Abstract-The role of serum uric acid as an independent risk factor for cardiovascular and renal morbidity is controversial.A better understanding of its relationship with preclinical organ damage may help clarify the mechanism(s) implicated in the development of early cardiovascular disease. We evaluated the association between uric acid and the presence and degree of target organ damage in 425 (265 males, 160 females) middle-aged, untreated patients with essential hypertension. Left ventricular mass index and carotid intima-media thickness were assessed by ultrasound scan. Albuminuria was measured as the albumin to creatinine ratio in 3 nonconsecutive first morning urine samples. Overall, patients with target organ damage had significantly higher levels of serum uric acid as compared with those without it (presence versus absence of left ventricular hypertrophy, Pϭ0.04; carotid abnormalities, PϽ0.05; microalbuminuria, PϽ0.004; and at least 1 versus no organ damage, PϽ0.03). In women, the occurrence and severity of each target organ damage we examined increased progressively from the lower to the upper serum uric acid tertiles (PϽ0.01). After adjustment for body mass index, age, creatinine clearance, and high-density lipoprotein cholesterol, each standard deviation increase in serum uric acid entailed a 75% higher risk of having cardiac hypertrophy and a 2-times greater risk of having carotid abnormalities. These results support the role of serum uric acid as an independent, modifiable marker of cardiovascular damage.

In patients with CKD, LVH is a strong predictor of the risk of poor CV and renal outcomes independent from LV geometry.

Arterial hypertension together with proteinuria is one of the most important factors associated with the progression of both diabetic and nondiabetic chronic kidney disease. In this review, the role of hypertension and proteinuria in renal disease progression, the BP target that should be achieved to slow the progression of renal damage, and the influence of baseline and current proteinuria on the renoprotective effects of antihypertensive therapy are discussed thoroughly. The interaction between the renoprotective effects of specific antihypertensive agents-mostly angiotensin-converting enzyme inhibitors and angiotensin receptor blockers-and the level of achieved BP also are evaluated. The body of evidence provided by several studies emphasizes the importance of both lowering BP and inhibiting the renin-angiotensin system as specific goals for renal and cardiovascular protection in chronic kidney disease.J Am Soc Nephrol 17: S98 -S103, 2006S98 -S103, . doi: 10.1681 C hronic kidney disease (CKD) is a worldwide public health problem. In the United States, there is an increasing incidence and prevalence of renal failure with poor outcome and high costs and an even higher prevalence of earlier stages of CKD (approximately 80 times greater than ESRD prevalence). Moreover, CKD is associated with elevated cardiovascular morbidity and mortality (1). Therefore, strategies that are aimed at identifying, preventing, and treating CKD and its related risk factors are needed.In the following sections, we focus on the role of hypertension and proteinuria as both independent and interdependent risk factors for renal disease progression. We also discuss BP targets that should be achieved to slow the progression of renal damage, the influence of baseline and current proteinuria on the renoprotective effects of antihypertensive therapy, and the interaction between the renoprotective action of specific antihypertensive agents-mostly angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB)-and the level of achieved BP. Role of Hypertension and Proteinuria on the Progression of Renal DiseaseHigh BP can be either a cause or a consequence of CKD. High BP may develop early in the course of CKD and can be associated with adverse outcomes such as worsening renal function and development of cardiovascular disease. Hypertension is a major promoter of the decline in GFR in both diabetic and nondiabetic kidney disease (2,3). Furthermore, large, observational, prospective trials in the general population showed that hypertension is a strong independent risk factor for ESRD. A strong relationship was observed between both systolic (SBP) and diastolic BP (DBP) and ESRD, regardless of other known risk factors, in men who were recruited in the Multiple Risk Factor Intervention Trial. The relative risk (RR) for ESRD was Ͼ20-fold higher for patients with stage 4 hypertension (SBP Ͼ 210 mmHg or DBP Ͼ 120 mmHg) than for patients with optimal BP levels (SBP Ͻ 120 mmHg and DBP Ͻ 80 mmHg) (4). The recent study by the Oki...

Background: In patients with chronic kidney disease (CKD), sarcopenia can be determined by a wide spectrum of risk factors. We evaluated the association of sarcopenia with nutritional, behavioral and inflammatory patterns in older patients with advanced CKD. Methods: we cross-sectionally evaluated 113 patients with CKD stages 3b-5. Sarcopenia was defined according to the EWGSOP2 criteria. We assessed: anthropometry, bioelectrical impedance analysis, physical, and psychological performance. Nutritional status was assessed using the Malnutrition Inflammation Score (MIS) and by verifying the eventual presence Protein Energy Wasting syndrome (PEW). Systemic inflammation was assessed by dosing: CRP, IL6, TNFα, MCP1, IL10, IL17, fetuin, IL12. Results: 24% of patients were sarcopenic. Sarcopenic individuals had lower creatinine clearance (18 ± 11 vs. 23 ± 19 mL/min; p = 0.0087) as well as lower BMI (24.8 ± 3.0 vs. 28.4 ± 5.5 Kg/m2; p < 0.0001) and a lower FTI (11.6 ± 3.9 vs. 14.4 ± 5.1 kg/m2, p = 0.023). Sarcopenic persons had higher prevalence of PEW (52 vs. 20%, p < 0.0001) and a tendency to have higher MIS (6.6 ± 6.5 vs. 4.5 ± 4.0, p = 0.09); however, they did not show any difference in systemic inflammation compared to non-sarcopenic individuals. Conclusions: CKD sarcopenic patients were more malnourished than non-sarcopenic ones, but the two groups did not show any difference in systemic inflammation.