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Pediatric nephrology (Berlin, Germany)

July 8, 2026 · via Europe PMC

Early-onset lipoprotein glomerulopathy in a 23-month-old boy with homozygous APOE Kyoto variant.

Donald JS, McCarthy HJ, Moghimi A, Lewis D.

Case ReportsAbstract only — full text under license

AI summary — for doctors, generated from the abstract only

Homozygous APOE Kyoto variant caused early-onset lipoprotein glomerulopathy in a toddler, and prompt biopsy and genetic testing redirected care from steroids to lipid-lowering therapy.

What was studied

Case report of a 23-month-old boy with nephrotic syndrome and severe anaemia, family history of kidney disease, parental consanguinity and enlarged echogenic kidneys.

Key findings

  • Early renal biopsy confirmed lipoprotein glomerulopathy
  • Genetic analysis showed homozygosity for the APOE Kyoto variant, prompting prednisolone discontinuation
  • Starting lipid-lowering therapy led to rapid clinical improvement

Clinical relevance

In atypical or steroid-resistant paediatric nephrotic syndrome, early biopsy and genetic testing can identify a treatable cause and avoid ineffective immunosuppression.

Who should care

NephrologyPediatric Nephrology

Limitations

Single case with no long-term follow-up reported in the abstract, so durability of response and kidney outcome are unknown.

Think of lipoprotein glomerulopathy in atypical early nephrotic syndrome, since targeted therapy can help.

This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.

Abstract

Lipoprotein glomerulopathy is a rare, inherited kidney disorder caused by pathogenic APOE variants that leads to obstruction of glomerular capillaries by lipoprotein thrombi, steroid-resistant nephrotic syndrome, and progressive chronic kidney disease. Immunosuppressive therapy is ineffective; instead, lipid-lowering measures reduce intraglomerular lipoprotein deposition and preserve kidney function. We describe a 23-month-old boy presenting with nephrotic syndrome and severe anaemia. Family history of kidney disease, parental consanguinity, and ultrasound showing enlarged echogenic kidneys led to early renal biopsy, which confirmed lipoprotein glomerulopathy. Genetic analysis revealed homozygosity for the APOE Kyoto variant and prompted discontinuation of prednisolone. Initiation of lipid-lowering therapy resulted in rapid clinical improvement. This case highlights the phenotype associated with homozygous APOE Kyoto variant and demonstrates how prompt kidney biopsy and genetic testing in atypical paediatric nephrotic syndrome can enable targeted treatment.

DOI

10.1007/s00467-026-07458-5

PMID

42417997

Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.

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