While IgA Nephropathy occurs in all age groups, it is usually diagnosed before the age of 30 years. It is common in children but the peak incidence is between 15-25 years. Usually, the passage of blood in the urine (macroscopic haematuria) making it coffee or tea coloured, is one of the signs for which the person sees a doctor. This is usually associated with a sore throat or respiratory infection or diarrhoea and vomiting, and may occur again in association with such infections.
For the individual patient with primary IgA nephropathy (IgAN), it remains a challenge to predict long-term outcomes for patients receiving standard treatment. We studied a prospective cohort of 332 patients with biopsy-proven IgAN patients followed over an average of 13 years.
IgA Nephropathy is sometimes called Berger's disease as a French doctor, Jean Berger, was the first to describe it. Nephropathy simply means kidney disease. The antibody IgA (Immunoglobulin A), derived from the lining of the throat, air passages and intestine is found in the kidney and has caused damage to the kidney. The precise mechanism is not yet certain and is the subject of much medical research. It is thought that some people produce too much IgA antibody when their body is fighting infections of the throat, tonsils, lungs and intestines and yet the antibody produced is not as efficient in eradicating the infection as it is in most people. As a result, the antibody combines with the infecting organism (antigen), circulates in the blood and lodges in the glomerulus (the filtering mechanism of the kidney) where it causes inflammation (nephritis) which may progress to more severe kidney damage, recognised as IgA Nephropathy.
In this paper, our goal was to use these three major risk factors to calculate a simple absolute renal risk (ARR) score allowing the accurate prediction of dialysis/death event at 10 and 20 years after disease onset, in adequately treated IgAN patients and in analogy to the well-known absolute cardiovascular (CV) risk of death/CV events at 10 years.
kidneyhospitalabroad@hotmail.com
For the individual patient with primary IgA nephropathy (IgAN), it remains a challenge to predict long-term outcomes for patients receiving standard treatment. We studied a prospective cohort of 332 patients with biopsy-proven IgAN patients followed over an average of 13 years.
IgA Nephropathy is sometimes called Berger's disease as a French doctor, Jean Berger, was the first to describe it. Nephropathy simply means kidney disease. The antibody IgA (Immunoglobulin A), derived from the lining of the throat, air passages and intestine is found in the kidney and has caused damage to the kidney. The precise mechanism is not yet certain and is the subject of much medical research. It is thought that some people produce too much IgA antibody when their body is fighting infections of the throat, tonsils, lungs and intestines and yet the antibody produced is not as efficient in eradicating the infection as it is in most people. As a result, the antibody combines with the infecting organism (antigen), circulates in the blood and lodges in the glomerulus (the filtering mechanism of the kidney) where it causes inflammation (nephritis) which may progress to more severe kidney damage, recognised as IgA Nephropathy.
In this paper, our goal was to use these three major risk factors to calculate a simple absolute renal risk (ARR) score allowing the accurate prediction of dialysis/death event at 10 and 20 years after disease onset, in adequately treated IgAN patients and in analogy to the well-known absolute cardiovascular (CV) risk of death/CV events at 10 years.
kidneyhospitalabroad@hotmail.com
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