Renal week 1 Thu & Fri
Terms
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- between which vertebral levels do kidneys lie?
- between T12 and L3
- the renal pelvis is lined by which type of epithelium?
- transitional epithelium
- what four elements are contained within the renal cortex?
-
(1) glomeruli
(2) tubules (make up nephron)
(3) blood vessels
(4) interstitial tissue - the kidneys receive what % of cardiac output?
- 25%
- the loop of Henle consists of which three things?
- thin desc limb, thin asc limb, thick ascending limb
- what is different about the loop of henle for superficial cortical nephrons?
- short loops of Henle which descend only into the outer medulla
- which has a higher GFR, the superficial cortical or the juxtamedullary nephron?
- the juxtamedullary nephron, because the glomeruli are larger
- each kidney contains approx how many glomeruli?
- 1 million (young adult)
- what is the normal thickness of the Glomerular Basement Membrane?
- 300-350 nm
- is the GBM normally permeable to small proteins?
-
yes, to light chains but impermeable to larger ones like IgG
becomes more permeable in disease, thus contributing to proteinuria - what are the four elements of the glomerular tuft?
-
(1) endothelial cells (capillary)
(2) GBM
(3) epithelial cells (podocytes)
(4) mesangium - function of podocytes
- filtration, maintenance of GBM, negative charge
- function of mesangium
- mechanical support, removal of macromolecules from phagocytosis, and contractility, thus playing a role in the regulation of glomerular blood flow
- Renal Clearance eqn
- C = (Ux * V) / Px
- what is used to measure renal plasma flow?
- PAH
- Renal Plasma Flow eqn
- RPF = (U(PAH) * V) / (RA(PAH) - RV(PAH))
- Effective RPF eqn
-
since RV(PAH) is approx 0
Effective RPF = C(PAH) - Renal Blood flow eqn
- RBF = RPF / (1 - Hct)
- what does angiotensin II do to RBF and GFR and how?
-
inc efferent renal constriction
thus:
- DEC RBF
- INC GFR - how does ureteral obstruction alter P(BS) and GFR?
- ureteral obstruction will DEC GFR because of INC P(BS)
- what is used to measure GFR?
- clearance of inulin
- Filtration fraction eqn
- GFR / RPF
- what happens to the plasma flow through the glomerular capillaries that is not filtered?
- circulates through the peritubular capillaries
- within the nephron where is sodium reabsorbed (include %'s)
- proximal convoluted tubule (67%), thick asc limb (25%), distal convoluted tubule (5%), collecting duct (3%)
- why does the proximal convoluted tubule exhibit isosmotic reabsorption?
- proportionality between sodium salt absorption and water reabsorption
- where does aldosterone work to regulate Na balance?
- late distal tubule and collecting duct
- why is the TALH called the diluting segment?
- because it reabsorbs NaCl without water
- furosemide
- a loop diuretic that inhibits the Na-K-2Cl cotransporter and NaCl reabsorption in the TALH
- why is the early distal tubule called the cortical diluting segment?
- like the TALH, it is also impermeable to water --> reaborbs 5% of filtered Na+ via a Na-Cl cotransporter
- thiazide diuretics
- inhibit the Na-Cl cotransporter of the early distal tubule
- K+-sparing diuretics
- act on the principal cells of the late distal tubule and collecting duct to inhibit Na+ channels
- aldosterone MOA
- steroid hormone --> goes to nucleus --> mRNA --> synth of Na channel in luminal membrane and Na-K ATPase
- what do acidosis and alkalosis do to K secretion in the renal distal tubule principal cell
- acidosis dec K secretion and alkalosis inc K secretion
- diuretics which inc flow rate to distal tubule do what to K secretion? exception?
-
inc K secretion
exception: K-sparing diuretics - what three things are needed to make hyperosmotic urine?
-
(1) corticopapillary osmotic gradient
(2) ADH
(3) vasa recta capillaries - what two things establish the cortico-papillary osmotic gradient?
- countercurrent multiplication and urea recycling
-
renal failure
- edema associated with what EABV & true volume - INC EABV & INC true volume
-
CHF
- edema associated with what EABV & true volume - DEC EABV & INC true volume
- T/F volume depletion always results in a DEC EABV
- T, caused by loss of sodium and water
-
physical findings related to loss of total volume:
1-10%
10-15%
15-25%
>40% -
loss of total volume:
1-10% INC pulse
10-15% orthostatic hypotension
15-25% supine hypotension
>40% shock - what happens to ADH if DEC EABV and hypoosmolarity both occur
- ADH is released despite low osmalality because volume always takes precedence
-
acute nephritic syndrome
- 5 clinical features -
(1) acute onset hematuria
(2) mild to moderate proteinuria
(3) azotemia
(4) edema
(5) hypertension -
nephrotic syndrome
- 5 clinical features -
(1) heavy proteinuria
(2) hypoalbuminemia
(3) severe edema
(4) hyperlipidemia
(5) lipiduria - what do prostaglandins, hypercalcemia, and Li+ do to the effect of ADH on water permeability
- inhibit ADH's effect
- desc the diurnal variation of GFR
- highest in the afternoon and lowest in the middle of the night
- does GFR inc or dec with pregnancy
- INC
- what is the normal BUN/Creatinine ratio? What is it in prerenal azotemia?
-
Normal: 10-15:1
Prerenal Azotemia: 20:1 - is creatinine a perfect measure of GFR?
- no, it's a good estimation. it actually slighly overestimates GFR a little bit in normals, and overestimates GFR in patients with impaired renal function
- FENa
-
fractional excretion of sodium -- % of filtered sodium that is excreted in the urine
in prerenal azotemia there is intense retention of sodium and the FENa is less than 1%
It is above 2% in renal disease and post renal diseases - FENa eqn
- (Una * Pcr * 100) / (Pna * Ucr)
- list 8 nonosmotic stimuli for ADH secretion
-
(1) pain
(2) nausea
(3) anesthesia
(4) CNS depressants
(5) nicotine
(6) cholinergic agents
(7) alpha-adrenergic agonists
(8) drugs - list 5 inhibitors of ADH secretion
-
(1) ECF volume expansion
(2) alcohol
(3) supraventricular tachycardia
(4) alpha-adrenergic agonists
(5) drugs - Rapidly Progressive Glomerulonephritis (2)
-
(1) loss of renal function in a few days
(2) active urine sediments (hematuria, dysorphic red cells, red cell casts) - acute renal failure (2)
-
(1) oliguria or anuria
(2) recent onset azotemia - chronic renal failure (2)
-
(1) final common pathway of all chronic renal diseases
(2) persistent signs and symptoms of uremia - Membranous Glomerulonephropathy is a classic example of which form of glomerular injury?
- circulating immune complex nephritis
- compare circulating immune complex nephritis and immune complex nephritis in situ with regards to ID'ing by IF and EM
-
circulating --> get granular deposits that can be seen by IF and EM
in situ --> linear and non-granular pattern can only be seen by IF - what is the classic example of immune complex nephritis in situ is what?
- Goodpasture's syndrome
- what is the most common cause of nephrotic syndrome in children?
- MCD
-
MCD
- pathogenesis
- lab -
disorder in which T cells release a cytokine or other factor that damages epithelial cell foot processes and possibly nephrin, leading to proteinuria
heavy proteinura; normal complement levels -
MCD
- main pathology finding
- treatment -
EM: foot processes appear "fused" or smeared over the outer side of GBM
children: usually good prognosis with steroid therapy - most common cause of adult nephrotic syndrome
- Membranous Glomerulonephropathy (MGN)
-
MGN
- pathogenesis - chronic immune-complex nephritis caused by circulating Ag-Ab complex entrapment in the GBM
-
MPGN
- pathogenesis
- clinical features -
circulating Ag-Ab complexes responsible
nephrotic syndrome -
MPGN
- lab
- pathology
- prognosis -
dec serum complement
"tram-track" appearance
uniformly poor prognosis -
Acute Proliferative (poststreptococcal, postinfectious) GN
- pathogenesis
- clinical features
- lab
- pathology -
deposition of IgG immune complexes in capillary loops, with complement (C3) activation
abrupt onset of nephritic syndrome with oliguria, hematuria, or tea-colored urine, red cells, white cells, and casts
enlarged hypercellular glomeruli; lumpy-bumpy pattern along capillary loops - Type I Crescentic GN
-
aka anti-GBM disease (Goodpasture's Disease)
IF shows linear deposition of IgG and C3 along GBM - Type II Crescentic GN
-
aka immune-complex-mediated crescentic GN
may be associated with any immune-complex type GN including SLE, IgA, nephropathy, or postinfectious GN
IF will reveal a course, granular, or "lumpy-bumpy" staining pattern - Type III Crescentic GN
- shows no anti-GBM Ab or immune-type complexes, either by IF or EM
- IgAN
-
associated with an error of IgA production and clearance
gross hematuria occurring coincidentally or immediately following a non-specific upper respiratory infection
IF: IgA prominent, diffeuse and granular in mesangium - Chronic Glumerulonephritis
-
aka CRGN
kidneys are grossly shrunken, and microscopically show widespread global glomerular sclerosis, with interstitial fibrosis and tubular atrophy -- "end-stage kidney" - major cations of ICF
- K+ and Mg2+
- major cation of ECF
- Na+
- major anions of ECF
- Cl- and HCO3-
- T/F At steady state, ECF osmolarity and ICF osmolarity are equal.
- T
- Filtered load =
- Filtered load = GFR x [plasma]
- Excretion rate =
- Excretion rate = V x [urine]
- is the late distal tubule, what do the alpha-intercalated cells do?
-
secrete H+ by a H+-ATPase, which is stimulated by aldosterone
reabsorb K+ by a H+/K+-ATPase