Abstract
BackgroundIgA nephropathy (IgAN) may progress to renal failure for some patients without any clinical risk factors and it is not unusual to find severe pathologic damage in clinically mild IgAN. We therefore investigated whether urinary kidney injury molecule-1 (KIM-1) was related to pathologic involvement in clinically mild IgAN.MethodsUrinary KIM-1/creatinine of 51 IgAN patients with normotension, normal renal function and proteinuria < 1.0 g/24 h were tested. Relationships between urinary KIM-1 and pathologic features were analyzed.ResultsEighteen of the 51 patients had elevated urinary KIM-1. The tubular atrophy/interstitial fibrosis was more severe in patients with elevated urinary KIM-1 than that in patients with normal urinary KIM-1 (T0/T1/T2, 13/5/0 vs. 33/0/0, P = 0.004). Proportion of glomeruli containing cresecents was higher in patients with elevated urinary KIM-1 than that in patients with normal urinary KIM-1 (50% vs. 18%, P = 0.026). Urinary KIM-1 correlated with the proportion of total crescents (R = 0.303, p = 0.031) and fibrous crescents (R = 0.456, p = 0.001), but did not correlate with the proportion of cellular crescents or fibrocellular crescents. Although the proportion of vascular lesions was higher in patients with elevated urinary KIM-1 (44.4%) than that in patients with normal urinary KIM-1 (18.1%), the difference was not significant (p = 0.057). There was no difference of the response to treatment between patients with and without elevated urinary KIM-1 during a short-term follow-up.ConclusionsUrinary KIM-1 is a reflection of tubularinstitial injury. For patients with clinically mild IgAN, high urinary KIM-1 is related to relatively severe pathologic involvement on renal biopsy.
Highlights
IgA nephropathy (IgAN) may progress to renal failure for some patients without any clinical risk factors and it is not unusual to find severe pathologic damage in clinically mild IgAN
Normotension was defined as systolic blood pressure
Patients were divided into two groups according to the level of urinary kidney injury molecule-1 (KIM-1) [i.e. patients with elevated urinary KIM-1 (>0.52 ng/ mg, n = 18) and patients without elevated urinary KIM-1 (≤0.52 ng/mg, n = 33)]
Summary
IgA nephropathy (IgAN) may progress to renal failure for some patients without any clinical risk factors and it is not unusual to find severe pathologic damage in clinically mild IgAN. We investigated whether urinary kidney injury molecule-1 (KIM-1) was related to pathologic involvement in clinically mild IgAN. Some clinical risk factors have been reported to link with progressive IgAN including hypertension, proteinuria >1.0 g/day, and reduced glomerular filtration rate (GFR), but it is not unusual to find patients with. Previous studies mainly focused on the value of the urinary KIM-1 in the prediction of renal survival and all these studies involved patients with IgAN from clinically trivial to very severe. The value of urinary KIM-1 in IgAN without clinical risk factors is unclear. We detected the levels of urinary KIM-1 in 51 IgAN patients with normotension, normal renal function and mild proteinuria, and analyzed the relationships between urinary KIM-1 and pathologic variables identified by the recently published Oxford classification of IgAN
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