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Increased Risk of Stroke from Concomitant Chronic Kidney Disease and Anaemia

Presence of both chronic kidney disease (CKD) and anaemia is associated with a marked increase in the risk of stroke. CDK without anaemia, however, leads only to a modestly increased risk of stroke, suggest results from a US study.

Jerome Abramson, PhD, Emory University School of Medicine, Atlanta, Georgia, United States, and colleagues involved 13,716 people who were enrolled in the Atherosclerosis Risk in Communities (ARIC) study. The subjects, who were community-based male and female African Americans and Caucasians with a mean age of 54.1 years, were followed up for 9 years for the occurrence of stroke.

Among patients with anaemia, the stroke rate in those who also had CKD was 10.53 per 1,000 person-years of follow up, compared with 1.52 for those without CKD. In patients without anaemia, the stroke rates in those with and without CKD were only slightly different -- 2.85 and 2.12, respectively.

The researchers defined anaemia as a haemoglobin level of less than 13 g/dL in men and less than 12 g/dL in women, and CKD as a serum creatinine clearance rate of less than 60 mL/min.

The association of anaemia and CKD with a significantly increased risk of stroke was also independent of a range of other risk variables, including: age; gender; race; education; prevalent coronary heart disease; diabetes; systolic and diastolic blood pressure; high- and low-density lipoprotein cholesterol; carotid intimal media thickness; and smoking.

Previous studies had found CKD to be associated with a higher risk of stroke in those with isolated systolic hypertension, among other groups. Other studies had identified anaemia as an independent risk factor for cardiovascular disease. Still other studies had demonstrated an interaction between CKD and anaemia leading to an increased risk of death in left-ventricular hypertrophy, the researchers said. The authors believe, however, that their data was "the first to examine how moderate CKD and anaemia interact to affect the risk of incident stroke among community-based persons".

The researchers note that the reasons for this manifestly increased risk were not yet clear. They put forward three possible explanations. The first is that anaemia often developed as a consequence of CKD, and that, rather than the two conditions interacting to increase the likelihood of stroke, long-lasting CKD was the risk factor and anaemia was just a marker for such long-lasting CKD.

The second explanation is that the two conditions each had independent pathways that led to stroke. Their co-existence creates an environment where ischaemia and left-ventricular hypertrophy were promoted, leading to an increased likelihood of stroke.

Finally, the researchers propose a mechanism based on the fact that increased levels of erythropoietin are normally produced to counter the adverse effect of anaemia on the brain. In cases of impaired renal function, the kidneys cannot produce as much erythropoietin, decreasing the degree of erythropoietin-mediated neuroprotection from anaemia-induced stroke. The authors note that no data on erythropoietin exist to support this hypothesis, and that it therefore remains speculative.

Whatever the reason, the increased risk of stroke when both anaemia and CKD is present is "notable", the researchers state. They conclude that, if confirmed, their results could help "in risk-stratifying community-based populations for the development of stroke."
Kidney Int 2003;64:2:610-5 "Chronic kidney disease, anemia, and incident stroke in a middle-aged, community-based population: The ARIC Study"

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