Evidence map›Paper›PMID 41356792›Full record

ArticleGlomerular diseases

Histopathological Features of Sickle Cell Nephropathy in the Arab-Indian Haplotype.

Basil Alnasrallah, Manaf Aljishi, Shatha Alfaraj, Abduallah Alqawain, Zainab Alkhuraidah, Eman Alabbad, Mohammad M Aljishi, Ahmed Ali Alnasser, Jafar Alrebh, Amein K Al-Ali and 1 more

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Article in Glomerular diseases. 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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5 · Who and what money

Authors and funding

11 authors.

Basil AlnasrallahQatif Central Hospital, Qatif, Saudi Arabia.
Manaf AljishiDr Sulaiman Alhabib Hospital, Alkhobar, Saudi Arabia.
Shatha AlfarajQatif Central Hospital, Qatif, Saudi Arabia.
Abduallah AlqawainQatif Central Hospital, Qatif, Saudi Arabia.
Zainab AlkhuraidahQatif Central Hospital, Qatif, Saudi Arabia.
Eman AlabbadQatif Central Hospital, Qatif, Saudi Arabia.
Mohammad M AljishiQatif Central Hospital, Qatif, Saudi Arabia.
Ahmed Ali AlnasserQatif Central Hospital, Qatif, Saudi Arabia.
Jafar AlrebhQatif Central Hospital, Qatif, Saudi Arabia.
Amein K Al-AliImam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia.
Husam AlzayerPrince Mohammed Bin Abdulaziz Medical City, Aljouf, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Sickle cell disease (SCD), an autosomal recessive disorder caused by hemoglobin S, leads to red blood cell sickling and multiorgan damage, including sickle cell nephropathy (SCN). While SCN histopathological changes are well described, data from the Middle East region, where the Arab-Indian (AI) haplotype is common, are limited. We hypothesized that SCN in patients in Saudi Arabia shows histopathological features similar to those in other regions, reflecting a shared renal injury mechanism. Methods: This single-center retrospective study analyzed kidney biopsies from adults with SCD in the Eastern Province of Saudi Arabia from 2012 to 2023. Histological specimens were examined using hematoxylin and eosin, periodic acid-Schiff stain, Masson trichrome stain, Jones silver stain, and immunofluorescence. Haplotype genotyping was performed using a nuclease allelic discrimination assay with target-specific primers and TaqMan probes labeled with VIC and FAM. Clinical and biochemical data were collected at the time of biopsy and at the last follow-up. Results: Twelve biopsies were included in the study (median age 44 years, 50% female). Median serum creatinine was 91.5 µmol/L (interquartile range [IQR] 59-130), and 24-h urinary protein was 3,300 mg (IQR 1,181-5,725). Of 9 patients tested, seven had homozygous AI haplotype, one had heterozygous AI, and one had BEN/CAR/CAM. Histopathology showed tubular hemosiderosis (92%), global sclerosis (75%), glomerular hypertrophy (75%), sickled red blood cells (58%), focal segmental glomerulosclerosis (42%), and glomerular basement membrane duplication (33%). These findings mirror SCN patterns in other haplotypes. Conclusions: In Saudi patients with SCD with predominant AI haplotype, SCN histopathological features align with those reported globally, suggesting a consistent renal pathogenesis across haplotypes. This study improves our understanding of SCN in the AI haplotype, supporting standardized treatment methods and further research into preventing progression.

Indexed as

Arab-Indian haplotypeChronic kidney diseasePathologyRenal biopsySickle cell diseaseSickle cell nephropathy

Identifiers

PMID41356792
PMCPMC12680401

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