Glomerular hematuria: IgA; Alport; thin basement membrane nephropathy

INTRODUCTION

Hematuria is a common finding in glomerular diseases. This is often associated with other abnormalities including red cell casts, proteinuria, edema, hypertension, and renal insufficiency. In some cases, however, the only manifestation is persistent hematuria similar to that seen with extraglomerular causes of bleeding such as prostatic disease and stones.

The patient should initially be reexamined over a period of weeks to months to ascertain that the hematuria is persistent. Transient hematuria is a relatively common finding over time in adults and may be induced by factors such as exercise or infection. (See "Etiology and evaluation of hematuria in adults" and "Exercise-induced hematuria".)

The presence of a glomerular disease in the patient with persistent hematuria is often suggested by the urinary findings of dysmorphic red cells and an occasional red cell cast. (See "Etiology and evaluation of hematuria in adults", section on 'Glomerular versus nonglomerular bleeding'.)

There are three disorders that account for most cases of persistent isolated hematuria due to glomerular disease: IgA nephropathy, hereditary nephritis (Alport syndrome), and thin basement membrane nephropathy (which accounts for most cases of what has been called benign familial hematuria) [1-6].

Although mild postinfectious glomerulonephritis can also lead to isolated hematuria, there is usually rapid resolution of the urinary abnormalities within three to six months in this setting. (See "Differential diagnosis and evaluation of glomerular disease", section on 'Hematuria following upper respiratory infection'.) Given the increasing availability of genetic testing, additional hematuric syndromes are likely to be described [7].