Renal Review Flashcards
Major Functions of the Kidney
- Fluid and ion balance
- Removal of metabolic waste and chemicals from the circulation
- Gluconeogenesis
- Endocrine function and hormone secretion (renin, prostaglandins, kinins, erythropoietin creation, Vit D activation, etc)
Release of erythropoietin is stimulated by
low pO2 sensed in the renal interstitial causes specialized cells to release it (may be due to anemia, chronic hypoxia, or low RBF)
Why does kidney failure lead to osteoporosis
Lack of vitamin D activation leads to decreased absorption of calcium from the GI tract.
Kidney pain is sensed through these fibers
SNS fibers from T10-L1
SNS innervation to the kidneys is provided by these fibers and causes this
Supplied by pre-ganglionic fibers from T8-L1. These terminate on B1 receptors. NE release onto the B1 receptors results in release of renin.
Ultimately this results in increased angiotensin II creation and increase in BP. Thus, BBs have antihypertensive qualities through this link of decrease in angiotensin II creation.
PSNS innervation to the kidneys is from
The vagus nerve, which terminates on the ureters
Kidneys represent __% of body weight but receive __% of the CO
0.4% body weight
25% of CO
Which layer of the kidney receives the most blood flow?
The cortex (outer layer) receives more than the medulla (inner layer). Cortex = 85% RBF Medulla = 15% RBF
Only 6% of RBF goes to the medulla, despite it being very metabolically active at the thick ascending limb d/t all that active transport going on. Average O2 tension here is 8mmHg.
Describe cortical vs. juxtamedullary nephrons
Cortical
- Receive 85% RBF
- Found in the outer/middle cortex
- Have SHORT loops
- Efferent arterioles drain into peritubular capillaries
Jextumedullary
- Found in the inner renal cortex
- Long loops
- Efferrent arterioles drain into the vasa recta (concentration system / counter current mechanism –> vasa recta rectify the concentration gradient. Remember that long loops = better concentrating ability)
Describe the pathway of blood within the kidney
Renal artery - interlobar artery - arcuate - cortical radial - afferent arteriole - glomerular cappillaries - efferent arteriole - peritubular arteries or vasa recta (depending on nephron type) - venous system (cortical veins)
Percentage of blood that filters into the bowman’s capsule
25% gets filtered into the capsule.
The remaining 75% moves on to the efferent arteriole
What are mesangial cells?
Smooth muscle cells that surround BVs in the kidney and function to regular blood flow through the capillaries.
Filtration based on size in the gomerulus
3.6nm or >60-70kDa get excluded from the filtrate (Hgb and albumin) –> these are not filtered unless the glomerulus gets fucked up d/t glomerulonephritis
These tubules have a high amount of metabolic activity (active transport) and are at risk for ischemia
Proximal convoluted tubules and the thick ascending limb
Where does reabsorption of water take place?
Proximal tubules = 65% (no drugs target this area)
Loop of Henle = 15% (powerful diuretics like Lasix work here)
Distal tubules = 10%
Collecting ducts = 10%
Things that happen in the proximal convoluted tubule
- 65% of filtered Na, K, Cl, and H2O gets reabsorbed via the Na/K/ATP pump. The active movement of sodium is very important here, because it results in the movement of most other things with it.
- Almost 100% of glucose and amino acids are actively reabsorbed
- H+ ions are secreted into the tubule in exchange for bicarb
- Ca++ gets reabsorbed under the influence of parathyroid hormone
- Waste products get actively secreted into this tubule (bile salts, rate, creatinine, dopamine, and drugs)
- High peritubular pressure will result in less reabsorption
Things that happen at the loop of Henle
- Formation of hypertonic fluid via the counter current mechanism
- Descending loop -> tubule is permeable to water and it freely exits the tubule as the peritubular concentration increases
- TAL –> metabolically active. Na/K/Cl/Bicarb are all pumped out of the tubule. High O2 consumption in this area.
What is the JG apparatus?
The distal TAL/initial portion of the distal tubule meets with the macula dense and efferent and afferent arterioles
The macula dense is made of these two types of cells
Mesangial cells (SM cells that contract in response to angiotensin II and other vasoconstrictive substances to decrease GFR)
Granular cells.
- These secrete renin in response to
1) Direct B1 stimulation
2) Decreased RBF. Decreased stretch of the granular cells (renal baroreceptors) causes renin release. Also decreased Na and Cl concentration releases prostaglandins on juxtaglomerular cells, resulting in renin release.
Renin also stimulates the release of
ADH from the posterior pituitary and aldosterone from the adrenal medulla
Things that happen in the distal convoluted tubule
- Na/Cl/H2O are reabsorbed here under the influence of ADH and aldosterone
- H+ and K+ are secreted into the tubule here
- ADH = movement of aquaporins to increase H2O reabsorption
- Aldosterone = Na and water reabsorption and K secretion
Things that happen in the collecting duct
- Water is reabsorbed under the influence of ADH
- H+ may be secreted
- Principle Cells = Reabsorb Na and water in exchange for K (principle cells are principally a Na/K pump)
- Intercalated cells = Secrete H+ and reabsorb bicarb (H-ATP pump)
Overall, the late distal tubule and collecting duct play an important role in acid-base regulation.
ADH release from the posterior pituitary is stimulated
high Na concentration, high osmolarity, arterial/atrial baroreceptor activation, and by stimulation of angiotensin II.
__% of the glomerular filtrate is reabsorbed into the vascular system
99% gets reabsorbed.
Therefore, only 1% of the filtrate ends up becoming urine.
Things that happen in response to hypovolemia
- SNS activation and release of angiotensin II results in vasoconstriction and decreased GFR, and increased Na reabsorption
- Aldosterone = Increased Na absorption and K secretion
- Vasopressin (ADH) - increased H2O absorption in the collecting duct
Things that happen in response to hypervolemia
- ANP release (d/t stretch in the atria, results in vasodilation and increase in GFR)
- Decreased SNS and angio II release (results in more dilation and higher GFR, and less Na reabsorption)
- Increased capillary hydrostatic pressure discourages Na reabsorption
- Decreased aldosterone decreases Na reabsorption in the distal tubule and collecting duct
- Decreased vasopressin (ADH) = less water reabsorbed in the collecting duct
Main two mechanisms of how unwanted substances are removed from the body
1) Filtration –> gets filtered in the glomerulus and is not reabsorbed
2) Secretion –> gets directly secreted from the plasma, through the epithelial cells, and into the tubular fluid.
Urine is made mostly of filtered substances, and a few secreted substances
What is normal GFR?
125mL/min
What is the lower limit of auto regulation for the kidney?
MAP of 80-85.
Below this, RBF is pressure dependent. This is a higher limit than the brain!
GFR is considered a measure of ____
glomerular function
What are the major determinants of filtration pressure?
Glomerular capillary pressure (from tone of afferent and efferent arterioles) and glomerular oncotic pressure
Degree of SNS tone and RAAS stimulation effects on GFR
Mild to moderate SNS tone = mainly efferent tone, resulting in increased GFR
High SNS tone = mainly afferent tone, resulting in decreased GFR.
In SNS, you need all the fluid you can get to maintain BP and perfuse things! When you’re relaxed, that’s when you have the time to increase your GFR and make pee.
Why is it important for GFR to be regulated?
Too slow = too much reabsorbed, resulting in no urine output
Too fast = too fast to be effectively reabsorbed substances that our bodies need
Auto regulation of RBF is possible between these MAPs
80-200.
Modulation of GFR is done mainly though ___ tone
afferent
Mechanisms of renal autoregulation
1) Myogenic
- Inherent property of muscle that causes it to constrict in response to increased stretch. Relaxation occurs in response to decreased stretch.
2) Tuboglomerular feedback via the JG apparatus.
- THIS IS THE MAIN MECHANISM!!!!**
- Feedback is based on the amount of NaCl delivery to the macular densa from the distal TAL
- Too much NaCl delivery (from dehydration, HTN, or failed concentration mechanisms in ARF) results in the release of renin and adenosine, resulting in afferent constriction.
- Too little NaCl delivery (d/t hypotension) means that catecholamine and renin levels are low, resulting in afferent dilation and efferent constriction to increase GFR
Importance of prostaglandins
- Protect against renal ischemia
- Produced by the actions of phospholipase A2 and COX
- Prostaglandins are released by the kidneys in response to renal ischemia, renal hypotension, and physiologic stress.
- Prostaglandins increased urine output and oppose the actions of angiotensin II, SNS stimulation, and ADH, which all try to decrease RBF.
What common anesthesia drug should be avoided because it blocks prostaglandin production and puts the kidneys at risk for ischemia?
TORODOL!
It’s an NSAID, and thus a COX inhibitor.
Note that NSAIDs are only nephrotoxic in the ischemic kidney, not to the normal kidney. NSAIDs like Toradol are bad for renal patients because they are usually dependent on their renal prostaglandins to maintain flow
What does ANP do?
- Gets released in response to atrial stretch (hypervolemia)
- Blocks the reabsorption of Na in the distal tubule and collecting duct (resulting in natriuresis!)
- Results in an overall increase in GFR d/t natriuresis, decreased renin release, and causes systemic vasodilation (overall reducing BP).