What is the management and treatment of azotemia?

Management and Treatment of Azotemia

Immediate Assessment and Diagnosis

The first priority in managing azotemia is to determine whether it is prerenal, intrinsic renal, or postrenal in origin, as this fundamentally directs treatment strategy. 1

Diagnostic Evaluation

• Prerenal azotemia is characterized by fractional excretion of sodium (FENa) <1%, urine sodium <10 mEq/L, and bland urine sediment 1
• FENa <1% has 100% sensitivity for prerenal causes, though specificity is lower at 14% 1
• Postrenal azotemia from urinary obstruction requires immediate restoration of urine flow through catheterization or other decompression methods 2
• Intrinsic renal disease typically shows FENa >1% and active urine sediment 1

Treatment Based on Etiology

Prerenal Azotemia Management

Prerenal azotemia typically responds to volume repletion and correction of the underlying hypoperfusion state. 1

• Restore intravascular volume with intravenous fluids 2
• Correct volume depletion before initiating or continuing ACE inhibitors or ARBs 3
• Temporarily discontinue or reduce ACE inhibitors, ARBs, and aldosterone antagonists in patients with worsening azotemia until renal function improves 4
• Prerenal azotemia is potentially reversible if the underlying cause of hypoperfusion is corrected 1

Postrenal Azotemia Management

Immediate therapy must be directed at restoring urine flow, as this is potentially life-threatening. 2

• Place urinary catheter or perform surgical decompression to relieve obstruction 5, 2
• Correct extracellular fluid volume deficits with intravenous fluids 2
• Minimize cardiac toxicity of hyperkalemia if present 2
• Ameliorate cardiovascular effects of metabolic acidosis 2
• Most patients respond quickly and completely to therapeutic intervention 2
• Dialysis may be postponed in extreme obstructive azotemia if there is evidence of residual renal function and obstruction can be promptly relieved 5

Drug-Induced Azotemia Management

Identify and discontinue the offending medication immediately. 6, 7

• Several drugs reduce renal perfusion and cause prerenal azotemia 6
• NSAIDs should be avoided in patients with heart failure or renal disease, as they inhibit renal prostaglandin production and promote sodium retention 8
• The combination of NSAIDs with ACE inhibitors and diuretics significantly increases the risk of renal failure 8
• ACE inhibitors can cause acute renal failure in patients with bilateral renal artery stenosis or stenosis to a solitary kidney by decreasing transglomerular hydrostatic pressure 4
• Clinically significant azotemia from ACE inhibitors is defined as >50% rise in serum creatinine that persists after correcting hypoperfusion states 4

Management in Heart Failure with Azotemia

Small or moderate elevations of blood urea nitrogen and serum creatinine should not lead to efforts to minimize the intensity of diuretic therapy, provided that renal function stabilizes. 4

Diuretic Management

• Progressive increments in loop diuretic dose are often required as heart failure advances 4
• Add a second diuretic with complementary mode of action (e.g., metolazone) if volume overload persists 4
• Hospitalization is generally required for further adjustment of therapy if outpatient management fails 4
• Intravenous dopamine or dobutamine may elicit marked increase in urine volume 4
• Diuresis is frequently accompanied by worsening azotemia, especially if patients are also being treated with an ACE inhibitor 4

Advanced Interventions

• If the degree of renal dysfunction is severe or edema becomes resistant to treatment, ultrafiltration or hemofiltration may be needed to achieve adequate control of fluid retention 4
• Mechanical methods of fluid removal can produce meaningful clinical benefits in patients with diuretic-resistant heart failure 4
• Ultrafiltration may restore responsiveness to conventional doses of loop diuretics 4

Neurohormonal Inhibitor Management

• Patients admitted with worsening azotemia should be considered for reduction in or temporary discontinuation of ACE inhibitors, ARBs, and/or aldosterone antagonists until renal function improves 4
• ACE inhibitors should not be initiated in patients with systolic blood pressure <80 mmHg or signs of peripheral hypoperfusion 4
• Small increases in blood urea nitrogen and serum creatinine are not an indication to discontinue ACE inhibitors or ARBs, as they have been shown to improve survival in patients with heart failure due to systolic dysfunction 4

Special Considerations in Cirrhosis

In patients with hepatic cirrhosis and ascites, diuretic therapy is best initiated in the hospital. 9

• Sudden alterations of fluid and electrolyte balance may precipitate hepatic coma 9
• If increasing azotemia and oliguria occur during treatment of severe progressive renal disease, furosemide should be discontinued 9
• Supplemental potassium chloride and aldosterone antagonists help prevent hypokalemia and metabolic alkalosis 9

Critical Pitfalls to Avoid

• Do not discontinue ACE inhibitors or ARBs for small increases in creatinine (<50% rise) in heart failure patients, as these medications improve survival 4
• Do not discharge heart failure patients from the hospital until a stable and effective diuretic regimen is established and ideally until euvolemia is achieved 4
• Do not combine NSAIDs with ACE inhibitors and diuretics in patients at risk, as this significantly increases renal failure risk 8
• Excessive diuresis in combination with initiation of ACE inhibitors or ARBs may result in increased blood urea nitrogen and serum creatinine 4