Chronic Interstitial Nephropathy
Slow, cumulative tubulointerstitial scarring — fibrosis, tubular atrophy and glomerulosclerosis with no discrete acute phase. The nitrosourea (carmustine/lomustine) lesion and delayed radioligand (radiation) nephropathy; often irreversible and detected only as a creeping creatinine months to years later.
Agents’ overall severity
Each agent’s whole-drug severity grade, not the severity of this lesion specifically — an agent whose signature injury is elsewhere can still be graded severe here.
Agents’ overall reversibility
Agents’ onset window
How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.
Management approach
Full framework →Largely preventive — cumulative-dose limits; established chronic interstitial fibrosis is often irreversible.
Drug-level levers
- Respect cumulative-dose thresholds (e.g., the nitrosoureas) and monitor for the delayed, creeping creatinine.
- Hold or avoid further exposure once progressive CKD appears.
Pharmacologic toolkit
- Supportive CKD care — Blood-pressure and proteinuria control, avoid added nephrotoxins; no specific reversal therapy exists.
When to biopsy
Consider to confirm chronic interstitial nephropathy and exclude treatable alternatives when the cause of progressive CKD is unclear.
Monitoring
- · Long-term creatinine / eGFR (months to years)
- · Blood pressure and proteinuria
Educational use only. Educational synthesis of the published literature — not a treatment protocol, dosing guide, or medical advice. Regimens and agents shown are illustrative of what the literature describes; verify against current guidelines (ASON / KDIGO / ASCO / NCCN) and individualize to the patient. Using this site creates no clinician–patient relationship.
Offending agents
Signature offenders
7Agents for which chronic interstitial nephropathy is the defining renal lesion.