Renal Flashcards
Features of Infection-associated glomerulonephritis
This is a nephritic syndrome.
It is a type 3 hypersensitivity reaction. Associated with hypocomplementemia (due to consumption).
Children-> due to group A strep (poststreptococcal glomerulonephritis), seen 2-4 weeks AFTER pharyngeal OR skin infections
Adults-> can be due to strep, but more commonly Staph, seen DURING the infection
This can progress to rapidly progressive (crescenteric) glomerulonephritis! BAD!
LM- glomeruli enlarged and hypercellular
IF- granular “starry sky” appearance and “lumpy bumpy” due to IgG, IgM, and C3 deposition in GBM and mesangium
EM- subepithelial IC humps
Features of Rapidly progressive (crescentric) glomerulonephritis:
what diseases contribute to this:
Nephritic
LM: Crescent moon shaped. has fibrin, plasma proteins, w/ macrophages
Linear IF: ab against GMB (type IV collagen): GOODPASTURE tx: plasmapharesis
Negative IF/Pauci-immune(no Ig/C3):
Proteinase3-ANCA/c-ANCA: GPA
MPO-ANCA/p-ANCA: microscopic polyangitis or Eosinophilic granulomatosis with polyangitis
Granular IF: PSGN or DPGN
Features of Diffuse proliferative glomerulonephritis:
Think SLE! DPGN and MPGN often present as nephrotic syndrome and nephritic at same time
LM: Wire looping of capillaries
IF: Granular
EM - subendothelial
can lead to rapidly cresecenteric glomerulonephritis
Features of IgA nephropathy (Berger disease)
episodic hematuria that occurs CONCURRENTLY with respiratory or GI tract infections
associated with IgA vasculitis (Henoch-Schhn purpura)
LM- mesangial proliferation
IF- IgA-based IC deposits in mesangium
EM- mesangial IC deposition
Features of Alport syndrome
mutation in type IV collagen causes irregular thinning and thickening and splitting of GBM
X-linked Dominant!
presents with eye problems, sensorineural deafness, and glomerulonephritis
EM- “basket-weave” appearance
features of Membrano-proliferative glomerulonephritis
Nephritic/nephrotic at same time :o
type I - who cares but might be secondary to hep infections
type 2 - C3 nephritic factor (IgG stabilizes C3 convertase – persistent complement activation – dec. C3 levels)
intramembranous deposits - dense deposit disease
Mesangial growth - GBM splitting – tram track appearance.
What is inflammation of the renal interstitium and how does this present?
Acute interstitial nephritis (tubulointerstitial nephritis). One of the causes of intrinsic renal failure!
Pyuria (eosinophils), and azotemia after administration of drug (NSAID, Penicillins, PPis, Rifampin).
Rash, fever, hematuria, CVA
What is inflammation of the renal interstitium and how does this present?
Acute interstitial nephritis (tubulointerstitial nephritis). One of the causes of intrinsic renal failure!
Pyuria (eosinophils), and azotemia after administration of drug (NSAID, Penicillins, PPis, Rifampin).
Rash, fever, hematuria, CVA
What are some causes for Prerenal Azotemia and how will this present? Urine osmolality? Urine Na? FeNa? Serum BUN/Cr
Hypovolemia, dec. CO, dec circulating volume (HF, liver failure)
Pt. will have oliguria (due to dec. RBF which leads to dec. GFR.)
Urine osmolality >500
Urine Na <20 (putting it back in blood)
FeNa <1%
Serum BUN/Cr >20 (more time to reabsorb due to low GFR)
How do thiazides work
block NaCl symporter in DCT
This reduces Na concentration inside the cells, which increases activity of basolateral Na-Ca exchanger. This puts Na inside the cell and Ca into serum
hypercalcemia
What is filtration fraction and how is this calculated
% of plasma that gets filtered through glomerulus.
FF = GFR/RPF
what is renal clearance and how is it measured
Compare the hypothetical outcome to GFR
the volume of plasma that is needed to completely clear a substance in the urine.
Cx = (UxV)/Px
If C > GFR : net tubular secretion of X
if C < GFR : net tubular reabsorption and/or not freely filtered
How to find RPF:
RPF= RBF(1-Hct)
Nuances about left kidney:
right kidney:
Left: receives 2 extra veins: left suprarenal and left gonadal. And longer renal vein (so the left is taken for transplant)
Right: slightly smaller
In anaphylaxis, what compartment is the plasma moving to and why
histamine release causes inc. permeability - fluid leaks from plasma and goes to interstitial space - edema
How is GFR, RPF, and FF changed with:
Afferent arteriole constriction
Efferent arteriole constriction
Afferent constriction:
Dec. GFR
Dec. RPF
- no change FF
Efferent constriction:
inc. GFR
Dec. RPF
inc. FF
How is GFR, RPF, and FF changed with:
Inc. plasma protein concentration:
Dec. Plasma protein concentration:
Inc. plasma protein concentration:
Dec. GFR
no change RPF
Dec. FF
Dec. Plasma protein concentration:
Inc. GFR
no change RPF
Inc. FF
Does plasma protein concentration affect RPF?
Does it affect tubular flow?
NO! doesn’t effect RPF - this is just amount of blood that is making its way to kidney
but YES it does effect the tubular flow because depending on the high/low solute concentration, it will move faster/slower (respectively)
How is GFR, RPF, and FF changed with:
constriction of ureter
Dehydration
Constriction of Ureter
Dec. GFR (inc hydrostatic pressure)
no change RPF
Dec FF
Dehydration:
Dec. GFR
SUper Dec RPF
Inc. FF
How to calculate reabsorption rate:
What does - value indicate?
What about +?
RR = filtered - excreted.
- RR indicates net secretion (more coming out of urine so must be from secretions)
+ RR indicates net reabsorption (less excretions so it had to have been reabsorbed)
2 Major ways of autoregulation done in Kidneys:
Myogenic: inc. arterial pressure – stretch of afferent arterioles – mechanical activation of vascular sm. m – vasoconstriction of afferent – dec. RPF
Tubuloglomerular: inc. NaCl or tonicity of filtrate sensed by macula densa – paracrine driven vasoconstriction of afferents – Dec. RPF
PTH works where in nephron
PCT - inhibits Na/PO4 cotransport – no phosphate being reabsorbed in blood to pick up calcium – inc. free calcium
DCT - Inc. Ca/Na exchange – inc. calcium reabsorption
Which parts of the nephron are impermeable to water
What is the significance
TAL and DCT
We’ve already left the medulla so now our urine becomes less concentrated. (keeping water in)
Aldosterone does WHAT
Kicks out H and K while bringing in Na to reabsorb it. What will this do to Cl and HC03 levels
Since H= is being put out in lumen - Cl- gets put out into lumen and Hco3 goes back into cell
So in Hypoaldosteronism (addisons)
Dec. aldosterone means less H in lumen, which means Cl gets stuck inside cell and Hco3 gets put in lumen
Features of Fanconi Synd:
How will pt. present
reabsorption defect in PCT – inc excretion of aminos, glucose, hco3, phosphate
This leads to RTA 2 (Bicarb not being reabsorbed into blood) Metabolic acidosis
Hypo everything
Pt will present
Young child with sx of diabetes but NO RISE IN SERUM GLUCOSE. growth retardation, rickets/osteopenia (frontal bossing, bow legged)
When can you detect autosomal dom. polycystic kidney disease?
What does it lead to as an infant?
What does it lead to later in life?
In utero! will see tiny cysts, and bilaterally enlarged kidneys.
Potter’s sequence.
If progresses.. HTN, portal HTN due to hepatic fibrosis,
What nerve might be impaired after multiple vaginal deliveries and what does this lead to?
Pudendal nerve injury (S2-S4) which controls external sphincter. (somatic)
STRESS INCONTINENCE
Internal/detrusor muscle are under autonomic control
