Renal Dysfunction in Pediatric Patients in Iraq With β-Thalassemia Major and Intermedia

Abstract

BackgroundWith optimum transfusion and chelation therapy, the survival of β-thalassemia patients and the incidence of various complications, including renal complications, have improved. ObjectivesTo investigate renal involvement in β-thalassemia patients using serum and urinary biochemical markers of glomerular and tubular dysfunction. MethodsThis case-control study included 69 β-thalassemia major (β-TM) patients, 23 β-thalassemia intermedia (β-TI) patients, and 100 healthy controls, all ranging from 1 to 16 years in age. Blood urea nitrogen (BUN), serum ferritin, serum and urinary levels of creatinine (Cr), uric acid (UA), calcium (Ca), phosphorus (Ph), magnesium (Mg), sodium (Na), and potassium (K), and the urinary albumin/creatinine ratio were evaluated. ResultsThe BUN level and the urinary Na/Cr, K/Cr, Ca/Cr, Mg/Cr, Ph/Cr, albumin/Cr, and UA/Cr ratios were significantly higher in the β-thalassemia patients than in the controls. In contrast, the serum Na, K, Ca, and Mg levels were significantly lower in the patients (P<0.05). An elevated urinary UA/Cr ratio was found in 61.9% of β-thalassemia patients, and an elevated urinary Ca/Cr, and urinary albumin/Cr ratio was found in 53.2%. An elevated Na/Cr ratio was found in 41.3%. The serum and urinary renal markers showed no significant differences between patients with β-TM and β-TI, except for microscopic hematuria, which was significantly higher in β-TI patients (34.8%) than in β-TM patients (13%), P>0.02. At an older age, high serum ferritin levels and deferoxamine therapy were associated with significant tubular and glomerular dysfunction in β-thalassemia patients. ConclusionsPediatric patients with β-thalassemia have significantly abnormal tubular and glomerular functions, necessitating early detection and monitoring to prevent/reverse renal function deterioration.

Novel biochemical markers for the prediction of renal injury in beta-thalassemia major pediatric patients

“…This reactive iron has the potential to trigger the generation of reactive oxygen species (ROS) and cause cellular damage. Consequently, there may be a defect in reabsorption, leading to increased urinary potassium excretion [32]. It is important to note that our study contradicts the findings, which reported a significant increase in serum potassium levels [37,38].…”

“…Our study's results indicate a significant decrease in serum potassium, although it remains within the normal range (P ≤ 0.05). These findings confirm previous research, including studies on thalassemia patients [30,32]. The decrease in serum potassium levels could be attributed to the fact that most potassium is reabsorbed in the loop of Henle and proximal tubule.…”

“…It should be noted that the growth retardation observed in patients with βTM could be attributed to a lack of muscle mass, which may affect the creatinine value. Some studies did not find a significant correlation between creatinine and βTM [31,32]. However, a study conducted by Mahmoud et al demonstrated a significant increase in creatinine levels in patients compared to controls [22].…”

Highlights on Deferasirox Use and its Renal Toxicity in Children with Beta Thalassemia Major

“…In previous studies by Aldudak et al (2) and Mohkam et al (14) on patients receiving DFO using common markers, early renal changes could not be demonstrated. As a result of chronic anemia, iron deposition, and/or drug like DFO cumulative toxicity, these studies have primarily shown the presence of proximal tubular compromise in those patients (2,14) . Papassotiriou et al (15) also reported slight changes of cystatin C level during deferasirox treatment in βthalassemia population.…”

“…Thalassemia patients may experience renal dysfunction as of DFO side effects, iron deposition in the kidney, or other causes such as lipid peroxidation, stress oxidation, generation of free radicals, and thrombosis (2,3) release free radicals and thrombosis (3) .…”