Strain vessel hypothesis: a viewpoint for linkage of albuminuria and cerebro-cardiovascular risk

Abstract

Albuminuria is closely associated with stroke and cardiovascular diseases (CVDs) as well as the salt sensitivity of blood pressure (BP). Although albuminuria may reflect generalized endothelial dysfunction, there may be more specific hemodynamic mechanisms underlying these associations. Cerebral hemorrhage and infarction occur most frequently in the area of small perforating arteries that are exposed to high pressure and that have to maintain strong vascular tone in order to provide large pressure gradients from the parent vessels to the capillaries. Analogous to the perforating arteries are the glomerular afferent arterioles of the juxtamedullary nephrons. Hypertensive vascular damage occurs first and more severely in the juxtamedullary glomeruli. Therefore, albuminuria may be an early sign of vascular damages imposed on 'strain vessels' such as perforating arteries and juxtamedullary afferent arterioles. Coronary circulation also occurs under unique hemodynamic conditions, in which the entire epicardial segments are exposed to very high pressure with little flow during systolic phases. From the evolutionary point of view, we speculate that such circulatory systems in the vital organs are mandatory for survival under the danger of hypoperfusion due to difficult access to salt and water as well as high risks of wound injuries. In addition, albuminuria would indicate an impairment of renal medullary circulation, downstream from the juxtamedullary glomeruli, and therefore an impaired pressure natriuresis, which would lead to salt sensitivity of BP. Our 'strain vessel hypothesis' may explain why hypertension and diabetes, unforeseen in the concept of evolution, preferentially affect vital organs such as the brain, heart and kidney.

Silent cerebral infarction is associated with the development and progression of nephropathy in patients with type 2 diabetes

“…Concerning the cardio-renal association in diabetic patients, as we discussed earlier, 17 albuminuria and cardiovascular disease share numerous risk factors that may help to explain the observed relationship between SCI and nephropathy in this study. Hemodynamic and anatomical aspects of renal and cerebral small vessels share many similarities, 25,26 and a common pathogenesis may contribute to both SCI and incident nephropathy in patients with type 2 diabetes. Another possible mechanism that may contribute to the association of SCI with albuminuria involves asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, which was shown to be associated with prevalent SCI in the Framingham offspring study.…”

Chronic kidney disease, 24-h blood pressure and small vessel diseases are independently associated with cognitive impairment in lacunar infarct patients

“…29 As the vascular supplies to the kidney and brain are similar, renal small vessel disease may also be indicative of the presence of small vessel disease in the brain. 30 On the other hand, levels of an endogenous inhibitor of nitric oxide synthase, asymmetric dimethylarginine, are increased in patients with impaired kidney function. 31 Such factors could accelerate extensive small vessel diseases in patients with CKD.…”

Neurocritical Care for Patients with Kidney Dysfunction

“…The arterioles of the kidney, retina, and brain are termed Bstrain arterioles^as they are relatively short, branch out from much larger arteries, and are exposed to blood pressure (BP) changes (Fig. 1) [16,17].…”