Arteriosclerosis is a common finding in pathology of IgA nephropathy. Hypertension has been indicated as the cause of the arterial change. The chronic changes, ie. glomerulosclerosis, tubulointerstitial fibrosis, is implied as the cause of hypertension. However, prominent arteriosclerosis can be seen in biopsies with mild chronic changes.A study by El Karoui et al. points out that a high percentage (53%) of IgAN patients also had thrombotic microangiopathy (TMA). These patients had poorer renal outcome than those with IgAN only, especially in IgAN+TMA patients who also had laboratory evidence of TMA (anemia, thrombocytopenia, schizocytes, etc...). They tend to have more proteinuria and hypertension. All patients with malignant hypertension had TMA. Renal bx in these patients also showed more severe chronic changes. In spite of this, the authors argued that TMA was rather the cause than the result of severe chronic parenchymal disease. A minority of patients showed TMA with only mild chronic changes.
TMA lesion in IgAN primarily involved arterioles and interlobular arteries. This is more similar to TMA lesion found in malignant hypertension and progressive systemic sclerosis rather than TMA lesion in hemolytic uremia syndrome (HUS) in which glomerular involvement was seen frequently.
Although the etiology of TMA in IgAN remains elusive, several hypotheses were proposed including decreased vascular endothelial growth factor (VEGF) due to presence of abnormal glycosylated IgA and the presence of antibody to endothelium.
In my opinion the cross sectional design of study prevents the conclusion that IgAN is the cause of TMA, eventhough other causes such as antiphospholipid antibodies or genetic factors had been excluded. It is still possible that the severe chronic changes seen in most patients with TMA could be the cause rather than the result of TMA.
Now it's time to pay close attention to the arteries when looking at the renal bx of IgAN.
