Cardiovascular (CV) risk assessment is not easy in chronic kidney disease (CKD) patients. Age, male sex, race, family history of CV disease, smoking status and diabetes should be considered as CV risk factors as the general population. It is also accepted that hypertension (HTN) is associated with the greater risk of CV complications in this population. However, there are some concerns in this issue.
First, supporting evidence for specific blood pressure (BP) targets in CKD is scarce. Many observational studies reported a J-shaped association between BP level and CV mortality unlike a linear association in the general population. Only few randomized trials (the MDRD, AASK, REIN-2 etc.) were conducted to draw conclusion about different BP targets and outcomes in CKD patients. Even in them, primary outcomes were focused on renal outcomes, and none of them had sufficient power to evaluate CV outcomes. In the last year, the Systolic Blood Pressure Intervention Trial (SPRINT) was reported, which partly included CKD patients with estimated glomerular filtration rate of 20 to less than 60 ml/min/1.73m2. Intensive BP treatment to systolic BP <120 mmHg led to a statistically significant 25% reduction in the composite CV outcome compared with standard BP treatment to systolic BP <140 mmHg. There was no interaction between treatment and CKD subgroup. In SPRINT, however, only 28% subjects had CKD and diabetic CKD patients were excluded. It is questionable whether its results could be safely applied to all CKD patients. Second, proteinuria level could modify the association between BP level and CV outcome. Until the late 2000 s, major guidelines recommended that the target BP was less than 130/80 mmHg in all CKD patients. However, recent randomized trials have been repeatedly failed to show the definite benefit of target BP below 130/80 mmHg in diabetic or non-diabetic CKD patients. Now, the lower target BP is recommended only for CKD patients with urinary albumin excretion >30 mg/day (or albumin/creatinine ratio >30 mg/g). Third, BP level may be influenced by measurement methods more largely in CKD patients than non-CKD patients. White coat effect as well as masked HTN are common in this population. Excessive reduction of BP only based on office BP could result in adverse events such as renal and cerebral ischemia.
Contrary to the general population, evidence supporting a linkage between obesity and CV outcomes is weak in CKD patients. Observational studies showed a relatively lower risk of death in patients with higher body mass index, so-called ’obesity paradox’. Beyond traditional risk factors, many non-traditional risk factors for CV disease have been suggested in CKD patients. Among them, anemia and mineral bone disease - especially serum phosphate and parathyroid hormone (PTH) levels - were strongly associated with CV outcomes in many observations. Now, treating anemia and controlling serum phosphate and PTH levels are one of the mainstay treatments in the care of CKD patients.