NEPHROLOGY

Chronic kidney disease: the canary in the coal mine

Chronic kidney disease (CKD) is a growing issue in New Zealand. Māori and Pacific peoples are overrepresented
in our CKD statistics which is concerning as it is a major driver of cardiovascular disease (CVD), and these groups
are already disproportionately affected by risk factors such diabetes, obesity and hypertension. Early detection of
CKD can be achieved via regular testing of at-risk people; this permits timely interventions to lower CVD risk and
slow or prevent the rate of kidney function decline.

KEY PR AC TICE POINTS:

Chronic Kidney Disease (CKD) is defined as defects in kidney – Guidelines vary in their recommendations about protein
structure or function, with negative implications for the restriction. A low protein diet is not necessary in most
patient’s health, over a period greater than three months. cases, and should only be undertaken with guidance
Damage associated with CKD is generally not reversible, from a nephrologist or dietitian with experience in
and this condition is associated with a substantial increase managing patients with CKD.
in CVD risk. Pharmacological management of CKD mostly involves
Patients can experience a marked reduction in kidney controlling blood pressure and reducing hyperglycaemia
function before symptoms become apparent. Therefore, (for patients with diabetes)
kidney function testing is recommended to initially identify – An angiotensin converting enzyme (ACE) inhibitor or
patients with CKD based on the presence of risk factors, e.g. angiotensin II receptor blocker (ARB) are the first-line
hypertension, diabetes, Māori/Pacific or South-Indo Asian antihypertensives for patients with CKD and a blood
ethnicity. pressure target of < 130/80 mmHg is generally
Testing for CKD involves checking serum creatinine appropriate
(to estimate glomerular filtration rate [eGFR]), urine – Early introduction of a sodium glucose co-transporter-2
albumin:creatinine ratio (ACR) and blood pressure every (SGLT-2) inhibitor is now recommended for patients
one to two years with CKD and diabetes (funded with Special Authority
If abnormal eGFR/ACR findings are detected (i.e. eGFR < approval) due to its dual kidney- and cardio-protective
60 mL/min/1.73m2 or ACR ≥ 3 mg/mmol), testing should properties. Evidence suggests that SGLT-2 inhibitors
be repeated over the next three months (see main text for may also benefit patients with CKD without diabetes,
specific recommendations) to confirm impaired kidney but this would require patients to self-fund treatment.
function
– Full classification of CKD is achieved by combining the Regular ongoing monitoring is important to assess the
patient’s eGFR grade (G1 – G5), degree of albuminuria efficacy of treatment and to detect progressive kidney
(A1 – A3) and the identified underlying cause; this function decline which may require secondary care referral.
information is used to inform management decisions Patients should also be advised of medicines to temporarily
avoid if they develop acute gastrointestinal illness (see main
Lifestyle changes are an important first step for all patients
text for details).
to reduce overall CVD risk and optimise CKD management,
e.g. weight loss, exercise, reducing salt intake

www.bpac.org.nz November 2022 1

 than doubled between 2000 and 2019.3, 8 As of 2020, there were
This is a revision of a previously published article.
reported to be a total of 3,004 people currently undergoing
What’s new for this update:
dialysis in New Zealand, and 2,199 people were living with a
A general article revision
successful kidney transplant (187 of which occurred during
Considerations when interpreting eGFR and ACR
2020).8 Approximately half of all people in New Zealand
results
requiring dialysis have diabetes as a primary cause of their
A discussion on low protein diets; there is no
condition and over half are Māori and Pacific peoples.3, 8
consistent recommendations in guidelines, they
are not considered to be standard practice and are Defining and classifying CKD
unlikely to be necessary for most patients unless
CKD itself is not considered a primary diagnosis. Instead, this
under dietitian or nephrologist supervision
term broadly describes any abnormality of kidney function
Update on blood pressure target for patients
or structure, present for at least three months, which has
with CKD; these are now lower than previously
implications for the patient’s health.9 More specifically, this can
recommended but there is still inconsistency
involve either:9, 10
between guidelines
Reduced kidney function: an estimated or measured
SGLT-2 inhibitors are recommended to be initiated
glomerular filtration rate (eGFR/GFR) < 60 mL/
early for patients with diabetes as well as for
min/1.73m2 that is present for three or more months with
patients with CKD without diabetes (if they are
or without evidence of kidney damage; or
able to self-fund)
Kidney damage: evidence of kidney damage with or
N.B. In January, 2022, the Kidney Disease: Improving Global
Outcomes (KDIGO) group announced their intention to evaluate without decreased eGFR that is present for three or more
and update the 2012 CKD Guidelines.1 The article presented here months. This “evidence” may include one or more of the
has been written prior to the updated KDIGO guidelines release following abnormalities:
and will be subsequently reviewed once it is available.
– Albuminuria (the most commonly assessed marker of
kidney damage)
Chronic kidney disease (CKD) in New Zealand – Haematuria after exclusion of urological causes
– Kidney tubular disorders, e.g. renal tubular acidosis,
Chronic kidney disease (CKD) is an umbrella term used to nephrogenic diabetes insipidus, renal potassium
describe any long-term condition that adversely affects kidney wasting
structure and function. However, declining kidney function is – Pathologic abnormalities detected by histology or
also a natural part of the ageing process.2 It is estimated that inferred; examples include glomerular conditions (e.g.
by the age of 70 years approximately 30% of the population diabetic nephropathy, autoimmune disease), vascular
will meet classification criteria for CKD.3 CKD is generally not conditions (e.g. hypertension, atherosclerosis),
reversible, and patients with untreated progressive disease tubulointerstitial conditions (e.g. urinary tract
have a substantially high risk of experiencing cardiovascular infections, stones, obstruction), cystic/congenital
disease (CVD).4 As such, early identification and intervention defects
for patients with CKD is essential. – Structural abnormalities detected by imaging, e.g.
polycystic kidneys, dysplastic kidneys, renal artery
CKD is a growing problem
stenosis
The worldwide prevalence of CKD is estimated to be 11 – 13%.5
While there is no overall prevalence data for CKD in New The Kidney Disease Improving Global Outcomes (KDIGO)
Zealand, regional estimates are consistent with these figures. criteria are used to further categorise patients according
An Auckland-based study involving the analysis of health to their eGFR grade (G1 – G5) and degree of persistent
records of over 25,000 patients in 2017 found the total sample albuminuria (A1 – A3; Table 1).9 This system can provide
prevalence of CKD to be 13%.6 There was significant variation predictive information on prognosis (see: “Patients with CKD
in rates of CKD between ethnicities; 17.8% of Samoan and have an increased risk of CVD events”), which can help guide
10.4% of Māori patients met the criteria for CKD, compared decisions around how intensely to monitor and treat patients.
with 7.1% of non-Pacific/non-Māori patients.6 An analysis of Prognostic assessment according to Table 1 does not require
electronic health records of over 200,000 patients in the Otago- determination of the underlying cause.9
Southland region in 2014 estimated the prevalence of CKD to
be 11.8%.7 Full classification of CKD according to KDIGO criteria can be
The impact of CKD on New Zealand communities is achieved by combining the patient’s eGFR grade and persistent
increasing and the number of people requiring dialysis more albuminuria category with an identified underlying cause; this

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will either be evident when considering the patients history/ increased cardiovascular risk in people with CKD.4 Patients
co-morbidities, or be determined during the diagnostic work- with established CKD often exhibit characteristic changes
up following abnormal laboratory findings (see: “Detecting in the myocardium, including myocardial fibrosis, collagen
patients with CKD in primary care”).9, 10 deposition and cardiac hypertrophy.4 Early detection of CKD
in groups with an already high CVD-risk, e.g. Māori and Pacific
Patients with CKD have an increased risk of CVD events peoples, should therefore be a priority.
Even in the early stages, CKD is a significant risk factor for CVD
events and death, and this risk increases further as kidney Distinguishing patients with progressive CKD from
function declines (Table 2). Patients with CKD are 20-times those with an age-related decline in kidney function
more likely to die as a result of a cardiovascular event than A key clinical challenge associated with CKD is differentiating
require a kidney transplant or receive dialysis.10 CVD risk patients with progressively deteriorating kidney function due
assessment tools can be used in patients with an eGFR ≥ 30 to disease from those with uncomplicated, age-related kidney
mL/min/1.73m2; those with CKD and an eGFR < 30 should be function decline. Age is a variable in the formula for calculating
assumed to have a five-year CVD risk of > 15% (see: bpac.org. eGFR; in the general population, eGFR therefore declines by
nz/2018/cvd.aspx).11 approximately 1 mL/min/year, and many older patients will
The association between CKD and CVD exists in part fulfil the criteria for grade G3a CKD (Table 1) without having
because two of the largest risk factors for CKD – diabetes any evidence of active or structural kidney disease.3
and hypertension – are also associated with left ventricular In general, progressive CKD can be distinguished as being
hypertrophy and left ventricular diastolic dysfunction, CKD in patients whose eGFR is declining at a rate > 5 mL/
both of which are predictive of myocardial infarction and min/year.3 Some regional HealthPathways define progressive
stroke.4 Vascular calcification, dyslipidaemia, inflammation, CKD in patients with an eGFR < 60 mL/min/1.73m2 which has
coagulopathy, altered blood viscosity and endothelial decreased ≥ 15 mL/min/1.73m2 within the previous 12 months,
dysfunction have also been suggested as mechanisms for the or an ACR > 250 mg/mmol (“nephrotic-range” proteinuria).

Table 1. Categorisation and prognostic risk* of patients with CKD according to eGFR (mL/min/1.73 m2) and persistent albuminuria
category (albumin:creatinine ratio [ACR], mg/mmol). Adapted from KDIGO clinical guidelines, 2012.9

Persistent albuminuria category (based on urine ACR)†

eGFR range A1 (normal) A2 (microalbuminuria) A3 (macroalbuminuria)

Description
(mL/min/1.73m2) < 3 mg/mmol 3 – 30 mg/mmol > 30 mg/mmol

G1 Normal or high ≥ 90
eGFR (kidney function) grade

G2 Mildly decreased 60 – 89

Mildly to moderately
G3a 45 – 59
decreased

Moderately to
G3b 30 – 44
severely decreased

G4 Severely decreased 15 – 29

G5 Kidney failure < 15 or dialysis

Prognostic risk: Low Moderate High Very High

* KDIGO guidelines broadly define prognostic risk as relating to “CKD outcomes”.9 This is a composite of various factors, including those relating to
progression (e.g. declining eGFR status, kidney failure), complications (e.g. CVD) and death. Such categorisation is intended to help clinicians triage
patients and inform on the intensity of management and monitoring required, as well as the need for nephrologist referral (see Figure 1 and “Patients
requiring a nephrologist referral” for further information). N.B. The specific risk percentage associated with individual outcomes is not given within general
risk categories.
† Some guidelines stratify ACR category thresholds by sex (e.g. defining macroalbuminuria as > 25 mg/mmol for males and > 35 mg/mmol for females).
However, the KDIGO group contends that this approach creates unnecessary complexity and that other variables may also affect assay precision, e.g.
ethnicity, diet, obesity.9

www.bpac.org.nz November 2022 3

Table 2. Risk of death due to a cardiovascular cause according to KDIGO criteria relative to a “healthy” person with an eGFR 90 – 105
mL/min/1.73 m2 and ACR < 1 mg/mmol. N.B. Data derived from a categorical meta-analysis, and the incidence rate of CVD death
was 4.5 per 1,000 person-years for the reference cell. Absolute risk can be determined by multiplying a cell’s relative risk by the
incidence rate for the reference cell. Adapted from KDIGO clinical guidelines, 2012.9

ACR < 1 ACR 1 – 2.9 ACR 3 – 29 ACR ≥ 30

eGFR > 105 0.9 1.3 2.3 2.1

eGFR 90 – 105 Reference value 1.5 1.7 3.7

eGFR 75 – 90 1.0 1.3 1.6 3.7

eGFR 60 – 75 1.1 1.4 2.0 4.1

eGFR 45 – 60 1.5 2.2 2.8 4.3

eGFR 30 – 45 2.2 2.7 3.4 5.2

eGFR 15 – 30* 14.0 7.9 4.8 8.1

* In general, increasing ACR correlates with a higher risk of cardiovascular mortality (and other prognostic outcomes, e.g. kidney failure, all-cause mortality).
However, in patients with a very low eGFR (e.g. < 30 mL/min/1.73m2) the opposite association is observed in this Table. This is likely to be because the
analysis was based on general-population cohorts and therefore not sufficiently powered to report accurate estimates for the relatively small number
of patients with severe eGFR grading.9 The confidence intervals for such eGFR categories (at any given ACR) are therefore substantially wider than for
higher eGFR categories and overlap.

Detecting patients with CKD in primary care

be appropriate when non-albumin proteinuria
People with CKD are generally asymptomatic in the early
is suspected (e.g. in patients with disorders of
stages and in some cases, kidney function can reduce by up
tubular function or myeloma).
to 90% before symptoms develop.10 Therefore, to increase the
detection of CKD in primary care, a risk-based approach to
investigation is recommended (Figure 1).3, 10 Investigation should occur every one to two years in most
patients with risk factors for CKD, e.g. hypertension, diabetes,
To investigate for CKD, request: people of Māori, Pacific or South/Indo Asian ethnicity (see
Serum creatinine, which automatically generates an Figure 1 for a full list of risk factors). A blood pressure
eGFR from the laboratory. measurement should also be included to contextualise these
markers of kidney health with respect to the patient’s overall
The eGFR reported from New Zealand laboratories
CVD risk.3, 10 These appointments can be an opportune time to
is usually calculated with the CKD-EPI algorithm
emphasise lifestyle changes which may reduce the likelihood
as this is now the recommended equation and
of CKD developing in people with risk factors (see: “Lifestyle
considered most accurate. N.B. The Cockcroft-
management of CKD”). If patients have established diabetes
Gault equation may be used to guide dose
or hypertension, investigation for CKD should take place at
adjustments for certain medicines, e.g. metformin
least annually.10 Population screening for CKD in isolation is
(see: “Glycaemic control”).
not recommended.
Urine ACR, to determine albuminuria status; if a first void
urine specimen, when the urine is most concentrated, is CKD symptoms and signs
not possible a random urine sample can be used The presence of symptoms or signs generally indicates more
advanced CKD but these are often non-specific. Patients
Albumin:creatinine ratio is preferable to
with grade 3 CKD may be asymptomatic, or report nocturia,
protein:creatinine ratio in most cases. ACR is
mild malaise or anorexia.10 If present, symptoms and signs of
considered to be a more sensitive and specific
grade 4 and 5 CKD are usually more overt, including nausea,
measure of changes in glomerular permeability
pruritus, restless legs and dyspnoea.10 Features resulting
than the total urinary protein:creatinine ratio.
from diminished kidney function may also become apparent
Evaluation of the protein:creatinine ratio may
in advanced disease, e.g. oedema. Cognitive impairment is

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 Patient with risk factors for CKD: Note: nephrology referral is generally
recommended for patients with:*
Diabetes or hypertension Prostatic syndrome or a urologic
eGFR < 30 mL/min/1.73m2
Established cardiovascular disease
Persistent macroalbuminuria (ACR > 30 mg/mmol)
disease Māori, Pacific or South/Indo Diabetes with eGFR < 45 mL/min/1.73m2
Family history of kidney disease Asian ethnicity eGFR decrease ≥ 20%
History of acute kidney injury Obesity (BMI ≥ 30 kg/m2) eGFR decline of > 15 mL/min/1.73m2 within 12
Age > 60 years Smoking months if initial eGFR < 60 mL/min/1.73m2
Nephrotoxic medicine use Suspected intrinsic kidney damage (see main text)
Haematuria in absence of urinary contamination
CKD and uncontrolled hypertension despite use of
three antihypertensives

Assess blood pressure

Patient with either and request laboratory
of the following evaluation of: Repeat
incidental laboratory Serum creatinine to assessments
findings determine eGFR every 1 – 2 years
Urine ACR Both normal (annually if patient
has diabetes or
hypertension)

Elevated urine ACR

eGFR < 60 mL/min/1.73m2
(≥ 3 mg/mmol)

Repeat relevant test twice within Consider need for

Reassess eGFR within 14 days
next three months other investigations
or referral
eGFR ACR

At least 3 At least 2/3

eGFR reduced eGFR stable or
reduced eGFRs elevated urine
≥ 20% from reduced < 20%
present for ≥ 3 ACRs over ≥ 3
previous from previous
months? months?

Consider possibility of acute

kidney injury; refer to nephrologist Yes No

Persistent albuminuria category (based on urine ACR)

eGFR range A1(normal) A2 (microalbuminuria) A3 (macroalbuminuria)
Description
(mL/min/1.73m2) < 3 mg/mmol 3 – 30 mg/mmol > 30 mg/mmol

G1 Normal or high ≥ 90
Monitor Refer
eGFR (kidney function)

G2 Mildly decreased 60 – 89
Mildly to moderately
G3a decreased
45 – 59 Monitor Monitor
grade

Moderately to severely
G3b 30 – 44 Monitor Monitor
decreased Refer
G4 Severely decreased 15 – 29
G5 Kidney failure < 15 or dialysis
Prognostic risk: Low Moderate High Very High
* Consider the individualised clinical benefit of
Perform any appropriate additional tests (see main text) to determine referral. In some cases (e.g. patients with a stable
the underlying cause/diagnosis isolated eGFR < 30 mL/min/1.73m2), formal referral
involving consultation and ongoing management
through a nephrology service may not be necessary;
nephrology advice may be all that is required along
with continued management in primary care.
Combine eGFR stage + albuminuria category + underlying diagnosis to
Age-dependent thresholds for certain criteria are
fully specify CKD e.g. grade G3a CKD with microalbuminuria due to hypertension currently being debated in the literature, however,
no consensus has been reached.

Figure 1. Algorithm for the initial detection and diagnosis of patients with CKD. Adapted from Kidney Health Australia.10

www.bpac.org.nz November 2022 5

also more common in patients with CKD than the general ACR
population, which can range in severity from mild cognitive Overestimation Urinary tract infection
dysfunction to dementia.12 Acute fever
Menstruation
Evaluating kidney test results Heart failure
Intense exercise within 24 hours
Decreased eGFR. If a patient is found to have an eGFR < before sample
60 mL/min/1.73 m2, serum creatinine should be measured Medicines, e.g. non-steroidal anti-
again within 14 days as small variations in eGFR are possible inflammatory drugs (NSAIDs)
and measurements in isolation are not always indicative of * The eGFR reported from New Zealand laboratories is usually calculated
kidney disease progression.13 If the reduced eGFR is confirmed, with the CKD-EPI algorithm; this is considered a more accurate estimate
and it is stable or decreased < 20% from the previous result, of true GFR compared with other equations, e.g. MDRD, Cockcroft-
Gault.14 N.B. The Cockcroft-Gault equation may still be used to guide
eGFR should be re-tested at least twice over the next three
dose adjustments for certain medicines, e.g. metformin (see: “Glycaemic
months (Figure 1).10 Patients with an eGFR < 45 mL/min/1.73 control”).
m2 are at higher risk of significant cardiovascular and kidney
Other tests to request when confirming CKD
consequences, e.g. end stage kidney disease or heart failure,
regardless of their age.10 N.B. Serum creatinine results within Following confirmation of consistently decreased eGFR and/
normal parameters does not exclude the possibility of CKD; or increased urine ACR over a three-month period, additional
kidney function decreases of > 50% can occur before serum tests should be requested to investigate and confirm the
creatinine values exceed the upper limit of normal.10 underlying cause (if not immediately apparent due to existing
co-morbidities/history).
Practice point: a reduction of ≥ 20% in eGFR from
baseline is considered clinically significant and may This may include:9, 10
indicate acute kidney injury (see: “Preventing acute Kidney ultrasound
kidney injury in patients with CKD”); nephrologist
Full blood count and CRP testing
referral is required.10
Glucose, lipids and HbA1C
Serum electrolytes
Increased ACR. If ACR is elevated, it should usually be repeated
Dipstick urine test to detect haematuria or pyuria;
twice within three months to confirm results (Figure 1).10
if positive, request urine microscopy, e.g. to detect
Albuminuria is classified according to the criteria in Table 1.
dysmorphic red cells, red cell casts or crystals

Considerations when interpreting eGFR/ACR results Other tests according to patient-specific risk factors and
There are numerous factors that can influence eGFR and clinical suspicion
ACR results other than CKD. These factors should always be
Patients requiring a nephrologist referral
considered, particularly for patients with borderline or isolated
abnormalities. This includes:10, 14 Decisions to refer patients with CKD to secondary care should
eGFR* be made on a case-by-case basis.10 A lower threshold for
referral is usually appropriate for younger patients, and for
Overestimation, Reduced skeletal muscle mass
i.e. true GFR likely decreases serum creatinine, e.g. Māori and Pacific peoples.10
to be lower anorexia nervosa, paraplegics,
amputees Nephrology referral is generally recommended for patients
Meat is the main exogenous source
with:3, 10
of creatinine (particularly red meat);
people who follow vegan/vegetarian eGFR < 30 mL/min/1.73 m2
diets have lower serum levels Persistent macroalbuminuria (ACR ≥ 30 mg/mmol)
Liver disease may reduce hepatic
Diabetes and an eGFR < 45 mL/min/1.73 m2
creatinine production
Underestimation, High red meat diets and creatine Suspected acute kidney injury, e.g. eGFR decrease ≥ 20%
i.e. true GFR likely supplementation between measurements
to be higher Increased muscle mass Suspected progressive CKD, e.g. eGFR decline of > 15 mL/
Medicines that limit creatinine min/1.73m2 within 12 months if initial eGFR < 60 mL/
excretion, e.g. fenofibrate or
trimethoprim min/1.73m2
Pregnancy Suspected intrinsic kidney disease, e.g. acute
Age < 18 years glomerulonephritis may be suspected in unwell patients

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 who are dehydrated, with rapidly rising creatinine, 2. Preventing or slowing CKD progression, primarily
increasing oedema and blood pressure, proteinuria and through pharmacological management of blood
haematuria pressure and hyperglycaemia (if the patient has
Haematuria in the absence of urinary contamination, e.g. diabetes)
bacteriuria
Resistant hypertension and/or significant issues with Software-based decision support, audit and patient recall
blood glucose and/or multiple vascular complications systems are an important part of best practice in the
management of CKD.3
Consider discussing patients with a nephrologist if there is any
uncertainty regarding referral. As CKD progresses, changes If you do not have an integrated CKD decision support
in bone mineral metabolism and calcium and phosphate installed in your patient management system (PMS), contact
metabolism develop.10 Anaemia will often occur in patients BPAC Clinical Solutions (bpacsolutions.co.nz/contact/) for
with severely reduced kidney function due to a reduction information about their CKD module.
in kidney synthesis of erythropoietin.10 Complications of
advanced CKD will be managed by a kidney team, e.g. acidosis, Complementary community-based care strategies involving
metabolic bone disease, anaemia, malnutrition, infection risk nurse-lead teams have been shown to improve short-term
and acute kidney injury.3 outcomes in patients with moderate CKD who are at high-risk
of progressing to kidney failure (see: “The utility of nurse-led
Managing patients with CKD in primary care management programmes: the DEFEND trial”).3, 19
The majority of patients with stable CKD can be fully managed
in primary care, particularly if they have stable grade G3 CKD In rare cases, a reversible cause of CKD may be present
or are aged over 75 years with early and stable grade G4 CKD.3 in patients with a recent diagnosis or be the driver of
Given that CKD rarely occurs in isolation, patients often have acute deterioration in those with established disease. If
other co-morbidities which may share common management corrected, this may lead to recovery of kidney function.
strategies and priorities.10 Examples include hypovolaemia, sepsis, urinary
tract obstruction and nephrotoxic medicine use, e.g.
The key aspects of CKD management in primary care are:9, 10 NSAIDs.9, 10 For further information, see: “Preventing
1. Lifestyle changes to optimise CKD management and the acute kidney injury in patients with CKD”.
associated CVD risk

CKD is a prominent risk factor for gout

Declining kidney function limits urate clearance, resulting Monitoring kidney function in patients with CKD and
in increased serum levels; once this passes the saturation gout is particularly important as many of the medicines
point, monosodium urate crystal deposition can occur in used to treat gout are potentially nephrotoxic, and initial
joints, resulting in gout symptoms for some patients.15 dosing decisions are made according to the patient’s eGFR
Up to 70% of patients with gout have an eGFR < 60 mL/ status.16 For example, patients with CKD who are receiving
min/1.73 m2, and gout further increases the CVD risk in urate lowering treatment require a lower starting dose of
patients with CKD.16 As with CKD, the prevalence of gout allopurinol, and more gradual dose escalation.15
increases with age and rates are significantly higher for
Māori and Pacific peoples.15 For further information on the medicines, dosing
Urate lowering treatment is indicated in patients with decisions and monitoring considerations involved in gout
symptomatic hyperuricaemia and grade ≥ G3 CKD (i.e. management, see:
eGFR < 60 mL/min/1.73m2) – kidney dysfunction alone bpac.org.nz/2021/gout-part1.aspx
is not an indication for urate lowering treatment in the bpac.org.nz/2021/gout-part2.aspx
absence of a gout flare.17, 18

www.bpac.org.nz November 2022 7

Lifestyle management of CKD Reducing alcohol consumption. All patients with
Lifestyle modifications are important for all patients with CKD CKD should be advised to have at least two alcohol-
as they can help to slow the rate of kidney function decline free days per week, and ideally only have one or two
and reduce the patient’s overall CVD risk.10, 20 These changes standard drinks on the days they consume alcohol.
can also be recommended to people who have risk factors for
CKD but do not yet have evidence of impairment, as part of a For further information on alcohol, see bpac.
general kidney health discussion. org.nz/2018/alcohol.aspx

Key examples of lifestyle changes and their benefits include:10, 20 Smoking cessation. Smoking is an important
modifiable risk factor for CKD progression and
Weight loss. Reducing BMI to at least ≤ 30 kg/m2 encouraging cessation should be a priority, if
with an ideal target of ≤ 25 kg/m2. Weight reduction relevant. The few studies that have been conducted
of 5.1 kg decreases systolic blood pressure by on the effects of smoking cessation in patients
approximately 4.4 mmHg. Central obesity is an with CKD have found that albuminuria decreases
important risk factor, and a waist circumference for significantly and the progression of diabetic
males of < 94 cm and for females < 88 cm should neuropathy slowed.21, 22
be targeted.
Achieving these recommendations may be difficult for some
For further information on weight loss, see: patients, and despite evidence for their efficacy in clinical trials,
“Weight loss: the options and the evidence” there is variable success in the real-world setting.20

Exercise. Performing 150 – 300 minutes/week of

Poor communication and planning has been
moderate intensity physical activity or 75 – 150
highlighted as a barrier to Māori engaging
minutes/week of vigorous intensity physical exercise
with interventions to promote kidney health. 23
is estimated to reduce systolic blood pressure by
Consideration must be given to whether lifestyle
3 – 5 mmHg. Strength/resistance training is advised
advice is culturally appropriate and tailored to their
on at least two days per week, e.g. lifting weights,
priorities.23 For example, nutritional changes may be
using a resistance band, stair climbing.
difficult for individuals to adopt when the sharing of
food has significant importance in engaging with their
Nutrition. Patients with CKD should be advised
whānau. Inclusion of family members in the planning
to eat a balanced diet which emphasises intake
process is one strategy to create an environment that
of fruits, vegetables, nuts, low-fat dairy products,
promotes long-term adherence.
whole grains and fish, e.g. the DASH diet. In addition,
the diet should include the following features:
Reduce sodium intake to no more than 2.3 g The jury remains out on low-protein diets
per day (≤ 6 g/day total salt); this change One of the most extensively studied dietary interventions
alone can help achieve a decrease in systolic for CKD is protein restriction, however, investigations have
blood pressure of 4 – 7 mmHg. Advise patients yielded mixed results over time. This approach is proposed to
to avoid adding salt during cooking or at the reduce progressive glomerular injury by reducing glomerular
table, and to select salt reduced packaged hyperfiltration.20 Several guidelines still recommend patients
food products, where possible. with CKD should maintain a normal daily intake of protein, i.e.
Avoid trans fats and minimise intake of 0.8 g/kg/day, and that low protein diets should be avoided as
processed meats, refined carbohydrates and insufficient dietary protein can lead to malnutrition, particularly
sweetened beverages in older patients.10, 13
Drink water to satisfy thirst but avoid The 2020 Kidney Disease Outcomes Quality Initiative
overconsumption (KDOQI) clinical guideline for nutrition in CKD recommended
High protein diets and creatine supplements that, under close supervision, stable patients with grades
should be avoided in patients with CKD. The G3 – 5 CKD (without diabetes and not on dialysis) consume
suitability of protein restriction continues to 0.55 – 0.6 g/kg/day of protein to prevent hyperfiltration and
be debated in the literature (see: “The jury kidney disease progression.24 This equates to 48 g of protein
remains out on low protein diets”) and is not per day for an 80 kg person, e.g. approximately 170 g of fillet
routinely recommended. steak, 150 g chicken breast or 190 g of canned tuna.25 However,

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other food sources also contribute to total protein intake and Overall blood pressure objective. There is variation between
these should be factored in when reviewing options, e.g. soy guidelines regarding the recommended blood pressure target
protein sources, grains, nuts and pulses.25 Vegetable-derived for patients with CKD:
proteins may induce lower levels of glomerular hyperfiltration Guidelines from the International Society of
than animal-derived protein, and can be more suitable in Hypertension and American College of Cardiology (ACC)/
certain situations, e.g. patients with hyperphosphataemia.20 American Heart Association (AHA) recommend a target
systolic blood pressure of < 130/80 mmHg26, 27; NICE
Recommendation of a low protein diet is not considered guidelines also recommend this target for patients with
standard practice in New Zealand for the treatment of CKD and albuminuria13
patients with CKD. If it is being considered, it should ideally KDIGO 2021 guidelines on blood pressure management
be under the guidance of a dietitian or nephrologist. Excessive in CKD recommend that for patients not undergoing
protein restriction (e.g. 0.3 – 0.4 g/kg/day) in particular is not dialysis, a more assertive systolic blood pressure
recommended unless under dietitian/nephrologist supervision target of < 120 mmHg is appropriate (N.B. diastolic
– complementary ketoacid analogue supplementation may be target not specified);28 they also place an emphasis
required.24 on using standardised methods for clinic blood
pressure measurements, and note that out-of-office
For further information on the nutritional content of foods, measurements (with at-home or ambulatory monitoring)
see: nutritionfoundation.org.nz/nutrition-facts/nutrients/ should be considered as a complementary strategy
protein/ wherever possible

Pharmacological treatment Evidence supporting systolic blood pressure targets of <

in patients with CKD 120 mmHg is more limited and, if being considered, is most
All patients with a new diagnosis of CKD should have their likely to benefit patients with CKD and multiple additional
current medicines reviewed for potential nephrotoxicity, CVD risk factors or those with proteinuric CKD. More lenient
and consider whether dose adjustments, switching or blood pressure targets (e.g. < 140/90 mmHg) may be more
discontinuation is required. Key examples include NSAIDs appropriate for some patient groups, e.g. frail patients or those
and certain antibiotics (e.g. aminoglycosides and penicillins).9 with a high burden of co-morbidities.
Also consider any use of over-the-counter NSAIDs or other
nephrotoxic substances, as well as complementary or First-line treatment: ACE or ARB.
alternative medicines. Decisions around nephrotoxic medicine Either an angiotensin converting enzyme (ACE) inhibitor or an
use can sometimes be challenging in the setting of CKD; while angiotensin II receptor blocker (ARB) should be used first-line
they may contribute to further deteriorating kidney function, for controlling blood pressure in patients with CKD.10, 28 ARBs
some are essential to the management of other pre-existing are often preferred due to the comparable efficacy and lower
conditions. If there is uncertainty, seek secondary care advice. risk of adverse effects. ACE inhibitors and ARBs also have an
antiproteinuric effect, which is most pronounced in patients
There are several traditional Rongoā Māori treatments on a low sodium diet.28 Following initiation, patients should
for kidney and urinary complaints. These include be monitored* for acute reductions in serum creatinine and
Kawakawa (Māori Pepper Tree), Karamu (Coprosma), hyperkalaemia (see: “Stopping an ACE inhibitor or ARB due to
Manuka (Red tea tree) and Kanuka (White tea tree). hyperkalaemia in a patient with CKD should be a last resort”)
While patients should generally be supported in the – ideally within one to two weeks in the first instance, then less
use of traditional healing remedies when there is no frequently once the target blood pressure is achieved.10, 28 If
evidence for harm, advise stopping use if there is following initiation serum creatinine reduces by ≥ 30% or eGFR
suspicion of nephrotoxicity or possible interactions decreases ≥ 25% from baseline, consider a dose decrease or
between the active ingredient and other conventional discontinuation and investigate possible non-pharmacological
medicines being taken. causes, e.g. a rapid deterioration may indicate possible renal
artery stenosis.28
* Other laboratory investigations such as renin, aldosterone and
angiotensin testing are not routinely required and would most likely be
Blood pressure management
arranged in secondary care, or after discussion with a nephrologist
Pharmacological treatment of blood pressure is a cornerstone
of CKD management, both to prevent or slow the rate of Concurrent use of an ACE inhibitor and ARB is not
disease progression and to bolster the effects lifestyle changes recommended in clinical guidelines,28 however, there is some
have on reducing overall CVD risk. evidence that dual ACE inhibitor/ARB treatment is effective

www.bpac.org.nz November 2022 9

for preventing end-stage kidney disease.29 This combination co-morbidities), as these increase serum potassium levels
should generally not be used unless under the guidance of a more significantly than ACE inhibitors/ARBs
nephrologist. Consider stopping/switching any other medicines and
supplements that impair kidney function or reduce
Escalating antihypertensive treatment: CCB is often the potassium excretion if hyperkalaemia is an issue
next step. Consider diuretics to increase potassium excretion by the
KDIGO guidelines recommend titrating the ACE inhibitor/ kidneys (e.g. frusemide), particularly if the patient has
ARB dose to the maximum (approved) tolerated level in resistant hypertension or volume overload
most patients with CKD to optimise their antiproteinuric Oral sodium bicarbonate can be used if the patient has
effect.* 28 This differs somewhat to the approach for managing metabolic acidosis
uncomplicated hypertension in international guidelines,
where there is increasing emphasis on the early use of low- Glycaemic control
dose dual antihypertensive treatment (i.e. avoiding early high One in two primary care patients with diabetes meet the
dose monotherapy). criteria for CKD.10 Glycaemic control is essential in patients
Ultimately, many patients with CKD will eventually with these co-morbidities to prevent or delay the progression
require multiple medicines to achieve blood pressure targets of microvascular complications (e.g. diabetic neuropathy) and
and this need increases as a patient’s eGFR declines.10 There reduce overall CVD risk.30
is little evidence to identify the optimal combination of
antihypertensives for patients with CKD. In those requiring Glycaemic target. A HbA1c target of < 53 mmol/mol is generally
treatment escalation, adding a calcium channel blocker (CCB) is appropriate for patients with CKD and diabetes, but more
a suitable next step.28 The efficacy of thiazide diuretics reduces lenient targets can be considered depending on individual
with worsening kidney impairment; loop diuretics may instead circumstances, e.g. older patients living alone, or those with
be beneficial, if required, particularly in patients with an eGFR multiple other co-morbidities or a limited life expectancy.10
< 30 mL/min/1.73m2. A beta-blocker may be considered as Given that hypoglycaemia becomes more common as eGFR
another option for combination treatment, particularly if decreases, less intensive glycaemic control may be appropriate
indicated for CVD co-morbidities (especially in patients with in patients with advanced grade G4 and grade G5 CKD.3, 10
diastolic dysfunction).28
* While the KDIGO guidelines do not specifically recommend against this Treatment strategy. The initial approach to glycaemic control
titration strategy in patients with advanced CKD (e.g. eGFR < 30 mL/ in patients with CKD and diabetes is lifestyle changes plus
min/1.73m2), they note that there is not yet sufficient RCT evidence metformin.30 The maximum dose of metformin in patients with
to guide use (most studies exclude such patients). Management
CKD will depend on their kidney function (Table 3).31, 32
decisions for patients with advanced CKD should ideally be made under
nephrologist guidance. If antihypertensive treatment is being initiated
while awaiting referral, a lower initial dose may be required depending Table 3. The maximum dose of metformin based on the
on the ACE inhibitor/ARB used (see the corresponding New Zealand
patient’s kidney function.31, 32
Formulary monograph for further information).
Patient eGFR Maximum recommended
(mL/min/1.73m2)* metformin dose
Stopping an ACE inhibitor or ARB due to hyperkalaemia in
a patient with CKD should be a last resort ≥ 60 2 g daily
Up to 10% of patients with CKD treated with ACE inhibitors/
30 – 59 1 g daily
ARBs in primary care develop hyperkalaemia and increases
in serum potassium of approximately 0.5 mmol/L are 15 – 29 0.5 g daily
common.10, 28, 30 In a long-term CKD management setting,
serum potassium levels up to 6.0 mmol/L are acceptable. < 15 Contraindicated

* While in many cases eGFR will be sufficient to estimate kidney function

Before lowering the dose or stopping use altogether, clinicians in patients taking metformin, the NZF recommends using the
should consider other options to reduce serum potassium in Cockcroft-Gault equation for a more accurate calculation of creatinine
patients with CKD if the increase is < 30% from the baseline clearance, which may be particularly useful in people with more severe
renal impairment.32 A calculator is available here: www.mdcalc.com/
value, including:28
creatinine-clearance-cockcroft-gault-equation.
Reduce dietary potassium intake
Stop or switch out beta-blocker if the patient is taking Escalating glycaemic control with a SGLT-2 inhibitor. If
one (if it will not compromise management of any metformin is insufficient for controlling HbA1c, use of a sodium
glucose co-transporter-2 (SGLT-2) inhibitor is recommended

10 November 2022 www.bpac.org.nz

as this has dual kidney- and cardio-protective effects.30
Empagliflozin is the only SGLT-2 inhibitor currently available
Preventing acute kidney injury in
in New Zealand; while KDIGO guidance states that a SGLT-2
patients with CKD
inhibitor should be initiated concurrently with metformin in
most patients,30 the Special Authority criteria for empagliflozin People with CKD have an increased risk of developing
requires that patients with diabetes and CKD have “an HbA1c acute kidney injury.10 Medicines are a common cause
level > 53 mmol/mol despite the regular use of at least one blood- and those with acute illness (e.g. a gastrointestinal illness,
glucose lowering agent (e.g. metformin, vildagliptin or insulin) for sepsis and respiratory or urinary tract infection causing
at least three months”. hypovolaemia) are at significant risk.
In people with CKD, some medicines should be used
SGLT-2 inhibitors may also be beneficial in non-diabetic with caution. For example, the “triple whammy” of NSAIDs,
patients with CKD. There is evidence that patients with ACE inhibitors (or ARBs) and diuretics can potentiate
proteinuric CKD without diabetes still benefit from SGLT-2 acute kidney injury by interfering with homeostatic
inhibitor use.33 However, under the current Special Authority mechanisms needed to preserve kidney perfusion during
criteria this would involve patients having to self-fund acute illness.10 Adequate fluid intake and electrolyte
treatment. This option should be discussed with patients, so maintenance are important in people with CKD who are
they have the opportunity to consider it depending on their acutely unwell.
individual circumstances, as appropriate.
The Mnemonic: SAD MANS can be used as a reminder of
Additional glucose lowering treatments. If further medicines which should be withheld in people with CKD
management is required, the addition of a glucagon-like during an acute illness:10
peptide-1 (GLP-1) receptor agonist can be considered as the Sulfonylureas
next step in management,30 however, dual SGLT-2 inhibitor/ ACE-inhibitors
GLP-1 receptor agonist treatment is not currently funded in
Diuretics
New Zealand. Alternatives include vildagliptin, pioglitazone
(unless the patient has heart failure), a sulfonylurea or insulin. Metformin
ARBs
For further information on:
NSAIDs
The management of diabetes, see: bpac.org.nz/2021/
SGLT-2 inhibitors
diabetes-management.aspx
SGLT-2 inhibitors and GLP-1 receptor antagonists, see:
bpac.org.nz/2021/diabetes.aspx Use of essential medicines (e.g. ACE inhibitors, ARBs,
metformin and SGLT-2 inhibitors) should then
recommence once the patient recovers from the acute
Additional medicines to consider illness.
Lipid management. Dyslipidaemia is common among
patients with CKD, particularly high triglyceride and low HDL-C Patients with CKD undergoing medical procedures.
levels.34 Given the high risk of CVD associated with CKD, the People with CKD are also at an increased risk of developing
benefits of statin treatment (starting with atorvastatin) should acute kidney injury when they undergo procedures
be discussed with patients.10, 34 Addition of ezetimibe (Special involving radiocontrast material and it may be necessary
Authority approval required) can be considered for patients to temporarily withdraw potentially nephrotoxic
whose LDL-C remains > 2 mmol/L despite the maximal medicines.10 The use of metformin is contraindicated
tolerated statin dose.10, 34 in patients undergoing procedures involving iodine-
containing X-ray contrast media due to the small risk of
Antiplatelet treatment. In general, long-term aspirin use lactic acidosis (particularly in elderly patients), e.g. when
should be considered for secondary prevention in patients investigating cancers.35
with CKD and established CVD.9, 30 Dual antiplatelet treatment
(e.g. aspirin + clopidogrel) may be considered for patients
with acute coronary syndrome or after percutaneous coronary
intervention.30 Aspirin may also be considered for primary
prevention in patients with a high risk of atherosclerotic events
unless there is an increased bleeding risk.9, 10

www.bpac.org.nz November 2022 11

Monitoring patients with established CKD
Acknowledgement: Thank you to Professor Rob Walker,
Patients with established CKD should have their eGFR and Nephrologist, Dunedin School of Medicine, University of
albuminuria assessed at least annually.10 Table 4 provides Otago for expert review of this article.
a recommended monitoring schedule for patients with
N.B. Expert reviewers do not write the articles and are not responsible for
established CKD according to severity. Patients with the final content. bpacnz retains editorial oversight of all content.
progressive grade G3 – 4 CKD have a much greater risk of South Link
Education Trust Article supported by the South Link Education Trust
developing kidney failure and require intensive management
with weekly or fortnightly review of risk factor management
until their condition is stable.3

Table 4. Monitoring and investigation schedule for patients with CKD.10

CKD parameters Frequency of review Clinical assessment Laboratory investigations

eGFR ≥ 60 mL/min/1.73m2 Annually; less frequent Blood pressure Serum creatinine

with microalbuminuria; or review may be appropriate Weight (eGFR), urine ACR, serum
eGFR 45 – 59 mL/min/1.73m2 if patient’s eGFR is stable Medicine use; avoid electrolytes, urea, HbA1c for
with normoalbuminuria and risk factors are well nephrotoxic options and patients with diabetes, lipids
controlled adjust doses to levels
appropriate for level of
eGFR 30 – 59 mL/min/1.73m2 Every 3 to 6 months kidney function Serum creatinine
with microalbuminuria; or (eGFR), urine ACR, serum
eGFR 30 – 44 mL/min/1.73m2 electrolytes, urea, HbA1c for
with normoalbuminuria patients with diabetes, lipids

Macroalbuminuria Every 1 to 3 months In addition to the above: In addition to the above:

irrespective of eGFR status; or checking for features plasma bicarbonate
eGFR < 30 mL/min/1.73m2 of advanced CKD, e.g.
Investigations will likely be
irrespective of albuminuria oedema
determined in conjunction
status
with a nephrologist

The utility of nurse-led management programmes for CKD: the DEFEND trial

General practice can help support improved outcomes was attributed to Māori and Pacific healthcare assistants
for patients at high risk of progressing to kidney failure providing culturally appropriate care, the more frequent
through relatively simple complementary nurse-led follow-up and prompting of patients to take medicines,
interventions involving the use of healthcare assistants. and reduced costs to patients because of home visits.36
The DElay Future End-stage Nephropathy due to After the intervention ended in 11 – 21 months,
Diabetes (DEFEND) trial involved 65 Māori and Pacific patients reverted back to routine medical care. In a 2015
patients aged 47 – 75 years with type 2 diabetes, moderate follow-up study, the initial short-term improvements
CKD and hypertension, living in Auckland.36 Patients in systolic blood pressure and proteinuria for the
received either routine medical care and follow-up or intervention cohort did not result in long-term reductions
nurse-led, community based, monthly assessments and in mortality and end-stage kidney disease rates compared
monitoring delivered by healthcare assistants.36 This study with the usual care group.37 These findings indicate that
found that community care resulted in clinically significant such community-based interventions may need to be
decreases in systolic blood pressure and proteinuria as initiated earlier and maintained throughout care to have
well as delayed progression of left ventricular hypertrophy a more meaningful impact for people with CKD.37
and diastolic dysfunction.36 The success of the programme

12 November 2022 www.bpac.org.nz

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