title: Relationship of renal histological damage to glomerular hypertension in patients with immunoglobulin A nephropathy.
abstract: OBJECTIVE
  Studies of experimental animals show glomerular hypertension to be important in the progression of glomerular disease. We evaluated this connection clinically by examining the relationship between glomerular hemodynamics and histological changes in patients with immunoglobulin (Ig)A nephropathy.
  
  
  METHODS
  The subjects were 23 patients with IgA nephropathy. All patients underwent renal biopsies. Glomerular hemodynamics, in terms of glomerular capillary hydraulic pressure (PGC) and the whole-kidney ultrafiltration coefficient, were calculated from the renal clearance, plasma total protein concentration, and pressure-natriuresis relationship. The severity of glomerulosclerosis, tubulointerstitial damage and mesangial matrix expansion was evaluated semiquantitatively.
  
  
  RESULTS
  PGC ranged from 33-69 mm Hg, and the mean arterial pressure (MAP) from 79-112 mm Hg. Their correlation was not significant (r= 0.29, P= 0.18). PGC was significantly correlated with the glomerulosclerosis score, and also with the score for tubulointerstitial damage (r= 0.65, P < 0.001 and rs = 0.59, P = 0.007, respectively), but not with the score for mesangial matrix expansion (r= 0.08, P= 0.72). MAP was significantly correlated only with the score for tubulointerstitial damage (rs = 0.63, P = 0.004). In multiple linear regression analysis of the histological changes and hemodynamics, the glomerulosclerosis score and the score for tubulointerstitial damage were correlated with PGC, but not with MAP.
  
  
  CONCLUSIONS
  These clinical results support the speculation that glomerular hypertension is involved in the glomerulosclerosis and tubulointerstitial damage that occurs in IgA nephropathy.
authors.affiliation: Department of Internal Medicine, Osaka City General Hospital, Osaka, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Konishi
authors.forename: M
authors.initials: M
authors.lastname: Imanishi
authors.forename: M
authors.initials: M
authors.lastname: Okamura
authors.forename: K
authors.initials: K
authors.lastname: Yoshioka
authors.forename: M
authors.initials: M
authors.lastname: Okumura
authors.forename: N
authors.initials: N
authors.lastname: Okada
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: S
authors.initials: S
authors.lastname: Fujii
authors.forename: G
authors.initials: G
authors.lastname: Kimura
mesh_terms: D000328:Adult; D001794:Blood Pressure; D002196:Capillaries / Q000503:physiopathology; D005260:Female; D005922:Glomerulonephritis, IGA / Q000150:complications*; D005923:Glomerulosclerosis, Focal Segmental / Q000209:etiology / Q000473:pathology; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology*; D007668:Kidney / Q000473:pathology*; D007678:Kidney Glomerulus / Q000098:blood supply / Q000503:physiopathology*; D007684:Kidney Tubules / Q000473:pathology; D008297:Male; D008875:Middle Aged