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Long‐term evolution of renal histology in slowly progressive patients with IgA nephropathy
Author(s) -
Abe A,
Kawamura T,
Utsunomiya Y,
Hamaguchi A,
Kitajima T,
Hosoya T
Publication year - 2001
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1046/j.1440-1797.2001.00016.x
Subject(s) - medicine , nephropathy , biopsy , renal biopsy , creatinine , urology , histology , arteriolosclerosis , pathology , renal function , glomerulosclerosis , kidney , glomerulonephritis , gastroenterology , endocrinology , proteinuria , diabetes mellitus , disease
Recent clinical trials indicate that non‐immunological mechanisms (e.g., glomerular hypertension or hypertrophy) may play a crucial role in the progression of patients with IgA nephropathy. Since the long‐term renal histological changes in an individual patient with IgA nephropathy are not well elucidated, we assessed the serial renal biopsy specimens from nine patients with IgA nephropathy (five males, four females) where serial biopsies were performed in an interval of more than 10 years (mean 12.8; range 10–20). Histological parameters (i.e. percentage of global sclerosis (GS), tubulo‐interstitial lesion (TI), patients (Pt) with cellular crescent (CC) or arteriolosclerosis (AS), mean glomerular area (MGA) and number of glomeruli per renal cortical area (glomerular density, GD)), were compared between the both specimens ( Table 1).Renal
biopsy Age
(year) Pt with HT
(%) UprV
(g/day) Ccr
(mL/min) GS
(%) Pt with CC
(%) MGA
(× 10 3 μmm) GD
(/mm 2 ) Pt with AS
(%) TI
(%)First 25 ± 8 22 0.6 ± 0.3 88 ± 17 10 ± 11 78 15 ± 6.0 3.9 ± 2.0 11 13 ± 8 Second 38 ± 8 78 * 1.3 ± 0.6 * 55 ± 21 * 25 ± 23 11 * 22 ± 8.4 * 2.0 ± 0.8 * 89 * 34 ± 16 *Mean ± SD, * P < 0.05 vs first biopsyAll patients had a slowly progressive course between the first and second biopsies as evidenced by the significant difference in the percentage of hypertension (HT), urinary protein excretion (UprV) and creatinine clearance (Ccr). Histological analysis of serial biopsy specimens revealed that the degrees of AS and TI were significantly enhanced at second biopsy, while acute glomerular lesions such as CC were remarkably diminished. Of note, a marked increase in MGA as well as a significant reduction in GD were observed during over 10 years. Moreover, at second biopsy, the values for MGA from individual patients negatively correlated with those for GD ( r = 0.77, P < 0.01) and Ccr ( r = 0.65, P < 0.01). These data indicate that patients with IgA nephropathy undergo glomerular hypertrophy subsequent to the reduction in nephron mass in the long‐term and glomerular hypertrophy may play an important role in the slow progression of patients with IgA nephropathy.