Renal Anatomy and Function

Renal blood flow progressively decreases from 1200 mL/minute at age 30 to 40 years to 600 mL/minute at age 80. The primary underlying factor is the decreased renovascular bed. However, the reduction in flow does not simply reflect decreased renal mass because flow per gram of tissue decreases progressively after age 30 to 40. This decrease is due to fixed anatomic changes rather than to reversible vasospasm, as shown by studies with vasoactive agents. Of significance is that cortical blood flow decreases and medullary flow is preserved, a finding consistent with histologic studies that show selective loss of cortical vasculature with age. These vascular changes probably account for the patchy cortical defects commonly seen on renal scans of healthy elderly persons.

A decrease in glomerular filtration rate is the most important functional defect caused by aging. The decrease is measured by creatinine clearance, which is stable until age 30 to 40 and then declines linearly at an average rate of about 8 mL/minute/1.73 m²/decade in about two thirds of elderly persons without renal disease or not undergoing treatment for hypertension. One third of elderly persons show no decrease in glomerular filtration rate. This variability suggests that factors other than aging may be responsible for the apparent reduction in renal function. For example, increases in blood pressure still within the normotensive range are associated with an accelerated, age-related loss of renal function.

Unless hypertension or marked vascular disease is present, the kidney maintains its relatively smooth contour. With age, however, renal mass progressively declines and renal weight decreases from 250 to 270 grams at about age 30 to 180 to 200 grams at about age 70. The loss of renal mass is primarily cortical, with relative sparing of the medulla. The number of identifiable glomeruli decreases, roughly in accordance with the decrease in renal weight. The proportion of sclerotic glomeruli increases from 1 to 2% between ages 30 and 40 to > 12% after age 70 and is proportionate to the amount of atherosclerosis occurring elsewhere in the body. The glomerular tufts become less lobulated, the number of mesangial cells increases, and the number of epithelial cells decreases, thus reducing the surface area available for filtration. However, glomerular permeability does not change with age.

Several minor microscopic changes occur in the renal tubule with age. Diverticula appear in the distal nephron, reaching a high of about three per tubule by age 90. These diverticula may become retention cysts, which are common in the elderly. Their clinical significance is unknown.

The walls of the large renal blood vessels undergo sclerotic changes with age. The sclerosis does not encroach on the lumen but is augmented when hypertension is present. Smaller vessels appear to be spared--only 15% of elderly normotensive persons have sclerotic changes in the renal arterioles. X-rays show that normotensive persons > 70 have an increasing prevalence of abnormalities (eg, abnormal tapering of interlobar arteries, abnormal arcuate arteries, increased tortuosity of intralobular arteries) similar to that of younger hypertensive persons.

Two age-related patterns of change occur in arteriolar-glomerular units. The first pattern, occurring primarily in the cortical area, is characterized by hyalinization and collapse of the glomerular tuft. The lumen of the preglomerular arteriole becomes obliterated, with a resultant loss in blood flow. The second pattern, occurring primarily in the juxtamedullary area, is characterized by glomerular sclerosis and the development of anatomic continuity between the afferent and efferent arterioles. The end point is shunting of blood flow from afferent to efferent arterioles and loss of glomeruli. Blood flow is maintained to the vasa recta, the medulla's primary vascular supply; these arterioles do not decrease in number with age.

Several proximal tubular functions--maximal excretion of p-aminohippurate and iodopyracet and maximal absorption of glucose--parallel the decline in glomerular filtration rate, suggesting that tubular function disappears in entire nephrons with age. The renal threshold for glycosuria, which relates inversely to the degree of splay in reabsorptive capacity of individual nephrons, increases with age. Thus, glucose generally spills into the urine at a higher blood glucose level in an older diabetic patient than in a younger one.

Unless a specific tubular defect exists, the ability to concentrate and dilute urine and to excrete acid also parallels changes in glomerular filtration rate in most persons. Although the renal tubular system responds normally to graded dosages of vasopressin, the maximum ability to concentrate urine decreases. This decrease seems to be due to a relative inability to maintain the solute (osmotic) gradient in the medullary portion of the kidney. The reason for this inability is unclear.