Medline ® Abstracts for References 84,85

of 'Antihypertensive therapy and progression of nondiabetic chronic kidney disease in adults'

84
TI
Blood pressure control, proteinuria, and the progression of renal disease. The Modification of Diet in Renal Disease Study.
AU
Peterson JC, Adler S, Burkart JM, Greene T, Hebert LA, Hunsicker LG, King AJ, Klahr S, Massry SG, Seifter JL
SO
Ann Intern Med. 1995;123(10):754.
 
OBJECTIVE: To examine the relations among proteinuria, prescribed and achieved blood pressure, and decline in glomerular filtration rate in the Modification of Diet in Renal Disease Study.
DESIGN: 2 randomized trials in patients with chronic renal diseases of diverse cause.
SETTING: 15 outpatient nephrology practices at university hospitals.
PATIENTS: 840 patients, of whom 585 were in study A (glomerular filtration rate, 25 to 55 mliters/min.1.73 m2) and 255 were in study B (glomerular filtration rate, 13 to 24 mliters/min.1.73 m2). Diabetic patients who required insulin were excluded.
INTERVENTIONS: Patients were randomly assigned to a usual blood pressure goal (target mean arterial pressure,<or = 107 mm Hg for patients<or = 60 years of age and<or = 113 mm Hg for patients>or = 61 years of age) or a low blood pressure goal (target mean arterial pressure,<or = 92 mm Hg for patients<or = 60 years of age and<or = 98 mm Hg for patients>or = 61 years of age).
MAIN OUTCOME MEASURES: Rate of decline in glomerular filtration rate and change in proteinuria during follow-up.
RESULTS: The low blood pressure goal had a greater beneficial effect in persons with higher baseline proteinuria in both study A (P = 0.02) and study B (P = 0.01). Glomerular filtration rate declined faster in patients with higher achieved blood pressure during follow-up in both study A (r = -0.20; P<0.001) and study B (r = -0.34; P<0.001), and these correlations were stronger in persons with higher baseline proteinuria (P<0.001 in study A; P<0.01 in study B). In study A, the association between decline in glomerular filtration rate and achieved follow-up blood pressure was nonlinear (P = 0.011) and was stronger at higher mean arterial pressure. In both studies, the low blood pressure goal significantly reduced proteinuria during the first 4 months after randomization. This, in turn, correlated with a slower subsequent decline in glomerular filtration rate.
CONCLUSIONS: Our study supports the concept that proteinuria is an independent risk factor for the progression of renal disease. For patients with proteinuria of more than 1 g/d, we suggest a target blood pressure of less than 92 mm Hg (125/75 mm Hg). For patients with proteinuria of 0.25 to 1.0 g/d, a target mean arterial pressure of less than 98 mm Hg (about 130/80 mm Hg) may be advisable. The extent to which lowering blood pressure reduces proteinuria may be a measure of the effectiveness of thistherapy in slowing the progression of renal disease.
AD
PMID
85
TI
Late escape from the antiproteinuric effect of ace inhibitors in nondiabetic renal disease.
AU
Shiigai T, Shichiri M
SO
Am J Kidney Dis. 2001;37(3):477.
 
Angiotensin-converting enzyme (ACE) inhibitors exert a renoprotective effect in both diabetic and nondiabetic renal disease with variable efficacy. Proteinuric patients with nondiabetic renal disease, normotension, and restricted protein and sodium intake were treated with ACE inhibitors without diuretics. Fifty-nine patients were treated with either lisinopril (10 mg/d; 36 patients) or enalapril (5 mg/d; 23 patients) over a period of 37.7 +/- 20.7 months. Urinary protein excretion decreased to less than 50% of pretreatment values after 1 to 37 months (6.9 +/- 8.8 months) of therapy in 33 patients (56%); in 29 patients, it reached less than 0.5 g/d of protein. Urinary protein levels remained low in 19 of the 33 patients (57.5%) throughout the entire posttreatment period (30.8 +/- 17.7 months). However, in the remaining 14 patients, escape from the antiproteinuric effect was detected after 19.2 +/- 13.4 months, evidenced by a decrease in the rate of change in creatinine clearance from 0.052 +/- 0.114 mL/min/mon during the low-proteinuria period to -0.697 +/- 1.101 mL/min/mon after the lapse of antiproteinuric effect (P:<0.001). Although ACE inhibitors reduce the severity of proteinuria in patients with nondiabetic renal disease, our results show that a proportion of patients escape the antiproteinuric effect and subsequently develop an exacerbation of renal dysfunction.
AD
Department of Internal Medicine, Toride Kyodo General Hospital, Ibaraki.
PMID