Background: IgA nephropathy (IgAN) is the most frequent glomerulonephritis in many countries including Estonia. There is no specific treatment for IgAN but renoprotection is indicated when proteinuria is >1 g/day. We aimed to assess the clinicopathological correlations of IgAN and to compare the follow-up outcome of the IgAN patients receiving renoprotection with the patients with other antihypertensive regimen treatments.
Methods: A retrospective kidney biopsy cohort study was carried out in consecutive 73 IgAN cases, using the new Oxford classification. The baseline and follow-up (FU, 4.1 years) clinical data were collected. The patients were divided into two main study groups according to their drug-treatment: the drug-treated and untreated patients' groups. Two subgroups among patients receiving two different antihypertensive drugs were formed and statistically analysed: Renin-angiotensin system (RASb, renoprotection) - and calcium-channel blockers (CCB)-receiving patients. Also, patient' subgroups with and without the presence of clinical and morphological risk factors were used for statistical analysis.
Results: The patients' mean age was 33.7 years (range 16-76). Proteinuria decreased at the end of FU (0.91 g/24 h to 0.79 g/24 h). Mean arterial pressure remained at the end of FU almost at the same level. Drug treatment was prescribed to the patients who had lower eGFR, higher proteinuria and more severe histological lesions (S1, T1/2), while the patients with minimal clinical symptoms and the ones with near-normal kidney function remained without drug treatment. The kidney function remained almost at the same normal level in untreated patients irrespective of the risk factors whereas in both treated patient' subgroups eGFR declined. The following statistically significant correlations in the IgAN cohort were found: correlations in patients with lower kidney function (eGFR <60 ml/min/1.73 m2), higher blood pressure (p = 0.00006) and proteinuria were found irrespectively of the fact whether the patients received (p = 0.006) or did not receive renoprotection (p = 0.001). The biggest significant eGFR change by Wilcoxon rank sum test was found among the patients who had clinical and morphological risk factors and received treatment. The result was confirmed by post hoc analysis and did not depend on the presence of treatment. In the investigation of the subgroups receiving RASb we found that the lowering of eGFR did depend on the presence of clinical and morphological risk factors.
Conclusions: Renoprotection is only effective in preventing the progression of IgAN when clinical and morphological risk factors are modest or missing.