Using cystatin C as an additional test will have financial implications (additional costs of testing but cost savings through reduced management costs). kidney disease; eGFR = estimated glomerular filtration rate; GFR = glomerular filtration rate. Pharmacotherapy Treatment strategies in CKD are aimed at reducing CVD risk, delaying CKD progression, addressing complications of CKD Arsonic acid and, where possible, managing the underlying cause. The treatment of specific causes of kidney disease, such as glomerulonephritis, is usually outside the scope of this guideline. Blood pressure control It is widely accepted that this progression of CKD is usually partly related to common secondary factors independent of the underlying cause of CKD. These factors include intra-glomerular hypertension, glomerular hypertrophy and proteinuria which lead to adaptive hyperfiltration, glomerular scarring and interstitial fibrosis.6 Numerous meta-analyses have demonstrated that intensive blood pressure lowering reduces progression of CKD in people with proteinuric CKD but not in those without proteinuria.7C9 Over-treatment of hypertension is also associated with an increased risk of adverse outcomes. Blood pressure target ranges are therefore recommended. These are shown in Table ?Table22. Table 2. Blood pressure targets in chronic kidney disease CKDBP 120C139/<90 mmHgCKD and diabetesBP 120C129/<80 mmHgCKD and ACR 70 mg/mmolBP 120C129/<80 mmHg Open in a separate window ACR = albumin to creatinine ratio; BP = blood pressure; CKD = chronic kidney disease. The role of renin-angiotensin system antagonists in diabetes associated with proteinuria is usually well established.10C12 Renin-angiotensin system antagonists also have specific reno-protective effects in proteinuric non-diabetic CKD independent of blood pressure control, reducing proteinuria and CKD progression as defined by doubling of baseline serum creatinine or development of end-stage kidney disease. The effect is usually greatest in those with higher levels of proteinuria.13 The indications for initiating renin-angiotensin system antagonists in CKD are summarised in Box ?Box1.1. Potassium and eGFR Arsonic acid should be measured before starting renin-angiotensin system antagonists and repeated 1 to 2 2 weeks after starting renin-angiotensin system antagonists and after each dose increase. Renin-angiotensin system antagonists should not be routinely offered to people with CKD if the pre-treatment potassium is usually >5.0 mmol/L, and stopped if the potassium increases to 6.0 mmol/L and other drugs known to promote hyperkalaemia have been discontinued. A combination of renin-angiotensin system antagonists should not be offered to people with CKD. Box 1. Indications for renin-angiotensin system antagonists in chronic kidney disease Diabetes and ACR 3 mg/mmolHypertension and ACR 30 mg/mmolACR 70 mg/mmol irrespective of hypertension or CVD Open in a separate window ACR = albumin MDS1 to creatinine ratio; CVD = cardiovascular disease Hypertension in people with CKD but without diabetes or ACR 30 mg/mmol should be managed according to the treatment recommendations in NICE guideline Hypertension in adults: diagnosis and management: NICE guideline [NG136].14 Other Arsonic acid strategies for renal protection There is some evidence that treatment of chronic metabolic acidosis with oral sodium bicarbonate may slow the progression to end-stage kidney disease.15 Consider oral sodium bicarbonate supplementation for people with both: a GFR <30 mL/min/1.73 m2 and a serum bicarbonate concentration <20 mmol/L. It is well established that glycaemic control in patients with diabetes mellitus can slow the development of albuminuria and CKD progression.16,17 There is also more recent evidence of a role for sodium-glucose co-transporter-2 inhibitors in reducing proteinuria and slowing the progressing of CKD in patients with type 2 diabetes.18 A detailed discussion of these findings is outside the scope of this article. Cardiovascular risk reduction Lipid lowering is usually important in CKD to reduce cardiovascular risk. Clinicians should follow the recommendations in NICE guideline Cardiovascular disease: risk assessment and reduction, including lipid modification: Clinical guideline [CG181],.