Acido úrico, aterosclerosis y calcificaciones vasculares en enfermedad renal crónica / Uric acid, atherosclerosis and vascular calcifications in chronic kidney disease

Estudios clínicos y epidemiológicos han demostrado que la enfermedad cardiovascular está relacionada con un aumento en la tasa de mortalidad en los pacientes con enfermedad renal crónica (ERC). Las complicaciones vasculares son principalmente secundarias a calcificaciones y ateroesclerosis. En los últimos años se ha renovado el interés por la asociación entre niveles de ácido úrico y riesgo cardiovascular. El objetivo de esta investigación fue relacionar la presencia de calcificaciones vasculares (CV) y aterosclerosis, evaluadas mediante ecografía carotídea, con niveles de ácido úrico en pacientes con ERC estadio 5 en diálisis. Se observaron CV en 56% de los pacientes; 46% tuvo criterios ecográficos para aterosclerosis con un promedio general de 0,89 mm (DE: ± 0,28), siendo mayor en los pacientes con hipertensión arterial y diabetes mellitus; este grupo también mostró mayor predisposición para CV (p= 0,01). Los niveles de urea (141,3 mg/dL) (p= 0,01) y ácido úrico (6,9 mg/dL) (p= 0,04) mostraron asociación estadísticamente significativa con la presencia de CV. Los eventos cardiovasculares adversos predominaron en los pacientes con aterosclerosis y CV (p= 0,01). Esta investigación demostró que un incremento en los niveles de ácido úrico por encima de 6 mg/L está relacionado con mayor riesgo de presentar calcificaciones y eventos cardiovasculares adversos en pacientes con ERC.

Epidemiological and clinical studies have shown that cardiovascular disease is associated with an increase in mortality in patients with chronic kidney disease (CKD). Vascular complications are mainly secondary to calcification and atherosclerosis. Interest in the association between uric acid levels and cardiovascular risk has been renewed in recent years. The objective of this research was to determine the relation between vascular calcification (VC) and atherosclerosis, through carotid ultrasound, with uric acid levels in patients with CKD in dialysis. VCs were observed in 56% of patients, 46% had ultrasound criteria for atherosclerosis with an overall average of 0.89 mm (SD ± 0.28), being higher in patients with hypertension and diabetes; this group also showed increased susceptibility to VC (p= 0.01). The levels of urea (141.3 mg/dL) (p= 0.01) and uric acid (6.9 mg/dL) (p= 0.04) showed significant association with the presence of VC. Adverse cardiovascular events were observed mainly in patients with atherosclerosis and VC (p= 0.01). This investigation showed that an increase in uric acid levels above 6 mg/dL is associated with an increased risk of calcification and cardiovascular adverse events in CKD patients in dialysis.

A Novel Biomarker of Coronary Atherosclerosis: Serum DKK1 Concentration Correlates with Coronary Artery Calcification and Atherosclerotic Plaques

DKK1 modulates Wnt signaling, which is involved in the atherosclerosis. However, no data exist regarding the usefulness of measuring serum DKK1 concentration in predicting coronary atherosclerosis. A total of 270 consecutive patients (62.8 +/- 11.2 yr; 70% male) were included. A contrast-enhanced 64-slice coronary MDCT was performed to identify the presence of atherosclerotic plaques. Agatston calcium scores (CS) were calculated to quantify the coronary artery calcification (CAC). DKK1 concentrations were measured by enzyme-linked immunosorbent assay. For each subsequent DKK1 quartile, there was a significant increase in CAC (P = 0.004) and the number of segments with coronary atherosclerosis (P or = 68.6 pg/mL demonstrated coronary atherosclerotic plaques even when they had low CS. Serum DKK1 concentrations correlate with the coronary atherosclerosis and play an independent role in predicting the presence of coronary atherosclerosis.

Tumoral calcinosis with hyperphosphatemia.

Tumoral calcinosis is a rare disorder of mineral metabolism among adolescents and young adults characterized by deposition of calcific masses around large joints. It is less commonly reported in pediatric population and commonly mistaken for bone tumors. Typical lab parameters include hyperphosphatemia with normal levels of serum calcium, parathyroid hormone (PTH) and alkaline phosphatase. A ten-year-old boy with typical features of tumoral calcinosis is presented.

Age-related Contribution of Lp (a) with Coronary Artery Calcification in Patients with Acute Coronary Syndrome: a Potential Role of Metabolic Disorder in Calcified Plaque

Lp (a) and coronary artery calcification (CAC) have recently been reported as predictors of plaque instability, but this is surrounded by much controversy. We investigated the influence of Lp (a) and CAC compared other acute coronary syndrome (ACS) risk factors. 698 patients diagnosed with at least minimal coronary artery obstructive disease from a coronary angiography were randomly selected using SPSS. Lp (a), other lipid profiles and past histories were checked, and CAC semi quantitatively graded on stored fluoroscopic images. The prevalence of CAC was significantly higher in the ACS than the non-ACS group (38.0% vs. 29.9%, p=0.026). The serum level of Lp (a) (26.89 +/- 30.64 vs. 20.85 +/- 21.63, p 35 mg/dl) was higher in the ACS group (24% vs. 15.7%, p 35 mg/dl. In the younger patients ( 60 years), CAC, but not the Lp (a), was an independent risk factor (OR=1.775, p=0.021, 95% CI; 1.090 - 2.890). Both the Lp (a) and CAC were risk factors for ACS, and they had a synergistic effect on its development. In the younger Lp (a), and the older CAC, was the more potent risk factor for ACS, respectively.

Serum and tissue glycoconjugates, digoxin and magnesium levels in chronic calcific pancreatitis.

BACKGROUND: Endogenous or exogenous digoxin can lead to membrane Na+,K+-ATPase inhibition and hypomagnesemia. Low magnesium levels can lead to increased glycosaminoglycans (GAG) concentration in many organs. Aim: To measure the serum levels of pancreatic GAG and glycoproteins, two major components of the extracellular matrix, in patients with chronic calcific pancreatitis (CCP). Serum levels of magnesium and digoxin were also assessed. METHODS: Patients with CCP and age- and sex-matched healthy control subjects (15 each) were studied. Serum GAG, Mg and digoxin levels were measured. RBC membrane Na+,K+-ATPase activity was also assessed. Pancreatic tissue obtained at autopsy from seven patients with CCP and sex- and age-matched healthy subjects who had died in accidents were also tested for GAG and glycoproteins. RESULTS: Total GAG levels were significantly increased in the serum and pancreas of patients with CCP. This was associated with lower serum Mg levels, increased serum digoxin levels and decreased RBC membrane Na+,K+-ATPase activity. CONCLUSION: Exogenous or endogenous digoxin-induced hypomagnesemia and the consequent altered glycoconjugate metabolism may be important in the pathogenesis of CCP.