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Renal 2 > Renal Pathophysiology > Flashcards

Renal Pathophysiology Flashcards

1
Q

How is GFR measured?

A

clearance of inulin or creatinine

estimates based on serum creatinine

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2
Q

azotemia

A

accumulation of nitrogenous waste products in the blood

i.e. urea

any rise in serum BUN or creatinine above normal

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3
Q

uremia

A

clinical syndrome or symptom compelx associated with severe impariment of renal function

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4
Q

specific gravity of urine

A

lower specific gravity correlated with low osmolarity (more dilute urine)

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5
Q
A

This is an example of a urine

1: Here a white cell with red blood cells around it

When you see cells in the urine you do not know if they have come from the kidney or someplace else in the urinary tract a

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6
Q
A

WBCs and bacteria in urine

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7
Q
A

tubular epithelial cell (not round like WBC)

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8
Q
A

squamous epithelial cells - from bladder ureter or urethra NOT kidney

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9
Q

casts

A

cylindrical masses of agglutinated material

formed in distal nephron, have to come from kidney

Tamm-Horsfall mucoprotein is the major protein constituent

Hyaline, granular or cellular

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10
Q

Where are casts formed?

A

distal nephron

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11
Q

Tamm-Horsfall mucoprotein

A

major protein constituent of casts

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12
Q
A

Hyaline cast

we think the hyaline cast and granular cast are degenerated cellular casts

There is a lot of other amorphous material here

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13
Q
A

tubular epithelial cell cast

you can see the shape of the cells here are not perfectly round which you would see in a white blood cell cast

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14
Q
A

broad cast

it was formed further down in the nephron, again there are red cells around this cast

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15
Q
A

coarse granular cast

notice the granules and degenerating cells

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16
Q
A

RBC cast

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17
Q
A

WBC cast

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18
Q
A

waxy cast (probably has cholesterol)

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19
Q
A

triple phosphate crystals

often in people with UTIs

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20
Q
A

calcium oxalate crystals

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21
Q
A

On the left there are stellar and amorphous Ca Phosphate crystals

On the right Ca Oxalate crystals

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22
Q
A

cysteine crystals

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23
Q
A

uric acid crystals

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24
Q

What does dipstick look for?

A

•Dipsticks (mainly picks up albumin, may miss low molecular weight and other nonalbumin proteins)

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25
Q

Heat and Acetic Acid for urine test?

A

take a specimen of urine and heat it up and if there’s protein you will see it form at the bottom of the test tube

The test tube has been heated (left) and as it cools you see the protein on the bottom

This is with heat and acetic acid but with sulfosalicylic acid it will look very similar

We don’t do this often, usually send sample off to the lab and they can measure protein or albumin

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26
Q

sulfosalicylic acid test for urine

A

detects all proteins in the urine

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27
Q

Microalbuminuria - how do we test?

A

dipsticks not positive until rel high

to find smaller amounts - use direct measrements of albumin secretion

microalbumin - to - creatinine ratio!

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28
Q

How do you determine the type of protein in the urine?

A

protein electrophoresis

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29
Q

glomerular proteinuria

A

increase in permeabilty of glomerular capillary wall leads to increased glomerular filtration of protein

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30
Q

tubular proteinuria

A

impaired reabsorption of normally filtered proteins

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31
Q

overflow proteinuria

A

increased production of smaller proteins in multiple myeloma and ther plasma cell issues

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32
Q

nephrotic syndrome

A

massive loss of normal serum proteins in the urine

  1. heavy proteinuria (>3.5)
  2. hypoalbuminemia
  3. edema
  4. hyperlipidemia
  5. sometimes HTN
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33
Q

hypoalbuminemia in nephrotic

A

urinary loss of protein

liver is making more but can’t keep up with loss

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34
Q

Why edema in nephrotic syndrome?

A

overfill hypothesis

glomerular disease/tubular inflammation leads to increased renal sodium retention (reabsorb mostly in collecting tubules

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35
Q

Why is there no hypertension in nephrotic syndrome?

A

Na retention USUALLY results in hypertension but nephrotic patients to not

MAY be secondary to hypoalbuminemia

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36
Q

Why hyperlipidemia in nephrotic syndrome?

A

elevated cholesterol, TG, phospholipids

low plasma albumin?

increased lipoprotein synthesis

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37
Q

lipiduria in nephrotic syndrome

A

oval fat bodies (tubular cells w fat drops)

maltese crosses (fat drops under polarized light)

on urinalysis

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38
Q
A

oval fat bodies in neprhotic synd urine

1: oval fat body (tubular cell that is filled with fat)

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39
Q
A

maltese crosses - polarized light on fat

lipid in urine in nephrotic

If you think a patient has nephrotic syndrome it is important to look at the urine for oval fat bodies and then look under polarized light

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40
Q

thromboembolic events

A

in nephrotic syndrome!

hypercoagulable state

DVT and renal vein thrombosis

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41
Q

Minimal Change Clinical Picture

A

acute onset

variable fluid retention

HTN infrequent

renal function is normal

EDEMA and protein in the urine!

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42
Q

urinalysis in minimal change disease

A

proteinuria (ALBUMIN - selective)

oval fat bodies

few cells

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43
Q

treatment for minimal change

A

high dose steroids - usually remission in 2-4 wks

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44
Q

membranous nephropathy presentation

A

insidious - asymptomatic proteinuria or microscopic hematuria

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45
Q

urinalysis in membranous

A

massive proteinuria (non selective - not just albumin)

HTN and azotemia if late

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46
Q

acute glomerulaonephritis presentation

A

follows GSA - pharyngitis or skin

gross hematuria and oligouria

edema and pulmonary congestion

flank pain

hypertension

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47
Q

when do you see congested circulation?

A

nephritic!!

renal retention of salt and water

decreased urine output

dyspnea, orthopnea, cardiomegaly, rales, gallop

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48
Q

urinalysis in acute glomerulonephritis

A

GAS rxn

hematuria (coca cola)

RBCs, RBC casts

prteinuria (low)

low urine sodium (retaining, vol overload)

very concentrated urine

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49
Q

treatment of acute glomerulonephritis

A

treat HTN

manage fluids and electrolytes

treat renal failure/dialysis

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50
Q

Hematuria in which syndromes/

A

gross - nephritic only

microscopic - sometimes nephrotic, always nephritic

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51
Q

hypertension in which syndromes

A

sometimes in nephrotic, always in nephritic

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52
Q

decreased GFR in which syndromes?

A

sometimes nephrotic

always nephritic

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53
Q

congestion in which syndromes

A

only nephritic

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54
Q

hypoalbuminemia in which syndromes

A

always nephrotic

rarely nephritic

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55
Q

urinalysis in UTI

A

pyuria and WBC casts

bacteria

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56
Q

urinalysis in pyelonephritis

A

WBCs and WBC casts

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57
Q

Urinalysis in acute interstitial nephritis

A

eosinophils

granular or WBC casts

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58
Q
A
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59
Q

systemic glomerulopathies

A

nephrotic

diabetes, amyloid

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60
Q

primary glomerulopathies

A

nephrotic

minimal change

fsgs

membranous

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61
Q

systemic nephritis

A

SLE

Endocarditis

MPGN

ANCA

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62
Q

kidney only nephritic

A

post infectious

IgA

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63
Q

congenital nephrotic syndrome of the newborn

A

finnish

severe NS at birth - all ESKD

need dialysis and transplant

because mutation in nephrin (in the podocyte slit diapragm)

how we learned about it!

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64
Q

secondary causes of minimal change

A

malignancy (Hodgkin and non-hodgkin lymphoma

drugs (NSAID, lithium, rifampin)

Infections (syphilis, malaria)

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65
Q

clinical presentation of minimal change

A

mostly children

explosive onset - edema, hypoalbuminemia

kidney biopsy to make diagnosis

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66
Q

treatment of minimal chagne

A

prednisone - usually dramatic and quick response

treat underlying secondary disease

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67
Q

urokinase plasminogen activating receptor (suPAR)

A

role in FSGS

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68
Q

Treatment for PRIMARY FSGS

A

steroids first line

most are steroid resistant

second = calcineurin inhibitors

some targetted thereapy?

recur post transplant!

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69
Q

secondary FSGS

A

secondary to other kidney disease and obesity

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70
Q

how does primary FSGS present?

A

NS or asymp prteinuria

normal or elevated BP

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71
Q

how does secondary FSGS present?

A

NON-nephrotic preinuria, decreased GFR

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72
Q

How do you treat secondary FSGS?

A

ACEI/ATR blocker

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73
Q

collapsing glomeruloathy etiology

A

variant of FSGS

characterized by dedifferentiation and proliferation of podocytes with collapse of glomerular tuft

HIV nephropathy (infects podocytes causing proliferation)

or infections, meds, malignanc

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74
Q

treatment of collpsing glomerulopathy

A

anti retroviral

correct underlying

ACEI/ARBs

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75
Q

APOL1

A

worse prognosis in FSGS, more likely to develop kidney failure in african americans

1 risk allele = prptection from trypanosomes

2 = risk for kidney failure

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76
Q

histopath of membraous nephropathy

A

characterized by C3, IgG deposits

SUBEPITHELIAL

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77
Q

how does membranous nephropathy present

A

NS or asymptomatic proteinuria

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78
Q

outcomes of membranous nephropathy

A

25% spontaneous remission

50% persistent proteinuria

25% renal failure

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79
Q

treatment for membranous nephropathy

A

ACEI/ARB

prednisone/calcineuron?

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80
Q

primary membranous nepropathy pathogenesis

A

IgG antibody to podocyte ag (PLA2R)

Ab fixes compliment and C3 is present in renal tissue

Here would be the podocyte (brownish stuff)

  • Expresses the antigen (phospholipase A2 receptor)
  • Ab is generated to that autoimmune antibody receptor that binds the receptor
  • That then activates complement à destroys the podocyte and gives you this disease
  • To remind you, an Ag-Ab complex can activate complement à which ultimately can form this membrane attack complex
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81
Q

PLA2R

A

phospholipase A2 receptor on the membrane of the podocyte

IgG ab bonds to it and fixes comp

Here would be the podocyte (brownish stuff)

  • Expresses the antigen (phospholipase A2 receptor)
  • Ab is generated to that autoimmune antibody receptor that binds the receptor
  • That then activates complement à destroys the podocyte and gives you this disease
  • To remind you, an Ag-Ab complex can activate complement à which ultimately can form this membrane attack complex
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82
Q

secondary membranous nephropathy pantogenesis

A

trapping of preformed antibody-angigen complexes leading to fixation of complement and podycte damage

SLE

syphilis

malaria

hep B

drugs

tumor

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83
Q

rapidly progressive glomerulonephritis (RPGB)

A

presentations OF nephritic syndrome that are emergent

based on percent of cresecents (not time!!)

require urgent treatment

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84
Q

post infectious glomerular nephritis

A

small circulating immune complexes of low-avidity antibody an oligovalent angigen (any infection can cause)

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85
Q

clinical presentation of post infections GN

A

nephritic syndrome 1-2 wks after strep infection (skin, throat)

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86
Q

pathology of post infectious GN

A

subepithelial deposition of immune complexes

granular on immunoflorscence

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87
Q

clinical course of post infectious gn

A

most recover in a couple weeks

control - BP, diuresis, infection

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88
Q

IgA nephropathy pathology

A

mesangial IC deposits

with IgA and usually C3 and IgG

  • Shown biopsy with immunofluorescence
  • Slice of kidney à primary Ab against IgA, IgG or IgF à secondary Ab with something that can be detected fluorescently
  • In this case see IgA deposited in kidney in mesangium and around glomerular capillaries (L piecture)
  • You also see complement (R picture)
  • This would be enough to give you a dx of IgA nephropathy
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89
Q

pathogenesis of IgA nephropathy

A
  1. incrased levels of galactose deficienct IgA
  2. production of unique auto antibodies
  3. formation of pathogenic IgA contianing ICs circulating
  4. mesangial deposition and glomerular injury

Somehow you get this galactose-deficient IgA à produce unique auto antibody à some systemic (maybe driven by a third factor like infection) à deposition of immune complex à activate immune response à inflammation

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90
Q

membranoproliferative glomerulonephritis causes

A

hep B, hep C, malignancy, eds

can present w systemic signs of vasculitis and renaly insufficiency and nephritic syndrome

skin rash etc

treat underlying

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91
Q

ANCA associated vasculitis

A

antibodies to proteins expressed in neutrophil

binding of abs to neutrophil plasma membrane leads to neutrophil activation which causes kidney disease

get autiantibodies by molecular mimicry - present protein that looks like self

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92
Q

treatment of ANCA-associated vasculitis

A

cancer model

inductions (steroids and abs)

plasmapheresis if severe renal impairment

interfere w immune system

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93
Q

anti-gbm mediated glomerularnephritis

A

i.e. goodpastures (+ pulmonary hemorrhage)

auto antibodies against alpha3 chain of collagen IV in renal and lung BM

ab activates compliment

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94
Q

presentation of anti-GBM mediated GN

A

oliguria

advanced renal failure

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95
Q

treatment for anti-gmb mediated gn

A

recovery of renal function is rare

can use aggressive drugs if fewer crescents

96
Q

primary GBM disease

A

alports! hereditary nephritis

97
Q

renal progression of alport’s

A
  1. hematuria
  2. proteinuria
  3. eskd (30s, 40s)
98
Q

pathophys of alports

A

genetic mutation in alpha 3/4 (ch 2) or alpha 5 or type IV collagen

inflammation

99
Q

treatment of alports

A

ACEI (before proteinuria) to protect GBM from damage from deposition

transplant

100
Q

C3 glomerulopathy

A

primary deposition of C3 in absence of IgG

was referred to MPGN2 or dense deposit disease DDD

alternative pathway!!!

101
Q

glomerulonephritis w dominant C3 - what can it be?

A

C3GN - DDD, C3GN without IC

post infectious GN
other

102
Q

DDD vs C3GN

A

DDD - younger, many more ESKD faster, more C3

C3GN - older, less end stage

both recur!!

103
Q

therapy for C3GN

A

monoclonal abs

104
Q

DDD treatment

A

alternate day steroids

abs

ACEI/ARB

105
Q
A
106
Q

role of hypothalamus

A

sense osmolality

control thirst

secrete/suppress ADH (post pit)

107
Q

ADH action on collecting duct

A

prinipal cell

AQP2, 3, and 4 are all affected by ADH. ADH attaches to the V2 receptor on the basolateral surface of principle cells in the collecting duct. That activates GTP-associated protein which activates adenylate cyclase. cAMP activates PKA in the cytoplasm and PKA in the nucleus. In the nucleus, PKA phosphorylates various transcription factors and increases the synthesis of AQP2, 3, and 4. Activation of PKA in the cytoplasm phosphorylates AQP2. AQP2 is located in a subapical region (in vesicles) and when it is phosphorylated, the aquaporin 2 moves to the apical membrane, fuses with it, and makes it water permeable. When AQP2 in the membrane is dephosphorylated, it moves back to the subapical region and vesicles accumulate. There is a shuttling of AQP2 between apical membrane and subapical region that is ultimately under the influence of ADH.

AQP3 and 4 are located on the basolateral surface and are not thought to shuttle between sub-basolateral membrane and membrane; they tend to stay on the membrane. You can see that water flows in the CD across AQP2 on the apical surface and out the basolateral membrane via AQP3 and 4. Exactly how water transport occurs through the cytoplasm is currently unknown.

108
Q

AQP 2

A

AQP2 is located in a subapical region (in vesicles) and when it is phosphorylated, the aquaporin 2 moves to the apical membrane, fuses with it, and makes it water permeable. When AQP2 in the membrane is dephosphorylated, it moves back to the subapical region and vesicles accumulate. There is a shuttling of AQP2 between apical membrane and subapical region that is ultimately under the influence of ADH.

109
Q

AQP

A

AQP2 is located in a subapical region (in vesicles) and when it is phosphorylated, the aquaporin 2 moves to the apical membrane, fuses with it, and makes it water permeable. When AQP2 in the membrane is dephosphorylated, it moves back to the subapical region and vesicles accumulate. There is a shuttling of AQP2 between apical membrane and subapical region that is ultimately under the influence of ADH.

AQP3 and 4 are located on the basolateral surface and are not thought to shuttle between sub-basolateral membrane and membrane; they tend to stay on the membrane. You can see that water flows in the CD across AQP2 on the apical surface and out the basolateral membrane via AQP3 and 4. Exactly how water transport occurs through the cytoplasm is currently unknown.

110
Q

causes of hypernaturemia

A

requires loss of hypotonic body fluid

AND

Absence of thirst

OR inability to get sufficient water

111
Q

management of hypernaturemia

A

replace water rapidly if acute (less than three days)

slowing if greater than 3 days or unknown

if there is hypernaturemia + Na deficit - replace sodium first (isotonic fluids) and then replace water

112
Q

hyperglycemia and Na

A

without insulin - glucose is in blood - shifts water from ICF to ECF

lowers Na by 1.6 mEq per 100 mg/dl glucose

hyperglycemia can entirely account for hyponaturemia or not

113
Q

water deficit equation

A

((Na/144) -1) x TBW

114
Q

hyperglycemia and Na equation

A

what degree hyperglycemia accounts for hyponaturemia

1.6 mEq/L for 100 mg/dL

115
Q

if hyponaturemia and increased Posm?

A

hyperglycemia!!

116
Q

role of Uosm in presence of hyponaturemia?

A

indicator of the relative roles of the kidney’s ability to dilute and fluid intake ans contributors to the hyponaturemia

117
Q

if Uosm is low, what is the role of fluid intake in hyponaturemia?

A

high!! kidney is not having trouble - problem is likely intake

118
Q

max dilute urine

A

50-100 mosm

119
Q

primary polydipsia

A

hyponaturemia despite max dilution of urine!

episodic drinking in excess of normal kidney’s ability to excrete water

polyuria, low Na in urine

120
Q

hyponaturemia and max dilution of urine

A

failure of defense of Posm after water intake - hyponautemia

primary polydipia

tea and toast diet (poor intake of protein and salt

drinking beer

renal failure (can’t dilute)

failure to suppress ADH (SIADH)

There are also patients that dilute normally but have a limitation in the amount of urine they can excrete. This is because they have a decrease in the number of osmoles in their urine– elderly people that eat tea and toast, very low protein diets or diets that primarily consist of beer— very low in Na, K; lots of sugars and very little or no protein. The number of osmoles in their urine are very low, a total of maybe 100 mOsm/day. These people can only excrete 2 L/day even though the urine has a Uosm of 50. This is a group of patients with dilute urine that becomes hyponatremic. 2 groups: primary polydipisa and decreased urinary solute.

121
Q

low ECFV, low EABV

A

diarrhea glycosuria diuretics

hyponaturemia

122
Q

high ECFV, low EABV

A

cirrhosis, CHF, nephrotic syndrome

123
Q

high ECFV high EABV

A

ARF

CRF

124
Q

if Uosm > 100 mOsm/kg

A

evidence of ADH effect

125
Q

hyponaturmia in decreased EABV

A

replenishment of decreased ECFV or decreased EABV with relatively more water than Na in the presence of reduced water (and Na) excretion due to

failure to filter normal amts of water (decreased GFR)

failure to deliver water and solute to TALH (increased proximal Na reabsorption)

failure to suppress ADH

126
Q

hyponaturemia in high ECFV and high EABV

A

intake of more water than Na in presence of reduced water (and Na excretion) due to ARF or CRF

failure to filture nomral amts of water due to decreased GFR

127
Q

SIADH

A

if exclude other causes of euvolemic hyponaturemia - increased hypothalamic release of ADH (pain, stress, pulm disease, drugs) or ectopic release of ADH (tumors)

hyponaturemia

high Uosm

clinically normal ECFV

suppression of Na reabsorption by water expansion of ECFV - effect on vol receptors

high urine Na!

DECREASED serum uric acid!!

128
Q

treatment of hyponaturemia

A

low ECFV - give NS to turn of ADH secretion

high ECFV - water restrict, diuretics, ACEI

129
Q

treatment of symptomatic SIADH

A

3% saline and sometimes Lasix

increase Osm enough t get rid of yptoms

desmopressin (DDAVP) to slow rate of correction

130
Q

treatment of asymptomatic SIADH

A

water restrict

Tolvaptam (ADH antagonist)

correct slowly!!! brain swelling

131
Q

osmotic demyelination syndrome

A

increase Na - opens BBB - C3 and cks get in and attack oligodendrocytes - demylination

rate of correction of chronic hyponaturemia is a risk

132
Q

Living Donor Kidney Pros

A

immediate funtion

longer lifespan

rapidly transplantable/able to plan

can avoid dialysis

elective scheduling

133
Q

deceased donor kidneys

A

delayed funtion

shorter lifespan

waitlist

unpredictable

134
Q

kidney graft survival

A

longer in living donors

135
Q

eligible for transplant?

A

GFR < 20

eval safety of immune suppression

eval safety

ensrure patient will be able to comply w regimen

136
Q

blood type w longest wait for transplant?

A

O - most common

137
Q

blood type with shortest wait for transplant

A

Ab

138
Q

heterotopic kidney

A

the new kidney is placed in the iliac fossa, native kidney remains in place

139
Q

meds post-transplant

A
  1. innunosuppresants (3)
  2. anti fungal, anti-viral, antibiotic
  3. anti hypertensives
140
Q

diet on dialysis

A

low sodium

low potassium

low phosphate

limited fluids

141
Q

immune response against transplant

A

once activated, t cells clonally expand - induce cytotoxic t cell activity, help b cellss make antibodies and help macrophages induce delayed hypersensivity

MHC!!

142
Q
A
143
Q

what can impair autoregulation?

A

NSAIDs, ACEi, vascular disase, CKD, chronically elevated BP

144
Q

impaired autoregulation threshold

A

when MAP <80 mm - autoregulation can’t work and GFR falls

145
Q

definition of ARF

A

ABRUPT fall in GFR by

increase creatinine by .5 or 50% over baseline

oliguria

decline in GFR to require dialysis

146
Q

causes of ARF

A

pre-renal

intrinsic

post-renal (obstruction)

147
Q

pre-renal definition

A

fall in RBF leading to fall P of glomerulus

148
Q

intrinsic ARF definition

A

fall in K(f)

fall in RBF

increase in P(t)

  • Intrinsic acute renal failure, which may result from anything happening in the kidney tissue/parenchyma itself
  • This may affect the ultrafiltration coefficient, e.g. the permeability or surface area of the membrane

It may result in a fall in renal blood flow, or a rise in tubular pressure

149
Q

post renal ARF definition

A

increase in Pt

  • Post-renal acute renal failure is typically caused by an obstruction to the flow of urine in the renal pelvis or distal to that
  • Obstruction initially increases the tubular pressure—the pressure increases proximal to the obstruction

When tubular pressure equals the glomerular pressure, filtration will stop

150
Q

Fe Na

A

percentage of filered Na that is excreted in the urine

U(na) x P(cr) / P(na) x U(cr)

x100

151
Q

pre renal urine

dipstick

micro

Uosm

FeNa

A

min protein

no micro

high osmolarity (low water)

lower Na

152
Q

interstitial urine

dipstick

micro

Uosm

FeNa+

A

tubular protein,

casts, RBC, WBC

low Uosm (a lot of water)

>1% Na - getting rid of Na

153
Q

post-renal urine

dipstick

micro

Osm

FeNa+

A

min protein

everything varies

154
Q

causes of low perfusion states

A

hypovolemia

low CO

distributive (sepsis, vasodilators)

renal (renal artery stenosis, drugs)

155
Q
A
156
Q

treatment of low perfusion states

A

effective treatment of vol loss, infection, reversible causes of impaired autoregulation

avoid additional insults (toxins, infections)

157
Q

Intrinsic ARF

A

ischemia and toxins

158
Q

sediment in prerenal vs ATN/AKI

A

pre renal - normal or occ hyaline

ATN - epithelial cells, grnular and muddy casts

159
Q

pathology of ATN/AKI

A

ischemia or toxins damage the tubular cells - leads to sloughing of brush border and cells into lumen w cast formation

decrease in GFR is out of proportion to pathological changes

160
Q

mechanisms of decreased GFR in ATN/AKI

A

hemodynamic (hypoperfusion or vasoconstriction of outer medulla)

alteration of tubule cell structure (necrosis and apoptosis)

tubular obstruction

activation of Tubulo Glomerular feedback

161
Q

ischemic damage to the tubule - where is it the worst?

A

the outer medulla! relatively hypoxic

oxygen demand is high because of transport

  • The cartoon shows the cortex, medulla and the thick ascending limb
  • In this portion of the kidney, in the thick ascending limb, there is a high oxygen demand because this is where the NKCC transporter lives
  • This transport takes up a lot of oxygen
  • In addition, the vasa recta are shunting blood around the ascending limb
  • This is how the medullary interstitial gradient is generated, which allows for concentration of the urine
  • In this segment of the kidney particularly, the balance between oxygen delivery and oxygen demand is pretty precarious
  • This segment is very sensitive to any decrease in oxygen supply
  • When oxygen demand exceeds oxygen supply, there is ischemic damage, ischemic reperfusion injury, free radicals, etc.
  • This is one possibility as to why ischemia causes tubular damage
162
Q

pathophysiology of ATN/AKI

A
  • This is a little more detailed view of the various mechanisms that are proposed to explain why GFR falls so much in tubular injury
  • Note: the peritubular capillary is shown at left
  • If you have shock, toxins, you have endothelial damage, an increase in adhesion molecules, and the inflammatory cells can enter the tubular lumen
  • There are cytokines that damage the tubular cells
  • In the proximal tubule (to the right of the peritubular capillary), you either lose the integrity of the cells, or lose cells entirely
  • When this occurs, there is nothing to protect the basement membrane from allowing the filtrate in the lumen to leak back into the circulation
  • You can filter urea, for example, but if it leaks back, it will not be excreted
  • These cells lose microvilli, some become necrotic or apoptotic and slough off in the tubular lumen à they no longer function like normal tubular cells
  • The image at right shows a region later on in the distal portion of the nephron
  • That image is a picture of tubular cells now contacting Tamm-Horsfall proteins, polymerizing with the protein, adhering to one another and forming a cast that now obstructs the tubular lumen and will prevent urine flow

It is a combination of ischemic damage, necrosis, loss of normal polarization of the tubular cells, cast formation, back leak à these all lead to renal failure when you have toxic or ischemic damage to the tubules

163
Q

alterations in tubule cell structure after ischemic AKI

A

loss of brush border and polarity

necrosis and apoptosis

sloughing off of cells w lumenal obstruction

dedifferentiation of viable cells

164
Q

tubuloglomerular feedback

A

decreased Na reabsorption in the proximal tubule increases delivery to the MD signalling the glomerulus to reduce GFR

165
Q

treatment of ATN/AKI

A

treat infection, support BP, avoid insults

duiretics to increase urine output

bicarb for acidosis if needed

limit Na, water, K intake

adjust meds for reduced GFR

166
Q

postrenal ARF

A

GFR falls when tubular pressure rises and gradient favoring filtration falls

for renal failure, obst must be bilat or in patient w only one kidney - not ruled out w normal urine output

167
Q

treatment of post-renal ARF

A

remove obstruction

168
Q

timecourse of glomerular hemodynamics in obstruction

A
  • The kidneys are designed to protect themselves
  • The first thing that happens in obstruction is the tubular pressure goes up
  • The kidneys think they may need more blood flow in order to overcome that
  • Afferent resistance will go down
  • Glomerular pressure will rise in an attempt to balance tubular pressure
  • Depending on how severe the obstruction is, the glomerular filtration rate (GFR) may not initially fall
  • If the tubular pressure stays very high, the kidney now knows any further perfusion will deleterious
  • Therefore, you have renal vasoconstriction that causes glomerular pressure to be lower and GFR falls still further
  • After you relieve the obstruction, it takes some time—not too long, but a little while—for the decrease in tubular pressure to be reflected in a decrease in afferent resistance
  • This is less than 24 hours, but you may not see an immediate increase in GFR
  • It may take time because the tubular obstruction has set off all of these compensatory mechanisms to try to initially maintain GFR and then prevent further damage
  • The take-home message in obstruction: tubular pressure goes up, GFR goes down
  • When you relieve the obstruction, this recovers within 24 hours
169
Q

Definition of chronic kidney disease

A

GFR < 60 for 3 months with or without kidney damage

OR

kidney damage for greater than 3 months with or without decreased GFR manifested by either pathologic abnormalities or markers of kidney damage

170
Q

end stage renal disease definiton

A

CKD requiring dialysis or transplant

171
Q

stages of CKD

A

1 - GFR > 90

2 60-89

3 GFR 30-59

4 15-29

5 less than 15

172
Q

ApoL1

A

african americans - 1 allele protects against trypanosomes

2 alleles increase the risk for kidney disease, FSGS and HIV nepropathy

circulating domain that pokes holes in trypanosimes

173
Q

major cause of death in CKD?

A

cardiovascular disease

174
Q

lipoprotein abnormalities in CKD

A

low cholesterol, low LDL, high TG

treat with a statin - lowers all cause mortality, CV death, non CV mortality

what is uremic toxin leads to heart disease?

175
Q

primary kidney disease

A

diabetes, GSFS MPGN IgA, membranous. post strep

always treat underlying kidney disease!

176
Q

secondary kidney disease

A

once a critical reduction of renal mass occurs, either by initiating disase or surgical removal of a kidney tissue, progressive rena; failure can ensue by a set of common mechanisms

177
Q

intact nephron hypothesis

A

lose nephrons as units

what remain are intact functional nephrons that must compensate for the loss of function of the lost neprons

try to compensate and damage themselves

increase single nephron GFR by increasing glomerular capillary P - hypertrophy

glomerular plasma low, pressure, filtrtion rate increases

178
Q

TGF beta in secondary ckd

A

endothelial cells: mechanical stretch activate EC to secrete factors that cause fibrosis

mesangial cell - mechanical stretch - narrowing

179
Q

how to decrease glomerular capillary pressure in CKD?

A
  1. control BP
  2. use ACEI as first line therapy
180
Q

How do we prevent the progression of CKD

A

inhibiting RAS

181
Q

how do we treat proteinuria in CKD

A

RAAS! antiprtoeinuric effects are due to direct effect of ATII on permeability barrier (podocyte) and decreas intraglomerular P

182
Q

how does proteinuria contribute to progression of ckd?

A

increased filtered albumin is taken up by PT

accumulate in cytoplasm - perturbation of cell function - recruit macrphages and T cells, activate TGF beta - bind to cells

fibroblast proliferation and matrix depositioon

183
Q

how do you treat proteinuria?

A

ACI, ARB

184
Q

causes that contribute to progression of renal failure

A

metabolic acidosis

high phosphate

smoking

obesity

hyperlipidemia

african american

185
Q

CKD and acedemia

A

CKD causes acidemia - increase interstitial fibrosis

This is just to highlight, because it is really important, that a lot of the things that you do, there’s not good data. There is good data for angiotensin system for progression. There is good data if you can decrease proteinuria. There is also data for treating the acidosis, for preventing progression. I mean, controlled trials that if you treat with bicarbonate and get the serum bicarbonate to normal, you will preserve kidney function. So ammonia can increase renal acid production, can activate complement, can activate a cytokine called endothelin.

186
Q

indicartions for starting dialysis

A

uremic symotms

hyperkalemia and acidosis

fluid overload or HTN

187
Q

30-20-10 rule

A

for GFR

30 - educate, referral for transplant

20 - create fistula

10 - start HD

188
Q

HIF-1

A

There is a transcription factor regulated by oxygen called HIF-1 (hypoxia inducible factor), which under normal conditions when oxygen is present, it is degraded. When oxygen is very low, the enzyme that causes it to get degraded, a prolyl hydroxylase, gets inhibited, and so HIF-1 is not degraded. It accumulates, it goes to the nucleus. It turns on erythropoietin, which then circulates and goes to the bone marrow, and commits RBCs to differentiate. If you don’t have kidney’s, your erythropoietin levels are low.

189
Q

anemia in CKD

A

kidney makes erythrpoetin - interstitial fibroblast senses O2 content/RBCs and if it decreases turns on erythropoetin

give recombinant erythropoeitin

190
Q

darbepoetin alfa

A

binds to same receptors with same mechanism as endogenous erythropoeitin

carb chains to increase half life

guidelines: do NOT go to Hgb> 12

191
Q

PO4 and PTH

A

So here is sort of the standard idea. As you lose kidney function, phosphorus goes up, it then will combine with calcium and precipitate in the bone. (Something about lay down in the bone and could be … go other ways? Could not make out sentence/clause). So high phosphorus will eventually lower in the serum the free ionized calcium. That sets (?) by the parathyroid gland and the parathyroid gland will make PTH, which then goes and circulates, and will stimulate and tell the osteoclasts to break down more bone and release calcium.

192
Q

Ca and Vit D

A

vitamin D needs to be activated by 2 ways, there is a 25 hydroxylase in the liver and then a one (hydroxylase?) in the kidney. So 1,25 (OH)2D is your active vitamin D. If you don’t have kidney function your 1,25 is decreased. That’s important for calcium reabsorption for the gut. So that’s another reason why your calcium could be low.

directly suppresses PTH in parathyroid

193
Q

tadeoff hypothesis

A

decreased nephron mass - decrease PO4 clearance - increased PO4 - decrease C, decreased D - increased PTH

also high FGF 23

194
Q

FGF 23

A

, fibroblast growth factor 23, this is actually one of the major stimuli for the kidney to decrease reabsorption of phosphorus. And it blocks phosphorus reabsorption by the kidney. So what happens is as you lose kidney function, phosphorus goes up, FGF23 is made to try to… is one of the other… maybe more important than PTH. FGF23 then causes increased phosphate loss, but FGF23 does a lot of other things. It can lower 1,25. It blocks the 1 hydroxylase. So it lowers vitamin D, which has its other effects.

195
Q

secondary hyperparathyroidism

A

increased osteoclast activation and bone resorption

196
Q

osteitis fibrosa cystica

A

painful bones - increased osteoclast - fractures

The disease that you get from hyperparathyroidism is a disease called osteitis fibrosa cystica where the osteoclasts are activated. They resorb bone and you get really painful bones, the patients will tell you their body aches all over. They can develop actual cysts in the bone and it can actually be crippling. That should never happen anymore, we can actually treat it. How do you treat it, really quickly?

197
Q

how do you treat hyperparathyroidism?

A

restrict phosphorus

oral phosphate binders (bind phosphate so not absorbed)

give vit d (decreases PTH syntehsiss and serum Ca levels)

198
Q
A
199
Q

What is removed in dialysis?

A

creatinine and urea

surrigates for uremic toxins

200
Q

mean survival of patients on hemodialysis

A

2.5 years

major COD is cardiovascular - HF, SCD, arrhythmias

atherolsclerosis but not by traditional risk factors

201
Q

Organic Anion Transporters

A

OATs

on cell membranes in PT and endothelium

transport many small protein bound solutes (? uremic toxins)

202
Q

indoxyl sulfate

A

candidate for uremic toxins - when administered to nephrectomized rats - accelerated renal scarring and changed the expression of many genes

mimics the effect of uremia on gene expression

gene dysregulation not corrected by dialysis (leading to cardiac death) may be due to IS which is poorly dialyzable!!!

203
Q

indoxyl sulfate mechanism

A

signals gene transcription (like a steroid hormone) in nucleus

transported by OAT in proximal tubule

204
Q

Anglerfish hypothesis

A

patients with end stage renal disease who rentain residual renal function (continue to produce urine) have better survival and less CV disease than patients who do not produce urine

? reflects activtiy of PT transporters and the small quantity of urine produced has IS (or another uremic toxin) elim of toxic products could serve survival function

205
Q

Where is indoxyl sulfate made?

A

in the gut! gut derived

binds albumin

206
Q
A
207
Q

hyperchloremic acidosis

A

gain of HCl!!

RTA (I, II, IV)

Diarrhea (loss of HCO3 = gain of HCl)

208
Q

anion gap acidosis

A

gain of HA, A is not Cl

ingestions

ketoacidosis

lactic acidosis

renal failure

209
Q

diarrhea acid-base abnormality

A

hyperchloemic metabolic acidosis

loss of stool (NaCl, KCl, NaHCO3) = gain of H+

decrease serum HCO3, decrease amt filtered

Kidney must reabsorb Na (esp bc high renin, low vol)

Renal Na reapsorption is accompanied by more Cl becaue no HCO3 is available!

210
Q

lactic acidosis acid-base abnormality

A

anion gap metabolic acidosis (gain of acid w non-Cl anion)

anaerobic metabolism

H+lactate- added to the plasma

H+ titrates HCO3 - decrease HCO3 - lactate replaces HCO3 in serum

211
Q

anion gap

A

electroneutrlity requires that cations = anions

Na + UC = Cl + HCO3 + UA

even thugh everything is measured we pretend it is not

212
Q

Anion gap calculation

A

Na - Cl - HCO3 = UA-UC = Anion Gap

nl = 6-12

(major UA is albumin)

213
Q

causes of anion gap metabolic acidosis

A

M — Methanol

U — Uremia (chronic kidney failure)

D — Diabetic ketoacidosis

P — Propylene glycol (“P” used to stand for Paraldehyde but this substance is not commonly used today)

I — Infection, Iron, Isoniazid, Inborn errors of metabolism

L — Lactic acidosis

E — Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.)

S — Salicylates

214
Q

Distal RTA (Type I)

A

distal tubular defect in H+ ion secretion (congenital or acquired)

decreased rate of H+ ion secretion - can’t get rid of daily proton load

urine pH > 5.5 (can’t acidify)

hyperchloremic metabolic acidosis (like gain of HCl)

H+ + Bone –> hypercalciuria and osteoporosis

215
Q

urine in type I RTA

A

high urine pH

high urine calcium

low urine citrate

calcium phosphate stones common bc citrate stops it!!

216
Q

Type II RTA

A

proximal tubular defect in H+ ion secretion

impaired HCO3 reabsorption in the PT

congenital or acquired - ocular abnormalities

still able to max acidify urine (pH < 5.5)

hyperchloremic acidosis but patients are in acid balance! To maintain Na - reabsorb Cl (really low HCO3)

No hypercalciuria or stones

if give HCO3 - pee it right out bc can’t reabsorb

217
Q

Urine in type II RTA

A

can max acidify urine!

hyperchloremic acidosis but still in acid balance (unlike distal) - no hypercalciuria or stones

reabsorb Cl with Na because no HCO3

218
Q

type IV RTA

A

hyporenin/hypoaldo is primary defect

conmmon in DM and with spiro/ACEI

hypoaldo –> hyperkalemia

hyperkalemia inhibits glutaminase activity and NH4 generation - no urinary buffer so urine is acidic

hyperchloremic metabolic acidosis

219
Q

urine in type IV renal failure

A

lack of urinary buffer (no NH3) leads to acidified urine

220
Q

acidosis of renal failre

A

GFR < 30

results from impaired ammonia synthesis because of reduced nephron mass in CKD

max acidified urine though patients are not in acid balance!! (remaining intact nephrons acidify urine)

lower GFR means less nephrons to get rid of acid

anion gap variable - depeneds on retention of SO4, PO4

221
Q

metabolic alkalosis

A

decrease in H due to increase in HCO3

2 components:

generation (cause of increased HCO3)

maintenence (reason kidney’s can’t excrete it)

i.e. eat HCO3 - usually NO maintenence (volume expansion - decrease in RAS - rapid excretion of HCO3_

222
Q

vomiting acid-base disorder

A

generation: Lose H, Cl

usually when secrete H into stomach, HCO3 goes into blood but in balance because HCO3 into duodenum so in balance

instead - no H entry into duodenum and no balance

high HCO3 in serum - urinary losses of Na and K - filtred HCO3 exceeds threshold of of PT

maintenence:

since lost Na and K - decrease in ECFV - increase in renin and aldo

increase serum HCO3 - Cl is low so reabsorb Na with HCO3

Cl responsive metabilic alkalosis (low Cl)

223
Q

urine in vomiting

A

low Cl!

Cl responsive!!

224
Q

Cl unresponsive metabolic alkalosis

A

UCl > 20

225
Q

paradoxic aciduria

A

during maintenence phase of vomiting, filtered HCO3 is being reabsorbed in proximal tubule - HCO3 is high but none in urine bc reabsorbing all of it

226
Q

Role of K in metabolic alkalosis maintenance

A

K loss leads to shift K out of cells and H in despite alkalosis

stim ammoniagenesis - H is being secreted so HCO3 reabsorption

227
Q

contraction alkalosis

A

loss of fluid relatively high in Cl

leads to a higher [HCO3]

does not account for the kidney!

diuretics cause

228
Q

diuretics and acid base disorders

A

Cl responsive metabolic alkalosis

  1. generation phase - loss of NaCl in TALK, higher [HCO2] results ue to loss of Cl - contraction alkalosis
  2. maintenance phase - decrease EABV - renin and AII and Aldo - Na distally leads to hypokalemia
229
Q

Gitelman syndrome

A

like taking thiazides

hypokalemic metabolic alkalosis - salt losing (hyperrenin/aldo)

230
Q

Bartter syndrome

A

like taking furosemide

hypokalemic hetabolic alkalosis

salt losing

hypomag

NOT hypocalciuria

231
Q

primary hyperaldo

A

Cl unresoonsive metabilic acidosis

continued NaCl delivery to CCD

Renin, ATII suppressed - turns off proximal Na reabsorption

NOT cl depleted so it’ won’t help

232
Q

conditions with LOW urine Cl

A

vomiting

diuretics (when not acting)

CF

low chloride intake

233
Q

conditions with HIGH urine Cl

A

primary hyperaldo

diuretics (acting)

alklai admin

bartters/gitelmans

severe hypokalemia

234
Q

treatment for low UCl

A

replete ECFV

replete Cl (NaCl, KCl)

235
Q
A

Renal 2 (4 decks)

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