From the Guidelines
For acute kidney injury (AKI) with active sediment, I strongly recommend immediate nephrology consultation along with supportive care, including fluid management, electrolyte correction, and avoidance of nephrotoxic medications, as the presence of active sediment suggests an inflammatory process that requires prompt intervention to prevent progression to chronic kidney disease or end-stage renal disease. Active sediment, such as red blood cells, white blood cells, and casts, indicates a renal cause of AKI, such as glomerulonephritis or vasculitis, rather than pre-renal or obstructive causes 1.
The initial management of AKI with active sediment should include a comprehensive workup, consisting of:
- Urinalysis to assess for proteinuria, hematuria, and casts
- Urine microscopy to evaluate for cellular casts and other abnormalities
- Protein-to-creatinine ratio to quantify proteinuria
- Complete blood count to assess for anemia, leukocytosis, or thrombocytopenia
- Comprehensive metabolic panel to evaluate electrolyte imbalances and renal function
- Serologic studies, including complement levels, ANCA, and anti-GBM antibodies, to diagnose specific renal diseases 1.
Blood pressure control is essential in the management of AKI, and medications like ACE inhibitors or ARBs may be used if appropriate, as they can help reduce proteinuria and slow disease progression 1. Depending on the underlying cause of AKI, immunosuppressive therapy may be necessary, such as corticosteroids (e.g., prednisone 1 mg/kg/day), cyclophosphamide, or rituximab 1.
Renal biopsy is frequently necessary to determine the specific pathology and guide treatment, as it can provide valuable information on the underlying cause of AKI and help identify potential targets for therapy 1. Patients should be monitored closely for worsening kidney function, with regular creatinine measurements and urine output tracking, to promptly identify any changes in renal function and adjust treatment accordingly 1.
From the Research
Acute Kidney Injury (AKI) with Active Sediment
- AKI refers to any acute decrease in glomerular filtration rate, regardless of etiology 2
- The staging of AKI is recommended to stratify AKI patients according to the severity of the condition, based on serum creatinine level and urine output 2
- Classification of AKI into prerenal, intrinsic renal, and postrenal etiologies is helpful in differential diagnosis and management 2, 3
Etiology and Pathogenesis
- AKI can result from decreased renal perfusion, drug-induced, contrast-associated, postoperative, and sepsis-associated causes 2
- Acute tubular necrosis, caused by either ischemia or nephrotoxicity, is common in the setting of AKI 3
- The timely and accurate identification of AKI and a better understanding of the pathophysiological mechanisms that cause kidney dysfunction are essential 3
Treatment and Management
- Appropriate treatment of AKI patients involves management of the underlying etiology, when possible, and use of nondialytic and dialytic therapies 2
- The use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) in AKI patients may decrease all-cause mortality, but increases the risk of acute kidney disease (AKD) 4, 5
- ACEI/ARB therapy is associated with a lower risk of recurrent adverse kidney events after AKI, but a higher risk of hyperkalemia 4
Clinical Outcomes
- AKI can result in many short- and long-term complications, including chronic kidney disease and end-stage renal disease 2
- The overall patient mortality rate in AKI patients is high, with a reported rate of 28.4% in one meta-analysis 4
- The use of ACEIs/ARBs in AKI patients may have a survival benefit, but requires close clinical monitoring due to the risk of hyperkalemia 4, 5