Nephrology Flashcards
What is the definition of acute kidney injury?
AKI defined as rise in serum creatinine or a decline in urine output that develops within hours to days (RIFLE, AKIN, KDIGO)
Increase in serum creatinine by ≥0.3 mg/dL within 48 hours
Increase to ≥1.5 times the presumed baseline value over 7 days
Decrease in UOP to <3 mL/kg over six hours
What is the differential for obstructive accute kidney injury?
Anatomical
Organ prolapse, gynecologic tumor
Drugs
Opiates, anticholinergics, antipsychotics
Operative
Pain, anesthesia
Neurological
Cord trauma, MS
Infectious
How do you manage obstructive AKI?
- Catherization if bladder volume > 400 cc
- Alpha blockers? Lower resting urethral pressure, but no difference vs placebo in success of voiding.
How do you treat Anti-GBM disease?
- Remove existin AB
- plasmapheresis for 1-2 weeks
- Prevention of new AB
- Cyclophosphamide dail for 3 months
- Pulse dose of prednisone for 3 days
What is rhabdomyolysis?
Syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation.
What are the causes of rhabdomyolysis?
- Trauma or Muscle Compression
- Non-traumatic Exertional
- Physically untrained, sickle cell trait, hypokalemia, metabolic myopathies
- Non-traumatic Non-exertional
- Drugs, toxins, infections
- Endocrine Disorders
- Diabetes, hypothyroidism
What are the clinical manifestation and physical exam findings in a patient with rhabdomyolysis?
- Symptoms:
- Classic triad: muscle pain, weakness, dark urine
- Physical Findings:
- Muscle tenderness/swelling/weakness, skin changes
- Be AWARE of compartment syndrome!
What are the laboratory findings in a patient with rhabdomyolysis?
- Elevated CK
- Urine studies
- Myogobulinuria
- Elevated LFTs
- Fluid and Electrolyte Abnormalities
- Hypovolemia
- Hyperkalemia and Hyperphosphatemia
- Hypocalcemia
- AKI
How do you manage a patient with rhabdomyolysis?
Volume repletion with isotonic fluids.
What is the differential for crescenteric glomerulonephritis on renal biopsy?
- Anti-GBM antibody disease
- Immune complex deposition; IgA nephropathy, post-streptococcal, lupus nephritis
- Pauci-immune; Necrotizing GN without immune deposits (i.e. ANCA vasculitis)
What is a crescent within the glomerulus?
Two or more layers of proliferating cells in Bowman’s space due to severe injury to glomerular capillary wall
What is the terminology of anti-glomerular basement membrane disease?
- Anti-GBM disease:
- Anti-GBM antibodies + GN
- Goodpasture’s disease:
- Anti-GBM antibodies + GN + pulmonary hemorrhage
- Goodpasture’s syndrome:
- GN + pulmonary hemorrhage
What is the epidemiology of anti-GBM disease?
- Rare - annual incidence of 0.5-0.9 cases per million
- White predominance
- Bimodal distribution: 3rd decade + 6th decade
- Older patients (> 50 years) more likely to have isolated GN without pulmonary hemorrhage
How do you diagnose anti-GBM disease?
- Look for Anti-GBM AB in the serum or kidney
- Renal biopsy looking at light microscopy and immunoflourescence
- There is a direct correlation between serum creatinine and percent of glomeruli with crescents.
How do you treat anti-GBM disease?
- Remove existing antibodies
- Plasmapheresis x 1-2 weeks
- 4L/day daily
- Improved mortality + morbidity since its introduction
- Monitoring anti-GBM antibodies
- Plasmapheresis x 1-2 weeks
- Prevent formation of new antibodies
- Cyclophosphamide x 3 months
- 2 mg PO/kg/day: IV vs. oral – unknown relative efficacy
- Rituximab as substitute
- Steroids x 6-12 months
- Pulse dose x 3 days à prednisone 1 mg/kg PO daily
- Cyclophosphamide x 3 months
- Treatment efficacy depends on kidney function at time of diagnosis
SCr < 5.7 (n = 19): 100% patient survival, 95% renal survival at 1 year
SCr > 5.7 but not HD dependent: (n = 13), 83% patient survival, 82% renal survival at 1 year
Dialysis-dependent (n = 39), 65% patient survival, 8% renal survival at 1 year
