Management of Acute Kidney Injury Due to Glomerular Causes
The management of AKI due to glomerular causes requires prompt identification of the underlying pathology and implementation of specific therapeutic interventions targeting both the glomerular disease and supportive care measures. 1
Diagnostic Approach
- Urinalysis and sediment examination: Look for hematuria, proteinuria, or abnormal urinary sediment which are key indicators of glomerular disease 2, 1
- Laboratory evaluation:
- Serum creatinine to stage AKI severity
- Urine protein quantification
- Serologic evaluation for glomerular diseases (complement levels, ANCA, anti-GBM antibodies)
- Kidney biopsy: Essential for definitive diagnosis of glomerular causes of AKI, particularly in cases of:
- Rapidly progressive glomerulonephritis
- Nephrotic syndrome with AKI
- Unexplained AKI with active urinary sediment 2
Specific Management Based on Glomerular Pathology
Rapidly Progressive Glomerulonephritis (RPGN)
Immediate immunosuppressive therapy:
Plasma exchange:
- Indicated for anti-GBM disease
- Consider for severe ANCA-associated vasculitis with pulmonary hemorrhage 1
Acute Interstitial Nephritis (AIN)
- Identify and discontinue offending agent (medications, infections)
- Corticosteroid therapy:
- Prednisone 1 mg/kg/day if no improvement after removing offending agent
- Taper over 4-6 weeks 1
Minimal Change Disease with AKI
- Corticosteroid therapy:
- Prednisone 1 mg/kg/day (maximum 80 mg)
- Continue until remission, then taper 2
Supportive Care Measures
Volume Management
- Assess volume status through clinical examination, vital signs, and weight changes 1
- Fluid management:
Medication Management
Discontinue nephrotoxic medications:
- NSAIDs
- Aminoglycosides
- ACE inhibitors/ARBs in the acute setting 1
Blood pressure control:
- Target BP <140/90 mmHg
- Once stabilized, consider ACEi/ARB for proteinuria >0.5 g/day 2
Nutritional Support
- Provide 20-30 kcal/kg/day total energy intake
- Protein intake of 0.8-1.0 g/kg/day in non-catabolic patients without dialysis
- Prefer enteral nutrition when possible 1
Electrolyte and Acid-Base Management
- Monitor and correct electrolyte abnormalities:
- Hyperkalemia
- Hypocalcemia
- Hyperphosphatemia
- Metabolic acidosis 3
Renal Replacement Therapy (RRT)
Indications for RRT
- Severe metabolic acidosis unresponsive to medical management
- Refractory hyperkalemia
- Volume overload unresponsive to diuretics
- Uremic symptoms (encephalopathy, pericarditis)
- Severe AKI with oliguria/anuria 2, 1
Modality Selection
- Continuous renal replacement therapy (CRRT): Preferred for hemodynamically unstable patients
- Intermittent hemodialysis: For stable patients
- Peritoneal dialysis: Alternative in pediatric patients or when other modalities unavailable 2, 1
Follow-up and Monitoring
Short-term monitoring:
- Serial measurements of serum creatinine every 2-4 days during hospitalization
- Monitor urine output and electrolytes
Long-term follow-up:
Common Pitfalls to Avoid
- Delayed diagnosis: Failure to recognize glomerular causes of AKI can lead to irreversible kidney damage
- Inadequate immunosuppression: Undertreating aggressive glomerular diseases can result in progression to kidney failure
- Overaggressive fluid resuscitation: Can worsen pulmonary edema in patients with glomerulonephritis and volume overload 2
- Failure to follow up: AKI due to glomerular causes carries significant risk for progression to CKD 4
By following this structured approach to management, clinicians can optimize outcomes for patients with AKI due to glomerular causes, reducing mortality and the risk of progression to chronic kidney disease.