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.