title: Dietary protein restriction, blood pressure control, and the progression of polycystic kidney disease. Modification of Diet in Renal Disease Study Group.
abstract: In the Modification of Diet in Renal Disease Study, a follow-up (mean, 2.2 yr) of 200 study participants with autosomal dominant polycystic kidney disease (ADPKD) was conducted to determine the effect of lowering protein intake and blood pressure on the rate of decline in GFR. The rate of decline was faster in participants with ADPKD than in persons with other diagnoses, reflecting, in part, faster disease progression in the ADPKD group. Baseline characteristics that predicted a faster rate of decline in GFR in persons with ADPKD were greater serum creatinine (independent of GFR), greater urinary protein excretion, higher mean arterial pressure (MAP), and younger age. In patients with initial GFR values between 25 and 55 mL/min per 1.73 m2, neither assignment to a low-protein diet group nor assignment to a low blood pressure group significantly reduced the rate of decline of GFR in ADPKD participants. Similarly, the decline in GFR was not related to achieved protein intake or MAP. In participants with GFR values between 13 and 24 mL/min per 1.73 m2, assignment to the low MAP group led to a somewhat more rapid decline in GFR. However, the more rapid decline in GFR did not appear to be due to a detrimental effect of low blood pressure or the antihypertensive agents used to reach the low blood pressure goal. Lower protein intake, but not prescription of the keto acid-amino acid supplement, was marginally associated with a slower progression of renal disease.
authors.affiliation: National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
authors.forename: S
authors.initials: S
authors.lastname: Klahr
authors.forename: J A
authors.initials: JA
authors.lastname: Breyer
authors.forename: G J
authors.initials: GJ
authors.lastname: Beck
authors.forename: V W
authors.initials: VW
authors.lastname: Dennis
authors.forename: J A
authors.initials: JA
authors.lastname: Hartman
authors.forename: D
authors.initials: D
authors.lastname: Roth
authors.forename: T I
authors.initials: TI
authors.lastname: Steinman
authors.forename: S R
authors.initials: SR
authors.lastname: Wang
authors.forename: M E
authors.initials: ME
authors.lastname: Yamamoto
mesh_terms: D000328:Adult; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D003131:Combined Modality Therapy; D003404:Creatinine / Q000097:blood; D018753:Diet, Protein-Restricted; D018450:Disease Progression; D004232:Diuretics / Q000627:therapeutic use; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D006977:Hypertension, Renal / Q000188:drug therapy / Q000209:etiology / Q000628:therapy*; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D010349:Patient Compliance; D010758:Phosphorus / Q000008:administration & dosage; D016891:Polycystic Kidney, Autosomal Dominant / Q000150:complications / Q000178:diet therapy / Q000503:physiopathology*; D011507:Proteinuria / Q000178:diet therapy / Q000209:etiology; D044469:Racial Groups
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D004232:Diuretics; D010758:Phosphorus; D003404:Creatinine