National guide to a preventive health assessment for Aboriginal and Torres Strait Islander people

Chapter 13: Chronic kidney disease prevention and management

Recommendations: Chronic kidney disease prevention and management
Preventive intervention type	Who is at risk?	What should be done?	How often?	Level/ strength of evidence	References
Screening	People aged 18–29 years without any chronic kidney disease (CKD) risk factors	Screen for CKD risk factors (smoking, obesity, hypertension, diabetes, history of acute kidney injury, family history of kidney disease)	As part of an annual health assessment	IIIB	^21, ³⁸
Screening	All people aged ≥30 years People aged 18–29 years with one or more of the CKD risk factors in Table 3	Screen for CKD with estimated glomerular filtration rate (eGFR) and urinary albumin– creatinine ratio (ACR; first void specimen preferred) If urine ACR is raised, repeat once or twice over three months (first void specimens if possible). For further quantification, consider collecting a timed specimen	Every two years (at least annual if CKD risk factor present)	IIIC	^21,²²
Behavioural	Adults with any risk factors for CKD (refer above)	Offer individualised, structured education about risk factor avoidance and management	Opportunistic	IIIB	³⁹
		Offer smoking cessation support (refer to Chapter 1: Lifestyle, ‘Smoking’) Advise avoidance of exposure to environmental tobacco smoke	Opportunistic	IIIB	^26,^31,⁴⁰
		Encourage regular physical exercise appropriate to physical ability and medical history (refer to Chapter 1: Lifestyle, ‘Physical activity’)	Opportunistic	IIIB	^29, ³¹
		If overweight or obese, encourage weight loss Offer group diet and exercise sessions if available, especially for patients with type 2 diabetes (refer to Chapter 1: Lifestyle, ‘Overweight and obesity’)	Opportunistic	IIIB	^31, ⁴¹
		Advise limiting dietary sodium intake to less than 100 mmol/day (6 g salt per day	Opportunistic	IIIB	³¹
	Adults with CKD stages 1–3 (Table 1)	Lifestyle risk factor management as above	Opportunistic	As above for each risk factor	^26, ^29, ^31, ^39–41
		Encourage a balanced diet rich in fruit, vegetables and dietary fibre	Opportunistic	IIC	³¹
		Advise consumption of the recommended daily intake of protein for adults (0.75 g/kg/day	Opportunistic	IIC	^31,⁴²
		Advise against salt substitutes that contain high amounts of potassium	Opportunistic	GPP	³¹
		A daily fluid intake of 2–2.5 L (including the fluid content of foods) is generally considered sufficient, although this might need to be varied according to individual circumstances	Opportunistic	IIIC	³¹
Chemo-prophylaxis	All persons with CKD	Regularly review medications to identify and avoid those with potential nephrotoxicity Advise patients taking an angiotensinconverting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) plus diuretic to avoid non-steroidal antiinflammatory drugs (other than low-dose aspirin if indicated)	Opportunistic at every medication change	GPP	^36, ⁴³
	Adults with albuminuria (Table 2)	Advise treatment with an ACE inhibitor or ARB, regardless of eGFR or blood pressure (BP) level. The goal is >50% reduction in albumin excretion without symptomatic hypotension Concurrently advise minimising salt intake to <6 g per day	At diagnosis	IA	^32, ^36, ⁴⁴
	Adults with albuminuria (Table 2)	An ACE inhibitor and ARB should not normally be prescribed together		IIB	³³
	Adults with CKD and diabetes	Blood glucose control in patients with CKD and diabetes should be optimised, aiming for an individualised glycated haemoglobin (HbA1c) target that takes into account factors such as capacity and safety considerations	Opportunistic	IA	^40, ⁴⁵
	Adults with CKD and BP consistently above 140/90 mmHg	Recommend lifestyle changes as noted above, plus drug treatment aiming at BP <140/90 mmHg. Note that aiming towards systolic BP <120 mmHg has shown additional benefit when well tolerated by the patient (The number of drugs required to achieve target BP tends to increase with declining GFR)	Opportunistic BP check at every visit	IA	⁴⁶
	Adults with CKD and BP consistently above 140/90 mmHg	In patients with diabetes or albuminuria, commence antihypertensive treatment with an ACE inhibitor or, if not tolerated, an ARB		IA	^32, ^46–48
	Adults with CKD	Patients with CKD who are not receiving dialysis should be offered statin therapy to reduce the risk of vascular events	At diagnosis	IA	^32, ³⁴
Environmental	Communities with high prevalence of scabies and pyoderma	Support the implementation of populationbased strategies for reduction of scabies and pyoderma among children (refer to Chapter 3: Child health, and Chapter 10: Acute rheumatic fever and rheumatic heart disease)		IIIB	^30, ⁴⁹

Table 1. Stages of chronic kidney disease
Stage	Description	GFR (ml/min/1.73 m² )
1	Kidney damage* with normal or increased GFR	>89
2	Kidney damage* with mild reduced GFR	60–89
3A	Moderately reduced GFR	45–59
3B	Moderately reduced GFR	30–44
4	Severely reduced GFR	15–29
5	Kidney failure	<15 or dialysis
_{GFR, glomerular filtration rate} _{*Kidney damage includes pathological abnormality or a marker of damage such as abnormalities in blood tests, urine tests or imaging studies degree}¹.

Table 2. Definitions of normal albumin excretion, microalbuminuria and macroalbuminuria
	Gender	Normal albumin excretion	Microalbuminuria	Macroalbuminuria
Urinary albumin–creatinine ratio (ACR)	Male	<2.5 mg/mmol	2.5–25 mg/mmol	>25 mg/mmol
	Female	<3.5 mg/mmol	3.5–35 mg/mmol	>35 mg/mmol
Urinary albumin excretion per 24 hours	Either	<30 mg/24 hours	30–300 mg/24 hours	>300 mg/24 hours

Table 3. Risk factors for chronic kidney disease³⁸
Modifiable	Non-modifiable
Smoking Obesity (BMI >30 kg/m² ) Hypertension Diabetes Severe socioeconomic disadvantage	Aboriginal or Torres Strait Islander aged >30 years Stage 5 CKD or hereditary kidney disease in a first-degree or second-degree relative History of acute kidney injury Established vascular disease
BMI, body mass index; CKD, chronic kidney disease

Background

Chronic kidney disease (CKD) in adults is defined as either kidney damage or a glomerular filtration rate (GFR) <60 ml/min/1.73 m², or both, persisting for at least three months. Kidney damage in this definition includes pathological abnormality or a marker of damage such as abnormalities in blood tests, urine tests or imaging studies.¹ CKD is classified into six stages depending on GFR, as outlined in Table 1.^1,2 Note that stage 2 CKD requires evidence of kidney damage in addition to reduced GFR, whereas stages 3A–5 are defined on the basis of GFR alone.

Aboriginal and Torres Strait Islander peoples have a greatly increased prevalence of CKD,³ and are approximately five times more likely than non-Indigenous Australians to develop end-stage kidney failure.⁴ Decline in GFR appears to be faster in Aboriginal and Torres Strait Islander individuals than in non-Indigenous individuals, and increased albumin excretion is a powerful predictor of GFR decline.⁵ However, there is great variation in prevalence between Aboriginal and Torres Strait Islander communities; rates are highest in remote areas and lowest in urban areas.^3,6 Rates also correlate strongly with socioeconomic disadvantage.^4,7 The reasons are multifactorial,⁸ but important modifiable risk factors in Aboriginal and Torres Strait Islander peoples are thought to be the same as those in non-Indigenous people: overweight and obesity, diabetes, hypertension and smoking.^3,4

Reduced GFR and raised urinary albumin excretion are independent risk factors for mortality.⁹ The bulk of this mortality is due to cardiovascular disease (CVD), and people with CKD are at higher risk of dying from CVD than they are of progressing to end-stage kidney disease (ESKD).^10,11 Even mild reduction in GFR is associated with excess cardiovascular and stroke risk,^12,13 while at any given level of kidney function, microalbuminuria or macroalbuminuria is associated with increased cardiovascular and stroke morbidity and mortality.^14,15

Interventions

GFR testing

In clinical practice, GFR is often estimated (eGFR) from serum creatinine and other parameters, including sex and age, using a formula such as that of the CKD epidemiology collaboration (CKD-EPI). This formula has been shown to perform well in Aboriginal and Torres Strait Islander people, both with and without diabetes.¹⁶ Care should be taken in accepting an eGFR at face value. Factors such as inter-current illness, certain diets, underweight, overweight, muscle diseases, high muscle mass or severe liver disease can bias the estimate.

Proteinuria and albuminuria testing

Abnormal proteinuria is an important marker of kidney damage. Urinary protein usually includes albumin, and the proportion of total protein that is albumin is typically increased at higher levels of proteinuria.¹⁷ In diabetes and under most other circumstances, measurement of urinary albumin is a more sensitive test for CKD than testing for proteinuria; in the AusDiab baseline study, only 8% of adults with proteinuria tested negative for albuminuria.¹⁷ The majority of Australian and international guidelines recommend screening for albuminuria rather than proteinuria for the detection of CKD.¹⁸ However, it is important to note that not all individuals with CKD exhibit abnormal albumin or protein excretion, and also that a small proportion of patients with abnormal proteinuria, such as those with tubulointerstitial disease or myeloma, may excrete abnormal amounts of non-albumin protein only.

Abnormal albumin excretion is classified as microalbuminuria (30–300 mg/24 hours) or macroalbuminuria (>300 mg/24 hours).¹⁸ A properly performed dipstick test, if negative, rules out macroalbuminuria but not microalbuminuria; a positive result requires confirmation by laboratory methods.¹⁹ It is often convenient to measure the albumin–creatinine ratio (ACR) on a spot specimen, preferably taken during first morning void. Table 2 provides definitions for microalbuminuria and macroalbuminuria based on ACR estimation. However, the relationship between this ratio and the albumin excretion rate is influenced by many factors, so that estimation of 24-hour excretion from the ACR value is not recommended.¹⁸

Albumin excretion may be increased by urinary tract infection, acute febrile illness, high dietary protein, heart failure, recent heavy exercise or some drugs. Menstruation or vaginal discharge may also increase urinary albumin levels. Definition of abnormal albuminuria requires at least two elevated ACR measurements in a three-month period, so that a single abnormal test should be repeated.¹⁸

Primary prevention

Evidence supports the efficacy and cost-effectiveness of screening for CKD risk factors (Table 3), and for CKD, in Aboriginal and Torres Strait Islander peoples.^20,21 In the absence of risk factors, current guidelines recommend measuring albumin excretion and eGFR at least biennially from the age of 30 years.^21,22 However, the 2012–13 Australian Aboriginal and Torres Strait Islander Health Survey found 17.9% of participants aged ≥18 years had indicators of CKD, so that biennial screening of all adults should be considered.²³ Measurement of albumin excretion and eGFR should be offered at least annually to patients with risk factors.

The robust epidemiological evidence and plausible biological explanations for the association of overweight and obesity, diabetes, hypertension and smoking with CKD suggest that interventions to prevent diabetes,^24,25 to promote exercise, healthy diet and normal weight, to limit salt intake and to discourage smoking have the potential also to reduce the incidence of CKD.^26–29 Programs to promote maternal health during pregnancy, and to prevent streptococcal infection in childhood, may also reduce future risk of CKD.³⁰

Secondary prevention

Active treatment of CKD, once detected, can slow progression to end-stage disease, and reduce cardiovascular endpoints. Patients should be assisted to quit smoking,²⁶ consume a healthy diet, reduce excess weight³¹ and take regular exercise.²⁹ Limiting dietary sodium intake to no more than 100 mmol
(approximately 6 g salt) per day may reduce both blood pressure and albumin excretion.³¹

An angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) is generally the first-line treatment for lowering blood pressure (BP) and protein excretion. These two classes of drug should not normally be prescribed together: although the combination may reduce both BP and proteinuria to a greater extent than monotherapy with either, it is associated with an increase in adverse effects and worse renal outcomes.^32,33
Statins lower death and major cardiovascular events in people with CKD not requiring dialysis.³⁴ The effects on stroke and progression of CKD are uncertain.

Referral to secondary care

The interventions in the ‘Recommendations’ are concerned with preventing kidney disease, detecting and slowing the progression of established CKD, and reducing the associated risks of CVD and stroke. While they are all amenable to delivery in the primary care setting, patients with more advanced disease or significant comorbidities, or at risk in other ways, are likely to benefit from referral to a secondary care nephrology service.³⁵ Australian guidelines recommend referral of patients with any of the following:^36,37

stage 4 or 5 CKD of any cause
persisting macroalbuminuria (Table 2)
a sustained decrease in eGFR of 25% or more, or a sustained decrease in eGFR of 15 mL/min/1.73 m² within 12 months
glomerular haematuria with albuminuria
CKD and elevated BP that is not at target despite at least three BP–lowering medications.

Resources
Kidney Health Australia, Chronic kidney disease (CKD) management in general practice: Guidance and clinical tips to help identify, manage and refer patients with CKD in your practice, 3rd edition Kidney Health Australia, Caring for Australasians with Renal Impairment (CARI), guidelines

National guide to a preventive health assessment for Aboriginal and Torres Strait Islander people

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