Unit 554

October 2018

Renal problems

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Renal problems
Unit 554 October 2018

About this activity 2

Case 1 Trisha’s rocky road 4

Case 2 Nick has high blood pressure 7

Case 3 Robyn’s kidney function has declined 11

Case 4 Hoon gets complicated 14

Case 5 Craig is nauseated 18

Multiple choice questions 22

The five domains of general practice

Communication skills and the patient–doctor relationship

Applied professional knowledge and skills
Population health and the context of general practice
Professional and ethical role
Organisational and legal dimensions
About this activity check Renal problems
About this activity
It is estimated that over 1.7 million
Australians have biomedical
indicators of kidney disease such as
albuminuria or reduced kidney
function.1 In 2013–14, 0.4 out of 100
general practice presentations
related to chronic kidney disease
(CKD).2 Many cases go undiagnosed,
and prevalence increases with age.3
The most frequent cause of CKD is
diabetes mellitus, followed by
glomerulonephritis and
hypertension.3 As diabetes frequently
results in albuminuria and a
reduction in estimated glomerular
filtration rate, approximately 50% of
patients with type 2 diabetes mellitus
have CKD.4
One form of kidney injury that can
lead to CKD is analgesic
nephropathy. Several decades ago,
analgesic nephropathy accounted
for 15–20% of cases of end-stage
renal failure. Although this has
fallen to 1%, the effect of analgesics
remains an important consideration
in kidney failure.5
The incidence of acute kidney injury
(AKI) is on the rise and prevalence
increases with age, with AKI leading
to 18,010 hospitalisations in 2012–13.6
AKI results in approximately 4,670
deaths per year, and mortality is 40%
greater in males than females.6
Urolithiasis affects up to 8% of
females and 15% of males, and many
patients initially present to a general
practitioners.7 Of patients who have
had one kidney stone, 50% will have
another at some point.7
References
1. Australian Bureau of Statistics.
Australian health survey: Biomedical
results for chronic diseases, 2011–12.
Canberra:
ABS, 2013.
2. Britt H, Miller GC, Henderson J,
et al. General practice activity in
Australia 2013–14. General practice
series no. 36. Sydney: Sydney
University Press, 2014. [Accessed 03
September 2018].
3. The Australian Kidney Foundation.
Chronic kidney disease management in
general practice. Melbourne: Kidney
Health Australia; 2015.
2
4. Thomas MC, Weekes AJ, Broadley OJ,
Cooper ME, Mathew TH. The burden of
chronic kidney disease in Australian
patients with type 2 diabetes (the
NEFRON study). Med J Aust
2006;185(3):140–44.
5. Yaxley J, Litfin T. Non-steroidal anti-
inflammatories and the development of
analgesic nephropathy: a systematic
review. Ren Fail 2016;38(9):1328–34.
6. Australian Institute of Health and
Welfare. Acute kidney injury in
Australia: a first national snapshot. Cat.
no. PHE 190. Canberra: AIHW, 2015.
7. Sewell J, Katz DJ, Shoshany O, Love C.
Urolithiasis: Ten things every general
practitioner should know. Aust Fam
Physician 2017;46(9):648–52. Available
at https://www.racgp.org.au/
afp/2017/september/urolithiasis/
[Accessed 3 September 2018].
Learning outcomes
At the end of this activity, participants
will be able to:
• outline the investigative process
used to diagnose urolithiasis
• summarise the management of
chronic kidney disease
• discuss the aetiology of analgesic
nephropathy
• describe the approach to managing
diabetic kidney disease
• identify the signs and symptoms of
acute kidney injury.
Authors
Karin Jandeleit-Dahm (Case 4) MD,
PhD, FRACP is an NHMRC senior
research fellow and Deputy Head of
the Diabetes Department at Central
Clinical School, Monash University.
Carol Lawson (Case 2) MBBS,
FRACGP is a general practitioner in
Brunswick, Victoria. Dr Lawson
previously worked in the Department
of General Practice at Monash
University and has an interest in
medical education.
Tahira Scott (Case 3) MBBS is a
nephrology registrar working at the
Townsville Hospital.
James Sewell (Case 1) is a Victorian
urology registrar currently practising
in Frankston. Dr Sewell has a special
interest in the medical and surgical
management of urolithiasis, as well
as an interest in academic surgery.
He enjoys teaching medical students
and junior doctors, and has published
on both benign and malignant
urological conditions. He is happy to
be contacted with questions about
the management of urolithiasis.
Merlin Thomas (Case 4) MBChB,
PhD, FRACP is a professor in the
Department of Diabetes, Monash
University, Melbourne and NHMRC
Senior Research Fellow. His research
is focused on exploring and
understanding the key pathways
involved in the development and
progression of diabetic
complications, and the development
of novel therapies for their prevention
and management. Professor Thomas
has published over 300 research
articles. He is also the best-selling
author of ‘The Longevity List’ and
‘Fast Living Slow Ageing’.
Katie Trinh (Case 5) BSc (Adv)
MBBS is a nephrology advanced
trainee at Westmead Hospital.
Julian Yaxley (Case 3) MBBS is a
nephrology registrar working at Gold
Coast University Hospital.
Peer reviewers
Karen Dwyer MBBS, PhD, FRACP is
professor of Medicine and Deputy
Head, School of Medicine at Deakin
University. She has trained as a
nephrologist and transplant
physician. Professor Dwyer currently
works clinically at University Hospital
Geelong and Epworth Geelong.
Jan Radford MBBS, MPsychMed,
MEd, FRACGP, FARGP,
AFANZAHPE is an associate
professor of general practice at the
University of Tasmania, based in
Launceston. Professor Radford has
worked as a general practitioner in
the same practice since 1986. She
has a specific clinical interest in
mental health care, which was the
basis for her FARGP. Her research in
chronic kidney disease stems from an
interest in the secondary use of
routinely collected electronic health
record data. Professor Radford is also
undertaking a PhD in medical
education.
 Renal problems check About this activity

Abbreviations
ABPM ambulatory blood
pressure monitoring
ACEI angiotensin converting
enzyme inhibitor
ACR albumin-to-creatinine ratio
AKI acute kidney injury
ARB angiotensin receptor blocker
BMI body mass index
CKD chronic kidney disease
CT computed tomography
CTKUB computed tomography of the
kidneys, ureter and bladder
DPP-4 dipeptidyl peptidase-4
DVT deep vein thrombosis
ECG electrocardiogram
eGFR estimated glomerular
filtration rate
FBE full blood evaluation
HBPM home blood pressure
monitoring
KDIGO Kidney Disease Improving
Global Outcomes
NSAIDs non-steroidal
anti‑inflammatory drugs
PPI proton pump inhibitor
PTH parathyroid hormone
SGLT2 sodium−glucose
cotransporter 2
T2DM type 2 diabetes mellitus
UTI urinary tract infection

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Case 1 check Renal problems

CASE Question 3

1
What further investigations would you organise?
Trisha’s rocky road

Trisha, a construction worker aged 56 years, is well

known to you from her regular visits with her children.
She presents to your clinic describing two episodes of
severe right flank pain over the past two weeks. She now
has frequent small, painful voids that have prevented her
from being able to work for the past two days.

Question 1
Further information
What history would you elicit? What investigation would you
Trisha’s creatinine is now 120 µmol/L (from a baseline of
do in your clinic room to help you differentiate the cause of
80 µmol/L), and her urine microscopy shows 80 erythrocytes,
Trisha’s symptoms?
20 polymorphs and no organisms. Computed tomography of
her kidneys, ureter and bladder (CTKUB) shows a 5‑mm
calculus at the right vesicoureteric junction with moderate-to-
severe proximal hydronephroureter. There are no other calculi
and no other abnormalities on her scan.

Question 4
What are the red flags for immediate referral to hospital for
treatment of renal colic?

Further information

Trisha has not had any symptoms of infection and has not
noticed any haematuria. She is a current smoker with a
40 pack-year history and is on irbesartan for hypertension.
She has not had urinary tract surgery or any other medical
history of note. She has tenderness in her right renal angle,
and her urine dipstick shows microhaematuria and leukocyte
esterase, but no nitrites.

Question 5
Question 2
Which criteria would you use to determine whether it is safe
What are your differential diagnoses for Trisha’s symptoms? to offer conservative management to Trisha?

4

Question 6
What instructions/medications would you give to Trisha if she
elected to pursue conservative management?
Further information
Trisha follows your advice regarding conservative
management but returns to you after three weeks with
ongoing pain. You refer her to a urologist, who inserts a
ureteric stent. She presents to you again with ongoing flank
pain, urinary frequency and haematuria.
Question 7
How will you manage Trisha?
Further information
Trisha undergoes a ureteroscopy and laser lithotripsy
(fragmentation of the calculus). Her postoperative ureteric
stent is subsequently removed. At her next visit to see you,
she asks you what she can do to prevent further episodes.
Question 8
What do you advise her?
Renal problems check Case 1
CASE 1 Answers
Answer 1
You should ask about fevers and infective symptoms, previous
episodes of pain, dysuria and haematuria.
A past history of urinary tract infections (UTIs), renal colic,
gallstones, previous urinary tract surgery, smoking, diabetes
and other forms of immunosuppression are all relevant.
A urine dipstick can be performed easily in the clinic and will
help to differentiate between potential causes of Trisha’s
symptoms.
Answer 2
From what you have gathered, it is likely that Trisha has
right ureteric colic. Classically, stranguria (painful small
voids) suggests that the stone is at the vesicoureteric
junction. However, cystitis and pyelonephritis remain
differentials.
Answer 3
In patients in whom the suspected diagnosis is renal colic, you
should organise CTKUB (non-contrast CT abdomen
performed prone). Ultrasonography of the renal tract should
be reserved for patients in whom ionising radiation must be
avoided. This includes pregnant women and young children.
Ultrasonography does not effectively visualise the ureters and
offers a poor estimate of stone size. Given that stone size and
location are two vital factors for determining management,
CTKUB should be performed.1
Trisha should also have a test of renal function and a formal
urine microscopy and culture arranged. 
Answer 4
Anatomical:
• Single functional kidney (congenitally or surgically absent
kidney, non-functional kidney)
• Bilateral ureteric obstruction
Systemic:
• Concurrent UTI or sepsis and obstruction
• Premorbid chronic kidney disease stages 4 or 5
• Anuric renal failure
Answer 5
Assuming the patient has none of the red flags listed in Answer 4,
there are some criteria that warrant referral for outpatient review
by a specialist rather than conservative management.
Patients who should be referred to a urologist or sent to an
emergency department include those with one or more of
the following:
• diabetes, particularly those with suboptimal control
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Case 1 check Renal problems

• an estimated glomerular filtration rate (eGFR) of Answer 8

≤30 mL/min/1.73 m2
• intractable pain and nausea.
It can often help to give your preferred urologist a phone call
about these patients, as the urologist may be able to arrange
for the patients to rapidly receive treatment if needed.
Most renal calculi are calcium oxalate stones (80%). You can
send the patient’s stone for calculus analysis to confirm the
composition.
Of patients who have had one stone, 50% will have another at
some point.4

Generally, it is appropriate to offer conservative management
to patients with stones that are 7 mm or smaller in size, as
approximately 60% of these stones should eventually pass.2
Answer 6
Provide a script for tamsulosin 400 µg daily for utereric
relaxation, paracetamol 1 g four times daily, indomethacin
50 mg orally, three times a day as needed, with or without
oxycodone 5 mg orally, four times a day as needed.3
Patients should remain hydrated sufficiently that the urine
remains clear. The actual amount of fluid will depend on the
time of year and the patient’s occupation, but looking at urine
provides easy feedback as to whether fluid intake is sufficient.
A low-salt diet will reduce urinary calcium (alteration of
dietary calcium is not helpful), and a low oxalate diet can also
be useful. Acidic urine promotes stone formation. In most
people, urine acidity is driven by protein intake, so a lower
protein diet helps to prevent stones.5

Advise Trisha to:

Resources for doctors
• present directly to emergency if she:
• Sewell J, Katz DJ, Shoshany O, Love C. Urolithiasis-Ten
–– develops a fever things every general practitioner should know. Aust Fam
Physician 2017;46(9):648–52; www.racgp.org.au/
–– becomes increasingly unwell
download/Documents/AFP/2017/September/AFP-2017-
–– starts vomiting 9-Focus-Urolithiasis.pdf

–– is unable to tolerate oral fluids

–– develops intolerable pain unresponsive to medication
• strain her urine to catch the stone
–– either urinate through a sieve or into a white plastic
container (eg an ice cream tub)
–– bring the stone in for calculus analysis and to confirm
stone passage.
Repeat the CT scan in four weeks if Trisha has not caught the
stone; if the stone is still present, she should be referred to a
urologist for intervention.
If the stone has not passed in six weeks, the risk of renal
damage from chronic obstruction increases, even though pain
is usually no longer a factor.1
References
1. Türk C, Neisius A, Petrik A, et al. EAU Guidelines on urolithiasis.
Arnhem, the Netherlands: European Association of Urology, 2017.
Available at https://uroweb.org/wp-content/uploads/EAU-
Guidelines-on-Urolithiasis_2017_10-05V2.pdf [Accessed 17 August
2018].
2. Coll DM, Varanelli MJ, Smith RC. Relationship of spontaneous
passage of ureteral calculi to stone size and location as revealed by
unenhanced helical CT. AJR Am J Roentgenol 2002;178(1):101–3.
3. Seitz C, Liatsikos E, Porpiglia F, Tiselius HG, Zwergel U. Medical
therapy to facilitate the passage of stones: What is the evidence?
Eur Urol 2009;56(3):455–71. doi: 10.1016/j.eururo.2009.06.012.
4. Macneil F, Bariol S. Urinary stone disease: Assessment and
management. Aust Fam Physician 2011;40(10):772–75.
5. Curhan GC, Willett WC, Rimm EB, Stampfer MJ. A prospective
study of dietary calcium and other nutrients and the risk of
symptomatic kidney stones. N Engl J Med 1993;328(12):833–38.

Answer 7
Urinary frequency, dysuria, haematuria from bladder irritation
and intermittent flank pain from refluxing urine are the classic
constellation of symptoms from stent pain but may often be
confused with the symptoms of a UTI.

Urine dipstick is not useful for the diagnosis of a UTI when

there is a stent in situ. If a named organism is grown on urine
culture, this can be treated.

The primary method for diagnosing UTI in a patient with a

stent should be assessing for signs of sepsis: tachycardia,
fever and elevated inflammatory markers.

In the absence of infection, stent pain can be managed with

non-steroidal anti-inflammatory drugs, tamsulosin (400 µg
daily), and oxybutynin (2.5–5 mg twice to three times per day,
remembering to warn about anticholinergic side effects).

6
 Renal problems check Case 2

CASE Question 3

2 Nick has high blood pressure

From the information available so far, what medical problems
will you need to address with Nick?

Nick, 64 years of age, is a recently retired retail manager.

He and his wife, Lucy, are planning a trip to Europe to
celebrate Nick’s retirement and their 40th wedding
anniversary. Lucy insisted he have a check-up before they
leave. Nick has attended your practice for many years but
comes very rarely. He smokes 10 cigarettes a day but has
no other significant past or family medical history. On
examination you note his blood pressure is 178/82 mmHg,
which decreases to 174/80 mmHg after 10 minutes.

Question 4
Question 1
Does Nick need any more tests?
Does Nick have hypertension?

Table 1. Nick’s test results

Further information
Result Normal range
Nick returns to your clinic a week later. He has checked his
Serum biochemistry
blood pressure twice at his local pharmacy and obtained
Sodium (mmol/L) 139 135–145
readings of 176/78 and 172/82 mmHg. The clinic reading
today is 178/84 mmHg. Potassium (mmol/L) 5.4* 35–5.2
Chloride (mmol/L) 107 95–110
Bicarbonate (mmol/L) 26 22–32
Question 2
Urea (mmol/L) 13.5* 3.0–9.0
What further assessments would you do now? Creatinine (µmol/L) 144* 60–110
Estimated glomerular filtration rate 43 ≥60
(mL/min/1.73 m2)
Urinary albumin studies
Albumin (mg/L) 127* <15
Creatinine (mmol/L) 4.0 4.0–15.0
Albumin-to-creatinine ratio (mg/mmol) 31.75* <2.5
Urine microscopy
Leucocytes (x106/L) 3 <2
Red blood cells (x106/L) 97 <13
Further information
Squamous epithelial cells Nil
Nick eats a reasonably balanced diet and walks 3–4 km most days.
Red blood cell morphology Glomerular
He drinks one or two glasses of wine with dinner most nights and
Serum lipids
more at weekends. His body mass index (BMI) is 23.5 kg/m2 and
his physical examination is normal apart from mild pitting oedema Total cholesterol (mmol/L) 5.9 <5.5
of his ankles. Urine dipstick shows a trace of blood and is strongly High-density lipoprotein (mmol/L) 1.1 >1.0
positive for protein. His haemoglobin is at the lower end of the Low-density lipoprotein (mmol/L) 4.2 <2.5
normal range and his fasting glucose and electrocardiogram (ECG)
Triglycerides (mmol/L) 1.4 <2.0
are normal. Further test results are outlined in Table 1.

7
Case 2 check Renal problems

Question 5 CASE 2 Answers

What lifestyle advice will you give Nick to help manage his
medical condition?
Answer 1
Criteria for the diagnosis of hypertension are shown in
Table 2. As yet, we do not have enough information to
diagnose Nick with hypertension. The diagnosis can be made
using measurements in the clinic (several measurements
taken on at least two separate occasions) or out of the clinic,
using regular home blood pressure monitoring (HPBM) or
24-hour ambulatory blood pressure monitoring (ABPM).1

Table 2. Criteria for the diagnosis of hypertension1

Method of measurement Systolic (mmHg) Diastolic (mmHg)

Clinic ≥140 ≥90

Question 6 ABPM daytime (awake) ≥135 ≥85

What medications would you recommend for Nick? ABPM night time (asleep) ≥120 ≥70

ABPM over 24 hours ≥130 ≥80

HBPM ≥135 ≥85

ABPM, ambulatory blood pressure monitoring; HBPM, home blood pressure monitoring

Answer 2
Nick now fits the diagnosis of hypertension. The diagnostic
process aims to:1

• identify all cardiovascular risk factors

• detect end-organ damage
• investigate any causes of secondary hypertension.
Question 7
Nick is a smoker. His other cardiovascular risks can be
What other management steps would you take? assessed by:2

• asking about his diet, alcohol consumption and level of

physical activity
• calculating his risk of diabetes using the Australian type 2
diabetes risk assessment tool, and having a fasting blood
glucose level checked if his risk is ≥12
• measuring his height, weight, BMI and waist circumference
• measuring his fasting lipids
• screening for renal disease
• calculating his absolute cardiovascular risk.
A thorough cardiovascular examination, as well as
Question 8
examination of the optic fundi and palpation of the kidneys
Should Nick be referred to a renal specialist? (for enlargement associated with polycystic kidneys), will help
identify end-organ damage and/or possible causes of
secondary hypertension. Laboratory investigations
recommended for all hypertensive patients comprise:1

• urine dipstick for blood (if abnormal, send for microscopy)

• urine albumin-to-creatinine ratio (ACR; first-void specimen
is recommended, but spot urine is acceptable)
• serum urea, electrolytes, creatinine and estimated
glomerular filtration rate (eGFR)
• haemoglobin and/or haematocrit
• 12-lead ECG.

8

Investigation for secondary causes of hypertension should be
considered in selected patients on the basis of clinical
suspicion or on specific findings in the history and/or
examination.1 Investigations could include:
• renal artery imaging in young females (to exclude fibromuscular
dysplasia), in older patients with known atherosclerotic disease
or in patients with a renal and/or femoral bruit1
• plasma renin-to-aldosterone ratio in patients with
moderate-to-severe hypertension, with hypertension that is
difficult to control or with hypokalaemia1
• plasma metanephrines in patients who have symptoms
suggestive of possible phaeochromocytoma, such as
episodic hypertension associated with headache,
palpitations and/or sweating.3
Answer 3
Nick may have chronic kidney disease (CKD); however, his
tests should be repeated in three months before making this
diagnosis. CKD is defined as:4
• a measured or eGFR of <60 mL/min/1.73 m2 that is present
for ≥3 months with or without evidence of kidney damage
or
• kidney damage with or without decreased eGFR that is
present for ≥3 months as evidenced by the following,
irrespective of the underlying cause:
–– albuminuria
–– haematuria after exclusion of urological causes
–– structural abnormalities (eg on kidney imaging tests)
–– pathological abnormalities (eg as determined by
renal biopsy).
Staging of CKD involves combining information about
eGFR and the level of albumin in the urine, as indicated
in Tables 3 and 4.4
If Nick has similar results on his repeat tests in three months, he
can be diagnosed with CKD stage 3b with macroalbuminuria.
In addition, he has a high absolute cardiovascular risk.
People with an eGFR of <45 mL/min/1.73 m2 and/or
macroalbuminuria have a high risk (>15% in the next five
years) of having a cardiovascular event.4 CKD is a more
important risk factor than diabetes for cardiovascular
disease (CVD).4 In fact, for people with CKD, the risk of dying
from cardiovascular events is up to 20 times higher than the
risk of requiring dialysis or transplantation.4
Answer 4
Nick should have his eGFR and ACR repeated within one
week; if eGFR is decreasing, you should suspect acute kidney
Table 3. Kidney function stages4
1 2 3a 3b 4 5
Glomerular ≥90 60–89 45–59 30–44 15–29 <15
filtration rate or on
(mL/min/1.73 m2) dialysis
Renal problems check Case 2
injury.4 To confirm the diagnosis of CKD, eGFR and ACR
should be repeated in three months.4
When CKD is first diagnosed, the underlying cause should be
investigated sufficiently to exclude treatable causes such as
obstruction, vasculitis, nephrotic syndrome and rapidly
progressive glomerulonephritis.5 In Australia, the most common
causes of CKD are diabetic nephropathy, glomerulonephritis,
hypertension and polycystic kidney disease.4
Diagnostic evaluation tests recommended for all people with
CKD are:5
• blood tests:
–– full blood evaluation (FBE)
–– erythrocyte sedimentation rate
–– C-reactive protein
–– fasting lipids and glucose
• urine microscopy and culture
• renal ultrasonography.
If eGFR is <60 mL/min/1.73 m2, iron studies and serum
calcium, phosphate, parathyroid hormone (PTH) and
vitamin D levels should be included in the blood tests.
Further testing will depend on the clinical features and initial
test results.
Answer 5
Smoking cessation has been shown to reduce blood
pressure and overall CVD risk.1 Stopping smoking is
recommended for all patients with CKD, to reduce the risk of
CKD progression.5
People with CKD should consume a healthy, balanced diet
and aim to maintain their BMI between 18.5 and 24.9 kg/m2.5
Low-protein diets and low-phosphate diets are not
recommended when eGFR is >30 mL/min/1.73 m2.5 A salt
intake of <6 g/day reduces blood pressure and albuminuria
in patients with CKD.5 Patients with persistent
hyperkalaemia may require dietary potassium restriction,
preferably under the guidance of a dietitian.5
No specific recommendations for physical activity are
available for people with CKD. However, Nick should be
encouraged to do at least 30 minutes of moderate physical
activity each day in line with Australian guidelines.6
In the absence of specific recommendations for alcohol
consumption for people with CKD, patients should be
advised to follow the National Health and Medical Research
Council (NHMRC) Australian guidelines to reduce health risks
from drinking alcohol.7 These guidelines recommend drinking
no more than two standard drinks on any day, to reduce the
risk of long-term alcohol-related harm.
Table 4. Albuminuria stages
Normal Microalbuminuria Macroalbuminuria
Urine albumin- Male <2.5 Male 2.5–25 Male >25
to-creatinine Female <3.5 Female 3.5–35 Female >35
ratio (mg/mmol)
9
Case 2 check Renal problems
Answer 6
CKD can cause and aggravate hypertension, and hypertension
can contribute to the progression of CKD.4 Maintaining blood
pressure below target levels is an important goal in the
management of CKD.4 Recommended targets are:5
• ≤130/80 mmHg in people with diabetes and those with
ACR >2.5 (men) or >3.5 (women)
• ≤140/90 mmHg for others with CKD.
Either an angiotensin converting enzyme inhibitor (ACEI) or
an angiotensin receptor blocker (ARB) should be used as
first‑line therapy unless potassium levels are significantly
elevated (>5.5 mmol/L).4 Combination therapy with ACEIs
and ARBs should be avoided.5 Note that eGFR can decrease
when treatment is initiated, but provided the reduction is
<25% within two weeks of starting therapy and not
progressive, the ACEI or ARB can be safely continued.4 If
eGFR declines by more than 25%, the ACEI or ARB should be
stopped and a nephrology referral should be considered.4
Serum potassium levels should be monitored.4
Beta adrenoceptor antagonists, calcium channel antagonists
and thiazide diuretics are all appropriate if high potassium levels
preclude the use of ACEI or ARB, or as second-line therapies.5
As Nick has peripheral oedema, a diuretic may be a good choice.
Given that Nick has a high absolute cardiovascular risk, he
should be started on a statin.4 Note that not all people with
CKD will qualify for subsidised lipid-lowering therapy under
the Pharmaceutical Benefits Scheme.8
Current guidelines do not recommend the routine use of
aspirin for CVD risk reduction or for the prevention of CKD
progression, as the risk-benefit ratio for patients with stages
1–3 CKD is uncertain.5
Answer 7
Nephrotoxic medication should be avoided in people with CKD.5
In particular, Nick needs to be aware that the combination of
ACEI or ARB with a diuretic and non-steroidal anti-
inflammatory drug (non-selective or selective cyclooxygenase-2
inhibitor) can result in acute kidney injury.4
Noting that Nick has CKD as a current medical problem in Nick’s
health record, including his electronic health record (e-HR) if he
has one, will assist in adjusting drug doses, as appropriate, and
avoiding the prescribing of nephrotoxic medications for Nick in
the future. The e-HR would need to provide the prescriber with
renal impairment alerts related to prescribing.
Placing a diagnosis in the e-HR will also assist in
systematising the monitoring of patients with CKD as this
population of patients can then easily be identified.
People with CKD and macroalbuminuria should be reviewed
at least every three months.4 The clinical assessment should
include weight and blood pressure measurement, and
assessing for the presence of any oedema. The following
indices should be monitored regularly:4
• urea, electrolytes, creatinine and eGFR
10
• urine ACR
• fasting lipids
• FBE
• calcium, phosphate and PTH.
Answer 8
The Kidney Health Australia–Caring for Australasians with
Renal Impairment guidelines5 recommend referral for
specialist assessment in the following situations:
• stage 4 or 5 CKD of any cause
• persistent significant albuminuria (ACR ≥30 mg/mmol)
• decline in eGFR of >5 mL/min/1.73 m2 over a six-month period
–– Because there can be variation of up to 15–20% between
consecutive individual eGFR measurements, the decline
should be confirmed on at least three separate readings.5
• glomerular haematuria with macroalbuminuria
• CKD with hypertension where target blood pressure is
difficult to achieve despite treatment with at least three
antihypertensive agents.
Nick has macroalbuminuria and glomerular haematuria and
therefore warrants specialist referral. Given his age, degree of
renal impairment and glomerular haematuria, Nick most likely
has IgA nephropathy.
References
1. National Heart Foundation of Australia. Guideline for the diagnosis
and management of hypertension in adults. Melbourne: National
Heart Foundation of Australia, 2016. Available at www.
heartfoundation.org.au/images/uploads/publications/PRO-167_
Hypertension-guideline-2016_WEB.pdf [Accessed 19 July 2018].
2. The Royal Australian College of General Practitioners. Guidelines
for preventive activities in general practice. 9th edn. Melbourne:
RACGP, 2016. Available at www.racgp.org.au/your-practice/
guidelines/redbook [Accessed 19 July 2018].
3. Blake M. Pheochromocytoma. Medscape, 2018. Available at
https://emedicine.medscape.com/article/124059-overview
[Accessed 15 July 2018].
4. The Australian Kidney Foundation. Chronic kidney disease
management in general practice. 3rd edn. Melbourne: Kidney
Health Australia, 2015. Available at https://kidney.org.au/cms_
uploads/docs/ckd-management-in-gp-handbook-3rd-edition.pdf
[Accessed 19 July 2018].
5. Johnson D, Atai E, Chan M, et al. KHA–CARI Guideline: Early
chronic kidney disease: Detection, prevention and management.
Nephrology 2013;18(5):340–50. doi: 10.1111/nep.12052.
6. Department of Health. Australia’s physical activity and sedentary
behaviour guidelines. Canberra: Commonwealth of Australia, 2018.
Available at www.health.gov.au/internet/main/publishing.nsf/
content/health-pubhlth-strateg-phys-act-guidelines#apaadult
[Accessed 19 July 2018].
7. National Health and Medical Research Council. Australian
guidelines to reduce health risks from drinking alcohol. Canberra:
Commonwealth of Australia, 2009. Available at www.nhmrc.gov.
au/health-topics/alcohol-guidelines [Accessed 19 July 2018].
8. Department of Health. Pharmaceutical Benefits Scheme: General
statement for lipid-lowering drugs prescribed as pharmaceutical
benefits. Canberra: Commonwealth of Australia, 2018. Available at
www.pbs.gov.au/info/healthpro/explanatory-notes/gs-lipid-
lowering-drugs [Accessed 19 July 2018].
 Renal problems check Case 3

CASE Question 3

3 Robyn’s kidney function

has declined
Which medications do we need to worry about?

Robyn, 69 years of age, is a retired dressmaker. She

visits you for a check-up and advice on pain relief.
Robyn has a long history of hand arthritis and now
complains of reproducible low back pain, which has
been slowly worsening over several years.

You note on examination that Robyn’s blood pressure

is elevated to 155/95 mmHg and there is mild lower
limb pitting oedema. You decide to order a baseline
set of pathology tests, which shows moderately
reduced renal function with a glomerular filtration
rate (GFR) of 40 mL/min/1.73 m2. Robyn’s last GFR
measurement six years ago was normal, and this new
decline is a surprise to her. Urine microscopy reveals
microscopic haematuria but no proteinuria.

Question 4
How do patients with analgesic nephropathy present?

Question 1
What are the possible diagnoses?

Question 5
Question 2 How would you investigate Robyn’s renal impairment?

What effect do analgesics have on the kidney?

11
Case 3 check Renal problems
Further information
Robyn confirms that she did consume small quantities of Bex
tablets in the distant past. Of greater relevance, Robyn also
says that for the previous five years she has required
paracetamol on most days because of progressive low back
pain and hand arthritis.
Urine microscopy reveals microscopic haematuria without
active sediment, as well as mild proteinuria. You refer Robyn
to a nephrologist and she subsequently has a kidney biopsy.
This shows non-specific chronic necrotic changes, consistent
with analgesic nephropathy in the correct context, but no
features diagnostic for glomerulonephritis or any other
identifiable cause.
Question 6
What treatment advice would you offer Robyn?
Question 7
What is Robyn’s prognosis?
Further information
Robyn is seen annually by her nephrologist for three years
with no change in her GFR. Her microscopic haematuria is
detected at the first year but resolves over the following
reviews. Robyn is discharged from the nephrologist’s care and
12
is awaiting an appointment with a urologist. You schedule
annual follow-up appointments with her. You control her
blood pressure by introducing ramipril 1.25 mg daily. Her low
back pain is thought to be musculoskeletal in nature and you
manage it successfully with physiotherapy and a small renally
adjusted dose of pregabalin.
CASE 3 Answers
Answer 1
An asymptomatic decline in renal function is common. More
than 1.7 million Australians have chronic kidney disease
(CKD), although most cases are undiagnosed.1 The prevalence
of CKD increases with age. In the Australian setting, the three
most frequently identified causes, in descending order, are
diabetes mellitus, glomerulonephritis and hypertension.1 A
significant minority of cases are unexplained and presumably
due to atherosclerosis and degenerative effects of ageing.
The presence of haematuria in a patient with renal impairment
should raise suspicion of urinary tract malignancies, although this
is relatively rare. In Robyn’s case, given her back pain, obstructive
uropathy from ureteric calculi is also a relevant possibility.
Analgesic nephropathy is an uncommon cause of CKD.
However, it is a diagnosis that merits consideration in patients
such as Robyn, where there is a potential history of heavy
analgesia medication consumption.
Answer 2
Many analgesic medicines are nephrotoxic and can produce
renal papillary necrosis and chronic inflammation of the renal
interstitium. It has therefore been observed that consistent
long-term consumption of analgesic agents may lead to CKD,
termed analgesic nephropathy.
The incidence of analgesic nephropathy is declining. It
accounts for only 1% of cases of end-stage renal failure in
current practice, compared with 15–20% of cases several
decades ago.2 However, incidence is difficult to quantify
because the condition is frequently overlooked, and
confirming a positive diagnosis is challenging.
Answer 3
The precise analgesic agents and quantities necessary to produce
CKD are unproven. It is thought that the minimum cumulative
dosage required to generate analgesic nephropathy is daily
consumption of analgesic medicines for two consecutive years.3
Analgesic nephropathy is most closely associated with
consumption of phenacetin, a non-opioid analgesic
medication that was gradually discontinued from the
Australian market in the 1980s after its link with
nephrotoxicity was realised.4 Phenacetin was previously
readily available as a compound preparation in Vincent
powder and Bex tablets, which were banned for sale over-the-
counter in Australia in 1977.5 There has been a steady decline

in the incidence of analgesic nephropathy in Australia
corresponding with their withdrawal from the market. Small
numbers of elderly patients today may still report a past
history of purchasing and consuming phenacetin products.
Nowadays, paracetamol is the most important drug believed to
be implicated in the development of analgesic nephropathy.4
This is, in fact, not surprising because paracetamol is a major
metabolite of phenacetin. It is even more harmful when
ingested in combination formulations with aspirin or codeine.4
The use of aspirin or codeine alone, without paracetamol, is
safe. Despite traditional teaching, long-term intake of non-
steroidal anti-inflammatory drugs (NSAIDs) is not associated
with an increased risk of CKD.2 Widely prescribed examples in
Australia include ibuprofen, celecoxib or naproxen.
It is prudent to mention, however, that NSAID use can cause
acute renal failure.2 Acute kidney injury (AKI) is estimated to
occur in between 1% and 5% of regular NSAID users, in a
roughly dose-related fashion, although this is variable
depending on other risk factors.3 NSAID-induced AKI is a
separate entity altogether from analgesic nephropathy and is
beyond the scope of this chapter.
Finally, analgesic drugs are only one of multiple medication
classes that are known to be correlated with CKD. Other
commonplace examples that should be considered include
proton pump inhibitors, lithium, transplant anti-rejection
medications, cancer chemotherapies and herbal extracts.
Answer 4
Most patients diagnosed with analgesic nephropathy are
middle-aged or elderly.6 The most common group of patients
are women in the seventh and eighth decades of life.3
Cases are typically identified incidentally on blood tests
performed for unrelated reasons. Occasionally, patients
complain of symptoms including flank pain, polyuria or
recurrent urinary tract infections. In most instances there is a
clear preceding history of long-term analgesia dependence,
generally for indications such as headaches or joint pain.
Medication use is commonly under-reported, although heavy
paracetamol consumption is the usual problem in contemporary
practice. Finally, most patients are hypertensive on examination.
Answer 5
Analgesic nephropathy is largely a diagnosis of exclusion.
Diabetes and longstanding hypertension should be excluded if
possible. Blood tests for renal function are obligatory and will
show an elevated creatinine level and reduced GFR. Anaemia of
CKD is often present, and it may be disproportionately severe
relative to the degree of kidney impairment. Proteinuria could be
detected and, if so, is associated with worse disease, although it
will very rarely reach nephrotic range (3.5 g per day). Computed
tomography (CT) is also a helpful test. Findings on non-contrast
CT can include small kidneys, with rough contours or with
papillary calcifications. The presence of at least one of these
features is 92% sensitive for analgesic nephropathy, and the
presence of all three is 100% specific.7 Kidney biopsy is non-
specific and demonstrates chronic interstitial nephritis.
Renal problems check Case 3
Answer 6
Robyn should be advised that analgesic nephropathy is the
most likely diagnosis, given her clinical history. She should be
instructed to cease regular paracetamol ingestion and limit
future intake where possible.
Generic strategies for CKD management should be applied.
This includes reduction of Robyn’s cardiovascular risk factors,
particularly optimisation of blood pressure and blood glucose.
Essentially, all patients with declining renal function should
have radiographic imaging for completeness, routinely with
ultrasonography or non-contrast CT, to exclude structural
abnormalities.
Robyn requires annual follow-up, including blood tests to
monitor renal function, and urine testing for proteinuria and
haematuria.
Robyn should also be referred to a urologist for evaluation for
urinary tract malignancy given her age and persisting
microscopic haematuria.
Answer 7
Robyn’s prognosis is good. Kidney function generally stagnates
after discontinuation of the offending agents or may continue
to decline slowly with age. Few patients with analgesic
nephropathy ever reach end-stage renal failure. The risk of
deterioration to end-stage renal failure, defined as a
GFR <15 mL/min/1.73 m2 or the need for dialysis, in patients
with a GFR of 15–60 mL/min/1.73 m2 is approximately 1.5%
per year.8 This is a rough estimate that applies to all causes of
CKD.
A significant minority of individuals with analgesic
nephropathy develop urinary tract cancers, usually one to two
decades after the onset of analgesic abuse.
References
1. The Australian Kidney Foundation. Chronic kidney disease
management in general practice. Melbourne: Kidney Health
Australia; 2015.
2. Yaxley J, Litfin T. Non-steroidal anti-inflammatories and the
development of analgesic nephropathy: a systematic review. Ren
Fail 2016;38(9):1328–34.
3. Lerma E, Berns J, Nissenson A. Current diagnosis and treatment:
Nephrology and hypertension. New York: The McGraw Hill
Companies, 2009.
4. Yaxley J. Common analgesic agents and their roles in analgesic
nephropathy: a commentary on the evidence. Korean J Fam Med
2016;37(6):310–16. doi: 10.4082/kjfm.2016.37.6.310.
5. Jefferies S, Saxena M, Young P. Paracetamol in critical illness: A
review. Crit Care Resusc 2012;14(1): 74–80.
6. Vadivel N, Trikudanathan S, Sing A. Analgesic nephropathy.
Kidney Int 2007;72(4):517–20.
7. Beers MH, Porter RS, Jones TV. The Merck manual of diagnosis
and therapy. 18th edn. Whitehouse Station: Merck Sharp and
Dohme Corp, 2006; p. 2418.
8. Hsu C, Vittinghoff E, Lin F, Shlipak M. The incidence of end-stage
renal disease is increasing faster than the prevalence of chronic
renal insufficiency. Ann Int Med 2004;141(2):95–101.
13
Case 4 check Renal problems

CASE Question 3

4
What additional tests will you order to help you confirm a
Hoon gets complicated diagnosis of diabetic kidney disease?

Hoon, 59 years of age, is an Asian businessman who

leads a very busy life. He comes to see you because
he has been feeling tired recently. Tests show that he
has an elevated fasting glucose level of 13 mmol/L,
confirming a diagnosis of type 2 diabetes mellitus
(T2DM). You discuss lifestyle modifications, including
dietary changes, increased physical activity and
weight loss1 and start him on daily metformin,
gradually increasing his dose to 2 g.

Recent pathology tests have noted that Hoon’s urinary

albumin-to-creatinine ratio (ACR) is elevated at
35 mg/mmol and his estimated glomerular filtration
rate (eGFR) is 62 mL/min/1.73 m2. You suspect he
has diabetic kidney disease.
Question 4
Having identified diabetic kidney disease, what is your
treatment strategy to reduce Hoon’s risk of kidney failure?

Question 1
What specific questions would you ask Hoon about his
kidneys and his risks for kidney problems?

Further information

One year later, Hoon presents to you feeling short of breath on

exertion. He says he has not had any chest pain. His
electrocardiogram shows left ventricular hypertrophy without
evidence of arrhythmia or prior infarction. On auscultation, he
has scattered bi-basal crackles in his lungs, and his chest
X-ray is consistent with heart failure. Blood tests taken at the
time of his presentation document a persistently elevated
glycated haemoglobin (HbA1c) level of 64 mmol/mol (8%) and
a reduced eGFR of 46 mL/min/1.73 m2. Hoon’s condition has
Question 2
become more complicated.
What specific issues would you look for in Hoon’s physical
examination?
Question 5
Having confirmed the presence of renal impairment, what is
your revised strategy to improve his glucose control?

14

Question 6
When would you consider it appropriate for Hoon to be
referred to a nephrologist?
CASE 4 Answers
Answer 1
Most individuals with chronic kidney disease (CKD) have no
symptoms relating to their kidneys until advanced stages of
kidney disease. This is why a diagnosis of CKD often comes
as a shock to patients. The most important clinical questions
to ask relate to the potential chronicity of any renal
impairment and prior exposure to common risk factors for
CKD including diabetes, dyslipidaemia, hypertension and
obesity. Hoon’s test results indicate T2DM is the leading risk
factor for kidney disease in this case. A prior history of
cardiovascular disease or microvascular complications, such
as eye or foot disease or erectile dysfunction, further supports
a diagnosis of diabetic kidney disease. The absence of
longstanding diabetes or prior poor glucose control does not
exclude the diagnosis of diabetic kidney disease. Indeed, at
least one-third of patients who have diabetes may have CKD
at the time of their diagnosis with diabetes.2
Alternative diagnoses should always be considered in a
patient initially presenting with CKD.3 A review of exposure
to potentially nephrotoxic agents (eg antibiotics,
chemotherapy, proton pump inhibitors, herbal medicines,
non-steroidal anti-inflammatory drugs [NSAIDs] or analgesic
combinations), especially in high doses or for prolonged
periods, or symptoms of urinary obstruction (pain,
prostatism) is appropriate. Family history should be explored
for familial diseases such as polycystic kidney disease and
some forms of glomerulonephritis. Finally, exploration of
non-renal causes of albuminuria may also be appropriate by
excluding a history of vigorous exercise or symptoms
consistent with a urinary tract infection (UTI) prior to their
last urinalysis.
Answer 2
On physical examination, most individuals with CKD have no or
few signs directly relating to their kidneys, although
hypertension, oedema and other signs of fluid overload are
increasingly common as renal function declines. In any
Renal problems check Case 4
individual with diabetes and CKD, a comprehensive eye
examination, foot examination (eg sensation, pedal pulses,
deformity, signs of inflammation or ulceration) and cardiac
examination should also be undertaken, as the risk for these
complications is markedly increased, compared with individuals
without CKD. Again, the presence of macrovascular or
microvascular complications of diabetes, such as eye or foot
disease or erectile dysfunction, supports a diagnosis of diabetic
kidney disease. However, renovascular disease is also common
in this setting and may be associated with a renal bruit or signs
of atherosclerotic disease in other vascular beds.
Answer 3
Initially, kidney function should be assessed by testing for
elevated albuminuria and a reduced eGFR in all people with
T2DM, from the time of their diagnosis.1
The urinary ACR obtained from a morning first-void sample
appears to provide the best predictive value for the future risk
of kidney failure. The finding of an elevated urinary ACR
(≥2.5 mg/mmol in men or ≥3.5mg/mmol in women), as in this
case, should be confirmed with a first-void urine collection
within the next three months to substantiate that the urinary
albumin excretion is persistently elevated. A third collection is
also warranted if the first test is abnormal, but the second
repeat urinalysis result is in the normal range.
If at least two urine tests show an elevated urinary
albumin excretion (between 2.5–25 mg/mmol in men or
3.5–35 mg/mmol in women), this is called moderately
increased albuminuria (the new terminology for what was
formerly called ‘microalbuminuria’). Urinary albumin excretion
above this level in at least two tests is considered to represent
severely increased albuminuria (the new terminology for
what was formerly called ‘macroalbuminuria’).4,5 The
importance of these categories rests in the markedly
increased absolute risk of complications associated with each
level of albuminuria.
GFR is automatically estimated on measurement of serum
creatinine. For patients without prior evidence of CKD,
repeat testing within seven days is essential in any individual
initially presenting with an eGFR of <60 mL/min/1.73 m2, to
exclude rapidly declining renal function, which may be
consistent with other renal pathologies. If renal function is
not declining rapidly (eg >20% loss) but the eGFR remains
<60 mL/min/1.73 m2, the test should be repeated within
three months. An eGFR persistently <60 mL/min/1.73 m2 for
three or more months denotes the presence of reduced
kidney function.
The presence of persistently elevated urinary albumin
excretion (as a sign of kidney damage) and/or persistently
reduced eGFR (as a sign of reduced kidney function) for at
least three months makes the diagnosis of CKD.2
In all patients presenting with CKD, a detailed urinalysis is
also appropriate to exclude glomerular haematuria (eg red
blood cell casts, dysmorphic red blood cells). A mid-stream
urine sample is sometimes appropriate to exclude chronic
UTI as a contributor to proteinuria. Serum protein
15
Case 4 check Renal problems
electrophoresis and urine protein electrophoresis are also
appropriate in older adults with proteinuria, to exclude
myeloma. Renal ultrasonography may also be an
appropriate assessment in patients with renal impairment
of uncertain duration to exclude obstruction or cystic
disease and assess chronicity.
Answer 4
The presence and severity of CKD is a strong risk factor for
adverse renal outcomes, including kidney failure, the
requirement for dialysis and premature mortality.6 Even in
individuals with established CKD, this risk can be
substantially reduced by improved and sustained diabetes
control, including better glucose, lipid and blood pressure
control, blockade of the renin-angiotensin-aldosterone system
and smoking cessation.1
In individuals with reduced kidney function, it is also important
to avoid, where possible, additional nephrotoxic insults (eg high
doses or prolonged use of over-the-counter painkillers, herbal
remedies, certain antibiotics, radiographic contrast material,
hypovolaemia, hypotension, dehydration). The implementation
of electronic health records with integrated clinical decision
support has the potential to automatically reduce these risks in
patients with established CKD, especially where multiple
practitioners are involved in their care.
Treatment with sodium-glucose co-transporter 2 (SGLT2)
inhibitors may reduce the risk of kidney disease progression in
patients with T2DM, beyond their glucose-lowering actions.7,8
Answer 5
Poor glucose control remains a significant risk factor for
adverse outcomes even in individuals with reduced kidney
function (eGFR <60 mL/min/1.73 m2).9 If glucose-lowering
can be achieved safely (eg without hypoglycaemia, heart
failure or other adverse drug reactions), it is still worth
pursuing in individuals with CKD. However, all classes of
glucose-lowering agents require some changes in their use
for individuals with reduced kidney function.
Metformin accumulates in renal impairment. However, in
most patients with CKD, metformin can still be safely used,
providing its dose is reduced appropriately. Metformin doses
for Hoon should be reduced to no more than 1 g/day to ensure
safe drug exposure and reduced risk of side effects. It is
recommended that metformin should eventually be
discontinued when eGFR is <30 mL/min/1.73 m2.1 Planning
to temporarily discontinue metformin therapy in the event of
significant illness is also important as part of sick-day rules.1
Sulphonylureas should be used with caution in individuals
with reduced kidney function because of the increased risk of
hypoglycaemia.1,10 Because of their kidney-cleared active
metabolites, glimepiride, glyburide and glibenclamide are not
recommended for patients with renal impairment. Gliclazide
is metabolised by the liver to inactive metabolites, so poses a
lower risk for severe hypoglycaemia; however, it is still
recommended to be stopped when eGFR falls to below
40 mL/min/1.73 m2.9
16
Dipeptidyl peptidase-4 (DPP-4) inhibitors are preferred in
patients with CKD because of comparable efficacy in patients
with renal impairment to that observed in patients with
normal renal function and a low incidence of adverse drug
reactions including hypoglycaemia. However, because of their
differing pharmacology, differing dosing strategies may be
required. Sitagliptin, alogliptin, and the major metabolites of
saxagliptin and vildagliptin are predominantly eliminated into
the urine, meaning some dose reduction is required (Figure 1).
Linagliptin requires no dose adjustment in renal impairment
because of its biliary metabolism.11 However, DPP-4 inhibitors
must also be used with metformin (or a sulphonylurea) to be
eligible for a Pharmaceutical Benefits Scheme subsidy, even
in patients with renal impairment. Using appropriately low
doses with sick-day rules usually makes this possible.
The glucose-lowering effects of SGLT2 inhibitors are small
or insignificant in patients with renal impairment because of
reduced glycosuria. Consequently, dapagliflozin may be used
if the eGFR is >60 mL/min/1.73 m2, and empagliflozin may
be used if the eGFR is >45 mL/min/1.73 m2.1 Notably, the
cardiac and renal effects of SGLT2 inhibition appear to be
independent of glucose-lowering and baseline renal function.7,8
Glucagon-like peptide 1 receptor agonists, such as exenatide,
are cleared by the kidneys, so renal impairment increases
dose-dependent nausea and other side effects.
Many practitioners reluctantly fall back on insulin therapy in
individuals with reduced kidney function, despite the ever-present
risks from hypoglycaemia due to altered insulin pharmacology,
inadequate compensatory gluconeogenesis and flattening of
the relationship between mean glucose control and HbA1c so
that the impact of intensification may be underestimated.
Answer 6
Early referral and care by nephrologists may be appropriate
for some individuals with diabetes and an eGFR
<30 mL/min/1.73 m2 in order to discuss and potentially plan
for renal replacement therapy.1
At higher levels of renal function, referral may also be
appropriate for those with CKD experiencing:
• a sustained decrease in eGFR of ≥25%
• a sustained decrease in eGFR of 15 mL/min/1.73 m2
within 12 months
Dosing of DPP-4 inhibitors in chronic kidney disease
Sitagliptin 100 mg qd 50 mg qd 25 mg qd
Alogliptin 25 mg qd 12.5 mg qd 6.75 mg qd
Saxagliptin 5 mg qd 2.5 mg qd
Vildagliptin 50 mg qd 50 mg qd
Linagliptin 5 mg qd
70 60 50 40 30 20
Estimated glomerular filtration rate (ml/min/1.73 m2)
Figure 1. Dosing of dipeptidyl peptidase-4 (DPP-4) inhibitors in
chronic kidney disease
 Renal problems check Case 4

• severely increased albuminuria (urinary ACR ≥25 mg/mmol

in men and ≥35 mg/mmol in women)

• anaemia
• volume overload that is difficult to control.

Conclusion
CKD is a common companion to T2DM. Approximately one in
every three patients with T2DM seen in Australian general
practice has increased albuminuria. Approximately one in every
four patients with T2DM has a persistent reduction in eGFR
below 60 mL/min/1.73 m2. Taken together, at least every
second patient with T2DM has CKD.2

The presence and severity of CKD identifies individuals at

increased risk of complications including renal failure,
cardiovascular disease and adverse drug reactions. Screening
for and identifying CKD in this setting provides an opportunity
to optimise therapy, increase patient safety and improve
clinical outcomes.

References
1. The Royal Australian College of General Practitioners. General
practice management of type 2 diabetes 2016–2018. Melbourne:
RACGP, 2016. Available at www.racgp.org.au/your-practice/
guidelines/diabetes/ [Accessed 17 August 2018].
2. Thomas MC, Weekes AJ, Broadley OJ, Cooper ME, Mathew TH.
The burden of chronic kidney disease in Australian patients with
type 2 diabetes (the NEFRON study). Med J Aust 2006;185(3):
140–44.
3. Teng J, Dwyer KM, Hill P, et al. Spectrum of renal disease in
diabetes. Nephrology 2014;19(9):528–36.
4. Kidney Disease Outcomes Quality Initiative. Definition and
classification of CKD. Kidney Int Suppl 2013;3(1):19–62.
5. The Australian Kidney Foundation. Chronic kidney disease
management in general practice. 3rd edn. Melbourne: Kidney
Health Australia, 2015. Available at https://kidney.org.au/cms_
uploads/docs/ckd-management-in-gp-handbook-3rd-edition.pdf
[Accessed 19 July 2018].
6. Afkarian M, Sachs MC, Kestenbaum B, et al. Kidney disease and
increased mortality risk in type 2 diabetes. J Am Soc Nephrol
2013;24(2):302–08.
7. Wanner C, Inzucchi SE, Lachin JM, et al. Empagliflozin and
progression of kidney disease in type 2 diabetes. N Engl J Med
2016;375(4):323–34. doi: 10.1056/NEJMoa1515920.
8. Thomas MC, Cherney DZI. The actions of SGLT2 inhibitors on
metabolism, renal function and blood pressure. Diabetologia
2018;61(10):2098–07.
9. Shurraw S, Hemmelgarn B, Lin M, et al. Association between
glycemic control and adverse outcomes in people with diabetes
mellitus and chronic kidney disease: A population-based cohort
study. Arch Intern Med 2011;171(21):1920–27.
10. National Kidney Foundation. KDOQI clinical practice guidelines for
diabetes and CKD: 2012 Update. Am J Kidney Dis 2012;60(5):850–86.
11. Agarwal V, Giri C, Solomon RJ. The effects of glucose-lowering
therapies on diabetic kidney disease. Curr Diab Rev 2015;11(3):191–200.

17
Case 5 check Renal problems

CASE Question 3

5
What investigations would you arrange for Craig to have?
Craig is nauseated

Craig is an office worker aged 58 years. He has

hypertension and takes a combination tablet
containing candesartan 32 mg and hydrochlorothiazide
12.5 mg once daily. He was diagnosed with type 2
diabetes mellitus (T2DM) 18 months ago and is on
metformin XR 1 g daily. He developed reflux symptoms
about one month ago and uses esomeprazole 20 mg
daily, which he bought over the counter. His reflux has
resolved but he presents with a one-week history of
malaise and nausea.

You request blood tests, which show normal full blood

count, liver function tests, thyroid function tests and
C-reactive protein. His biochemistry is significant for
urea (12.8 mmol/L; normal range 2.5–6.5 mmol/L) and
creatinine (170 µmol/L; normal range 60–110 µmol/L).
Question 4
Six months ago Craig’s creatinine level was 70 µmol/L
and estimated glomerular filtration rate (eGFR) What else should you advise Craig before he leaves to have
≥90 mL/min/1.73 m2. his investigations?

Question 1
What is your interpretation of Craig’s blood test results?

Further information

Further information Craig tells you that his only symptoms are malaise and nausea.
He has not had any recent infections or commenced any other
You recall Craig for urgent review.
medications. He has been drinking but not eating much
because of his nausea, and passed urine normally this morning.
His blood pressure is lower than usual at 110/75 mmHg, with
Question 2
no postural drop, and his temperature and heart rate are
What further questions should you ask in your history and normal. He appears only mildly dehydrated but examination is
look for in your examination? otherwise unremarkable.

You refer him to a local medical imaging centre for an

urgent renal ultrasound, which shows normal-sized kidneys
with echogenic parenchyma and no hydronephrosis,
suggestive of an acute kidney injury (AKI) of non-obstructive
aetiology. His blood tests are sent off urgently. Basic tests
return first:

• Urinalysis shows 1+ protein and 2+ blood.

• Biochemistry shows his creatinine has now risen to 234 µmol/L.

18
 Renal problems check Case 5

Question 5 Further information

What would you do next? Craig wants to know how to protect his kidney from further insults.

Question 8
What should you advise him?

Further information

Craig returns to you a week later with a discharge summary

from hospital. He was admitted under the care of a
nephrologist and had an urgent renal biopsy, which showed
evidence of acute interstitial nephritis. Esomeprazole was
suspected to be the likely cause. The medication was ceased
and his renal function subsequently improved. He was CASE 5 Answers
discharged yesterday with a creatinine of 90 µmol/L and
eGFR 80 mL/min/1.73 m2.
Answer 1
Craig asks you for repeat prescriptions of his medications, but
admits he is not sure what he should still be taking. The Kidney Disease Improving Global Outcomes (KDIGO)
guidelines define AKI as an increase in serum creatinine by
≥26.5 µmol/L within 48 hours; or an increase in serum
Question 6 creatinine by ≥1.5 times the baseline, which is known or
presumed to have occurred within the past seven days; or if
What do you advise him?
urine output is <0.5 mL/kg/h for six hours.1 By contrast,
KDIGO defines chronic kidney disease (CKD) as abnormalities
of kidney structure or function that are present for more than
three months.2

Given that Craig’s last blood test was six months ago, this
result may be reflective of CKD. Repeat evaluation can
confirm the diagnosis of AKI or CKD, the timing of which
requires clinical judgement and suspicion for AKI.2 In the
context of his acute illness, it may be inferred that Craig has
AKI and he should be re-evaluated early.

Answer 2
Further information
The KDIGO guidelines recommend that patients be evaluated
Craig is worried that this event has caused permanent promptly to determine the cause of AKI.1 History and
damage to his kidneys. examination are important in determining the aetiology of
AKI. Pre-renal AKI is caused by renal hypoperfusion, such as
in hypovolaemia, sepsis and reduced effective arterial blood
Question 7
volume (eg heart failure, decompensated liver failure). Intrinsic
What do you tell Craig? How should you monitor his causes of AKI include acute glomerulonephritis, acute
progress? interstitial nephritis, acute tubular necrosis (due to prolonged
renal hypoperfusion), vasculitis and nephrotoxins. Post-renal
AKI due to obstruction of the urinary tract may be caused by
kidney stones, prostatic hypertrophy or malignancy.

Assessment should be targeted towards assessing Craig’s

volume status and the cause of his AKI. Craig’s fluid status
should be determined by measuring his weight, temperature,
blood pressure and heart rate (supine and standing to look for
postural hypotension) and assessing his mucosal membranes,
skin turgor, capillary refill and jugular venous pressure.

19
Case 5 check Renal problems

You should ask Craig about his oral intake, fluid losses (such
Table 1. Commonly used oral drugs in adults requiring
as vomiting or diarrhoea) and urine output.
dose reduction or caution in renal impairment7
To determine the aetiology of his AKI, you could ask Craig
Drug Dosing recommendations and comments
questions about:
Anticoagulants used to prevent emboli in atrial fibrillation
• symptoms of acute illness (eg vomiting, diarrhoea, infection)
• systemic symptoms, such as rash or arthralgia, which may Apixaban No renally adjusted dosing
be suggestive of systemic vasculitis or a rheumatological Contraindicated when CrCl <25 mL/min
condition Rivaroxaban Standard dose: 20 mg once daily
• recent changes in medications (including supplements and CrCl 30–49 mL/min: 15 mg once daily
over-the-counter medications), and in particular non- CrCl <30 mL/min: contraindicated
steroidal anti-inflammatory drugs (NSAIDs), proton pump
Dabigatran Standard dose: 150 mg twice daily
inhibitors (PPIs) and antibiotics
(or 110 mg twice daily if >75 years)
–– you should also enquire if Craig has had recent studies CrCl 30–50 mL/min: 110 mg twice daily
with intravenous contrast CrCl <30 mL/min: contraindicated
• flank pain, which may be due to kidney stones Hypoglycaemic drugs
• obstructive lower urinary tract symptoms, such as in
Metformin Should be withheld in acute illness and if at risk of
prostatic hypertrophy.
further deterioration of renal function.
You could also examine Craig for clues to the underlying Maximum doses based on stable renal function
aetiology of his AKI, such as rash, joint swelling or a palpable CrCl 60–90 mL/min, 2 g daily
bladder. Signs of heart failure or decompensated liver failure CrCl 30–60 mL/min, 1 g daily
may also be suggestive but are unlikely in Craig’s case. CrCl 15–30 mL/min, 500 mg daily*
*In practice, metformin is generally not used if
Answer 3 CrCl <30 mL/min)4

Urine should be collected for urinalysis, microscopy/culture/ Gliclazide Dose reduction is required in severe renal impairment
Glipizide because the risk of hypoglycaemia is increased
sensitivity, red cell morphology, casts and quantification of
creatinine, albumin and protein. Urinary sodium, if low Sitagliptin Standard dose: 100 mg daily
(<20 mmol/L), may suggest pre-renal azotemia rather than CrCl 30–50 mL/min: 50 mg daily
acute tubular necrosis. However, interpretation of this would be CrCl <30 mL/min: 25 mg daily
difficult in Craig’s situation because he is on a diuretic, which
Empaglifozin Standard dose: 10 mg once daily, up to 25 mg daily
increases urinary sodium excretion. Renal ultrasonography
CrCl <45 mL/min: contraindicated
should be performed to look for urinary obstruction.3,4 Blood
tests to look for other underlying pathology should also be Analgesia
considered if there are suggestive features in the history,
Oxycodone Reduce initial dose if CrCl <30 mL/min
examination and initial urine investigations (eg dysmorphic red
Example: oxycodone/naloxone
blood cells, active urinary sediment, including red and white
Standard dose: 5/2.5 to 10/5 mg every 12 hours
blood cell casts). These blood tests may include C3, C4,
CrCl <30 mL/min: start with 2.5/1.25 mg every
antinuclear antibodies, extractable nuclear antigen, anti-double
12 hours
stranded DNA, anti-neutrophil cytoplasmic antibodies, serum
electrophoresis and serum free light chains. Pregabalin Standard dose: initially 75 mg twice daily,
up to maximum 300 mg twice daily
Answer 4 CrCl 30–60 mL/min, initially 75 mg daily,
maximum 300 mg daily
It is very important that Craig’s medications are reviewed to CrCl 15–30 mL/min, initially 25–50 mg daily,
prevent further exacerbation of his AKI, prevent toxicity of maximum 150 mg daily
renally excreted drugs that may accumulate in renal failure, and CrCl <15 mL/min, initially 25 mg daily,
cease any drugs that may be the primary cause of his AKI. maximum 75 mg daily

You should tell Craig to stop taking his combined
antihypertensive tablets until further notice. AKI can be
exacerbated by medications such as antihypertensives,
(especially angiotensin converting enzyme inhibitors [ACEIs]
or angiotensin II receptor blockers [ARBs]), diuretics and
NSAIDs. These medications can further exacerbate
hypovolaemic states and renal hypoperfusion.
Given his acute illness, Craig should be advised to withhold
metformin. In general, patients with eGFR <30 mL/min/1.73 m2
should also be advised to withhold metformin to reduce the risk
Drugs for gout prophylaxis
Allopurinol Use lower starting doses in renal impairment
eGFR >60 mL/min/1.73 m2: 100 mg daily
eGFR 30–60 mL/min/1.73 m2: 50 mg once daily
eGFR 15–30 mL/min/1.73 m2: 50 mg alternate days
eGFR <15 mL/min/1.73 m2: 50 mg twice a week
Colchicine Standard dose: 500 µg once or twice daily
CrCl <30 mL/min: initially 250 µg daily
CrCl, creatine clearance; eGFR, estimated glomerular filtration rate

20
 Renal problems check Case 5

of lactic acidosis.5 Commonly used medications that may also Answer 7

require dose adjustment include allopurinol, pregabalin and
opioids (Table 1).
Finally, you should ask Craig to stop taking esomeprazole.
PPIs are a common cause of acute interstitial nephritis.6
Answer 5
Craig should be referred for urgent nephrology review. He has
stage 3 AKI (as his current creatinine of 234 µmol/L is more than
three times his baseline of 70 µmol/L six months ago) of unclear
aetiology and his results suggest that there may be an additional
diagnosis requiring specialist treatment. Staging criteria are shown
in Table 2. The presence of proteinuria and microhaematuria
may suggest an underlying diagnosis such as interstitial
nephritis or glomerulonephritis, requiring specialist input.
The National Institute for Health and Care Excellence
guidelines recommend that you discuss the management of
AKI with a nephrologist if there is:3
• a possible diagnosis requiring specialist treatment (eg
vasculitis, glomerulonephritis)
• no clear cause of AKI
• inadequate response to treatment
• presence of complications associated with AKI
• stage 3 AKI
• history of stage 4 or 5 CKD
• history of renal transplant.
Kidney function may show full, partial or no recovery on repeat
testing. AKI is associated with an increased risk of CKD, which
can subsequently lead to end-stage kidney disease and the need
for renal replacement therapy.8 In general, Kidney Health Australia
recommends that patients who have had AKI should have a
kidney health check annually for at least three years, then continue
with screening every second year.4 A kidney health check includes
measuring kidney function, urine albumin-to-creatinine ratio and
blood pressure. However, some patients may require more
frequent monitoring, depending on the clinical context.
Answer 8
Craig is at higher risk of developing AKI. Risk factors for AKI
include advanced age, pre-existing CKD and other comorbid
conditions, such as diabetes, hypertension and cardiovascular
disease.8 Craig should be aware of risk factors for AKI, such
as acute illnesses that predispose to hypovolaemia or
hypotension (eg infection, vomiting, diarrhoea, reduced oral
intake). It is recommended that he restrict use of NSAIDs. In
the event of acute illness, consideration should be given to
withholding his antihypertensive medications (especially
ACEIs or ARBs) until he has improved.3
Resources for patients
• Kidney Heath Australia, Acute Kidney Injury fact sheet;
https://kidney.org.au/cms_uploads/docs/acute-kidney-
injury-fact-sheet.pdf

Answer 6
Medication review is very important in the context of renal
impairment. Craig should discontinue esomeprazole and avoid
PPIs. His blood pressure should be assessed prior to
recommencing antihypertensive medications. Given his renal
function has improved and eGFR is 80 mL/min/1.73 m2,
candesartan and hydrochlorothiazide could be re-introduced
(with ongoing monitoring of renal function). If there is evidence of
persistent renal dysfunction, ACEIs, ARBs and diuretics should
be avoided until renal recovery. In such a situation, alternative
agents such as non-dihydropyridine calcium channel blockers,
including amlodipine, may be used to manage his blood pressure.
It should be safe for Craig to continue using his metformin with
his current eGFR of 80 mL/min/1.73 m2. Dose reduction and
further additions to his T2DM management should be considered
in the context of his renal impairment.
Table 2. Staging of acute kidney injury in adults1
Stage Serum creatinine Urine output
1 1.5–1.9 times baseline, or <0.5 mL/kg/h for 6–12 hours
≥26.5 µmol/L increase
References
1. Kidney Disease: Improving Global Outcomes Acute Kidney Injury
Work Group. KDIGO clinical practice guideline for acute kidney
injury. Kidney Inter Suppl 2012;2:1–138.
2. Kidney Disease: Improving Global Outcomes Acute Kidney Injury
Work Group. KDIGO 2012 clinical practice guideline for the
evaluation and management of chronic kidney disease. Kidney
Inter Suppl 2012;3:1–150.
3. The National Institute for Health and Care Excellence. Acute
kidney injury: Prevention, detection and management. London:
NICE, 2013. Available at www.nice.org.uk/guidance/cg169
[Accessed 17 August 2018].
4. The Australian Kidney Foundation. Chronic kidney disease
management in general practice. 3rd edn. Melbourne: Kidney
Health Australia, 2015. Available at https://kidney.org.au/cms_
uploads/docs/ckd-management-in-gp-handbook-3rd-edition.pdf
[Accessed 20 August 2018].
5. The Royal Australian College of General Practitioners. General
practice management of type 2 diabetes 2016–18. Melbourne:
RACGP, 2016. Available at www.racgp.org.au/download/
Documents/Guidelines/Diabetes/2015diabetesmanagement.pdf
[Accessed 17 August 2018]
6. Geevasinga N, Coleman PL, Webster AC, Roger SD. Proton pump
inhibitors and acute interstitial nephritis. Clin Gastroenterol
Hepatol 2006;4(5):597–604.

2 2.0–2.9 times baseline
3 3.0 times baseline, or
increase in serum creatinine
to ≥353.6 µmol/L, or
initiation of renal
replacement therapy
<0.5 mL/kg/h for ≥12 hours
<0.3 mL/kg/h for ≥24 hours,
or
Anuria for ≥12 hours
7. Australian Medicines Handbook 2018. Adelaide: Australian
Medicines Handbook Pty Ltd, 2018. Available at https://
amhonline.amh.net.au/ [Accessed 20 August 2018].
8. Chawla LS, Eggers PW, Star RA, Kimmel PL. Acute kidney injury
and chronic kidney disease as interconnected syndromes. N Engl J
Med 2014;371(1):58–66. doi: 10.1056/NEJMra1214243.

21
Multiple choice question check Renal problems
ACTIVITY ID 141821
Renal problems
This unit of check is approved for six Category 2
points in the RACGP QI&CPD program. The expected
time to complete this activity is three hours and
consists of:
• reading and completing the questions for each
case study
–– you can do this on hard copy or by logging on to
the gplearning website, http://gplearning.racgp.
org.au
• answering the following multiple choice questions
(MCQs) by logging on to the gplearning website,
http://gplearning.racgp.org.au
–– you must score ≥80% before you can mark the
activity as ‘Complete’
• completing the online evaluation form.
You can only qualify for QI&CPD points by
completing the MCQs online; we cannot process
hard copy answers.
If you have any technical issues accessing this activity
online, please contact the gplearning helpdesk on
1800 284 789.
If you are not an RACGP member and would like to
access the check program, please contact the
gplearning helpdesk on 1800 284 789 to purchase
access to the program.
Case 1 – Vincent
Vincent, 38 years of age, presents to you complaining
of severe pain in his right flank, which started the day
before and has been unresponsive to analgesics. Since
the onset of pain, he has frequently felt the need to
urinate, but has only been able to pass small amounts
and that is also painful. He has also been feeling
nauseous. A urine dipstick shows haematuria but no
nitrites or signs of infection. You suspect that Vincent
might have renal colic. Vincent has no past or other
current medical history of note.
Question 1
To further investigate Vincent’s condition, you should
initially organise for him to have:
A. an ultrasound scan
B. computed tomography of the kidneys, ureter and
bladder (CTKUB)
C. CT of the abdomen
D. X-ray KUB.
22
Question 2
Which of the following features of Vincent’s presentation
warrant referral to hospital for treatment?
A. Urinary frequency
B. Painful small voids
C. Intolerable flank pain and nausea
D. All of the above
Case 2 – Maria
Maria, 50 years of age, is one of your regular patients and was
diagnosed with type 2 diabetes mellitus (T2DM) two weeks
ago. At the time of T2DM diagnosis, you advised Maria to have
an eye examination and you requested blood and urine tests to
check her kidney function. The results show that her estimated
glomerular filtration rate (eGFR) is 64 mL/min/1.73 m2 and her
urinary albumin-to-creatinine (ACR) is 40 mg/mmol.
Question 3
Maria’s test results indicate that she:
A. has moderately increased albuminuria
B. has severely increased albuminuria
C. will need repeat testing within the next three months
D. will need repeat testing within seven days.
Further information
Maria had initially opted for lifestyle modification to control her
blood glucose levels, but this proved inadequate, so you prescribed
metformin 1 g. Repeat urine tests three months after the initial
tests showed no change in eGFR and urinary ACR, confirming
severely increased albuminuria. Testing a year later shows eGFR
has decreased to 55 mL/min/1.73 m2 and remains decreased on
repeat testing. HbA1c has increased to 69 mmol/mol (8.5%).
Question 4
To manage Maria’s glucose levels, you should:
A. increase her metformin dose to 2 g
B. switch from metformin to glibenclamide
C. switch from metformin to dapagliflozin
D. add linagliptin to her current dose of metformin.
Case 3 – Conrad
Conrad is 58 years of age and was diagnosed with hypertension
five years ago and asthma when he was 18 years of age. His
blood pressure has been controlled with perindopril and he uses
a steroid preventer for his asthma. He has also had regular
monitoring of his kidney function. His eGFR and urinary ACR had
been stable at around 65 mL/min/1.73 m2 and 27 mg/mmol
respectively, but his last test results, two weeks ago, showed that
eGFR and urinary ACR had deteriorated to 57 mL/min/1.73 m2
and 45 mg/mmol respectively. His blood pressure has increased
to 148/98 mmHg.

Question 5
Lifestyle changes that you could recommend to help with
reducing Conrad’s blood pressure include:
A. a low-phosphate diet
B. a low-protein diet
C. reduction of salt intake to <6 g/day
D. all of the above.
Further information
Repeat testing three and six months later shows eGFR results
of 55 and 50 mL/min/1.73 m2 respectively. Urinary ACR has
remained at about 45 mg/mmol. Conrad’s blood pressure
remains increased at 148/98 mmHg despite his being on the
maximum dose of perindopril. You prescribe a second
antihypertensive agent and refer Conrad to a nephrologist.
Question 6
Which of the following antihypertensive agents would be an
appropriate addition to Conrad’s antihypertensive regimen?
A. Candesartan
B. Irbesartan
C. Atenolol
D. Hydrochorothiazide
Case 4 – Tracy
Tracy, 50 years of age, presents with a two-day history of
exhaustion, nausea and loss of appetite. Three months ago,
she had presented with swelling and pain in her right calf and
ankle, which she had attributed to running on concrete for
about an hour four or five times a week. Initially, she was
prescribed naproxen 750 mg to relieve the pain and
inflammation, and esomeprazole 20 mg to prevent any
gastrointestinal side effects of the naproxen. However, further
testing confirmed a diagnosis of deep vein thrombosis (DVT)
and she is currently on treatment with rivaroxaban 20 mg.
She had been on naproxen and esomeprazole for three days
before her DVT diagnosis. She no longer takes naproxen, but
finds esomeprazole helpful for bouts of gastric reflux, which
she has been having more frequently in the past two months.
Occasionally, she uses ibuprofen for pain relief.
You request blood tests, which show that serum creatinine is
elevated. You note that her serum creatinine level, measured
three months ago, was 85 µmol/L. Urinalysis shows proteinuria
and microhaematuria. Urine output is also reduced. You
suspect that Tracy has Stage 3 acute kidney disease (AKI).
Question 7
Stage 3 AKI means that Tracy’s current serum creatinine level
would be in the range of:
A. 128–150 µmol/L
B. 135–160 µmol/L
Renal problems check Multiple choice question
C. 170–240 µmol/L
D. 255–360 µmol/L
Further information
You arrange for an urgent referral to a nephrologist, who
admits Tracy to hospital for treatment. She recovers fully and,
after being discharged, returns to see you for a follow-up
appointment. You advise Tracy that she will need ongoing
monitoring of her kidney function. You also discuss her
medications and risk factors for AKI.
Question 8
In Tracy’s case, the most likely cause of her AKI is:
A. esomeprazole
B. naproxen
C. rivaroxaban
D. ibuprofen.
Case 5 – Trini
Trini, 56 years of age, has had chronic back pain for the past
five years, after falling from a ladder. She has been taking a
combination of paracetamol and codeine, and sometimes a
non-steroidal anti-inflammatory drug (NSAID) for pain relief.
She comes to see you as she now needs a prescription for
the paracetamol/codeine combination. You request blood
tests, which show that eGFR is 45 mL/min/1.73 m2. Trini’s
notes show that her last eGFR reading, 18 months ago, was
80 mL/min/1.73 m2. From her clinical history, you consider a
possible diagnosis of analgesic nephropathy.
Question 9
Which of the following is not a feature of analgesic
nephropathy?
A. Proteinuria
B. Anaemia
C. Urinary red blood cell casts
D. Interstitial nephritis
Further information
Further investigations confirm a diagnosis of analgesic
nephropathy and, on your advice, Trini ceases regular use of
paracetamol/codeine.
Question 10
What follow-up would you organise for Trini?
A. Annual monitoring of kidney function
B. Absolute cardiovascular risk assessment
C. AUSDRISK assessment
D. All of the above
23
Independent learning program for GPs

Independent learning program for GPs