Renal adaptation Flashcards
Renal responses to various abnormalities
Deficient nephrons
Reduced renal mass
Reduced Nephron function
T or F
Deficient nephrons can be seen at birth
T
developmental abnormalities like hypoplastic kidney
CAKUT congenital abnormalities of the kidney and urinary tract
Low nephrons at birth
Autosomal recessive kidney disease
Urinary tract abnormalities with abnormal kidney
Dysplastic or Hypoplastic kidneys
kidney mass below two standard
deviations of age-matched normal or a
combined kidney mass of less than half
normal for the patient age
Dysplastic or hypoplastic kidneys
FACTORS CONTIRBUTING TO LOW NEPHRON
Decrease growth in utero
Low birth weight mothers= low birth weight babies
Calorie restrictions
Protein restrictions
Hi-fat intake prone to hypertension and renal fibrosis
Deficiency in Na, Zn, Fe, Vit A
Drugs taken during preg
T or F
persistence of hyperglycemia can actually delay the kidney development and decrease in
the number of nephrons developed
T
calorie restriction of mothers may predispose their child to _____
albuminuria
Protein restriction decreases lifespan by
200mdays
Drugs that could contribute to deficient numbers of nephron
Dexamethasone
ACEI and ARBS
Gentamicin
Nsaids
This postulates what the kidney does when an
individual is born with deficient number [of
nephrons].
BENNER HYPERFILTRATION HYPOTHESIS
becomes maladaptive as it leads to progressive anatomical and functional deterioration of the kidney
BENNER HYPERFILTRATION HYPOTHESIS
adaptation in chronic kidney kidney injury
Counterbalance Hypertrophy systemic adap: -potassium -sodium -Acid-base homeostasis -mineral metabolism
an attempt on the part of the less injured or uninjured portion of the kidney to take over the work of the more injured portion
Counterbalance
growth or compensation due to overstimulation
acquired reserve
related to increase in renal blood flow due to dilatation of the renal arterioles due to Nitric oxide production
increased size of the glomeruli and hyperfiltration
Hypertrophy
factors implicated in compensated hypertrophy after nephron loss
inc renal blood flow inc tubular absorption of Na with dec distal delivery and decreased afferent arterial resistance due to adaptive tubuloglomerular feedback Hepatocyte growth factor Gluc transporters Inc renal nerve activity Insulin like growth factor Mammalian target of rapamycin signalling pathway activation Transforming growth factor beta
potassium is reabsorbed in the ______ and secretion determined by _____
proximal tubule; distal nephron
hyperkalemia promotes potassium secretion by the principal cell of the _______
collecting duct
Increases the density and activity of the
basolateral Na-K-ATPase and the
number of Na channels in the apical
membrane of the collecting duct
aldosterone
In CKD: positive feedback=
increase distal delivery = increased filtration
acid-base metabolism normal:
excrete 1 mEq/kg/day of dietary acid load
adaptation to decreased mass (acid-base metab)
Increased H excretion
o Enhanced nephron ammoniagenesis
o Increased distal H ion secretion (RAS and endothelin-1)
Mineral-metabolism response
• Increased secretion of PTH and FGF-23 • Stimulate phosphaturia • Reduces levels of Na-phosphate cotransporter NaPi2a and NaPi2c
mineral metabolism Maladaptive response:
• Downregulation of Klotho-fibroblast growth factor I resulting to a decrease in the ability of FGF-23 to downregulate PTH production • Persistent elevation leads to soft tissue calcification, left ventricular hypertrophy and subsequent increased mortality in CKD.
Activation of intrinsic defense mechanisms
to cope with pathologic conditions
PRECONDITIONING
renders the organ resistant to subsequent ischemic injury
ISCHEMIC PRECONDITIONING
Protection afforded in one vascular bed by
ischemia in another vascular bed in the
same organ or a different organ
remote ischemic preconditioning
adenosine
akt (protein kinase b)
antioxidants
autophagy
bradykinin
dec in genes regulating inflammation
extracellular single-related kinase
hypoxia induced factors
heat shock proteins
protein kinase c
JAK stat pathways
Jun N terminal kinase
Mitochondrial connexin
Nitric oxide
Opioids
Sirtuin activity
Adaptive response to acute injury
Hypoxia
Acute renal success
Tubulogromerular feedback
Hypoxia-induced factor 1 alpha
Induces upregulations of genes whose
protein products are involved in energy
metabolism, angiogenesis, and apoptosis
Hypoxia-induced factor 1 alpha
ADAPTIVE RESPONSE TO TOXIC INJURY SPECIFIC TO THE PROXIMAL TUBULES
Response of the proximal tubule cells to direct
injury by Diphtheria toxin producing repair with minimal sequela.
