CORRELATION BETWEEN GLOMERULAR MORPHOLOGY AND RENAL HEMODYNAMIC-RESPONSE TO AMINO-ACID ADMINISTRATION IN PATIENTS WITH IGA NEPHROPATHY

Rationale. To establish relationship, if any, between renal morphology and renal haemodynamic response to amino acids. Design and methods. W e investigated the correlation between renal haemodynamic regulation a nd morphology in a group of 15 patients with primary IgA nephropathy ( IgAN) (age 26 +/- 2 years, BMI 24.4 +/- 1, GFR 64 +/- 5 ml/min, RPF 37 7 +/- 34 ml/min, FF 0.17 +/- 0.02). Twelve normal subjects (age 30 +/- 3 years, BMI 24 +/- 1, GFR 82 +/- 6 ml/min, RPF 421 +/- 42 ml/min, FF 0.19 +/- 0.02) were studied as controls. IgA patients were divided in to two groups according to the histological staging of glomerular lesi ons: group I (n=7) stage II, and group II (n=8) stage III-IV. Results. In the basal state GFR was similar in the two groups and averaged 64 +/- 9 and 64 +/- 6 ml/min respectively. In contrast, FF was significan tly lower in group II (0.14 +/- 0.01) (P < 0.05) in comparison to grou p I (0.21 +/- 0.03) and controls (0.19 +/- 0.02). In order to evaluate the renal functional reserve, all study groups underwent to an intrav enous amino-acid infusion designed to increase plasma amino acid level s twofold (total from 2096 +/- 145 to 4301 +/- 221 mu mol/1 in IgA nep hropathy patients and from 2272 +/- 83 to 3844 +/- 238 mu mol/l in con trols). In response to aminoacid infusion, GFR rose significantly in g roup I (GFR 20 +/- 2% and RPF 37 +/- 4% versus basal) and controls (GF R 20 +/- 2% and RPF 20 +/- 3% versus basal) (both P < 0.01 vs basal). In contrast, in patients with more severe glomerular lesions (group II ) neither GFR nor RPF rose significantly (GFR -1 +/- 4% and RPF -8 +/- 6% versus basal) (P NS versus basal, P < 0.01 versus group I and cont rols). Conclusions. The data show that in IgA nephropathy: severe form s of glomerular lesions are associated with a complex alteration of gl omerular haemodynamic regulation, characterized by lower basal FF and loss of haemodynamic response to hyperaminoacidaemia.