Renal Flashcards

1
Q

Features of Infection-associated glomerulonephritis

A

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

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2
Q

Features of Rapidly progressive (crescentric) glomerulonephritis:
what diseases contribute to this:

A

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

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3
Q

Features of Diffuse proliferative glomerulonephritis:

A

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

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4
Q

Features of IgA nephropathy (Berger disease)

A

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

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5
Q

Features of Alport syndrome

A

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

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6
Q

features of Membrano-proliferative glomerulonephritis

A

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.

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7
Q

What is inflammation of the renal interstitium and how does this present?

A

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

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7
Q

What is inflammation of the renal interstitium and how does this present?

A

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

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8
Q
What are some causes for Prerenal Azotemia and how will this present?
Urine osmolality?
Urine Na?
FeNa?
Serum BUN/Cr
A

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)

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9
Q

How do thiazides work

A

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

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10
Q

What is filtration fraction and how is this calculated

A

% of plasma that gets filtered through glomerulus.

FF = GFR/RPF

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11
Q

what is renal clearance and how is it measured

Compare the hypothetical outcome to GFR

A

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

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12
Q

How to find RPF:

A

RPF= RBF(1-Hct)

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13
Q

Nuances about left kidney:

right kidney:

A

Left: receives 2 extra veins: left suprarenal and left gonadal. And longer renal vein (so the left is taken for transplant)
Right: slightly smaller

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14
Q

In anaphylaxis, what compartment is the plasma moving to and why

A

histamine release causes inc. permeability - fluid leaks from plasma and goes to interstitial space - edema

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15
Q

How is GFR, RPF, and FF changed with:
Afferent arteriole constriction
Efferent arteriole constriction

A

Afferent constriction:
Dec. GFR
Dec. RPF
- no change FF

Efferent constriction:
inc. GFR
Dec. RPF
inc. FF

16
Q

How is GFR, RPF, and FF changed with:
Inc. plasma protein concentration:
Dec. Plasma protein concentration:

A

Inc. plasma protein concentration:
Dec. GFR
no change RPF
Dec. FF

Dec. Plasma protein concentration:
Inc. GFR
no change RPF
Inc. FF

17
Q

Does plasma protein concentration affect RPF?

Does it affect tubular flow?

A

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)

18
Q

How is GFR, RPF, and FF changed with:
constriction of ureter
Dehydration

A

Constriction of Ureter
Dec. GFR (inc hydrostatic pressure)
no change RPF
Dec FF

Dehydration:
Dec. GFR
SUper Dec RPF
Inc. FF

19
Q

How to calculate reabsorption rate:
What does - value indicate?
What about +?

A

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)

20
Q

2 Major ways of autoregulation done in Kidneys:

A

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

21
Q

PTH works where in nephron

A

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

22
Q

Which parts of the nephron are impermeable to water

What is the significance

A

TAL and DCT

We’ve already left the medulla so now our urine becomes less concentrated. (keeping water in)

23
Q

Aldosterone does WHAT

A

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

24
Q

Features of Fanconi Synd:

How will pt. present

A

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)

25
Q

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?

A

In utero! will see tiny cysts, and bilaterally enlarged kidneys.
Potter’s sequence.
If progresses.. HTN, portal HTN due to hepatic fibrosis,

26
Q

What nerve might be impaired after multiple vaginal deliveries and what does this lead to?

A

Pudendal nerve injury (S2-S4) which controls external sphincter. (somatic)
STRESS INCONTINENCE
Internal/detrusor muscle are under autonomic control