2. Introduction
• CKD is common but silent and under recognised condition in Malaysia
• CKD is a strong risk factor for mortality and coronary events
• If CKD is detected early and treated early, the deteorarion of kidney
function can be reduced as 50%
• CKD is a progressive reduction of functioning renal tissue such that
the remaining kidney mass can no longer maintain the body’s
internal environment.
7. Staging of CKD
•Markers of kidney damage is defined as either:
o albuminuria (AER ≥30 mg/24 hours or ACR ≥3 mg/mmol)
o urine sediment abnormalities
o electrolyte and other abnormalities due to tubular disorders
o abnormalities detected by histology
o structural abnormalities detected by imaging
o history of kidney transplantation
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8. Classification of CKD
•Classification of CKD should be based upon cause, GFR category and
albumin category (CGA).
o Cause
‒ Presence or absence of systemic disease and location within the kidney of observed or
presumed HPE findings
oGFR category
oAlbuminuria category
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15. Established
1. Optimal BP
control
2. Proteinuria
reduction
3. RAS blockers
4. Glycaemic
control
Need more
evidence
1. Life style
modifications
2. SGLT-2
inhibitors
3. Uric acid
reduction
Not proven
1. Dual RAS
blockade
2. Lipid lowering
3. Vitamin D
analogue
4. Pentoxyfylline
5. Traditional
medicine
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Strategies to delay CKD progression
17. Optimal blood pressure control
• The majority of CKD patients (70 - 80%) have
hypertension (usually systolic) which is more severe than
non-CKD patients.9
• BP lowering has an impact on all-cause mortality,
cardiovascular (CV) events, stroke risk and progression of
kidney disease.
• Any class of antihypertensive agents can be used to
control BP in CKD.9
• However, some antihypertensive agents have additional
antiproteinuric effect [e.g. Angiotensin-Converting
Enzyme Inhibitor (ACEi)/Angiotensin Receptor Blocker
(ARB)].
9. MoH, Malaysia. Management of CKD in Adults. Putrajaya: MoH; 2011
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20. Glycaemic control for renoprotection
• Optimal glycaemic control should be attained to reduce the
complications of diabetes.
• Aggressive glycaemic control in patients with established CVD
may increase the risks of hypoglycaemia and death due to
impaired drug metabolism.9
• Regular blood glucose measurements are advised for more
accurate assessment of diabetic control as HbA1c maybe falsely
low in CKD due to anaemia.9
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23. Dietary protein restriction
•Proteinuria is an independent CV risk factor and
an independent predictor for renal disease
progression.9
•Protein restriction is one of the supportive
measures to delay CKD progression.9
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24. Sodium-glucose co-transporter-2 (SGLT-2)
inhibitors
•Potential agent
•Recent trials (EMPA-REG, CANVAS/CANVAS-R) on sodium-glucose co-
transporter-2 (SGLT2) inhibitors have been shown to improve CV
outcomes and may have renoprotective effect.39, 40
•Avoid if eGFR <45 ml/min due to reduced efficacy in lowering HbA1c.
•39. Wanner C, et al. N Engl J Med. 2016;375(4):323-34
•40. Neal B, et al. N Engl J Med. 2017;377(7):644-57
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25. Uric acid reduction
•There is emerging evidence to suggest uric acid reduction (e.g. by
allopurinol, febuxostat) is a potential strategy to delay CKD
progression.45, 46, 47
•However, more RCTs are needed to confirm the renoprotective effect.
45. Kanji T, et al. BMC Nephrol. 2015;16:58
46. Bose B, et al. Nephrol Dial Transplant. 2014;29(2):406-13
• 47. Sircar D, et al. Am J Kidney Dis. 2015;66(6):945-50
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