title: Correlation between glomerular morphology and renal haemodynamic response to amino-acid administration in patients with IgA nephropathy.
abstract: 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.
authors.affiliation: Istituto di Medicina Interna e Nefrologia, Seconda Università di Napoli, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Pluvio
authors.forename: E
authors.initials: E
authors.lastname: de Pascale
authors.forename: M
authors.initials: M
authors.lastname: Giordano
authors.forename: D
authors.initials: D
authors.lastname: Cirillo
authors.forename: M
authors.initials: M
authors.lastname: Carone
authors.forename: M
authors.initials: M
authors.lastname: Pluvio
authors.forename: P
authors.initials: P
authors.lastname: Castellino
authors.forename: C
authors.initials: C
authors.lastname: Giordano
mesh_terms: 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
chemical_list: D000596:Amino Acids; D007328:Insulin; D005934:Glucagon; D010130:p-Aminohippuric Acid