[Clinical and pathological analysis of IgA nephropathy with acute kidney injury]

M G Chen, X H Ye, H Y Liang, Q Yang
Zhonghua Er Ke za Zhi. Chinese Journal of Pediatrics 2016, 54 (8): 610-3

OBJECTIVE: To investigate the incidence, etiology, clinico- pathological characteristics and prognosis in primary IgA nephropathy (IgAN) children with acute kidney injury (AKI).

METHOD: Retrospective analysis of the clinical and pathological manifestations and follow-up results of 19 Chlidren, who were associated with AKI in 196 cases of children with IgA nephropathy treated in our department from January, 1996 to Jun, 2012 was performed.

RESULT: (1) The 19 cases associated with AKI accounted for 9.7% of all 196 Chlidren with IgAN. Within the 19 cases, there were gross hematuria in 17 cases, massive proteinuria in 16 cases, hypoalbuminemia in 10 cases, edema in 10 cases and hypertension in one case. The peak serum creatinine was from 94.5 μmol/ L to 282 μmol/L. (2) Histological changes: with the formation of crescent in 10 cases, diffuse endocapillary proliferation in 5 cases, 15 cases had renal tubular injury, 10 cases had red blood cell and protein cast, 1 case with acute interstitial nephritis. (3) The cause of IgA nephropathy with AKI: 13 patients had severe glomerular damage, including crescentic glomerulonephritis and diffuse endocapillary proliferation; 1 case was complicated with acute interstitial nephritis after being treated with antibiotics, 2 patients had decreased glomerular filtration rate because of taking benazepril or oral indomethacin, 1 case with renal tubular injury induced by gross hematuria, and the other two cases the reason was not clear. (4) Multivariate Logistic regression analysis showed that massive proteinuria was independent risk factor of IgAN in children with AKI (OR=27.370, 95% confidence interval was 3.151-237.740, P<0.01). (5) None of the patients were on dialysis, steroid therapy was used in 13 cases (including 7 cases of methylprednisolone pulse therapy), 6 cases were treated with combined cyclophosphamide treatment. Except 1 cases no significant improvement, the renal functiones of all patients recovered or improved within 1-2 months after treatment. Follow-up period was from 1 month to 7 years, 3 cases had renal function improved, but 2 cases were lost to follow-up for 3 years and then entered the chronic renal failure, 1 case had renal function loss after 32 months and repeated renal biopsy showed glomerular sclerosis of 32% during the follow-up period.

CONCLUSION: In children with IgAN, AKI accounted for about 10%, except glomerular severe lesion, the onset of AKI is also relevant to clinical medication and repeated gross hematuria, and the heavy proteinuria is an independent risk factor. Based on clinical observation, the short-term prognosis of IgAN children with AKI is optimistic.

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