How should kidney function be monitored during Temsirolimus therapy?

Baseline and periodic urinalysis / UPCR or UACR for proteinuria; Serum creatinine and eGFR; Serum phosphate and potassium; Fasting glucose and lipid panel (metabolic class effects); Blood pressure.

How can kidney injury from Temsirolimus be prevented?

Optimize blood pressure and avoid concurrent nephrotoxins

Who is at higher risk of kidney injury from Temsirolimus?

Pre-existing CKD or baseline proteinuria; Reduced renal mass (post-nephrectomy / solitary kidney in RCC); Diabetes or hypertension; Prior or concurrent VEGF-pathway-targeted therapy; Hypoalbuminemia.

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Printable monograph

mTOR inhibitor

Temsirolimus

Q: What kind of kidney injury does Temsirolimus cause?

Glomerular Injury / Proteinuria — Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade. Other reported patterns: Electrolyte Disturbance.

Q: How common is kidney injury with Temsirolimus?

Approximately 5% (grade ≥3) — Not firmly quantified for temsirolimus specifically. Proteinuria is the recognized mTOR-inhibitor glomerular signal, but for temsirolimus it is documented mostly at the class/case level rather than in drug-specific renal endpoints (everolimus proteinuria runs high yet is usually grade 1-2 — e.g., 96% all-grade in one first-line mRCC cohort). In the pivotal temsirolimus ARCC trial, metabolic lab abnormalities (hyperglycemia, hyperlipidemia, hypophosphatemia) dominated and frank nephrotoxicity was uncommon; drug-specific AKI and nephrotic syndrome appear only in case reports. Reported rate: grade >=3 hypophosphatemia in 5% — 82 East Asian (Sun 2012, PMID 22844126). (Source: Sun et al., Jpn J Clin Oncol 2012 (grade >=3 hypophosphatemia; drug-specific proteinuria/AKI still not separately quantified — class/case context from Land et al., J Oncol Pharm Pract 2014 and Heras et al., Nefrologia 2009)).

Q: Is kidney injury from Temsirolimus reversible?

Variable. Typical onset: Subacute — typically weeks to months into weekly dosing; not firmly characterized for temsirolimus..

Torisel · TEM

mTOR inhibitor · approved 2007 · 10 citations

Dated evidence· through 2016

Fairly sourced4/9 · 4 signals

Met: 10 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
Not met: Current through 2016
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.

The IV rapalog whose kidney signal is podocyte proteinuria — real for the class, thinly quantified for the drug.

MildmTOR inhibitor

Advanced (poor-prognosis) renal cell carcinomaRelapsed/refractory mantle cell lymphoma (EU approval)

§01

Signature kidney injury

Signature lesion

Glomerular Injury / Proteinuria

Representative grade ≥3 incidence5%

Not firmly quantified for temsirolimus specifically. Proteinuria is the recognized mTOR-inhibitor glomerular signal, but for temsirolimus it is documented mostly at the class/case level rather than in drug-specific renal endpoints (everolimus proteinuria runs high yet is usually grade 1-2 — e.g., 96% all-grade in one first-line mRCC cohort). In the pivotal temsirolimus ARCC trial, metabolic lab abnormalities (hyperglycemia, hyperlipidemia, hypophosphatemia) dominated and frank nephrotoxicity was uncommon; drug-specific AKI and nephrotic syndrome appear only in case reports. Reported rate: grade >=3 hypophosphatemia in 5% — 82 East Asian (Sun 2012, PMID 22844126).Source: Sun et al., Jpn J Clin Oncol 2012 (grade >=3 hypophosphatemia; drug-specific proteinuria/AKI still not separately quantified — class/case context from Land et al., J Oncol Pharm Pract 2014 and Heras et al., Nefrologia 2009)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Typically weeks to months into weekly dosing; not firmly characterized for temsirolimus.

Distilled from: “Subacute — typically weeks to months into weekly dosing; not firmly characterized for temsirolimus.” · PMID 17538086 (opens PubMed in a new tab)

§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.

Glomerular Injury / Proteinuria#1 · Signaturequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

5%grade ≥3 incidence

SeverityMild

ReversibilityVariable

Evidence10 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Proximal Tubule

Distal Tubule / Collecting Duct

Glomerular Injury / Proteinuria

Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

§03

Kidney injury

Mechanism of kidney injury

Inferred largely from the sirolimus/everolimus class (temsirolimus is a sirolimus prodrug): mTORC1 (and secondary mTORC2) inhibition in podocytes down-regulates slit-diaphragm proteins (nephrin, TRPC6) and the Nck/actin cytoskeleton, and disrupts the autophagic flux podocytes depend on for maintenance and repair — producing proteinuria and FSGS-type lesions. Reduced VEGF signaling with an antiproliferative effect on glomerular endothelium can add a thrombotic-microangiopathy-like component. Proximal-tubular phosphate wasting contributes to the class-typical hypophosphatemia.

Clinical presentation

Usually asymptomatic proteinuria found on urinalysis or urine protein/creatinine ratio, occasionally nephrotic-range with edema; sometimes a modest creatinine rise. Rare acute kidney injury is reported at case level. Hypophosphatemia (and less often hypokalemia) plus the metabolic derangements hyperglycemia and hyperlipidemia are common lab findings, distinct from primary renal parenchymal injury.

Management

Quantify proteinuria with a UPCR/UACR. Low-grade proteinuria can usually be continued with monitoring; add an ACEi or ARB for its antiproteinuric effect. Reduce dose or hold for grade 3-4 or nephrotic-range proteinuria or a rising creatinine, and discontinue for persistent nephrotic syndrome or progressive decline. Refer to nephrology and consider biopsy for nephrotic-range proteinuria or atypical AKI. Replace phosphate and manage hyperglycemia/hyperlipidemia. For rare AKI, hold the drug and correct prerenal/GI-loss contributors with supportive care.Lesion-level management framework

Risk factors

Pre-existing CKD or baseline proteinuria
Reduced renal mass (post-nephrectomy / solitary kidney in RCC)
Diabetes or hypertension
Prior or concurrent VEGF-pathway-targeted therapy
Hypoalbuminemia

Prevention

Optimize blood pressure and avoid concurrent nephrotoxins

Anticancer mechanism· how it treats cancer

Temsirolimus is an IV ester prodrug of sirolimus (rapamycin). It binds FKBP-12, and the complex inhibits mTORC1, lowering HIF-1alpha/VEGF and cyclin D1 to arrest tumor cells in G1 and blunt angiogenesis.

Note · IV ester prodrug of sirolimus; renal profile largely extrapolated from the sirolimus/everolimus class. Temsirolimus-specific renal incidence is not firmly quantified — claims are hedged to case-level and class evidence.

§04

Clinical depth

Renal dose adjustment

No specific renal dose adjustment is recommended in the label — temsirolimus and its active metabolite sirolimus are cleared by hepatic CYP3A4 metabolism and biliary excretion, not renal elimination, so renal impairment does not mandate a dose change (efficacy/safety in severe renal impairment are not established; use caution). Hepatic impairment, not renal, drives dose reduction (and severe hepatic impairment is a contraindication). Standard RCC dosing is 25 mg IV weekly.

Dialyzability & ESKD dosing

Not meaningfully dialyzable. Sirolimus (the active moiety) has a large volume of distribution, extensive tissue and erythrocyte partitioning, and high protein/lipoprotein binding, so hemodialysis is not expected to remove clinically significant amounts; direct data are limited.

Differential diagnosis

Separate drug-induced podocytopathy/proteinuria from RCC-associated paraneoplastic glomerulopathy (membranous nephropathy, minimal-change disease), diabetic nephropathy, and hypertensive nephrosclerosis. In sequenced RCC regimens, concurrent or prior VEGF-pathway inhibitors can cause overlapping proteinuria/TMA. For an acute creatinine rise, weigh prerenal azotemia from GI losses/dehydration and ischemic/contrast ATN. Hypophosphatemia has its own differential (poor intake, other tubular toxins).

Monitoring

Baseline and periodic urinalysis / UPCR or UACR for proteinuria
Serum creatinine and eGFR
Serum phosphate and potassium
Fasting glucose and lipid panel (metabolic class effects)
Blood pressure

Key trials & series

GLOBAL ARCC (Hudes et al., NEJM 2007) — pivotal phase 3 in poor-prognosis metastatic RCC establishing 25 mg IV weekly; hyperglycemia, hyperlipidemia and hypophosphatemia were prominent while frank nephrotoxicity was uncommon and renal-specific proteinuria was not systematically captured
Phase 3 mantle-cell-lymphoma program — higher 175/75 mg dosing with a different, mostly hematologic/GI safety profile (Bouabdallah et al., Curr Opin Oncol 2013)

Clinical pearls

Temsirolimus is the IV ester prodrug of sirolimus — its renal footprint is inferred mainly from the sirolimus/everolimus class literature rather than temsirolimus-specific trials.
Proteinuria (podocyte slit-diaphragm down-regulation plus autophagy disruption, with FSGS in some cases) is the signature mTOR-inhibitor renal signal, but the temsirolimus-specific incidence is not firmly quantified — hedge.
The pivotal ARCC trial foregrounded hyperglycemia, hyperlipidemia and hypophosphatemia; frank nephrotoxicity was uncommon and creatinine changes modest.
An ACEi/ARB plus dose reduction usually controls proteinuria; nephrotic-range proteinuria or a rising creatinine warrants holding the drug and nephrology input.
Watch for additive glomerular injury when temsirolimus is sequenced with VEGF-pathway agents in RCC.

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

Class-level context for the major non-renal toxicities of mtor inhibitors.

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Non-infectious pneumonitis

Endocrine

Thyroiditis, hypophysitis, diabetes

Hyperglycemia, hyperlipidemia

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Stomatitis

Immune / Infusion

CRS, infusion reactions, irAEs, anaphylaxis

Immunosuppression / infection

§05

References

9 primary references — trials, cohorts, mechanism, and reviews. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

9 references · 2007–2016 · 2 since 2014

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.

Case reports — ranked by strength· 1

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseB · ModerateTemsirolimus-induced glomerulopathy.Izzedine H et al. · Oncology 2009 · PMID 19212144Nephrotic-range proteinuria with biopsy-documented glomerulopathy attributed to the mTOR inhibitor temsirolimus, a podocyte/glomerular injury phenotype.

FDA label — boxed warning & renal dosing· renal impairment

Quoted verbatim from this agent's current FDA label (Dec 2025) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

No clinical studies were conducted with TORISEL in patients with decreased renal function. Less than 5% of total radioactivity was excreted in the urine following a 25 mg intravenous dose of [ 14 C]-labeled temsirolimus in healthy subjects. Renal impairment is not expected to markedly influence drug exposure, and no dosage adjustment of TORISEL is recommended in patients with renal impairment. TORISEL has not been studied in patients undergoing hemodialysis.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 4,502 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· 7 signals

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 2026-08-21.

What reporting says about this profile's documented lesions

Glomerular Injury / Proteinuriacorroborated · ROR 7.6 — on the terms that name the lesion (ROR 2.36)
Electrolyte Disturbancecorroborated · ROR 5.25 — on the terms that name the lesion (ROR 4.04)

Glomerular Injury / Proteinuria

ROR 7.6095% CI 5.70–10.14· 47 reports

Electrolyte Disturbance

ROR 5.2595% CI 4.56–6.03· 207 reports

SIADH / Hyponatremia

ROR 3.6295% CI 2.82–4.66· 62 reports

Acute Tubular Necrosis

ROR 2.8595% CI 1.28–6.34· 6 reports

Thrombotic Microangiopathy

ROR 2.1195% CI 1.00–4.42· 7 reports

Hemorrhagic Cystitis

ROR 1.8995% CI 1.30–2.74· 28 reports

Hypertension

ROR 1.6395% CI 1.37–1.93· 133 reports

FAERS outcomes & reporting trend· 21.5% of reports w/ death · 44.5% w/ hospitalization

21.5%

Reported with a death outcome

967 of 4,502 reports

44.5%

Reported with hospitalization

2,002 of 4,502 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 4,502 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 2026-08-08.

Disproportionality (acute kidney injury):ROR 0.9895% CI 0.69–1.39· 32 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Renal & urinary

Blood Creatinine Increased102Renal Failure96

Gastrointestinal

Nausea190Diarrhoea189Vomiting177Stomatitis156Mucosal Inflammation112

Blood & lymphatic

Anaemia188Thrombocytopenia164Febrile Neutropenia126Neutropenia106

Respiratory

Dyspnoea215Pleural Effusion125Interstitial Lung Disease111Pneumonitis108

General / constitutional

Fatigue206Pyrexia179Asthenia124

Metabolic & electrolyte

Dehydration162Decreased Appetite113

Immune / infection

Pneumonia190

Skin

Rash143

Vascular

Hypertension100

Guidelines & consensus· 12

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 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 Temsirolimus 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

Everolimus

Afinitor · mTOR inhibitor

Profile

Podocyte injury with proteinuria/FSGS; occasional thrombotic microangiopathy.

GLOMTMALYTE

Moderate#1 · 71% phenotype match

Cetuximab

Erbitux · Anti-EGFR antibody

Profile

TRPM6 magnesium wasting.

LYTEGLOM

Mild#2 · 64% phenotype match

Panitumumab

Vectibix · Anti-EGFR antibody

Profile

TRPM6 magnesium wasting — heavier than cetuximab.

LYTEGLOM

Mild#3 · 64% phenotype match

mTOR inhibitors (everolimus · temsirolimus)

mTOR inhibitor

Profile

Podocyte injury → proteinuria and FSGS.

GLOMATNTMA

Mild#4 · 62% phenotype match

Sirolimus

Rapamune · mTOR inhibitor

Profile

Proteinuria, cast nephropathy, delayed graft recovery.

GLOMATN

Moderate#5 · 61% phenotype match

Ibandronate

Boniva · Bisphosphonate

Profile

Lower renal risk than zoledronate.

ATNLYTEGLOM

Mild#6 · 60% phenotype match

Compare Temsirolimus 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 mTOR inhibitors

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.

1Temsirolimus· this agentGLOM — Glomerular Injury / ProteinuriaMild
2mTOR inhibitors (everolimus · temsirolimus)GLOM — Glomerular Injury / ProteinuriaMild
3SirolimusGLOM — Glomerular Injury / ProteinuriaFAERS AKIModerate
4EverolimusGLOM — Glomerular Injury / ProteinuriaFAERS AKIModerate

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.

Who studies this

The leading contributors to Temsirolimus’s clinical kidney literature on PubMed, ranked by a blend of publication volume and citation impact — filtered toward clinical work via the PubMed Humans heading and clinical publication types (trials, cohorts, case reports, guidelines, reviews). Names link to that author’s work on Temsirolimus.

Ranked by publication volume and citation impact (NIH iCite) on this agent’s renal literature — bibliometric context, not an endorsement or a measure of clinical authority.