Acute Tubulointerstitial Nephritis

Question 1

What is the definition?

Answer 1

Acute inflammation of the renal interstitium and tubules that causes a decline in the renal function over a period of days to weeks

Question 2

What is the pathophysiology?

Answer 2

Inflammatory infiltrates → tissue edema and tubular cell damage → compromised tubular flow

Acute obstruction: crystals (from e.g., uric acid, medications) or proteins (e.g., light chains) obstruct tubules

Allergic interstitial nephritis: drugs act as haptens → type IV hypersensitivity reaction

Question 3

What is the aetiology?

Answer 3

Medications (most common) - antibiotics, NSAID’s, PPI’s, loop diuretics and thiazides, anticonvulsants

Infection - E. coli, viruses (HIV, cmv, EBV, HSV), parasites, fungi

Autoimmune - sjogrens disease, sarcoidosis

Question 4

What are the clinical features?

Answer 4

Morbiliform rash
Fever
Arthalgias
Flank pain

Question 5

What is the diagnosis?

Answer 5

Blood tests - BMP - increased BUN and creatinine
CBC - increased eosinophils

Urinalysis - sterile pyuria, sub nephrotic range proteinuria, microscopic Hematuria
Urine microscopy - WBC casts, RBC casts, waxy casts, granular casts, tubular epithelial casts

Renal ultrasound to rule other causes of (acute kidney damage). Findings - often normal, many demonstrate enlarged kidneys with increased echogenicity, reflecting interstitial oedema

Renal biopsy - findings - diffuse or patchy peritubular inflammatory cell infiltrates, interstitial oedema, sparing of glomeruli and vessels

Question 6

What is the DD?

Answer 6

Other causes of intrinsic AKI eg vasculitis, acute tubular necrosis
Prerenal AKI
Postrenal AKI

Question 7

What is the treatment?

Answer 7

Stop causative agents or treat underlying systemic disease.
Provide supportive care for AKI.
Consider systemic glucocorticoids under specialist guidance.
Monitor kidney function; evaluate for indications for acute dialysis.