Acute tubulointerstitial nephritis
Definition
Acute tubulointerstitial nephritis (ATIN) is an acute inflammation of the renal interstitium and tubules that causes a decline in renal function over a period of days to weeks.
Etiology
Medications (most common)
- Antibiotics: β-lactams, sulfonamides, rifampin, fluoroquinolones
- NSAIDs
- Proton pump inhibitors and H2 blockers
- Loop diuretics and thiazides
- Anticonvulsants: phenytoin, valproate, carbamazepine, phenobarbital
- Other: allopurinol
Pathophysiology
- Immune-mediated tubulointerstitial damage (allergic interstitial nephritis) is the most widely accepted theory.
- Inflammatory infiltrates → tissue edema and tubular cell damage → compromised tubular flow
- Allergic interstitial nephritis: drugs act as haptens → type IV hypersensitivity reaction
- Acute obstruction: crystals (from e.g., uric acid, medications) or proteins (e.g., light chains) obstruct tubules
Clinical features
Clinical features of acute kidney injury, with or without:
- Morbilliform rash
- Fever
- Arthralgias
- Flank pain
Tip
The classic triad of fever, morbilliform rash, and eosinophilia is present in < 10% of patients with ATIN, but their presence can help to guide the diagnosis.
Diagnostics
- Blood tests
- BMP: ↑ BUN and creatinine
- CBC: ↑ eosinophils (more common in drug-induced ATIN)
- Urine studies
- Urinalysis
- Sterile pyuria
- Subnephrotic-range proteinuria
- Microscopic hematuria
- Urine microscopy
- WBC casts , RBC casts , waxy casts , granular casts , tubular epithelial casts
- Urine eosinophils (low sensitivity and specificity for ATIN)
Tip
Although frequently cited as a diagnostic clue, in clinical practice, urine eosinophils lack sensitivity and specificity for reliably confirming ATIN.
Treatment
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Crystalline nephropathies
Definition: a type of kidney injury that is triggered by crystal deposition and may lead to crystal-induced AKI, crystal-induced CKD, or urolithiasis
Epidemiology
Etiology
Drug-induced: e.g., acyclovir, indinavir, ciprofloxacin, methotrexate
Pathophysiology
Precipitation of minerals (crystallization) → phagocytosis of crystals → activation of the inflammasome → renal damage
Clinical features
Diagnostics
Crystals may be seen on urine microscopy.
Treatment
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Chronic tubulointerstitial nephritis
Chronic tubulointerstitial nephritis (CTIN) is a condition of chronic inflammation of the renal tubules and interstitium and can progress to end-stage renal disease (ESRD) after months or years.
Pathophysiology
- Analgesic nephropathy (e.g., resulting from NSAIDs use)
- Inhibition of prostacyclin synthesis → vasoconstriction of the medullary blood vessels → papillary ischemia and papillary necrosis
- Associated with an increased risk of urothelial carcinoma; can progress to ESRD
Etiology
- Medications
- Analgesic nephropathy: combination analgesics , NSAIDs, and acetaminophen
Clinical features
- Painless hematuria, pyuria, oliguria, or polyuria
- Colicky flank pain
Diagnostics
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- Blood tests: ↑ BUN and creatinine, ↓ K+ or ↑ K+; normal anion gap ; anemia of CKD
- Urine chemistries in tubulointerstitial diseases (findings similar to ATIN): sterile pyuria, proteinuria, hematuria, RBC casts, WBC casts
- Renal biopsy: tubulointerstitial fibrosis and tubular atrophy
Renal papillary necrosis
Renal papillary necrosis is ischemic, coagulative necrosis of the renal medullary pyramids and papillae and is a feature of various conditions.
Epidemiology
Etiology
- Often multifactorial
- Sickle cell disease and sickle cell trait
- Acute pyelonephritis
- Obstruction of the urinary tract
- Tuberculosis
- Cirrhosis of the liver
- NSAIDs (due to inhibition of prostaglandin-mediated vasodilation in the vasa recta)
- Diabetes mellitus
Pathophysiology
Usually bilateral
Clinical features
- Flank pain, colicky pain
- Hematuria (microscopic or macroscopic)
- Proteinuria
Diagnostics
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Treatment
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