A. Festa et al., Inflammation and microalbuminuria in nondiabetic and type 2 diabetic subjects: The Insulin Resistance Atherosclerosis Study, KIDNEY INT, 58(4), 2000, pp. 1703-1710
Background. Microalbuminuria is a risk factor for cardiovascular disease, b
ut the underlying pathomechanisms are still poorly understood. A relationsh
ip between C-reactive protein (CRP), a sensitive marker of inflammation, an
d atherosclerotic disease has been reported recently.
Methods. We hypothesized that microalbuminuria might be associated with chr
onic inflammation and investigated the relationship of urinary albumin excr
etion, as assessed from the albumin-to-creatinine ratio (ACR), in an untime
d morning urine specimen, and two inflammatory markers (CRP and fibrinogen)
in the large, triethnic population of the Insulin Resistance Atheroscleros
is Study (IRAS). After exclusion of subjects with macroalbuminuria, 1481 su
bjects were studied.
Results. Both inflammatory markers were related to urinary ACR (r = 0.17 fo
r CRP and r = 0.14 for fibrinogen, both P = 0.0001), an association that re
mained significant after adjustment for demographic variables, diabetic sta
tus, smoking, and use of angiotensin-converting enzyme inhibitors (P < 0.01
). Mean levels of CRP and fibrinogen were elevated in microalbuminuric (N =
262) versus normoalbuminuric (N = 1219) subjects (5.37 +/- 0.47 vs. 3.80 /- 0.15 mg/L and 295.7 +/- 4.0 vs. 278.2 +/- 1.6 mg/dL, both P < 0.0001). T
he associations were consistent among nondiabetic and type 2 diabetic subje
cts and among the three ethnic groups of the IRAS (non-Hispanic whites, bla
cks, Hispanics). In a logistic regression model, fibrinogen was independent
ly associated with microalbuminuria (P = 0.047), along with hypertension, f
emale gender, waist circumference, and fasting blood glucose, while CRP was
not independently related to microalbuminuria in this model (P = 0.26).
Conclusion. We have shown an association of CRP and fibrinogen with urinary
albumin excretion in the microalbuminuric range in type 2 diabetic and non
diabetic individuals. Chronic inflammation therefore emerges as a potential
mediator between microalbuminuria and macrovascular disease.