What is Renal Artery Stenosis (RAS, Renovascular disease, Ischemic nephropathy)

Renal Artery Stenosis is a disease of the renal arteries.

This name of this condition describes the narrowing (stenosis) of the main arteries of the kidneys, most often due to artherosclerosis (accumulation of cholesterol in arteries resulting in their hardening.) In younger women, the condition may arise from structural abnormalities of the arterial wall called fibromuscular dysplasia.

Statistics on Renal Artery Stenosis (RAS, Renovascular disease, Ischemic nephropathy)

In the UK, this condition was found in 18% of those aged 65-74 and in 42% of those aged over 75 years. The condition affects both renal arteries in half of all cases found with this condition. In younger women, the condition may arise from structural abnormalities of the arterial wall called fibromuscular dysplasia.

Risk Factors for Renal Artery Stenosis (RAS, Renovascular disease, Ischemic nephropathy)

As the primary cause of disease is atherosclerosis, the risk factors for this condition align with that of renal artery stenosis:

1. Age – The condition occurs more commonly with advancing age.
2. Elevated blood pressure.
3. Diet – High in cholesterol and saturated fats.
4. Smoking.
5. Physical inactivity.

Progression of Renal Artery Stenosis (RAS, Renovascular disease, Ischemic nephropathy)

The onset of disease depends on the cause of renal artery stenosis. A late onset of disease is expected with atherosclerosis whereas an early onset of disease will be seen in fibromuscular dyplasia of the renal arteries. Both causes result in the narrowing the renal arteries, which then cannot provide a sufficient blood supply to the kidneys. Over time, this inadequate blood supply will result in ischaemic changes to the kidney supplied by this artery and also hormonal problems. The kidney will nromal release a hormone called “renin” if its blood supply is compromised. This hormone acts to increase the blood pressure in a number of ways to maintain blood flow through the narrowed part of the renal artery. Perfusion of the affected kidney is improved by this hormone. Blood pressure throughout the body, however, increases to ensure good kidney blood flow. The condition will therefore ultimately result in the development of hypertension (elevated blood pressure) and the complications of this disease, unless adequately treated.

How is Renal Artery Stenosis (RAS, Renovascular disease, Ischemic nephropathy) Diagnosed?

The initial assessment of this condition includes blood tests to assess renal function and an ultrasound to detect any changes in the size and shape of the kidney that occurs with renal artery stenosis.

Prognosis of Renal Artery Stenosis (RAS, Renovascular disease, Ischemic nephropathy)

The prognosis of this condition is good, if diagnosed at an early stage of development. Because of the gradual nature of this disease, the signs and symptoms may go unnoticed for many years, resulting in significant kidney damage prior to diagnosis. The prognosis of renal artery stenosis induced by fibromuscular dysplasia has a more favourable prognosis as the ocndition occurs at birth with diagnosis made in the first few months of life. In the atherosclerosis cases, renal arterial stenosis continues to be a significant cause of long term renal disease in modern society.

How is Renal Artery Stenosis (RAS, Renovascular disease, Ischemic nephropathy) Treated?

The priorities of therapy are to control blood pressure in the first instance while arrangements are made to dilate the affected renal artery and restore blood flow to the affected kidney. A surgical procedure will be required to exapnd the affect segment of renal artery and restore sufficient blood flow to cease the disease process.

Renal Artery Stenosis (RAS, Renovascular disease, Ischemic nephropathy) References

[1] Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison’s Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001.
[2] Cotran, Kumar, Collins 6th edition. Robbins Pathologic Basis of Disease. WB Saunders Company. 1999.
[3] Kumar P, Clark M. CLINICAL MEDICINE. WB Saunders 2002 Pg 545-549.
[4] Longmore M, Wilkinson I, Torok E. OXFORD HANDBOOK OF CLINICAL MEDICINE. Oxford University Press. 2001.