Introduction: Chronic kidney disease is associated with increased morbidity and
mortality in cardiovascular disease. Apart from traditional risk factors, chronic
inflammation, and increased left-ventricular wall tension related to hypervolemia are
important in cardiovascular disease development in renal patients. B-type natriuretic
peptide (BNP) is a cardiac neurohormone specifically secreted bycardiac ventricles
in response to volume expansion and pressure overload. High sensitivity C-reactive
(hsCRP) have been found to reflect chronic inflammation and significantly elevated in
hemodialysis patients.Aim of the work:To assess the relationship between left
ventricular filling pressure (using plasma BNP levels) and inflammation (using
plasma hsCRP levels) in patients with chronic renal failure and their relationship
with renal echogenisity detected by ultrasonography.Patients and methods: Plasma
BNP and hsCRP were measured on the same day in 38 pre-dialysis patients. Patients
were classified into 5 groups according toultrasonographic renal echogenisity into
Group 1(no=3) with grade 0, group 2 (no=2)with grade I, group 3 (no=15) with
grade II, group 4 (no=14) with grade III renal echogenisity and group 5 (no=4) with
complete loss of the medulla and cortex of the kidney.Result: Plasma levels of BNP
and hsCRP were significantly higher in patients with chronic renal failure in
comparison with controls (274.3±97.1 pg/ml versus 33.7±8.0 pg/ml and 11.4±3.9
mg/L versus 2.7±1.0 mg/L respectively P <0.0001 for each). Comparing plasma
levels of BNP and hsCRP with ultrasonograghic renal echogenisity, which reflect
severity of renal disease, showed that the plasma levels of BNP were 104.7±15.0
pg/ml, 148.0±67.9 pg/ml, 248.5±72.0 pg/ml, 310.1±39.2 pg/ml and 436.0±10.0 pg/ml
in the five groups of patients respectively and hsCRP were 4.7±0.6 mg/L, 5.5±0.7
mg/L, 10.3±3.2 mg/L, 13.6±1.8 mg/L and 16.0±0.8 mg/L in the same previous groups
respectively. It was clear that the plasmalevels of both biomarkers were significantly
higher in patients with more severe renal affection (P< 0.0001 for each). There was,
also, highly significant positive correlation between plasmalevels of BNP and hsCRP
in all groups of patients (r= 0.9, P<0.0001) and significant negative correlation
between both markers and serum albumin (r=-0.4, P<0.001 and r=-0.5, P<0.0001
respectively) and significant negative correlation between both markers and
hemoglobin levels (r=-0.8, P< 0.0001 and r=-0.8, P< 0.0001 respectively).
Conclusion: The present results suggest a link between left ventricular pressure and
inflammation in patients with chronic renal failure. The importance of strict volume
control in these patients, in order to reduce left ventricular pressure and therefore
inflammation, should be considered. Both BNP and hsCRP could provide
complementary diagnostic and prognostic information regarding future
cardiovascular disorders in renal patients.