title: The influence of familial factors on the progression of IgA nephropathy.
abstract: BACKGROUND
  Vascular risk factors in first degree relatives of patients with insulin dependent diabetes mellitus are known to increase the risk of that patient developing diabetic nephropathy. We explored the influence of vascular risk factors in first degree relatives on patients with stable (serum creatinine < 150 mumol/l for > 5 years) and progressive (serum creatinine > 200 mumol/l, and > 150% serum creatinine at presentation, after minimum follow-up at 2 years) IgA nephropathy (IgAN).
  
  
  METHODS
  We compared sodium-lithium countertransport activity (SLC Vmax), plasma lipoprotein(a) and von Willebrand factor (vWf) concentrations, incidence of vascular disease, and incidence of hypertension in 37 first degree relatives of 23 patients with stable IgAN and 33 first degree relatives of 17 patients with progressive IgAN. The two groups of relatives were comparable with respect to other risk factors: age, smoking, blood pressure, and plasma glucose, creatinine, cholesterol and triglyceride concentrations.
  
  
  RESULTS
  SLC Vmax was higher in relatives of stable patients (mean 0.37 mmol/h/l RBC [S.D. 0.18] vs 0.30 [S.D. 0.09]; P = 0.034 two-sample t-test). There was no difference between the relatives of stable and progressive patients in plasma lipoprotein(a) concentration (median 11.5 mg/l vs 13.0: P = 0.45; 95% C.I. -12 to 3; Mann-Whitney test), plasma vWf concentration (149.4 IU/dl [S.D. 55.6] vs. 163.2 IU/dl [S.D. 57.3]; P = 0.31 two-sample t-test), or incidence of hypertension (13/37 [35.1%] vs 10/33 [30.3%]; chi 2 = 0.185; P = 0.667). Relatives of patients with progressive IgAN had a slightly higher incidence of vascular disease (10/33 [30.3%] vs 8/37 [21.6%]; chi 2 = 0.688; P = 0.407).
  
  
  CONCLUSIONS
  Familial vascular risk may increase the likelihood of progressive renal failure in patients with IgAN but the influence is likely to be small and unrelated to the factors we measured. SLC Vmax was significantly higher in relatives of patients with stable disease which contrasts with data from other studies and is unexplained.
authors.affiliation: Renal Unit, Glasgow Royal Infirmary, UK.
authors.forename: C C
authors.initials: CC
authors.lastname: Geddes
authors.forename: G L
authors.initials: GL
authors.lastname: Warwick
authors.forename: I
authors.initials: I
authors.lastname: Tulloch
authors.forename: J M
authors.initials: JM
authors.lastname: Boulton-Jones
mesh_terms: D000328:Adult; D000368:Aged; D017920:Antiporters / Q000378:metabolism; D018450:Disease Progression; D005260:Female; D005922:Glomerulonephritis, IGA / Q000235:genetics* / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000235:genetics; D015994:Incidence; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D008875:Middle Aged; D014652:Vascular Diseases / Q000453:epidemiology / Q000235:genetics; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D017920:Antiporters; D017270:Lipoprotein(a); C045885:sodium-lithium countertransporter; D014841:von Willebrand Factor