Evidence map›Paper›PMID 42495511›Full record

ArticleCureus2026

Severe Hypophosphatemia and Renal Phosphate Wasting Presenting as Atraumatic Bilateral Hip Pain: Suspected Hypophosphatemic Osteomalacia.

Adonai James Chery, Atta Ur Rehman Ilham

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In one paragraph

Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

2 authors.

Adonai James CheryMedicine and Surgery, Escuela Latinoamericana de Medicina, Port-au-Prince, HTI.
Atta Ur Rehman IlhamOrthopaedics and Trauma, Northwick Park Hospital, London, GBR.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypophosphatemic osteomalacia is an uncommon metabolic bone disorder that may present with nonspecific musculoskeletal symptoms, resulting in delayed diagnosis across orthopedic and emergency care pathways. We describe a 55-year-old man who presented through a National Health Service (NHS) orthopedic pathway with progressive atraumatic bilateral hip and groin pain, worsening mobility, proximal muscle weakness, and functional decline, initially managed as presumed mechanical musculoskeletal pain. Plain hip and pelvic radiographs did not identify a structural explanation for the severity of his symptoms. Initial laboratory investigations demonstrated profound hypophosphatemia (0.32 mmol/L) with markedly elevated alkaline phosphatase (428 IU/L), mildly reduced corrected calcium (2.18 mmol/L), elevated parathyroid hormone, and vitamin D insufficiency. Because the severity of hypophosphatemia appeared disproportionate to the degree of vitamin D deficiency, extended metabolic bone investigations were undertaken. Further testing demonstrated renal phosphate wasting with reduced tubular maximum phosphate reabsorption corrected for glomerular filtration rate (TmP/GFR 0.42 mmol/L) and C-terminal fibroblast growth factor 23 (FGF23) above the laboratory reference range (248 RU/mL), supporting suspected FGF23-mediated phosphate-wasting osteomalacia; localization imaging and definitive etiologic classification remained pending at the time of reporting. Severe hypophosphatemia with elevated alkaline phosphatase in patients presenting with unexplained atraumatic bilateral hip or groin pain, proximal weakness, or progressive mobility impairment should prompt consideration of metabolic bone disease and renal phosphate wasting. This case also illustrates that clinically significant osteomalacia may occur despite only mildly reduced calcium concentrations and initially nondiagnostic radiographs. Early biochemical recognition may facilitate timely specialist referral and help reduce diagnostic delay and downstream skeletal morbidity in patients with phosphate-wasting disorders.

Indexed as

atraumatic hip painbilateral hip painfgf23hypophosphatemiametabolic bone diseaseorthopedic diagnosisosteomalaciaphosphate wasting disorderphosphate-wasting osteomalaciarenal phosphate wasting

Identifiers

PMID42495511
PMCPMC13392624

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