Management of chronic kidney disease (CKD) can be divided into four phases: diagnosis, prevention of progression, management of complications such as metabolic bone disease or anemia, and renal replacement therapy with dialysis or renal transplantation. The latter two phases are best managed by nephrologists. A brief summary of the diagnostic approach to CKD appears in "Evaluation of patients with chronic kidney disease" and a brief summary of how to prevent or slow its progression appears below.

Slowing progression of CKD

Summary:
Consideration should be given to the use of an ACE inhibitor or Angiotensin receptor blocker, tight blood pressure control (<130/80), use of a statin in patients with dyslipidemia, recommending smoking cessation, and optimization of glycemic control in patients with diabetes mellitus. Multiple antihypertensive medications and dietary sodium restriction may be required to achieve the blood pressure target. Patients with GFR <60 ml/min/1.73m2 should avoid NSAIDS, COXIBs and other nephrotoxins such as intravenous contrast if possible.

1. Why use an ACE inhibitor or angiotensin receptor blocker in CKD?

Drugs which interrupt the renin-angiotensin system have been repeatedly shown to slow or prevent progression to end-stage renal disease. Although blood pressure reduction is critical for management of CKD, the advantages of ACE inhibitors and angiotensin receptor blockers are additional to those seen with tight blood pressure control achieved with other drugs. Although they are most effective in renal diseases with proteinuria, they seem to be advantageous in almost all forms of CKD.

2. Is it safe to use an ACE inhibitor or angiotensin receptor blocker in CKD?

Aside from general considerations which apply to all patients (the possibility of allergy, angioedema etc), the major risks of using these drugs in CKD are:

  a. precipitating an acute deterioration in kidney function (see below)

  b. hyperkalemia

These agents are generally safe for use in CKD providing that follow-up monitoring is performed. In all CKD patients, a low starting dose should be used, and the serum electrolytes and serum creatinine rechecked within 7-10 days. The dose can then be titrated up, rechecking serum electrolytes and serum creatinine within 5-7 days of each dose increase.

ACE inhibitors or angiotensin receptor blockers should be used with caution in CKD patients with known renal artery stenosis, pre-existing hyperkalemia. For patients currently receiving potassium supplements, consideration should be given to discontinuing these prior to starting an ACEi or ARB.

3. What should I do if kidney function deteriorates after starting an ACE inhibitor or angiotensin receptor blocker?

Declines in kidney function of up to 25% (i.e. a rise of serum creatinine of <25% or a fall in estimated GFR of 25%) following introduction of an ACE inhibitor or angiotensin receptor blocker are acceptable, provided that kidney function stabilizes at this level. This is the expected response, since ACEi / ARB will reduce intraglomerular pressure. If kidney function continues to deteriorate, however, the agent should be discontinued and kidney function rechecked. In the unlikely event that kidney function does not improve, Nephrology referral should be considered.

4. What should I do if hyperkalemia develops after starting an ACE inhibitor or angiotensin receptor blocker?

Mild hyperkalemia (serum potassium of 5.1 - 5.8 mmol/l) is common in patients with CKD who receive these agents. If the rate of rise has been very rapid or the absolute increase has been high, consideration should be given to stopping the agent or decreasing the dose. Otherwise, it is generally safe to recheck serum potassium in a few days.

More severe hyperkalemia should be managed by stopping the agent or decreasing the dose, and considering other appropriate treatment of hyperkalemia (depending on the serum potassium level). The addition of a thiazide or loop diuretic may also help lower serum potassium levels while maintaining the use of the ACE inhibitor or angiotensin receptor blocker.

5. What is the optimal blood pressure in patients with CKD?

The answer to this question is not known with certainty. Tight blood pressure control is certainly beneficial, and it is clear that multiple drugs will be required to achieve good control. Many patients will require three or four drugs, and dietary sodium restriction is essential. Current guidelines recommend reduction of blood pressure to <130/80, and <130/80 for patients with significant proteinuria (more than 1 g per day; equivalent to an albumin:creatinine ratio > 35 mg/mmol).

6. Why prescribe a statin to patients with CKD?

Patients with CKD are at high risk for cardiovascular events, and CKD is considered a cardiovascular risk equivalent (like diabetes mellitus). Statins are safe and effective for preventing cardiovascular events in most patients with CKD, and may also slow the rate of kidney function loss. To minimize the risk of toxicity, statins should be started at a low dose in people with CKD, and combined use of statins and fibrates should be avoided.

7. What drugs should be avoided in patients with CKD?

Iatrogenic declines in kidney function are common in patients with CKD. Common offending agents include NSAIDS and COXIBs, radiocontrast, and aminoglycoside antibiotics. Many agents are safe for use in patients with CKD, but will require dose reduction. It is good practice to look up the dose of all drugs when prescribing for CKD patients to ensure that dose reduction is not required. Aspirin, in low dose (75-325 mg/day), is generally safe in CKD and may reduce cardiovascular risk.

8. Why recommend smoking cessation to CKD patients?

Aside from general considerations about the benefits of smoking cessation, smokers with CKD appear to have more rapid kidney function loss, compared to non-smokers. Therefore, recommending smoking cessation may also preserve kidney function.

9. What is the target for glycemic control in patients with CKD and diabetes mellitus?

The targets for glycemic control are the same in patients with and without CKD. However, it is important to realize that hypoglycemic agents (including insulin) are cleared by the kidney, and so gradual dose reductions may be necessary, particularly in patients whose kidney function deteriorates. Unexpected hypoglycemia in patients with CKD should trigger measurement of kidney function, since hypoglycemia may represent accumulation of hypoglycemic agents due to increased severity of renal dysfunction.