Correlation between glomerular morphology and renal haemodynamic response to amino-acid administration in patients with IgA nephropathy.
BACKGROUND
To establish relationship, if any, between renal morphology and renal haemodynamic response to amino acids.


METHODS
We investigated the correlation between renal haemodynamic regulation and 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 377 +/- 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 into two groups according to the histological staging of glomerular lesions: 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 significantly lower in group II (0.14 +/- 0.01) (P < 0.05) in comparison to group 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 intravenous amino-acid infusion designed to increase plasma amino acid levels twofold (total from 2096 +/- 145 to 4301 +/- 221 mumol/l in IgA nephropathy patients and from 2272 +/- 83 to 3844 +/- 238 mumol/l in controls). In response to amino-acid infusion, GFR rose significantly in group I (GFR 20 +/- 2% and RPF 37 +/- 4% versus basal) and controls (GFR 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 controls).


CONCLUSIONS
The data show that in IgA nephropathy: severe forms of glomerular lesions are associated with a complex alteration of glomerular haemodynamic regulation, characterized by lower basal FF and loss of haemodynamic response to hyperaminoacidaemia.
Pluvio
C
C
Istituto di Medicina Interna e Nefrologia, Seconda Università di Napoli, Italy.
de Pascale
E
E
Giordano
M
M
Cirillo
D
D
Carone
M
M
Pluvio
M
M
Castellino
P
P
Giordano
C
C
D000328:Adult; D000596:Amino Acids / Q000008:administration & dosage* / Q000097:blood; D001794:Blood Pressure; D005215:Fasting; D005919:Glomerular Filtration Rate; D005922:Glomerulonephritis, IGA / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D005934:Glucagon / Q000097:blood; D006339:Heart Rate; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007262:Infusions, Intravenous; D007328:Insulin / Q000097:blood; D007668:Kidney / Q000502:physiology*; D007678:Kidney Glomerulus / Q000473:pathology; D017595:Renal Plasma Flow; D014655:Vascular Resistance; D010130:p-Aminohippuric Acid / Q000097:blood
D000596:Amino Acids; D007328:Insulin; D005934:Glucagon; D010130:p-Aminohippuric Acid