Congenital or acquired nephron number reduction and diabetes mellitus
both induce hyperfiltration and intrarenal hypertension, These hemodyn
amic factors have been suggested to play an important role in the init
iation and progression of diabetic and nondiabetic glomerulopathies, I
n a prevalence cohort of all 50 albuminuric (greater than or equal to
300 mg/24 hr), non-insulin-dependent diabetic mellitus (NIDDM) patient
s (aged <66 years) attending a diabetic clinic during 1987, we identif
ied four patients with acquired oligonephropathy who had developed dia
betic nephropathy, Three patients only had a single functioning kidney
(nephrectomy in two cases), and the remaining patient had unilateral
severely reduced kidney function and elevated plasma renin concentrati
on, These patients represent 8% of our NIDDM population with albuminur
ia, and are the only patients in our NIDDM population younger than 66
years (n = 363) known to have single kidneys, However, systematic reno
graphy screening was not performed. During the observation period, whi
ch ranged from 16 to 100 months, albuminuria increased from 2.3 g/24 h
r (range, 1.2 to 3.4 g/24 hr) to 3.2 g/24 hr (range, 0.7 to 9.4 g/24 h
r), glomerular filtration rate decreased to 6 mL/min/yr (range, 4 to 1
2 mL/min/yr), and blood pressure remained stable at 142/92 mm Hg, Thre
e patients received antihypertensive medication, Two of the patients d
ied after 16 and 26 months of observation, respectively, due to acute
myocardial infarction and stroke, The results of our study of NIDDM pa
tients support the concept that reduced nephron number predisposes pat
ients to the development of diabetic nephropathy. (C) 1995 by the Nati
onal Kidney Foundation, Inc.