Renal Dysfunction in Beta-Thalassemia Patients
Summary
Beta-thalassemia encompasses a spectrum of inherited disorders characterised by defective synthesis of the β-globin chains of haemoglobin, leading to chronic anaemia and compensatory erythroid hyperplasia. Advances in transfusion programmes and iron-chelation therapy have markedly improved survival but have unveiled a range of long-term complications, among which renal dysfunction has emerged as a significant contributor to morbidity. Renal involvement in beta-thalassemia may manifest as glomerular hyperfiltration, proximal and distal tubular defects, reduced concentrating ability and microalbuminuria. Underlying mechanisms include chronic hypoxia, iron deposition in renal parenchyma, oxidative stress and nephrotoxic effects of chelating agents. These processes promote tubular cell injury, interstitial fibrosis and progressive decline in glomerular filtration rate. Clinical presentation can be subtle, with early signs detectable only by sensitive biomarkers such as neutrophil gelatinase-associated lipocalin and kidney injury molecule-1. Timely recognition of renal impairment is essential, as even mild dysfunction can exacerbate anaemia management, increase cardiovascular risk and reduce quality of life. Multidisciplinary care integrating regular assessment of renal function, optimisation of transfusion regimens, individualised chelator dosing and emerging antioxidant strategies holds promise for preserving kidney health and improving long-term outcomes.
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Renal Dysfunction in Beta-Thalassemia Patients publication trend
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Technical terms
Ineffective erythropoiesis: A condition in which erythroid precursors proliferate in the bone marrow but fail to mature into functional red cells.
Hemosiderosis: Accumulation of excess iron in tissues, often secondary to repeated blood transfusions.
Glomerular filtration rate (GFR): A measure of kidney function indicating the volume of plasma filtered per unit time.
Tubular dysfunction: Impairment of renal tubule processes, affecting reabsorption and secretion of electrolytes and water.
Iron chelation: The use of agents that bind excess iron to facilitate its excretion and prevent tissue damage.
Oxidative stress: Cellular injury caused by an imbalance between production of reactive oxygen species and antioxidant defences.
References
- Early Kidney Damage Markers after Deferasirox Treatment in Patients with Thalassemia Major: A Case‐Control Study. Oxidative Medicine and Cellular Longevity (2019).
- Beta-thalassemia: renal complications and mechanisms: a narrative review. Hematology (2019).
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