age-associated changes in renal function
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Introduction
Renal function declines with age (variable)
Pathology
- impaired renal autoregulation
- prerenal aoztemia resulting in intrinsic renal damage is more common in the elderly[5]
- diminished thirst, especially with cognitive impairment, contributes to prerenal azotemia
- diuretics, prescribed for hypertension, contribute to prerenal azotemia
Physiology
- decreased kidney mass & volume
- decreased synthesis of calcitriol
- increased thickness of glomerular basement membrane
- loss of renal glomeruli
- hyalinization & collapse of glomerular tufts occurs in renal cortex
- glomerulosclerosis
- increased number of sclerotic glomeruli occurs in juxtaglomerular region
- sclerosis of pre- & postglomerular arterioles
- renal tubular atrophy
- decreased number & length of tubules
- diminished tubular secretion & reabsorption parallels decline in glomerular filtration rate
- increase in tubular basement membrane thickness
- renal interstitial fibrosis
- decreased renal blood flow & glomerular filtration rate
- cortical blood flow decreases
- medullary blood flow is maintained
- 1/3 of elderly show no decrease in GFR
- decreased NO production
- increased dependence on NO & prostaglandins to maintain perfusion
- diverticula appear in the distal nephron
- may become retention cysts, common in elderly
- significance unknown
- decreased creatinine clearance
- decreased serum creatinine (if renal function is unchanged)
- decreased maximum urine osmolality
- decreased responsiveness to volume depletion
- Na+ homeostasis
- decreased basal & stress-induced renin & aldosterone
- blunted response to Na+ restriction
- increase in basal & stimulated ANP levels
- decreased renal response to ANP (cGMP)
- decreased distal tubular Na+ reabsorption
- susceptibility to hyponatremia
- K+ homeostasis
- decrease in total body K+
- increased frequency of hyporeninemic hypoaldosteronism
- increased use of pharmaceuticals that impair K+ excretion
- increased risk of hyperkalemia
- impaired secretion of H+ & NH4+
- impaired ability to resorb glucose
- susceptibility to metabolic acidosis
- water regulation
- increased basal & osmolality-stimulated vasopressin
- diminished renal tubule response to vasopressin[3]
- maximum urine concentration decreases
- diminished thirst to hyperosmolality
More general terms
Additional terms
References
- ↑ Essentials of Clinical Geriatrics, 4th ed, Kane RL et al (eds) McGraw Hill, NY, 1999
- ↑ UCLA Intensive Course in Geriatric Medicine & Board Review, Marina Del Ray, CA, Sept 29-Oct 2, 2004
- ↑ 3.0 3.1 The Merck Manual of Geriatrics, 3rdh ed, Merck & Co, Rahway NJ, 2000
- ↑ Taffet GE, Physiology of Aging, In: Geriatric Medicine: An Evidence-Based Approach, 4th ed, Cassel CK et al (eds), Springer-Verlag, New York, 2003
- ↑ 5.0 5.1 Geriatric Review Syllabus, 7th edition Parada JT et al (eds) American Geriatrics Society, 2010
Geriatric Review Syllabus, 8th edition (GRS8) Durso SC and Sullivan GN (eds) American Geriatrics Society, 2013
Geriatric Review Syllabus, 10th edition (GRS10) Harper GM, Lyons WL, Potter JF (eds) American Geriatrics Society, 2019 - ↑ Denic A, Glassock RJ, Rule AD. Structural and Functional Changes With the Aging Kidney. Adv Chronic Kidney Dis. 2016 Jan;23(1):19-28. Review. PMID: https://pubmed.ncbi.nlm.nih.gov/26709059 PMCID: PMC4693148 Free PMC Article https://pmc.ncbi.nlm.nih.gov/articles/PMC4693148/
- ↑ Papacocea RI, Timofte D, Tanasescu MD et al Kidney aging process and the management of the elderly patient with renal impairment (Review). Exp Ther Med. 2021 Mar;21(3):266. PMID: https://pubmed.ncbi.nlm.nih.gov/33603873 PMCID: PMC7851660 Free PMC article. Review. https://pmc.ncbi.nlm.nih.gov/articles/PMC7851660/