Evidence map›Paper›PMID 40291173›Full record

ArticleCureus2025

Managing Ifosfamide-Induced Arginine Vasopressin Resistance: Diagnostic and Treatment Strategies.

Avia A Williams, Arslan I Pir Muhammad, Rupam Ruchi, Rozina Ali

Abstract readCase Reports
In one paragraph

Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Avia A WilliamsInternal Medicine, Cornwall Regional Hospital, Montego Bay, JAM.
Arslan I Pir MuhammadMedicine, Ziauddin University, Karachi, PAK.
Rupam RuchiNephrology, Hypertension, and Transplantation, University of Florida-College of Medicine, Gainesville, USA.
Rozina AliNephrology, Hypertension, and Transplantation, University of Florida-College of Medicine, Gainesville, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The early recognition of ifosfamide-related renal dysfunction, including arginine vasopressin resistance (previously referred to as diabetes insipidus), which is characterized by polyuria due to the inability of the collecting duct to concentrate urine, as well as direct proximal tubular injury, which is characterized by numerous metabolic disturbances including hypophosphatemia, metabolic acidosis, hypokalemia, and glucosuria, is paramount to timely initiation of treatment and titration of desmopressin. In this report, we present a case of a 42-year-old female with a history of spindle cell carcinoma of the left thigh, who was referred to the inpatient nephrology consult service for acute kidney injury, polyuria, and metabolic derangements following her sixth cycle of doxorubicin-ifosfamide chemotherapy. The patient was treated with supratherapeutic doses of desmopressin, with successful improvement of her polyuria. We review the pathophysiology of different forms of ifosfamide-associated nephrotoxicity, including arginine vasopressin resistance, the challenges of diagnosing arginine vasopressin disorders, and the utility of desmopressin in the management of arginine vasopressin resistance. This case also highlights the clinical implications of using copeptin in the diagnosis of arginine vasopressin resistance, leading to effective treatment and improving patient outcomes.

Indexed as

acute kidney injuryarginine vasopressin deficiencyarginine vasopressin disorderarginine vasopressin resistancediabetes inspidusdrug induced fanconi syndromehypernatremiaifosfamidepolyuriaproximal tubulopathy

Identifiers

PMID40291173
PMCPMC12025348

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.