Acute Allergic Interstitial Nephritis Flashcards
• Usually occurs within 2 weeks of therapy
Acute Allergic Interstitial Nephritis
the prototype
Methicillin-induced
presentation of Acute Allergic Interstitial Nephritis
Fever, maculopapular rash, eosinophilia, arthralgia, and
oliguria.
– Tubular dysfunction may be manifested by acidosis,
hyperkalemia, salt wasting, and concentrating defects
NSAID induced AIN
6-months, 70% have nephrotic
syndrome (proteinuria >3.5 g/day
the most definitive method for diagnosis For AIN
Renal biopsy
Pathogenesis of Acute Allergic Interstitial Nephritis
allergic sensitivity response,
granulomas and tubular epithelial cell necrosis are
common
• Risk factors:
Acute Allergic Interstitial Nephritis
No specific risk factors (idiosyncratic hypersensitivity
reactions)
– Individuals with other drug allergies may have increased
risk
Prevention of Acute Allergic Interstitial Nephritis
: monitor patient carefully, discontinuing the
offending drug
Managment of AIN
corticosteroid (prednisolone), monitor
kidney function
Chronic Interstitial Nephritis
- Lithium:
- Cyclosporine & Tacrolimus
- Aristolochic acid
Usually occurs after 10 to 20 years of treatment
lithium
– Nephrogenic diabetes insipidus is seen in up to 87% of patients
lithium
Presentation of lithium
Polydipsia
polyuria
20%, fibrosis in the first 5 years of therapy
Pathogenesis of lithium
Impaired ability to concentrate urine is a result of a
decrease in collecting duct response to antidiuretic hormone, which
may be related to downregulation of aquaporin 2 water channel
expression
risk factors of lithium
: long term therapy, age
Prevention of lithium CKD
Maintaining lithium concentrations as low as
therapeutically possible, avoiding dehydration, and
monitoring kidney function.
– Amiloride: prevention and treatment of nephrogenic diabetes
insipidus, since it blocks epithelial sodium transport of lithium into the
cortical collecting duct
Management of lithium
Discontinuation of lithium therapy or start with amiloride 5
to 10 mg daily during lithium therapy
– Monitor kidney function and lithium serum concentrations
– Delayed nephritis after several months of therapy and can
result in irreversible kidney disease
- Cyclosporine & Tacrolimus
– ESRD develops within 6 to 24 months of exposure
. Aristolochic acid
Can use chromic & acute Interstitial Nephritis & DI
lithium
Presentation of 3. Aristolochic acid
: hypertension, mild proteinuria, glucosuria, high
Scr, anemia
Pathogenesis of . Aristolochic acid
metabolites bind to DNA and cause direct DNA
damage and may lead to proximal tubular atrophy and
apoptosis
• Implies inflammation of the vessel wall, capillaries, or
glomeruli and is typically classified according to vessel
size
Renal Vasculitis
presentation of renal vasculitis
Patients present with hematuria, proteinuria, oliguria,
and red cell casts, frequently along with fever, malaise,
myalgias, and arthralgia
Treatment of Renal Vasculitis
: D/C the offending drug, administer
corticosteroids or other immunosuppressive therapy
Outpatient setting, nephrotoxicity is recognized by
the symptoms of
malaise, anorexia, vomiting, volume overload (shortness of breath
or edema), and hypertension
Outpatient setting, nephrotoxicity is recognized by
the symptoms of
malaise, anorexia, vomiting, volume overload (shortness of breath
or edema), and hypertension
Nephrotoxicity may also be evidenced by
y primary alterations in
renal tubular function: proteinuria, biomarkers
Many toxic substances including drugs are filtered through kidney
High concentration in the kidney, i.e., aminoglycosides, cisplatin
Directly affect on glomerular membranes
Immunologic reaction, gold, penicillamine
increase uric acid
increase chance to
crystal formation
The primary agents associated with this type of injury are↓↓1-Tubular Epithelial Cell Damage
A.Aminoglycosides B. radiocontrast media C. cisplatin, D. amphotericin B E. foscarnet F. osmotically active agents such as immunoglobulins, dextrans, and mannitol
Typically seen within 5 to 10 days of therapy
A.Aminoglycoside
Presentation:↓↓ of aminoglycosiodes
• Nonoliguria, microscopic hematuria and proteinuria
sometimes
pathogenesis of aminoglycosides
Accumulation of high drug conc within proximal tubular cells, and
generation of reactive oxygen species that produce mitochondrial injury,
which leads to cellular apoptosis and necrosis.
The number of cationic groups appears to correlate with the
nephrotoxicity: neomycin > gentamicin > tobramycin > amikacin
aminoglycosides cause renal vasoconstriction and mesangial contraction
Prevention of aminoglycosides
Follow up the patient and switch to another antibiotic as
fluoroquinolones (e.g., ciprofloxacin or levofloxacin) and
third-or fourth-generation cephalosporins (e.g., ceftazidime
or cefepime).
– Avoid volume depletion and other nephrotoxic drugs.
– Aminoglycoside dose adjustment
– concurrent use of antioxidant compounds such as alpha- lipoic acid, vitamin E and N-acetylcysteine
management of amionoglycosides
D/C aminoglycoside or the dosage regimen revised if AKI is evident. Usually reversible after drug D/C D/C other nephrotoxic agents Hydration Short-term RRT may be necessary
• Third leading cause of hospital-acquired AKI, accounting
for 10-13% of case
Contrast media-induced nephrotoxicity
- Increased risk in patients with CKD or DM
* 5x increased risk of death
Contrast media-induced nephrotoxicity
Presentation Contrast media-induced nephrotoxicity
s nonoliguria with kidney injury apparent within 24
to 48 hrs of administration
– Scr peaks between 3 and 4 days and recovers after 7-10 days
– Urine: Casts with low Na
(rise in
SCr of at least 0.5 mg/dL (44 μmol/L) or a 25% increase in Scr within 48
hours of contrast administration.
Contrast media-induced nephrotoxicity
