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

Chapter 13: Chronic kidney disease prevention and management
☰ Table of contents

Recommendations: Chronic kidney disease prevention and management

Preventive intervention type

Who is at risk?

What should be done?

How often?

Level/ strength of evidence



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
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


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


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
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
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


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



GFR (ml/min/1.73 m2 )


Kidney damage* with normal or increased GFR



Kidney damage* with mild reduced GFR



Moderately reduced GFR



Moderately reduced GFR



Severely reduced GFR



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 degree1.

Table 2. Definitions of normal albumin excretion, microalbuminuria and macroalbuminuria



Normal albumin excretion



Urinary albumin–creatinine ratio (ACR)


<2.5 mg/mmol

2.5–25 mg/mmol

>25 mg/mmol



<3.5 mg/mmol

3.5–35 mg/mmol

>35 mg/mmol

Urinary albumin excretion per 24 hours


<30 mg/24 hours

30–300 mg/24 hours

>300 mg/24 hours

Table 3. Risk factors for chronic kidney disease38



  • 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


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


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.



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


  1. Stevens PE, Levin A. Evaluation and management of chronic kidney disease: Synopsis of the kidney disease: Improving global outcomes 2012 clinical practice guideline. Ann Intern Med 2013;158(11):825–30.
  2. Johnson DW, Atai E, Chan M, et al. KHA‐CARI guideline: Early chronic kidney disease: Detection, prevention and management. Nephrology 2013;18(5):340–50.
  3. Australian Institiute of Health and Welfare. Cardiovascular disease, diabetes and chronic kidney disease – Australian facts: Aboriginal and Torres Strait Islander people. Canberra: AIHW, 2015.
  4. Australian Institiute of Health and Welfare. Incidence of end-stage kidney disease in Australia 1997–2013. Canberra: AIHW, 2015.
  5. Maple-Brown LJ, Hughes JT, Ritte R, et al. Progression of kidney disease in Indigenous Australians: The eGFR follow-up study. Clin J Am Soc Nephrol 2016;11(6):993–1004.
  6. Preston‐Thomas A, Cass A, O’Rourke P. Trends in the incidence of treated end‐stage kidney disease among Indigenous Australians and access to treatment. Aust N Z J Public Health 2007;31(5):419–21.
  7. Cass A, Cunningham J, Snelling P, Wang Z, Hoy W. End-stage renal disease in Indigenous Australians: A disease of disadvantage. Ethn Dis 2002;12(3):373–78.
  8. Cass A, Cunningham J, Snelling P, Wang Z, Hoy W. Exploring the pathways leading from disadvantage to end-stage renal disease for indigenous Australians. Soc Sci Med 2004;58(4):767–85.
  9. Matsushita K, van der Velde M, Astor BC, et al. Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: A collaborative meta-analysis. Lancet 2010;375(9731):2073–81.
  10. Weiner DE, Tighiouart H, Amin MG, et al. Chronic kidney disease as a risk factor for cardiovascular disease and all-cause mortality: A pooled analysis of community-based studies. J Am Soc Nephrol 2004;15(5):1307–15.
  11. Keith DS, Nichols GA, Gullion CM, Brown J, Smith DH. Longitudinal follow-up and outcomes among a population with chronic kidney disease in a large managed care organization. Arch Intern Med 2004;164(6):659–63.
  12. Di Angelantonio E, Chowdhury R, Sarwar N, Aspelund T, Danesh J, Gudnason V. Chronic kidney disease and risk of major cardiovascular disease and non-vascular mortality: Prospective population based cohort study. BMJ 2010;341:c4986.
  13. Lee M, Saver JL, Chang KH, Liao HW, Chang SC, Ovbiagele B. Low glomerular filtration rate and risk of stroke: Meta-analysis. BMJ 2010;341:c4249.
  14. Lee M, Saver JL, Chang KH, Liao HW, Chang SC, Ovbiagele B. Impact of microalbuminuria on incident stroke: A meta-analysis. Stroke 2010;41(11):2625–31.
  15. Schmieder RE, Schrader J, Zidek W, et al. Low-grade albuminuria and cardiovascular risk: What is the evidence? Clin Res Cardiol 2007;96(5):247–57.
  16. Maple-Brown LJ, Ekinci EI, Hughes JT, et al. Performance of formulas for estimating glomerular filtration rate in Indigenous Australians with and without type 2 diabetes: The eGFR Study. Diabet Med 2014;31(7):829–38.
  17. Atkins RC, Briganti EM, Zimmet PZ, Chadban SJ. Association between albuminuria and proteinuria in the general population: The AusDiab Study. Nephrol Dial Transplant 2003;18(10):2170–74.
  18. Australasian Proteinuria Consensus Working Group. Chronic kidney disease and measurement of albuminuria or proteinuria: A position statement. Med J Aust 2012;197(4):224–25.
  19. White SL, Yu R, Craig JC, Polkinghorne KR, Atkins RC, Chadban SJ. Diagnostic accuracy of urine dipsticks for detection of albuminuria in the general community. Am J Kidney Dis 2011;58(1):19–28.
  20. Mathew T, Corso O. Early detection of chronic kidney disease in Australia: Which way to go? Nephrology 2009;14(4):367–73.
  21. Toussaint N. Caring for Australasians with Renal Impairment (CARI) guidelines: Screening for chronic kidney disease. Sydney: Kidney Health Australia, 2012. [Accessed 12 December 2017].
  22. The Royal Australian College of General Practitioners. Guidelines for preventive activities in general practice. 9th edn. East Melbourne, Vic: RACGP, 2016.
  23. Australian Bureau of Statistics. Australian Aboriginal and Torres Strait Islander Health Survey: Biomedical results 2012–13. [Accessed 12 December 2017].
  24. Paulweber B, Valensi P, Lindstrom J, et al. A European evidence-based guideline for the prevention of type 2 diabetes. Horm Metab Res 2010;42(Suppl 1):S3–36.
  25. Lindstrom J, Ilanne-Parikka P, Peltonen M, et al. Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: Followup of the Finnish Diabetes Prevention Study. Lancet 2006;368(9548):1673–79.
  26. Jones-Burton C, Seliger SL, Scherer RW, et al. Cigarette smoking and incident chronic kidney disease: A systematic review. Am J Nephrol 2007;27(4):342–51.
  27. Forman JP, Stampfer MJ, Curhan GC. Diet and lifestyle risk factors associated with incident hypertension in women. JAMA 2009;302(4):401–11.
  28. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med 2001;344(1):3–10.
  29. White SL, Dunstan DW, Polkinghorne KR, Atkins RC, Cass A, Chadban SJ. Physical inactivity and chronic kidney disease in Australian adults: The AusDiab study. Nutr Metab Cardiovasc Dis 2011;21(2):104–112.
  30. Hoy WE, Kincaid-Smith P, Hughson MD, et al. CKD in Aboriginal Australians. Am J Kidney Dis 2010;56(5):983–93.
  31. Chan M, Johnson D. Caring for Australasians with Renal Impairment (CARI) guidelines: Modification of lifestyle and nutrition interventions for management of early chronic kidney disease. Sydney: Kidney Health Australia, 2012.  [Accessed 12 December 2017].
  32. Phoon R, Johnson D. Caring for Australasians with Renal Impairment (CARI) guidelines: Medical therapies to reduce chronic kidney disease progression and cardiovascular risk. Sydney: Kidney Health Australia, 2012.  [Accessed 12 December 2017].
  33. Mann JF, Schmieder RE, McQueen M, et al. Renal outcomes with telmisartan, ramipril, or both, in people at high vascular risk (the ONTARGET study): A multicentre, randomised, double-blind, controlled trial. Lancet 2008;372(9638):547–53.
  34. Palmer SC, Navaneethan SD, Craig JC, et al. HMG CoA reductase inhibitors (statins) for people with chronic kidney disease not requiring dialysis. Cochrane Database Syst Rev 2014;(5):CD007784.
  35. Black C, Sharma P, Scotland G, et al. Early referral strategies for management of people with markers of renal disease: A systematic review of the evidence of clinical effectiveness, cost-effectiveness and economic analysis. Health Technol Assess 2010;14(21):1–184.
  36. 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 edn. [Accessed 12 December 2017].
  37. Johnson D. Caring for Australasians with Renal Impairment (CARI) guidelines: When to refer for specialist renal care. Sydney: Kidney Health Australia, 2012.  [Accessed 12 December 2017].
  38. Johnson D. Caring for Australasians with Renal Impairment (CARI) guidelines: Risk factors for early chronic kidney disease. Sydney: Kidney Health Australia, 2012. Available at [Accessed 12 December 2017].
  39. Atai E, Johnson D. Caring for Australasians with Renal Impairment (CARI) guidelines: Education strategies. Sydney: Kidney Health Australia, 2012.  [Accessed 12 December 2017].
  40. Chadban S, Howell M, Twigg S, et al. Prevention and management of chronic kidney disease in type 2 diabetes. Nephrology 2010;15:S162–94.
  41. Steinsbekk A, Rygg LO, Lisulo M, Rise MB, Fretheim A. Group based diabetes self-management education compared to routine treatment for people with type 2 diabetes mellitus: A systematic review with meta-analysis. BMC Health Serv Res 2012;12:213.
  42. Robertson L, Waugh N, Robertson A. Protein restriction for diabetic renal disease. Cochrane Database Syst Rev 2007(4):CD002181.
  43. Thomas MC. Diuretics, ACE inhibitors and NSAIDs: The triple whammy. Med J Aust 2000;172:184–85.
  44. D’Elia L, Rossi G, Schiano di Cola M, Savino I, Galletti F, Strazzullo P. Meta-analysis of the effect of dietary sodium restriction with or without concomitant renin-angiotensin-aldosterone system-inhibiting treatment on albuminuria. Clin J Am Soc Nephrol 2015;10(9):1542–52.
  45. Inzucchi SE, Bergenstal RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: A patient-centered approach: Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care 2012;35(6):1364–79.
  46. National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults, 2016. Melbourne: National Heart Foundation of Australia, 2016.
  47. Cheng J, Zhang W, Zhang X, et al. Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: A meta-analysis. JAMA Intern Med 2014;174(5):773–85.
  48. Xie X, Liu Y, Perkovic V, et al. Renin-angiotensin system inhibitors and kidney and cardiovascular outcomes in patients with CKD: A Bayesian network meta-analysis of randomized clinical trials. Am J Kidney Dis 2016;67(5):728–41.
  49. Andrews RM, Kearns T, Connors C, et al. A regional initiative to reduce skin infections amongst Aboriginal children living in remote communities of the Northern Territory, Australia. PLoS Negl Trop Dis 2009;3(11):e554.