title: Impact of lisinopril and atenolol on kidney function in hypertensive NIDDM subjects with diabetic nephropathy.
abstract: Diabetic nephropathy is characterized by hypertension and a relentless decline in kidney function. Angiotensin-converting enzyme inhibitors have been claimed to preserve kidney function better than an equal blood pressure (BP) reduction with conventional antihypertensive treatment (renoprotection). We compared the effect on kidney function of lisinopril (10-20 mg/day) and atenolol (50-100 mg/day) in hypertensive NIDDM patients (mean age 60 +/- 8 years) with diabetic nephropathy. Forty-three (21 lisinopril and 22 atenolol) patients were enrolled in a 1-year randomized double-blind parallel study. Eight patients dropped out, and the results for the remaining 35 patients (16 lisinopril and 19 atenolol) are presented. Diuretics were required in 10 of 16 lisinopril patients and 12 of 19 atenolol patients. The following variables were measured: 24-hour ambulatory BP (Takeda TM2420), albuminuria (enzyme-linked immunosorbent assay), fractional albumin clearance, and glomerular filtration rate (GFR) ([51Cr]EDTA technique). The average reduction in mean arterial BP during the 12 months was identical in the two groups 12 +/- 2 vs. 11 +/- 1 mmHg in the lisinopril and atenolol group, respectively. Albuminuria was on average reduced 45% in the lisinopril group vs. 12% in the atenolol group (P < 0.01), and fractional albumin clearance was on average reduced 49% in the lisinopril group vs. 1% in the atenolol group (P < 0.05). GFR declined identically in the two groups 11.7 +/- 2.3 vs. 11.6 +/- 2.3 ml.min-1.year-1 in the lisinopril and atenolol groups, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Steno Diabetes Center, Gentofte, Denmark.
authors.forename: F S
authors.initials: FS
authors.lastname: Nielsen
authors.forename: P
authors.initials: P
authors.lastname: Rossing
authors.forename: M A
authors.initials: MA
authors.lastname: Gall
authors.forename: P
authors.initials: P
authors.lastname: Skøtt
authors.forename: U M
authors.initials: UM
authors.lastname: Smidt
authors.forename: H H
authors.initials: HH
authors.lastname: Parving
mesh_terms: D000419:Albuminuria; D001053:Apolipoproteins / Q000032:analysis; D053241:Apoprotein(a); D001262:Atenolol / Q000009:adverse effects / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002940:Circadian Rhythm; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000503:physiopathology*; D004311:Double-Blind Method; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology*; D017270:Lipoprotein(a); D017706:Lisinopril / Q000009:adverse effects / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D012083:Renin / Q000097:blood; D012709:Serum Albumin / Q000378:metabolism; D012964:Sodium / Q000097:blood; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001053:Apolipoproteins; D017270:Lipoprotein(a); D012709:Serum Albumin; D014280:Triglycerides; D001262:Atenolol; D012964:Sodium; D017706:Lisinopril; D053241:Apoprotein(a); D012083:Renin; D011188:Potassium