title: Pregnancy and progression of diabetic nephropathy.
abstract: OBJECTIVE
  Pregnancy could damage kidney function in diabetic nephropathy. We investigated the long-term impact of pregnancy on the progression of diabetic nephropathy.
  
  
  METHODS
  Our observational follow-up study included all women patients with Type I (insulin-dependent) diabetes mellitus who developed diabetic nephropathy between 1970 and 1989 at Steno Diabetes Center (n = 93). Follow-up lasted 16 years (range 3-28) from the onset of diabetic nephropathy until death or the year 2000. A total of 26 women became pregnant after the onset of diabetic nephropathy (group A). The remaining 67 served as control subjects (group B). All patients received aggressive antihypertensive treatment (blood pressure goal < 140/90 mmHg).
  
  
  RESULTS
  The two groups were comparable at onset of diabetic nephropathy regarding blood pressure, albuminuria, s-cholesterol, smoking, retinopathy and s-creatinine (mean 79(SD 23) micromol/l). The slopes of 1/s-creatinine (1000.l.micromol(-1).year(-1)) during the whole observation period were -0.39(0.40) compared with -0.41(0.70) (group A vs B-NS). The slopes of 1/s-creatinine before and after pregnancy were similar. Decline in creatinine clearance (ml/min/yr) was 3.2 (3.4) compared with 3.2 (5.1) (group A vs B -NS). At the end of follow-up, 35 % (95 %-CI:17-53) of the pregnant women had died and 19 % (7-39) had reached end stage renal disease compared to 34 % (23-45) and 24 %(14-34) of the control subjects, respectively(NS). Group A and B had similar blood pressure levels during the whole observation period: 136(13)/83(7) vs 139 (14)/85(7) mmHg (NS).
  
  
  CONCLUSIONS
  Pregnancy has no adverse long-term impact on kidney function and survival in Type I diabetic patients with well-preserved kidney function (normal serum creatinine) suffering from diabetic nephropathy.
authors.affiliation: Steno Diabetes Center, Niels Steensens Vej 2, DK-2820 Gentofte, Denmark. krossing@dadlnet.dk
authors.forename: K
authors.initials: K
authors.lastname: Rossing
authors.forename: P
authors.initials: P
authors.lastname: Jacobsen
authors.forename: E
authors.initials: E
authors.lastname: Hommel
authors.forename: E
authors.initials: E
authors.lastname: Mathiesen
authors.forename: A
authors.initials: A
authors.lastname: Svenningsen
authors.forename: P
authors.initials: P
authors.lastname: Rossing
authors.forename: H-H
authors.initials: HH
authors.lastname: Parving
mesh_terms: D000328:Adult; D001794:Blood Pressure; D003404:Creatinine / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000503:physiopathology*; D003937:Diagnosis, Differential; D018450:Disease Progression; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D015994:Incidence; D007676:Kidney Failure, Chronic / Q000453:epidemiology / Q000503:physiopathology; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000503:physiopathology*; D012189:Retrospective Studies
chemical_list: D003404:Creatinine