia with ECG changes should be treated therefore at risk of developing pre-renal failure unless
immediately with calcium gluconate (to stabilise cardiac
their fluid balance is managed carefully.
myocytes) and insulin-dextrose (causes a redistribution
of K+ intracellularly).
• Acute renal failure can be caused by pre-renal (e.g.
hypovolaemia), renal (e.g. GN) and post-renal
(e.g. obstruction) causes.
PART 2: CASES