Abstract
Primary IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide [1,2]. Although IgAN was considered a benign condition for many years, we now know that many cases eventually progress to end-stage renal failure. According to recent reviews, the actuarial renal survival at 10 years is 80–85% in most studies. Moreover, 30–40% of affected individuals develop end-stage renal failure within 20 years from the apparent onset of the disease [1,2]. Impairment of renal function, severe proteinuria and arterial hypertension are the strongest predictors of an unfavourable outcome. Among histological parameters, proliferative glomerulonephritis with crescents or advanced lesions (glomerulosclerosis and interstitial fibrosis) are the most reliable prognostic markers. Despite considerable progress in our understanding of IgA biology, the aetiology and fundamental pathogenic mechanisms of mesangial IgA deposition have remained unsolved [2]. For this reason, treatment options of IgAN patients currently lack a disease-specific approach. Furthermore, progression to irreversible renal parenchymal damage follows a final common pathway in most cases of chronic proteinuric nephropathies that is relatively independent of the initial insult. IgAN is no exception in that regard. The risk factors for progression of IgAN are the same as in most other chronic glomerulopathies, including hypertension, proteinuria, smoking and early elevation of serum creatinine. Hypertension is the most well known, the most frequently examined and probably also the most important of the risk factors for renal disease progression. This commentary will focus on the epidemiology and pathophysiology of hypertension, on the value of 24 h ambulatory blood pressure measurement (ABPM), on target blood pressures and on treatment options for hypertension in chronic IgAN.
Published Version
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