Skip to content
The Injury Atlas
FANC

Fanconi Syndrome

Global failure of proximal tubule reabsorption — glucosuria, phosphaturia and acidosis, classically from ifosfamide.

3signature agents

Where it strikes

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

See it on the nephron

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.

Severe· 2Moderate· 1

Agents’ overall reversibility

Often irreversible· 1Partially reversible· 1Reversible· 1
Does the kidney recover? Cross-drug outcomes

Agents’ onset window

How soon each agent’s kidney toxicity typically appears — a whole-drug tempo, not specific to this lesion.

Acute (days)· 1Subacute (weeks)· 1Variable· 1

Real-world reporting for this lesion

FAERS across all lesions →

Agents with a disproportionate FAERS reporting signal for fanconi syndrome (reporting odds ratio with a 95% CI lower bound above 1) — a spontaneous-reporting signal, not incidence or proven causation. FAERS carries reporting and indication biases and has no denominator.

4Corroborated

Documented in the atlas profile and carrying a FAERS signal — the strongest claim the atlas makes.

5Documented, FAERS-silent

Documented in a profile with no reporting signal. Mostly expected: naming this lesion on a report can require a biopsy, and silence is not evidence against the literature.

12Not attributable

A real reporting signal that is not evidence for this drug-lesion pair: no MedDRA term names it, the naming subset asked alone came back flat, or the 2026-08 review attributed the reporting to the population, co-therapy, or class-level literature.

7Reported by name

The terms that name this lesion are disproportionate, but no profile documents it for that agent. Most are echoed by a sibling agent in the same class. Leads for review, never lesions the atlas claims.

23 agents with a significant FANC reporting signal.

Management approach

Full framework →

Supportive electrolyte and acid–base repletion; often partially irreversible, so prevention (cumulative-dose limits) matters.

Drug-level levers

  • Hold or avoid further exposure once Fanconi features appear.
  • Respect cumulative-dose limits; use caution in young children and after prior cisplatin exposure.

Pharmacologic toolkit

  • Electrolyte repletion — Phosphate, bicarbonate or citrate (for proximal renal tubular acidosis), and potassium replacement.
  • Supportive — Monitor growth in children; some proximal tubular dysfunction persists long-term.

When to biopsy

Usually clinical (glucosuria with normal serum glucose, phosphaturia, proximal RTA); biopsy not routinely required.

Monitoring

  • · Phosphate, bicarbonate, potassium, glucose
  • · Growth in children

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.

Signature offenders

3

Agents for which fanconi syndrome is the defining renal lesion.

IfosfamideAcute tubulopathy during therapy; chronic Fanconi/CKD can emerge months–years later.Subclinical tubular dysfunction is common while overt Fanconi is not, and the gap is the point. In 183 children investigated prospectively at least 5 years out — none of whom received any platinum, so the toxicity is attributable — the tubular threshold for phosphate was reduced in 24% and glycosuria detected in 37%, yet glycosuria exceeded 0.5 g/24 h in only 5%, bicarbonate and calcium were normal in every patient, and 89.5% had normal tubular function overall at a median 10 years. GFR was abnormal in 21.5%. Ifosfamide dose and time since therapy both predicted tubulopathy. Rates elsewhere span 0% to 84% depending on the definition and cohort used, so a single figure is only meaningful with its threshold attached.SevereStreptozocinWithin weeks of therapy; worsens with cumulative dose; abrupt AKI possible on re-challenge.Nephrotoxicity is the major dose-limiting toxicity; transient proteinuria, tubular dysfunction and azotemia are common and a sizable minority develop clinically significant renal impairment, though precise rates are not uniformly quantified. Reported rate: decrease in estimated glomerular filtration rate of at least 25% during treatment in 30% — 111 patients (27 prospective + 84 retrospective) with locally advanced or metastatic well-differentiated digestive… (Legoux 2021, PMID 33751987).SevereAzacitidineDuring treatment cycles (days to weeks).Proximal tubular dysfunction (proximal/type 2 renal tubular acidosis, polyuria, and glucose/amino-acid/electrolyte wasting) was described with higher-dose azacitidine; with current low-dose subcutaneous/IV regimens overt AKI is uncommon and renal incidence is not well quantified (case-level).Moderate