Chronic kidney disease (CKD) increases cardiovascular (CV) disease risk, including transient ischemic attacks (TIA) and stroke. ESRD is associated with a 10- to 20-fold larger rate of CV mortality and advanced carotid atherosclerosis compared with the general population. In the British Regional Heart Study a serum creatinine level over 1.3 mg/dL significantly increased the risk of stroke, even after adjustment for several CV risk factors. Among patients with isolated systolic hypertension, higher creatinine levels increased the odds-ratio (OR) for stroke.
Lacunar silent brain infarcts correlate independently to estimated declining glomerular filtration rates (GFR). A glance at less advanced renal dysfunction in selected patients with chronic heart disease followed-up for incidental ischemic stroke or TIA over years showed that those with CKD (ie eGFR<60 mL/min/1.73 m2) had a 1.54-fold OR (CI 95%:1.13 to 2.09) of incident ischemic stroke and TIA. Cumulative ischemic stroke or TIA-free curves decline by increasing serum creatinine levels. Increased CV risk is explained by anemia, oxidative stress, hypercalcemia, hyperphosphatemia and secondary hyperparathyroidism, increased homocysteine, inflammation, atherosclerosis, endothelial dysfunction, and coagulation promotion; this last one most associated with nephrotic syndrome.
In nephrotic syndrome, prophylactic anticoagulation is recommended when plasma albumin is below 3 g/dL.
Intracerebral, subdural, and subarachnoid hemorrhage (SAH) yield a mortality index of up to 60% in CKD. It is related to platelet dysfunction, altered platelet-vessel wall interaction, arterial hypertension, head trauma, polycystic kidney disease, use of anticoagulants, and platelet antiaggregants. Subdural hematomas may clinically resemble encephalopathy. Management includes minimal or heparin-free HD, switch from HD to PD (not requiring anticoagulation), and surgery.
Reference:
Lacerda et al. Neurologic Presentations of Renal Diseases. Neurol Clin 28 (2010) 45–59.
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