There’re several impacts of aging upon the renal system. Renal mass declines by 25 -30 % between the 30 & 80 ys of age, with the maximum decline after

 

AN AGING KIDNEY

 

There’re several impacts of aging upon the renal system. Renal mass declines by 25 -30 % between the 30 & 80 ys of age, with the maximum decline after the age of 50. Furthermore, fat & fibrous tissues may replace some of the remained functional tissues. Renal losses involve primarily the renal cortex & the nephrons most crucial to produce a concentrated urine. Senescent cells are commonly observed with increased age in donor kidney cortex that suggests the role of senolytic agents may improve age-related drop in kidney function.

 

Physiological aging is accompanied by a decline in functional glomeruli of about 50 %, as observed with the comparison of a kidney from donor aged 18-29 with those aged 70-75 ys. Nephrons’ atrophy & resorption may contribute to the aging impact more than glomerular diffuse sclerosis. The remainder of the glomeruli may show diminished filtering activity, despite the single nephron reports declared a preserved filtration rate until the age of 70. Intrarenal vascular alterations include spiralling of the afferent arterioles, narrowed large arteries, fibrosed intima, and shunting between afferent & efferent arteriole allowing blood flowing to bypass the glomerulus. Nephrosclerosis (global glomerulosclerosis, fibrosed interstitium, & sclerosed arteries) was recognized in donor kidney offered for kidney transplant in 3 % of donors 18-29 ys old & in 73 % of donors aging 70-77 ys.

 

Basically, renal blood flow is 40 % lower in healthy normotensive older males as compared to young males. Moreover, this difference is currently exaggerated under conditions stimulating renal VD (vasodilation). Recent reports suggest that aging kidney may be kept in a status of vasodilation to override the lost vasculature. Vasodilator Pg are elevated at baseline in normal elderly that may augment (nearly doubled) the risk of AKI with NSAID administration in elderly.

 

CrCl decline with aging (7.5-10 mL/min/decade), despite the variable values in decline observed in longitudinal reports in healthy old subjects. Almost one 1/3^rd show no changes in eGFR estimation, one 1/3^rd show slight drop, and 1/3^rd show a more vigorous decline. Creatinine production diminishes with age & tubular secretions of creatinine rises, so that the SCr may remain stable despite the decline in GFR. Almost all the currently applied equations to estimate the CrCl factor age into the formulae; the eGFR given by some electronic health reports require to be dealt with caution, particularly with those above 90.

 

Cystatin C-based testing of kidney function can be informative if an accurate evaluation in an old subject is warranted. In healthy elderly, a rise of almost 50 % in Cystatin C levels is observed from the age of 40-80. Elevations in Cystatin C track vigorously with functional decline in longitudinal reports. Of note, old males with more physical activity show 👉better preservation of the GFR.

 

Fluid & electrolyte homeostatic maintenance is relatively well preserved with aging, in absence of stressful challenges. However, ptns ability for maximum dilution of urine and excretion of water load is currently compromised with difficulty in volume regulation ability during stress. During dehydration states, for example, the minimum urine flow rate is twice as much in those > 70 as compared to those < 40, and the maximal urine osmolality is also declined with age. Added to this diminished ability to retain water & solute, the older kidney has also declined ability to maintain amino acids & glucose levels.

 

Added to the functional alterations in renal system, is the diminished urine acidification ability with diminished excretion of acid load. Moreover, an older kidney is more vulnerable to nephrotoxicity induced by medications, chemotherapeutics, or IV contrast. The older kidney with AKI is also less amenable for recovery. Furthermore, older kidney is more prone for ischemic injury, with a higher number of cells may undergo post-ischemic events apoptosis as compared to younger kidney. Tubular cell appears to exhibit lowered ability for repopulation of the tubules after an acute ischemic event.

 Renal changes with aging 👉

Hormonal function of the kidney can be also deranged by aging process including 👉:

1)    Lowered vit D hydroxylation in old female, its response to PTH infusion is diminished.

2)    Downregulated RAAS has been observed in normal & HT elderlies.

3)    EPO production in response to HB levels seems to be unchanged with age.

4)    Finally, kidney is a primary source for klotho, a protein with vital role in aging. Renal production of klotho declines with aging and genetic polymorphisms that increase its levels are accompanied with higher longevity.