Acute Allergic Interstitial Nephritis

Question 1

• Usually occurs within 2 weeks of therapy

Answer 1

Acute Allergic Interstitial Nephritis

Question 2

the prototype

Answer 2

Methicillin-induced

Question 3

presentation of Acute Allergic Interstitial Nephritis

Answer 3

Fever, maculopapular rash, eosinophilia, arthralgia, and
oliguria.
– Tubular dysfunction may be manifested by acidosis,
hyperkalemia, salt wasting, and concentrating defects

Question 4

NSAID induced AIN

Answer 4

6-months, 70% have nephrotic

syndrome (proteinuria >3.5 g/day

Question 5

the most definitive method for diagnosis For AIN

Answer 5

Renal biopsy

Question 6

Pathogenesis of Acute Allergic Interstitial Nephritis

Answer 6

allergic sensitivity response,
granulomas and tubular epithelial cell necrosis are
common

Question 7

• Risk factors:

Acute Allergic Interstitial Nephritis

Answer 7

No specific risk factors (idiosyncratic hypersensitivity
reactions)
– Individuals with other drug allergies may have increased
risk

Question 8

Prevention of Acute Allergic Interstitial Nephritis

Answer 8

: monitor patient carefully, discontinuing the

offending drug

Question 9

Managment of AIN

Answer 9

corticosteroid (prednisolone), monitor

kidney function

Question 10

Chronic Interstitial Nephritis

Answer 10

1. Lithium:
2. Cyclosporine & Tacrolimus
3. Aristolochic acid

Question 11

Usually occurs after 10 to 20 years of treatment

Answer 11

lithium

Question 12

– Nephrogenic diabetes insipidus is seen in up to 87% of patients

Answer 12

lithium

Question 13

Presentation of lithium

Answer 13

Polydipsia
polyuria
20%, fibrosis in the first 5 years of therapy

Question 14

Pathogenesis of lithium

Answer 14

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

Question 15

risk factors of lithium

Answer 15

: long term therapy, age

Question 16

Prevention of lithium CKD

Answer 16

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

Question 17

Management of lithium

Answer 17

Discontinuation of lithium therapy or start with amiloride 5
to 10 mg daily during lithium therapy
– Monitor kidney function and lithium serum concentrations

Question 18

– Delayed nephritis after several months of therapy and can

result in irreversible kidney disease

Answer 18

2. Cyclosporine & Tacrolimus

Question 19

– ESRD develops within 6 to 24 months of exposure

Answer 19

. Aristolochic acid

Question 20

Can use chromic & acute Interstitial Nephritis & DI

Answer 20

lithium

Question 21

Presentation of 3. Aristolochic acid

Answer 21

: hypertension, mild proteinuria, glucosuria, high

Scr, anemia

Question 22

Pathogenesis of . Aristolochic acid

Answer 22

metabolites bind to DNA and cause direct DNA
damage and may lead to proximal tubular atrophy and
apoptosis

Question 23

• Implies inflammation of the vessel wall, capillaries, or
glomeruli and is typically classified according to vessel
size

Answer 23

Renal Vasculitis

Question 24

presentation of renal vasculitis

Answer 24

Patients present with hematuria, proteinuria, oliguria,
and red cell casts, frequently along with fever, malaise,
myalgias, and arthralgia

Question 25

Treatment of Renal Vasculitis

Answer 25

: D/C the offending drug, administer

corticosteroids or other immunosuppressive therapy

Question 26

Outpatient setting, nephrotoxicity is recognized by

Answer 26

the symptoms of
malaise, anorexia, vomiting, volume overload (shortness of breath
or edema), and hypertension

Question 26

Outpatient setting, nephrotoxicity is recognized by

Answer 26

the symptoms of
malaise, anorexia, vomiting, volume overload (shortness of breath
or edema), and hypertension

Question 27

Nephrotoxicity may also be evidenced by

Answer 27

y primary alterations in

renal tubular function: proteinuria, biomarkers

Question 28

Many toxic substances including drugs are filtered through kidney

Answer 28

High concentration in the kidney, i.e., aminoglycosides, cisplatin

Question 29

Directly affect on glomerular membranes

Answer 29

Immunologic reaction, gold, penicillamine

Question 30

increase uric acid

increase chance to

Answer 30

crystal formation

Question 31

The primary agents associated with this type of injury are↓↓1-Tubular Epithelial Cell Damage

Answer 31

A.Aminoglycosides
B. radiocontrast media
C. cisplatin,
D. amphotericin B
E. foscarnet
F. osmotically active agents such as immunoglobulins, dextrans, and
mannitol

Question 32

Typically seen within 5 to 10 days of therapy

Answer 32

A.Aminoglycoside

Question 33

Presentation:↓↓ of aminoglycosiodes

Answer 33

• Nonoliguria, microscopic hematuria and proteinuria

sometimes

Question 34

pathogenesis of aminoglycosides

Answer 34

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

Question 35

Prevention of aminoglycosides

Answer 35

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

Question 36

management of amionoglycosides

Answer 36

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

Question 37

• Third leading cause of hospital-acquired AKI, accounting

for 10-13% of case

Answer 37

Contrast media-induced nephrotoxicity

Question 38

• Increased risk in patients with CKD or DM

* 5x increased risk of death

Answer 38

Contrast media-induced nephrotoxicity

Question 39

Presentation Contrast media-induced nephrotoxicity

Answer 39

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

Question 40

(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.

Answer 40

Contrast media-induced nephrotoxicity