Hubungan antara Kadar Serum Hepcidin dengan Kreatinin pada Pasien Thalassemia Beta Mayor di Rumah Sakit Universitas Airlangga

Hassan, Naja Maulana (2026) Hubungan antara Kadar Serum Hepcidin dengan Kreatinin pada Pasien Thalassemia Beta Mayor di Rumah Sakit Universitas Airlangga. Undergraduate thesis, Universitas Muhammadiyah Surabaya.

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Abstract

Thalassemia beta mayor merupakan kelainan genetik yang ditandai oleh gangguan sintesis rantai globin, sehingga pasien memerlukan transfusi darah seumur hidup. Transfusi berulang dapat menyebabkan kelebihan zat besi yang menumpuk di berbagai organ vital, termasuk ginjal. Penumpukan besi menimbulkan stres oksidatif melalui pembentukan reactive oxygen species yang berpotensi merusak jaringan ginjal. Hepcidin, hormon yang mengatur homeostasis zat besi, berperan penting dalam mekanisme ini, sedangkan kreatinin digunakan sebagai penanda fungsi ginjal. Penelitian ini bertujuan untuk mengetahui hubungan kadar serum hepcidin dengan kreatinin pada pasien thalassemia beta mayor di Rumah Sakit Universitas Airlangga. Penelitian ini merupakan penelitian analitik observasional dengan pendekatan cross sectional. Sampel terdiri dari pasien thalassemia beta mayor berusia 16–47 tahun yang memenuhi kriteria inklusi. Data primer berupa kadar serum hepcidin diukur menggunakan metode Enzyme-Linked Immunosorbent Assay, sedangkan kadar kreatinin diukur dengan Enzymatic Colorimetric Test. Analisis data dilakukan menggunakan uji korelasi pearson karena kedua variabel berskala rasio. Hasil uji korelasi Pearson menunjukkan nilai koefisien korelasi (r) sebesar -0,061 dengan nilai signifikansi (p) sebesar 0,715 pada 38 sampel penelitian. Nilai tersebut menunjukkan bahwa hubungan antara kadar serum hepcidin dan kreatinin pada pasien thalassemia beta mayor bersifat sangat lemah dan tidak signifikan secara statistik (p > 0,05).
Tidak terdapat hubungan yang bermakna antara kadar serum hepcidin dengan kreatinin pada pasien thalassemia beta mayor di Rumah Sakit Universitas Airlangga.
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Beta thalassemia major is a genetic disorder characterized by impaired globin chain synthesis, requiring lifelong blood transfusions. Repeated transfusions can lead to excess iron accumulation in various vital organs, including the kidneys. Iron accumulation causes oxidative stress through the formation of reactive oxygen species (ROS), which can potentially damage kidney tissue. Hepcidin, a hormone that regulates iron homeostasis, plays a key role in this mechanism, while creatinine is used as a marker of kidney function. This study aimed to determine the relationship between serum hepcidin and creatinine levels in patients with beta thalassemia major at Universitas Airlangga Hospital. This was an observational analytical study with a cross-sectional approach. The sample consisted of beta thalassemia major patients aged 16–47 years who met the inclusion criteria. Primary data, serum hepcidin levels, were measured using the Enzyme-Linked Immunosorbent Assay (ELISA), while creatinine levels were measured using the Enzymatic Colorimetric Test. Data analysis was performed using the pearson correlation test because both variables are rasio. The Pearson correlation test showed a correlation coefficient (r) of -0.061 with a significance value (p) of 0.715 in 38 research samples. These findings indicate that the relationship between serum hepcidin levels and creatinine in patients with beta-thalassemia major was very weak and not statistically significant (p > 0.05). There was no significant relationship between serum hepcidin levels and creatinine in patients with beta-thalassemia major at Universitas Airlangga Hospital.

Item Type: Thesis (Undergraduate)
Uncontrolled Keywords: Thalassemia, Hepcidin, Kreatinin, Thalassemia, Hepcidin, Creatinine
Subjects: Q Science > QP Physiology
R Medicine > RB Pathology
R Medicine > RC Internal medicine
Divisions: 05. Fakultas Kedokteran > Pendidikan Dokter
Depositing User: NAJA MAULANA HASSAN
Date Deposited: 03 Jul 2026 09:18
Last Modified: 03 Jul 2026 09:18
URI: https://repository.um-surabaya.ac.id/id/eprint/12698

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