title: Hypertriglyceridaemia and hyperuricaemia are risk factors for progression of IgA nephropathy.
abstract: BACKGROUND
  The prognosis of IgA nephropathy (IgAN) is variable and about 10-20% of patients progress to end-stage renal disease (ESRD) in 10 years. Hypertension, proteinuria and renal insufficiency at the time of diagnosis are risk factors associated with poor prognosis. Lipid abnormalities may have a role in the progression of glomerulonephritides, and glomerulosclerosis and atherosclerosis may have similar pathophysiological mechanisms. We therefore evaluated factors associated with cardiovascular diseases, especially hypercholesterolaemia, hypertriglyceridaemia, and hyperuricaemia, as predictors of the progression of IgAN.
  
  
  METHODS
  A total of 223 patients with IgAN (141 men, 82 women; median age 41 years, range 8-78 years) were studied. The following parameters were recorded at the time of renal biopsy: presence of hypertension or diabetes, smoking habits, body mass index (BMI), serum creatinine, total and HDL-cholesterol, triglycerides, and urate and 24-h urinary protein excretion. The patients were followed up for 0.2-17 years (median 10 years) with respect to progression of renal disease defined as elevation of serum creatinine above 125 micromol/l in men or 105 micromol/l in women, and over 20% elevation from baseline.
  
  
  RESULTS
  Forty-one patients (18%) showed progression. Hypertriglyceridaemia and hyperuricaemia were significantly more common at the time of renal biopsy in patients with progressive than in those with stable disease. In patients with normal renal function at the time of diagnosis initial hypertriglyceridaemia, hyperuricaemia, hypertension and proteinuria were independent risk factors for progression of IgAN in the Cox regression hazard model.
  
  
  CONCLUSIONS
  Our results show that hypertriglyceridaemia and hyperuricaemia at the time of diagnosis are important, previously underestimated predictors of poor outcome in IgAN, although causality between these factors and progression cannot be inferred from the present study.
authors.affiliation: Department of Medicine, Tampere University Hospital and Medical School, University of Tampere, Tampere, Finland.
authors.forename: J
authors.initials: J
authors.lastname: Syrjänen
authors.forename: J
authors.initials: J
authors.lastname: Mustonen
authors.forename: A
authors.initials: A
authors.lastname: Pasternack
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002648:Child; D005260:Female; D005922:Glomerulonephritis, IGA / Q000097:blood* / Q000150:complications*; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications; D015228:Hypertriglyceridemia / Q000150:complications*; D007676:Kidney Failure, Chronic / Q000209:etiology; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012307:Risk Factors; D014527:Uric Acid / Q000097:blood*
chemical_list: D008055:Lipids; D014527:Uric Acid