Mr. U, a 54 years old gentleman who is known to have suffered from systemic hypertension for 15 years and was not on regular medications was detected to have azotemia (Creatinine 2.2 mg%) with normal-sized kidneys on an ultrasonogram. There was no history of oedema, hematuria, oliguria or intake of nephrotoxic medications. He had no proteinuria and hematuria. He underwent a renal biopsy.

Renal biopsy:

Light microscopy showed 17 glomeruli, 2 sclerosed. There was no significant abnormality in the viable glomeruli, except for ischemic wrinkling of the tuft. There were small areas of chronic tubule interstitial damage but the major changes were in the blood vessels. There was arteriolar hyalinosis. The arteries show mucoid intimal thickening, duplication of the internal elastic lamina and severe luminal narrowing.

The above features are consistent with benign nephrosclerosis. It is an age-related change due to hypertension. The basic change is a pink homogenous hyaline thickening of the walls of the arterioles. This leads to a decrease in vessel wall lumina with a decrease in blood flow leading to ischemic atrophy of the glomeruli and the tubules. The glomeruli hence become globally sclerosed with interstitial fibrosis and tubular atrophy.

Benign nephrosclerosis is the end organ damage that is secondary to long-standing uncontrolled hypertension. Generally, this is associated with other end organ damages like hypertensive heart disease, retinopathy, etc. If the kidneys are contracted and echogenic kidney biopsy is not possible.

In our patient, the kidney size was normal, hence a renal biopsy was performed.

Pathophysiology:

It is generally due to blood vessel changes related to long-standing uncontrolled hypertension. Because of the luminal narrowing in the blood vessels, there is glomerular shrinkage and ischemia. This causes some of the glomeruli to become sclerotic and the remaining glomeruli to hyperfiltrate. This results in increased intraglomerular pressure in these glomeruli and they gradually undergo sclerosis.

This is a vicious cycle and there is progressive glomerular sclerosis. The nonsclerotic glomeruli undergo hyperfiltration and sclerosis.

Hypertensive nephrosclerosis is the second common cause of ESRD (End Stage Renal Disease) worldwide, next to Diabetic nephropathy. It is estimated to comprise 15 to 20 % of ESRD cases. Lifestyle modification, good control of blood pressure will not only prevent kidney damage, but it will also slow down the progression of all end organ damage including the kidneys.

Dr. Balasubramaniam Raju,
Chief Nephrologist