How should kidney function be monitored during Sacituzumab govitecan therapy?

CBC for neutropenia (a marker of SN-38 exposure/UGT1A1 status); Urinalysis/urine protein if AKI is disproportionate to volume status (AIN screen); Serum creatinine and volume status each cycle.

How can kidney injury from Sacituzumab govitecan be prevented?

Aggressive antidiarrheal management (loperamide) and hydration Consider UGT1A1 genotype in patients with severe early toxicity

Who is at higher risk of kidney injury from Sacituzumab govitecan?

Severe diarrhea/vomiting and dehydration; UGT1A1*28 homozygosity (reduced SN-38 glucuronidation); Pre-existing CKD; Concurrent nephrotoxins.

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Printable monograph

Antibody-drug conjugate (Trop-2/SN-38)

Sacituzumab govitecan

Trodelvy · SG

Antibody-drug conjugate (Trop-2/SN-38) · approved 2020 · 5 citations

Up to date· through 2026

Fairly sourced4/9 · 4 signals

Not met: 5 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 9y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
Not met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

A Trop-2/SN-38 conjugate whose diarrhea can drive prerenal AKI — with a rare biopsy-proven interstitial nephritis signal.

ModerateAntibody-drug conjugate

Triple-negative breast cancerHR+/HER2- breast cancerUrothelial carcinoma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

AKI is mainly prerenal, driven by the severe diarrhea/nausea and neutropenia that dominate the ASCENT safety profile; renal-specific incidence is not well quantified. A biopsy-proven severe acute tubulointerstitial nephritis requiring hemodialysis has also been reported (case-level).Source: Guarin et al., BMC Nephrol 2024 (case); Bardia et al., N Engl J Med 2021 (ASCENT)

Onset & rechallenge

Time to injuryVariable / unpredictable

Prerenal AKI tracks GI toxicity across treatment cycles.

Distilled from: “Variable; prerenal AKI tracks with GI toxicity during treatment cycles.”

§02

Renal toxicities, ranked

This agent's kidney lesions ordered by prominence — the #1 signature lesion first, then secondary and rare patterns. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Prerenal / Hemodynamic AKI#1 · Signatureno population incidence denominator
Predominant AKI mechanism is prerenal, driven by GI toxicity (diarrhea/vomiting) PMID 39522022 (opens PubMed in a new tab)
Acute Tubular NecrosisSecondaryno population incidence denominator
Trop-2 expressed in proximal tubule/collecting duct; SN-38 direct tubular toxicity (UGT1A1*28 homozygotes at higher risk) PMID 39522022 (opens PubMed in a new tab)
Acute Interstitial NephritisRareno population incidence denominator
Biopsy-proven acute tubulointerstitial nephritis requiring hemodialysis — single case report PMID 39522022 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityVariable

Evidence5 citations

Nephron map

Vasculature / Endothelium

Proximal Tubule

Distal Tubule / Collecting Duct

Interstitium

Prerenal / Hemodynamic AKI

Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

Predominantly hemodynamic: GI toxicity (diarrhea, vomiting) causes volume depletion and prerenal AKI, which can progress to ischemic ATN. SN-38 toxicity (and thus diarrhea/neutropenia severity) is amplified in UGT1A1 poor metabolizers, e.g. UGT1A1*28 homozygotes. Trop-2 is expressed in collecting ducts and, to a lesser extent, proximal tubule; a rare immune-mediated acute tubulointerstitial nephritis has been described on biopsy, expanding the renal differential beyond pure prerenal physiology.

Clinical presentation

AKI in the setting of diarrhea/dehydration with bland sediment; in the reported AIN case, severe AKI with nephrotic-range proteinuria requiring dialysis, responsive to corticosteroids and renal replacement therapy. Watch for concurrent grade 3-4 neutropenia.

Management

Rehydrate, manage diarrhea and neutropenia, and hold drug for significant AKI; for steroid-responsive features or AKI out of proportion to volume status, pursue kidney biopsy and consider corticosteroids for biopsy-proven AIN, with supportive care/dialysis as needed.Lesion-level management framework

Risk factors

Severe diarrhea/vomiting and dehydration
UGT1A1*28 homozygosity (reduced SN-38 glucuronidation)
Pre-existing CKD
Concurrent nephrotoxins

Prevention

Aggressive antidiarrheal management (loperamide) and hydration
Consider UGT1A1 genotype in patients with severe early toxicity

Anticancer mechanism· how it treats cancer

Antibody-drug conjugate targeting Trop-2 and delivering SN-38, the active topoisomerase I-inhibitor metabolite of irinotecan, via a hydrolyzable linker with a high drug-to-antibody ratio. Approved for metastatic triple-negative and HR+/HER2- breast cancer and urothelial carcinoma.

§04

Clinical depth

Renal dose adjustment

No established renal dose adjustment; pivotal trials did not define renal cutoffs and the active SN-38 is hepatically glucuronidated (UGT1A1), not renally cleared. Use clinical judgment in advanced CKD/ESKD given limited data.

Dialyzability & ESKD dosing

The intact ADC and protein-bound SN-38 are not appreciably dialyzed; HD in reported cases was for AKI support, not drug removal.

Differential diagnosis

Distinguish prerenal/ischemic ATN from diarrhea (fluid-responsive, bland sediment, FeNa low then rising) from drug-induced AIN (AKI out of proportion to volume loss, possible sterile pyuria, steroid-responsive on biopsy). UGT1A1*28 status helps explain unusually severe GI toxicity.

Monitoring

CBC for neutropenia (a marker of SN-38 exposure/UGT1A1 status)
Urinalysis/urine protein if AKI is disproportionate to volume status (AIN screen)
Serum creatinine and volume status each cycle

Key trials & series

ASCENT (Bardia NEJM 2021, metastatic TNBC)
Guarin BMC Nephrol 2024 (biopsy-proven AIN requiring HD)

Clinical pearls

The everyday renal risk is dehydration from diarrhea — but remember the rare biopsy-proven AIN if AKI does not track with volume status.
UGT1A1*28 homozygotes get more SN-38, more diarrhea/neutropenia, and therefore more prerenal AKI risk.
Trop-2 is expressed in the collecting duct, providing a plausible substrate for the reported interstitial injury.

Beyond the kidney — non-renal toxicities· 4 organ systems

Class-level context for the major non-renal toxicities of the Antibody-drug conjugate (Trop-2/SN-38) class.

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression (payload-dependent)

Ophthalmic

Keratopathy, uveitis, retinopathy

Keratopathy (belantamab, mirvetuximab, tisotumab)

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Interstitial lung disease (deruxtecan ADCs)

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Peripheral neuropathy (MMAE payloads)

§05

References

5 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

5 references · 2017–2026 · 3 since 2024

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Jun 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: NEUTROPENIA AND DIARRHEA TRODELVY can cause severe, life-threatening, or fatal neutropenia. Withhold TRODELVY for absolute neutrophil count below 1500/mm 3 or neutropenic fever. Monitor blood cell counts periodically during treatment. Primary prophylaxis with G-CSF is recommended for all patients at increased risk of febrile neutropenia [see Dosage and Administration (2.4) ] . Initiate anti-infective treatment in patients with febrile neutropenia without delay [see Warnings and Precautions (5.1) ]. TRODELVY can cause severe diarrhea. Monitor patients with diarrhea and give fluid and electrolytes as needed. At the onset of diarrhea, evaluate for infectious causes and, if negative, promptly initiate loperamide [see Warnings and Precautions (5.2) ]. If severe diarrhea occurs, withhold TRODELVY until resolved to ≤ Grade 1 and reduce subsequent doses [see Dosage and Administration (2.4) ]. WARNING: NEUTROPENIA AND DIARRHEA See full prescribing information for complete boxed warning . TRODELVY can cause severe, life-threatening, or fatal neutropenia. Withhold TRODELVY for absolute neutrophil count below 1500/mm 3 or neutropenic fever. Monitor blood cell counts periodically during treatment. Primary prophylaxis with G-CSF is recommended for all patients at increased risk of febrile neutropenia. Initiate anti-infective treatment in patients with febrile neutropenia without…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 4,518 of them for this agent. Nobody counts the patients who were fine, so none of these numbers is an incidence, a risk, or a rate: they describe what gets reported, shaped by a drug's fame, its indication, and who was watching. How these numbers work.

Reporting odds ratio (ROR) — is kidney injury named in this agent's reports more often than in every other drug's? Above 1 means yes, disproportionately.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
Outcomes — a share of this agent's own reports, not of patients: how many were filed as involving a death or a hospitalization. Not a case-fatality rate.

FAERS reported renal phenotypes· 1 signal

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-10-01.

What reporting says about this profile's documented lesions

Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Acute Interstitial NephritisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.
Acute Tubular NecrosisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.

Electrolyte Disturbance

ROR 2.1195% CI 1.71–2.61· 86 reports

FAERS outcomes & reporting trend· 20.6% of reports w/ death · 27.2% w/ hospitalization

20.6%

Reported with a death outcome

929 of 4,518 reports

27.2%

Reported with hospitalization

1,231 of 4,518 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 4,518 reports

Bars rank systems by summed reaction-term mentions (a report counts once per term it names) — an ordinal “more vs less reported” cue, not a tally of distinct reports. Renal & urinary first. As of 2026-10-01.

Disproportionality (acute kidney injury):ROR 1.0495% CI 0.74–1.45· 34 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Neutropenia510Febrile Neutropenia203Thrombocytopenia135Neutrophil Count Decreased132Anaemia129

Gastrointestinal

Diarrhoea561Nausea265Vomiting139Constipation120Abdominal Pain89

General / constitutional

Fatigue265Asthenia206Malaise126Weight Decreased117Pyrexia104

Skin

Alopecia170

Respiratory

Dyspnoea96

Immune / infection

Sepsis91

Guidelines & consensus· 13

Each recommendation below is this atlas's faithful summary of the source, not a quotation from it — follow the PubMed link for the wording the society published. Summaries may be superseded; consult the current full text and individualize to the patient.

General onco-nephrology references

ADQIThe nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupNat Rev Nephrol 2026 · PMID 41361704Provides expert-based statements (modified Delphi) on preventing and managing cisplatin/platinum-associated AKI, including isotonic IV hydration, attention to volume status and concomitant nephrotoxins, and incorporates evidence that IV magnesium supplementation may reduce cisplatin-associated AKI; emphasizes risk stratification and standardized AKI definitions.SIRMSIRM-SIN-AIOM: appropriateness criteria for evaluation and prevention of renal damage in the patient undergoing contrast medium examinations-consensus statements from Italian College of Radiology (SIRM), Italian College of Nephrology (SIN) and Italian Association of Medical Oncology (AIOM)Radiol Med 2022 · PMID 35303246Recommends eGFR-based renal risk assessment and pre/post-contrast isotonic saline or sodium bicarbonate hydration; advises maintaining a 5-7 day interval between iodinated contrast administration and cisplatin in cancer patients to reduce additive nephrotoxicity.KDIGOKDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerKidney Int 2020 · PMID 33126977Identifies platinum compounds (especially cisplatin) as leading cytotoxic causes of acute tubular injury, AKI, and electrolyte/magnesium wasting; calls for interdisciplinary onco-nephrology care, accurate GFR estimation, and individualized drug dosing in patients with reduced kidney function.KDIGOKDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationKidney Int 2020 · PMID 33276867Addresses chemotherapy-associated AKI/CKD in hematologic cancer, GFR estimation and chemotherapy dosing in patients with reduced kidney function, and management priorities and research gaps for onco-nephrology care.ADDIKDIntegrating International Consensus Guidelines for Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) into everyday practiceEClinicalMedicine 2025 · PMID 40290844Provides GRADE-based, drug-specific dose-adjustment recommendations for anticancer agents in kidney dysfunction (illustrated for methotrexate, cisplatin, carboplatin and nivolumab); the recommendations build on Part 1's standardised CKD-EPI eGFR assessment rather than Cockcroft-Gault creatinine clearance.ADDIKDAligning kidney function assessment in patients with cancer to global practices in internal medicineEClinicalMedicine 2025 · PMID 40290845Three consensus recommendations: assess kidney function by GFR (measured GFR or CKD-EPI eGFR), classify it using KDIGO categories, and use this uniform approach to dose anticancer drugs — moving cancer medicine away from Cockcroft-Gault estimated creatinine clearance.ADDIKDA methodology for determining dosing recommendations for anticancer drugs in patients with reduced kidney functionEClinicalMedicine 2025 · PMID 40290846Establishes that, where RCT evidence is lacking, anticancer drug dosing recommendations in kidney dysfunction should be derived by critically appraising observational literature via GRADE combined with structured international multidisciplinary consensus voting.KDIGODiagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Crit Care 2013 · PMID 23394211Defines/stages AKI by serum creatinine and urine output; emphasizes avoiding nephrotoxins, maintaining euvolemia/perfusion, dose-adjusting drugs to kidney function, and monitoring high-risk patients — the framework applied to nephrotoxic anti-cancer agents.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknownsKidney Int 2024 · PMID 38519239Evaluate and risk-stratify CKD, manage to delay progression and its complications, and practise explicit medication management and drug stewardship — the framework the atlas's G1–G5 eGFR banding and every renal dose-adjustment recommendation sit inside. Because the guideline excludes dialysis and transplant recipients by its own statement of scope, its recommendations do not carry to those settings, where this atlas's dialyzability and post-transplant guidance rests on other sources.KDIGOExecutive summary of the KDIGO 2021 Guideline for the Management of Glomerular DiseasesKidney Int 2021 · PMID 34556300Provides the staging/treatment framework for drug-associated glomerular lesions (e.g., bisphosphonate- and interferon-related collapsing FSGS, VEGF-inhibitor podocytopathy/proteinuria), including immunosuppression and supportive RAAS-blockade strategies.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of ANCA-Associated VasculitisKidney Int 2024 · PMID 38388147Updates immunosuppressive induction (rituximab/cyclophosphamide), incorporates avacopan and lower-dose or glucocorticoid-sparing regimens — the management framework for drug- and checkpoint-inhibitor-associated ANCA/pauci-immune glomerulonephritis.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisKidney Int 2024 · PMID 38182299Updates first-line lupus nephritis therapy to combination immunosuppression with the addition of belimumab or a calcineurin inhibitor (voclosporin) — informs management of immune-complex/lupus-like glomerulonephritis encountered with immunotherapy.KDIGOExecutive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV)Kidney Int 2025 · PMID 40975525Encourages liberal kidney biopsy and stricter proteinuria control (<0.5 g/d, ideally <0.3 g/d) with RAAS blockers, SGLT2 inhibitors, and targeted-release budesonide — the framework for IgA-dominant glomerular lesions, including those triggered by immune-modulating cancer therapy.

Where Sacituzumab govitecan sits in nephrotoxicity space — each dot is an anti-cancer agent, positioned so neighbors share a kidney-injury phenotype. Its 6 closest are filled and lead to a numbered marker, matching the numbered cards below.

Position is a 2-D projection (MDS) of each agent's injury signature, nephron target, severity, and class, so two dots can sit close on the page while differing on an axis the projection flattened — the numbered ranking is computed from the full metric, not from the distance you see. Open the full map.

Phenotype-similar agents· the numbered markers on the map above

Tarlatamab

Imdelltra · Bispecific (DLL3×CD3)

Profile

2024 small-cell lung BiTE; CRS-driven AKI risk.

PREATN

Moderate#1 · 70% phenotype match

Mirvetuximab soravtansine

Elahere · Antibody-drug conjugate (FRα/DM4)

Profile

Ocular toxicity dominates; renal involvement indirect/case-level (GI volume loss).

PRE

Mild#2 · 63% phenotype match

Lifileucel

Amtagvi · Tumor-infiltrating lymphocyte (TIL) therapy

Profile

2024 cellular therapy; high-dose IL-2 conditioning → capillary leak AKI.

PREATNLYTE

Moderate#3 · 62% phenotype match

Gemtuzumab ozogamicin

Mylotarg · Antibody-drug conjugate (CD33/calicheamicin)

Profile

Tumor lysis and veno-occlusive disease.

PRELYTEXTAL

Moderate#4 · 62% phenotype match

Inotuzumab ozogamicin

Besponsa · Antibody-drug conjugate (CD22/calicheamicin)

Profile

Tumor lysis and VOD in ALL.

PRELYTEXTAL

Moderate#5 · 62% phenotype match

Tretinoin (ATRA)

Vesanoid · Retinoid (differentiating agent)

Profile

Differentiation syndrome → capillary leak and AKI.

PREATN

Moderate#6 · 62% phenotype match

Compare Sacituzumab govitecan with its nearest agents

Nearest agents by kidney-injury phenotype (shared injuries, nephron target, severity, class) — a similarity approximation, not a claim of shared drug identity or mechanism.

Kidney risk across Antibody-drug conjugates

Same-class agents ordered by their documented kidney-injury profile — atlas severity, an acute-kidney-injury FAERS signal, and how many injury types each is documented to cause. Agents nearer the top carry the lighter documented renal profile.

A comparison of documented kidney-injury data within one drug class — not a substitution recommendation. Efficacy, indication, and non-renal toxicity differ between these agents and are out of scope here. Educational only, not medical advice.