Tubulointerstitial and Vascular Disease
Core concepts
This domain covers acute interstitial nephritis (AIN), chronic tubulointerstitial nephritis, and vascular diseases: thrombotic microangiopathy (TMA), renal artery stenosis, hypertensive nephrosclerosis, scleroderma renal crisis, and atheroembolic disease.
AIN classically presents with AKI, sterile pyuria, WBC casts, and eosinophiluria after drugs (NSAIDs, PPIs, beta-lactams, sulfonamides, checkpoint inhibitors). Fever, rash, and eosinophilia are present in a minority-absence does not exclude it. Treatment is withdrawal of the culprit; steroids may help if diagnosed early.
TMA (schistocytes, thrombocytopenia, elevated LDH, low haptoglobin) requires distinguishing TTP (ADAMTS13 <10%, plasma exchange) from HUS (Shiga toxin; supportive care) from complement-mediated aHUS (eculizumab) and drug/transplant-associated TMA.
Atheroembolic disease follows vascular instrumentation or anticoagulation in atherosclerotic patients: blue toes, livedo, eosinophilia, eosinophiluria, and delayed, progressive renal failure with normal complement; biopsy shows cholesterol clefts.
Traps
Eosinophiluria is nonspecific. Do not attribute AKI after starting an NSAID only to hemodynamics-AIN is a possibility. Scleroderma renal crisis presents with malignant hypertension and microangiopathic hemolysis; ACE inhibitors are first-line, unlike in other scleroderma settings where they are used cautiously.
Rule of thumb
New AKI + sterile pyuria + drug exposure = stop the drug and consider AIN before dialysis-dependent progression.
Worked example
A 65-year-old develops creatinine rise 3 weeks after cardiac catheterization with livedo and eosinophilia. Diagnosis: atheroembolic disease; management is supportive, avoid further instrumentation.