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IgA nephropathy, characterized by the deposition of immunoglobulin A (IgA) in the kidneys, presents an estimated incidence of 2 to 10 cases per 100,000 individuals per year. Diagnosis typically occurs during the second and third decades of life, with a male-to-female ratio of 2 to 3:1 in North America and a 1:1 ratio in Asia. Notably, in Mexico, reported prevalence figures have reached up to 7% in small renal biopsy registries among patients aged 18 to 30 years.
IgA nephropathy often remains asymptomatic until the patient manifests gross hematuria, hypertension, significant proteinuria, or renal insufficiency. The majority of patients exhibit an asymptomatic clinical course, characterized by asymptomatic proteinuria (23.2%), microscopic hematuria (13.7%), and subnephrotic proteinuria (39%). The presence of proteinuria exceeding 0.75 to 1 gram is associated with renal progression. Recent findings have indicated that arterial hypertension, obesity, and glucose irregularities serve as factors that expedite disease progression.
The primary objective of this study is to present a comprehensive overview of the clinical characteristics at the time of diagnosis within a cohort of Mexican patients diagnosed with IgA nephropathy at a single medical center.
This investigation adopted a cross-sectional analytical approach, enrolling 12 patients who were diagnosed with IgA nephropathy through renal biopsy. Quantitative variables were depicted according to their respective distributions, and qualitative variables were characterized in terms of frequencies.
Eighty-three percent of the cohort was comprised of male patients, with a median age of 32 years (interquartile range: 20-40) and an average body mass index (BMI) of 28±4.1 kg/m². A subset of patients, specifically 33%, initially presented with a clinical triad consisting of microscopic hematuria, arterial hypertension, and headaches, while 60% exhibited bromuria, 25% experienced lumbalgia, and 17% displayed gross hematuria. Notably, two patients presented with Schönlein-Henoch purpura. Four patients within the cohort went on to develop acute kidney injury, and one of these necessitated renal replacement therapy. Comorbidities associated with IgA nephropathy in this study encompassed diabetes mellitus, dry eye, HIV, and hypothyroidism. Significantly, no patients reported any antecedent gastrointestinal or respiratory disturbances prior to the onset of their symptoms. At the time of diagnosis, the median serum creatinine level stood at 1.5 mg/dL (range: 1.23-2.4), with an average urinary protein excretion of 2.4±1 g/24 hours. Median glucose, urea, uric acid, and albumin levels measured 101 (range: 51-102) mg/dL, 47.2 (range: 42.5-85) mg/dL, 6.3 (range: 6.9-13.8) mg/dL, and 3.9±0.3 g/dL, respectively. Additionally, 50% of the patients exhibited a modest elevation in serum IgA levels. Two patients displayed elevated c-ANCA levels, although only one of them developed vasculitis, accompanied by diminished C3 and C4 complement fractions. The lipid profile was as follows: triglycerides (96±7 mg/dL), cholesterol-HDL (45.5±10 mg/dL), LDL (79.55±16.3 mg/dL), and VLDL (39±3 mg/dL). The incidence of IgA nephropathy at our center stood at 7.3.
This study revealed that the clinical characteristics of patients diagnosed with IgA nephropathy in Mexico were akin to those observed in the Asian population. These findings underscore a 40% risk of renal disease progression within one year of diagnosis, with many patients exhibiting risk factors for such progression, notably obesity and systemic arterial hypertension. Of note, the average proteinuria levels observed in this study, 2.4±1 g/24 hours, significantly exceeded those reported in the VALIGA study (European population, average of 1.8 g/24 hours) and mirrored those of the TORONTO study (Asian population, mean of 2.4 g/24 hours).