Structure - Function Flashcards
What is the cup shaped around the glomerulus
BOWMAN’S CAPUSULE
Smooth muscle cells found between / supporting glomerular capillaries, which can contract to regulate blood flow into the glomerulus.
They also have phagocytic properties similar to monocytes and release inflammatory cytokines and growth factors.
Mesangial Cells
What is special about the glomerular capillaries
They are fenestrated, and allow large amounts of solute-rich fluid (Ions and large molecules, not protein or blood cells) to pass through
They have podocytes - which make up the visceral epithelium of bowman’s capsule
Where does the filtrate enter the (bowman’s) capsular space
Filtration slits of the podocytes
Clefts between the foot processes of the podocytes
Filtration slits
Most nephrons are _____ They are the “hard workers” and have a shorter loop of henle
Cortical Nephrons
About 15% of nephrons are ______ They have a long loop of henle
Juxtaglomerular Nephrons
What do juxtaglomerular nephrons specialize in
CONCENTRATING URINE
Where does renal filtration occur?
Glomerulus
Where does renal reabsorption and secretion occur?
Tubules
Name the two kinds of capillaries found in nephrons
Glomerular - filtration!
Peritubular -
The only capillaries in the body that are fed and drained by an arteriole
Glomerular capillaries
When filtrate reabsorbed by the tubules, how does it return to the blood stream
via peritubular capillaries
What allows the blood pressure in the glomerular capillary bed to be so high?
The fact that these glomerular capillaries are fed and drained by an arteriole
On what forces does glomerular filtration depend
STARLING forces - hydrostatic and osmotic pressures
What makes glomeruli efficient filters?
- large surface area
- Surface is very permeable to water
- High glomerular BP (55 mmHg) (higher than capsule pressure)
Glomerular BP?
55mmHg
What opposes glomerular filtration?
Osmotic pressure in the plasma from protein
Fluid pressure in Bowman’s space
- Increase plasma protein (dehydration, polycythemia)
- Increase BS pressure
- Decrease BP
What favors glomerular filtration?
Glomerular capillary BP
- raise systemic BP
- Decrease pressure in BS
- Decrease plasma protein (blood loss, no transfusion)
Tubular cells are joined by _____ through which substances can _______
Tight junction, diffuse
Percentage of urea reabsorbed
44%
Percentage of Na reabsorbed
99.5%
Percentage of water reabsorbed
99%
Examples of things which are secreted in the tubules
H+
K+
Organic anions
Tubule secretion is particularly important for which homeostatic mechanism
Controlling blood pH (H+ secretion)
Normal GFR
90/120 ml/min
< 60 = disease
GFR affected by
- Filtration surface area
- Membrane permeability and Net Filtration Pressure (NFP)
- Blood pressure / flow to glomerulus
Key mechanisms kidneys use to regulate water and ions
Water reabsorption
Na reabsorption / secretion
Range of daily urine volume
400 - 2500mL
Renal salt wasting
Hypo-aldosteronism
Order of operations in nephron
Afferent arteriole > glomerulus > Prox convoluted tubule > Descending loope of henle > Loop > thin ascending loop > thick ascending loop > distal convoluted tubule > (cortex, medulla) > Collecting duct > papilla of renal pyramid > minor and major calyces >renal pelvis (Hilum) > Ureter
What makes up the renal corpuscle
Glomerulus, bowman’s capsule, mesangial cells
Major disorders that disrupt the glomerular filtration barrier
DMII, HTN, Glomerulonephritis (autoimmune)
Where does sodium reabsorption occur and how is it transported?
Occurs in all tubular segments EXCEPT the descending loop of Henle (for the countercurrent!)
Transported passively, by diffusion, from the tubular lumen to the epithelial cells. Then transported actively, via Na/K pump, from the epithelial cells to the systemic capillaries
By what mechanism is water reabsorbed
Osmosis (passive) - but ** determined by the movement of sodium and presence of aquaporins **
Sites for water / Na balance
Renal Tubules
Where would one find aquaporins?
Proximal convoluted tubule +++
Descending, loop, ascending?
NONE in collectinge ducts UNLESS YOU HAVE ADH
ADH is produced where and alongside what?
Produced in HYPOTHALAMUS
STORED in POSTERIOR PITUITARY
alongside oxytocin
How does ADH lead to increased aquaporins
increased plasma osmolarity > ADH from post pituitary >
binds receptors on basolateral membrane of COLLECTING DUCTS >
increased cAMP / PO4 >
AQP fuse w luminal membrane
How is sodium transported in renal tubules?
Transported passively, by diffusion, from the tubular lumen to the epithelial cells.
Then transported actively, via Na/K pump, from the epithelial cells to the systemic capillaries
Why is active transport of Na out of the tubule epithelial cells necessary?
To keep intracellular Na low and drive the diffusion gradient
Things which might disrupt the homeostasis of passive / active Na reabsorption and subsequent H20 / glucose drafting?
Broken AQPs
Lack of ATP in kidney
Tubular damage w interstitial fibrosis
How to baroreceptors in the atria and carotid arteries affect ADH
Lower BP at carotid / atrial baroreceptors will inhibit ADH, so the kidneys will hold on to water and increased blood volume / BP
How does SIADH affect fluid homeostasis
- Too much ADH > too much water reabsorbed / retained
2. High BP, low Na
How does Diabetes Insipidus affect fluid homeostasis?
- Not enough or ineffective ADH
- Low BP, high Na
- Large, dilute volumes urine
Where does concentration of urine happen/
Loop of Henle
What special function does the special structure of the loop of henle provide?
Countercurrent Multiplier
Osmolarity of filtrate in proximal tubule and beginning of descending loop vs plasma
IT’S THE SAME IT’S THE SAME
Describe how the osmolarity of filtrate changes throughout the tubules
PCT and beginning of descending loop (same as plasma)
Osmolarity increases (concentration) as filtrate travels down the descending limb - because only water is reabsorbed here. Impermeable to solutes.
Osmolarity decreases (dilutes) as filtrate travels up the ascending limb - because Na is reabsorbed. Permeable to solutes.
Filtrate entering the DCT is very dilute - as low as 70mOsm
Osmolarity either increases, decreases, or stays the same as filtrate travels down collecting duct - depending on body’s needs, presence of ADH etc
What contributes to the medullary osmotic gradient
Urea recycling
How dilute can filtrate be by the time it reaches the DCT ?
Very dilute - as low as 70mOsm
How concentrated can urine become?
1200 mOsm
Key controller of Na reabsorption?
Aldosterone
Aldosterone site / action
Steroid, from adrenal cortex
Increases Na reabsorption from distal tubules and collecting ducts
** fine- tuning here - bulk reabsorption already happening in earlier tubules **
Increases Na reabsorption from distal tubules and collecting ducts by dumping K
Aldosterone
Hold Na, at the expense of K
JGA consists of
JG cells + Macula Densa
Enlarged, specialized smooth muscle cells that secrete renin and control blood flow to glomerulus
JG cells
Are JG cells considered endocrine?
YES
What kind of receptors to JG cells use to detect BP shifts in afferent arteriole?
Mechanoreceptors
How to renin and aldosterone relate?
JG cells detect Low BP > JG cells secrete Renin > Angiotensinogen / I / II > Aldosterone
A group of tall, closely packed cells in the DCT which detect changes in Na / osmolarity via chemoreceptors
Macula Densa
What does low Na in the DCT mean for Macula Densa?
Low Na = decreased filtration»_space; JG cells release renin (Paracrine signaling!!)
What controls aldosterone?
Renin, Angiotensin II»_space;
Adrenal Cortex >
Aldosterone >
Na and H20 retention
Three triggers for Renin release
- Low BP (JGA, less stretch = more renin)
- Low Na (Macula)
- SNS stimulation (JG)
Atrial Natriuretic Peptide and Na
Increased BP > cardiac distention > ANP released
ANP > decreased aldosterone > Na dumped
ANP > afferent dilation, efferent constriction > Increased GFR
Major extracellular buffering system
CO2 / HCO3 system
Major intracellular buffers
Phosphate and proteins
How do the kidney’s alter the body’s pH?
By altering the plasma HCO3 concentration
HCO3 is filtered, then reabsorbed or secreted in tubules according to body’s pH needs
Normally, all filtered HCO3 is “reabsorbed” (H exchange mechanism)
A “low oxygen” environment, this area of the kidney is particularly prone to ischemia
Medulla!
The structure of this area makes it particularly vulnerable to deposition of immune complexes, compliment fixation, and damage from HTN and glycosylation
Glomerulus!
highly vascular, fenestrated structure
This area gets clogged by things that shouldn’t have made it through the glomerulus and is therefore prone to ischemia
Tubules!
RBC, WBC, Protein, Fat, Stones
These structures are more prone to malformation, obstruction, and masses
“Post renal” structures - ureters, bladder
Renal medulla is particularly prone to what kind of problem
Ischemia
Glomerulus is particularly prone to what kinds of problems
Due to fenestrated vasculature:
Deposition of immune complexes, complement
HTN damage
Glycosylation
Tubules are particularly prone to
Ischemia, clogged by large molecules that make it through damaged glomeruli (WBC, RBC, protein etc)
Post renal structures are particularly prone to what kinds of problems
Malformation
Obstruction
Masses
What “pre renal” structures can cause renal problems?
Vascular - Renal Artery
General blood volume / perfusion
DRUGS (NSAIDs, ACEi, diuretics)
Heterogenous group of disorders characterized by rapid deterioration of renal function (GFR), rapid elevation of BUN, and S Cr, oliguria
ACUTE renal failure
Acute Renal Failure, Pre-renal causes (30%)
CV, volume depletion (ischemia)
Drug induced (NSAIDs, ACE, diuretics)
Acute Renal Failure, Intrarenal causes (60%)
Inflammatory diseases
Acute Tubular Necrosis
Acute Renal Failure, Post Renal causes (10%)
OBSTRUCTION
Cancer
Congenital abnormalities
60% of acute renal failure is caused by
Intrarenal problems, mostly Acute Tubular Necrosis
*ATN, when blood supply to kidney is severely reduced or blocked. Tubular cells slough off and form casts
30% of acute renal failure is caused by
Pre renal, hemodynamic
10% of acute renal failure is caused by
Post renal, OBSTRUCTION
Slow, progressive loss of renal function associated with:
Systemic diseases (HTN, DM, SLE) or
Intrinsic kidney disease (kidney stones, acute kidney injury, chronic glomerulonephritis, chronic pyelonephritis, obstructive uropathies, or vascular disorders)
Chronic Kidney Disease
Clinical definition of CKD
GFR less than 60 ml/min/1.73 m2 for 3 months or more
Irrespective of the initial cause of the renal damage
Anatomical changes to kidney in CKD
Granular surface
Smaller size
Decreased function
high urine protein
Stage 1 CKD
GFR > 90
No obvious disease. GFR being compensated by higher kidney pressure
Stage 2 CKD
GFR 60-89
Early evidence of bone disease (VD3)
Creeping SrCr
EPO anemia
Mild HTN
Stage 3 CKD
GFR 30-59
Elevated SrCr and Urea
Mod HTN
High Triglycerides
Metabolic Acidosis
Stage 4 CKD
GFR 15-29
Hyperkalemia
Na / H2O retention
Increasing SrCr / Urea
Stage 5 CKD
GFR 0-14
Significant Uremia
Death
GFR for Kidney Failure
< 15
When do symptomatic changes appear in renal failure
Not until renal function declines to < 25% of normal (75% loss) - when adaptive reserves have bee exhausted
What causes the symptoms of renal failure
Symptoms result from:
increased levels of creatinine, urea, and potassium
alterations in salt and water balance
Intact nephron hypothesis
when nephrons are lost, the surviving nephrons step up their game to sustain normal kidney function
