Chronic Kidney Disease Darrow CIS Flashcards
(84 cards)
1
Q
Stage 3 for 3 months is considered to be
A
Chronic kidney disease
2
Q
stage 2 symptoms
A
htn
3
Q
stage 3 symptoms
A
Increaase pth
anema
4
Q
increase 4 symptoms
A
increase phosphorous
acidosis and hyperkalemia
5
Q
stage 5 symptoms
A
uremic syndrome
6
Q
chronic renal disease causes
A
70% of cases are caused by diabetes or hypertension with GNand the cystic diseases accounting for another 12%. Prostatic obstructionand the tubulointerstitialdiseasesmake up the rest.
7
Q
list of symptoms for chronic renal disease
A
- Hypertension, edema, CHF
- Bone disease
- Anemia
- Isosthenuriaand broad waxy casts
- Acidosis
- Hyperkalemia
- Progressive azotemia over months to years (end stage: fatigue weakness, malaise, nausea, vomiting, etc.)
- Paresthesias
- Bilateral small kidneys
8
Q
what causes htn edem and chf in chronic renal disease
A
na and h20 retention
9
Q
A patient with severe diabetes and renal failure presents with
complaints of proximal muscle weakness and bone pain in the arms
and legs.
Bun is 60 with creatinineof 6 mg/dL. K is 5.5 mg/dL. Phosphorus is 5.9
meq/l (n = 2.4-4.1). Calcium is 7.2 mg/dL(n= 8-11).
What is causing renal osteodystrophyand bone pain in this patient?
A
PTH
10
Q
What is the mechanism of the bone disease in CRF?
A
(increased P, decreased Ca and VitD, increased PTH, acidosis)
11
Q
Renal disease=
A
decrease GFR = increase phosphate= decrease calcium*(#1)
*Calcium is decreased due to
increased P and decreased vitD.
12
Q
Renal disease = decrease 1-alpha hydroxylaseactivity =
A
decrease vitamin D production(#2
13
Q
Both hypo and hyper magnesemiaresult in
A
decreased PTH
production and secretion and thus hypocalcemia
14
Q
Continuouslyelevated PTH drives
A
the osteoblastto produce RANKL
and thus more osteoclastactivity with bone resorption, ie. osteitis
fibrosacystica! In the mean time, low vitamin D levels produce
osteomalacia!
At the same time, the acidosis(H+) of renal
disease leads to bone resorptiondue to
buffering by carbonate and phosphates.
- Osteoclast activity also increased by hyponatremia
15
Q
Anemia in chronic renal disease
A
decreased epo
16
Q
itothenuria and broad waxy casts in chronic renal disease
A
tubular destruction
17
Q
acisosi in chronic renal disease
A
hyperchloremic versus anion gap
18
Q
hyperkaliemia in chornic renal disease
A
not secreting
19
Q
progressive azotemia over months to years in chronic renal disease
A
(
20
Q
paresthesias in chronic renal disease
A
uremic toxins
21
Q
bilateral small kidneys in chronic renal disease
A
fibrosis
22
Q
releasing proinflammatory tnf il6 il1
this is what youre trying to fight
A
dendritic cell macrophage endothelial cell mesangial cell podocyte tubular epithelial cell
23
Q
Chronic renal failure
Nephritic Spectrum Glomerular Diseases
A
- PostinfectiousGlomerulonephritis(GN)
- IgA nephropathy
- Henoch-Schönlein
- Pauci-immune GN
- Anti-glomerular Basement membrane GN
- Cryoglobulin-Associated GN
- MembranoproliferativeGN
- Hepatitis C Infection
- SLE
24
Q
A 16 y/o male, who has a ventriculoperitonealshunt, presents with a two week history of febrile episodes and pedal edema. Three days ago he noticed the onset of blood in his urine. Urinalysis confirms dysmorphicred blood cells, red cell casts and mild proteinuria. Serum complement level is low. Electron microscopy shows subepithelialdeposits (“humps”) of IgGand C3. This is most likely which type of glomerulonephritis?
A
•E. Immune complex
This is post infectious GN.
25
Subepithelial“humps”
of trapped immune complexes
seen with
glomerulonephritis
26
An 18 y/o male patient presents with cola colored urine one day after onset of a URI. Urine dipstick is positive for blood and protein. Urine protein/creatinineratio is 2.0 (N=
synpharyngitichematuria.
IGA nepropathy
no complement and IGA doesnt go through that
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200 mg protein per
24 hours
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complement pathwasy
ci1q is normal that goes to c243
c3 right away (alternative)
letin pathway
29
IGA is concurrent with
infection
30
Berger’s disease –IgAnephropathy
Deposits of aberrant IgA1 which exhibits galactosedeficiency in the O-linked glycansin the
hinge region of the heavy chain resulting in antibody formation and immune complexes.
Complexes with galactose-deficient IgA1 induce
cultured human mesangialcells to proliferate,
secrete extracellular matrix components, and release
humoralfactors such as TNFα, IL-6, and TGFβ.
31
This patient’s level of proteinuriaindicates that he will most
likely go on to develop HTN and chronic renal failure. He is
certainly a candidate for ACE inhibitors, steroids and possibly
even cyclophosphamide and azathioprine.
If the above patient presented with additional complaints of
arthralgias, nausea, colic, melena, and the following palpable rash,
it would be compatible with:
Henoch-Schöleinpurpura
32
Henoch-Schöleinpurpura
IGA skin vasculitis
IgA nephropathy with glycosylated IgA*
deposits may also be found in
hepatic cirrhosis, HIV, CMV and Celiac
disease, as well as part of HSP
33
IGA vasculitis
inflammation of glomerular capillaries
iga deposits in glomerulus viewed by immunofluorescence microscopy
34
IGA skin vasculitis
inflammation of small vessels in the skin
igan deposits in small vessels in the skin viewed by immunofluorescence microscopy
35
This patient with palpable purpurahas fever, weight loss, and hematuria. History is negative for asthma or eosinophilia. RBC casts are found on UA. Blood test show P-ANCA to be present. Renal biopsy shows rapidly progressive GN. This patient has:
microscopic polyangitis.
36
Pauci-immune Glomerulonephritis: The ANCAs
This is an ANCA associated or Pauci-immune GMN (ANCAs lead to neutrophilicactivation* which along with a cell mediated immune response results in vessel damage/vasculitis.
ethanol fixation
37
P-ANCA (perinuclear antimyeloperoxidase neutrophilcytoplasmicantibodies)
= Churg-Strauss and Microscopic Polyangitis. MPA does not have granulomatous inflammation and does not involve the upper respiratory tract as does granulomatosis with polyangitis.
ie, anti-MPO
abs
38
C-ANCA (cytoplasmic antiproteinase-3 antibodies) =
granulomatosiswith polyangitis(formerly Wegener’s granulomatosis)
PR3
39
ChurgStrauss is actually now classified as
an eosinophilic(IL 5) disease.
40
Priming causes PR3 and MPO to be expressed on neutrophilmembrane
where binding with antibodies is facilitated, thus resulting in the production of reactive oxygen species and release of proteolyticenzymes.
41
Anti-GlomerularBasement Membrane Disease
The principal target for the anti-GBM antibodies (which are
typically IgG1 and 3) is the NC1 domain of the alpha-3
chain of type IV collagen(alpha-3(IV) chain), one of six
genetically distinct gene products found in basement
membrane collagen.
Linear anti-basement membrane
antibodies as in Goodpasturesor
anti-GBM GN
hemoptysisand hematuria
42
This patient presented with hematuria, arthralgias, and hepatosplenomegaly, having spent a coldnight at the ballpark one week ago. Serum complement levels are depressed and RF is positive. There are RBC cast present in the urine. The patient is hepatitis C positive. Renal biopsy shows a cresenticpattern This patient has:
essential mixed cryoglobulinemia
43
essential mixed cryoglobulinemia
goes to crescented
44
cold agglutinin disease.
associated with anemia mono
45
Type I
occurs at the same time as cancers of the blood and immune system. Multiple myeloma,
chronic lymphocytic leukemia and Waldenstrom’smacroglobulinemiaare all cancers of this
type
46
Types II and III
are associated with diseases which include autoimmune diseases such
as systemic lupus erythematosusor Sjogren’ssyndrome, and virusessuch as hepatitis C* or HIV.
47
A 23 y/o female with a recent URI presents with gross hematuria and mild proteinuria. There is no edema. She is mildly hypertensive. C3 and C4 are low. Renal biopsy and immunofluorescence microscopy shows Ig + C3 depositisin the mesangiumand subendothelialcapillary wall. Electron microscopy shows “tramtracking”. Best initial treatment should
ACE inhibitor. - treats proteinuria by dialating the efferent arteriole
tramtracking so it is mebranoproliferative
48
MembranoProliferativeGN
Type I
Discrete immune complexes* are found in the mesangium, subendothelial
(and subepithelial) space. Immune complexes are combinations of antigens, antibodies, and
complement which bind to each other and then become lodged in the kidney This activates
the immune system, which causes inflammation and damage to the kidney itself. C3 and C4
are low.
“Tramtracking” seen in capillary wall remodeling.
49
Hepatitis C is associated with 3 glomerulopathies:
1. Immune complex mediated MPGN (nephritic, type I)
2. Mixed CryoglobulinemicGN (nephritic)
3. MembraneousNephropathy (nephrotic)
50
MembranoProliferativeGN
TypeII
This is also called dense deposit disease* with immunoglobulin staining for only C3.
When viewed under the microscope, continuous, dense ribbon-like deposits are found along
the basement membranes of the glomeruli,
tubules, and Bowman’s capsule. C3 is low.
complement is not blocked or getting broke down called c3 nephropathy
51
Treatment for Nephritic Diseases
1. Treat hypertension with ACE inhibitors.
2. Treat proteinuria with ACE inhibitors.
3. Add methylprednisolone for proteinuria > 1 gm/d and GFR > 70 mL/min. (for minimal change disease)
4. Add cyclophosphamide or mycophenolatemofetilfor GFR
52
Factor H
is not deactivating complement factor type IIc3 nephritic factor
53
Chronic Renal Failure
NephroticSpectrum Diseases in Primary Renal Diseases
Minimal change disease (children*)
Focal segmental glomerulosclerosis(FSGS)
Membranous
54
3 things found in nephrotic syndrom
proteinuria
hypoalbuminemia
hyperlipidemia
55
Focal segmental glomerulosclerosis(FSGS) predisposing factors
afroamerican hiv and heroin
56
An AfroAmericanHIV patient on heroin is referred to you from the ED after presenting with pedal, periorbitaledema, hypertension, and urine analysis showing oval fat bodies.
Renal biopsy shows podocyteinjury with areas of sclerosis. What is the most likely diagnosis?
Focal segmental glomerulosclerosis
57
oval fat bodies. think
think nephrotic syndome
58
Focal Segmental GlomeruloSclerosis
Idiopathic disease may be related to heritable abnormalities of any of several podocyteproteins, to polymorphisms in the APOL1gene* in those of African descent, or to increased levels of soluble urokinasereceptors. Additionalycalled C1q nephropathy. Also seen in UV reflux, morbid obesity, heroin abuse, and HIV.
*APOL1polymorphisms is also a variable in increased risk for HIV-associated nephropathy.
59
A 55 y/o male with non-Hodkinslymphoma presents with peripheral edema, 40 pound weight gain, and a history of recurrent infections over the past 6 months. The patient’s abdomen is prominent and he complains of dyspnea.
Urinalysis is shown. Serum vitamin D levels are low and albumin is 1.6 gm/dL. Spot urine for protein/creatinineratio is 6.5 (6.5 gm/24 hours). Kidney biopsy shows thickened GBM with “spike and dome pattern” of subepithelialdeposits. This patient has which type of renal nephroticpathology?
membranous
60
Membranous nephropathy
(as with lymphoma, carcinoma,
penicillamine, gold, SLE, MCTD, thyroiditis, hepatitis B and C,
endocarditis, syphilis), is caused by immune complex deposition (IgG
and C3 with “spike and dome”) in the subepithelialarea.
61
stage 1 membranous nephropathy
In Stage I, there are subepithelial, electron dense deposits with no projection of basement membrane; Stage II: well-defined
projections of basement membrane between deposits; Stage III: deposits are surrounded by basement membrane; Stage IV:
electron dense material fades creating 'holes' in the GBM; Stage V: repair of membrane.
62
The antigen in primary membranous nephropathy is
phospholipase A2 receptor
on the podocytemembrane. Secondary cases are due to infections(HepB and C,
endocarditis, syphilis), autoimmune diseases(SLE, MCTD, thyroiditis), carcinomas
and certain drugs(NSAIDs, captopril).
63
The above patient suddenly develops nausea and vomiting with
flank pain. Ultrasound shows bilateral kidney enlargement. The
patient has developed renal
vein thrombosis.
64
In nephroticsyndrome there is loss
of antithrombinIII, protein C and S, as well as increased fibrinogen, increased production of *lipoprotein (a) and increased platelet aggregation (with the latter three being due to low albumin)
see increased B or lp(a), fibrinogen on electrophoresis
65
Amyloidosis
NephroticSpectrum Diseases from Systemic Disorders
Amorphic, eosinophilic, PAS negative or scantly positive, extracellular substance not only
in glomeruli, but also in the wall of arteries and arterioles.
66
Diabetic Nephropathy
NephroticSpectrum Diseases from Systemic Disorders
number 1 cause of nephrotic
67
HIV –Associated Nephropathy
collapsing sclerosis
NephroticSpectrum Diseases from Systemic Disorders
68
Pauci-immune overview
vascular necrosis
ckd, proteinuria and haematuria
focal necrotizind glomerulonephritis and anca associated vasculitis
69
subendothelial immune complex deposits overview
endothelial cell injury
ckd, proteinurea and haematuria
lupus nephritis class 3 and 4
70
c3 depsotion overview
glomerular cell injury
asymptomatic proteinuria and microscopic haematuria
c3 glomerulopathy and ahus
71
mesangial immune complex depsotis
mesangial cell injury
asymptomatic proteinuria and microscopic haematuria
iga enphropathy and lupus nephritis class I and II
72
Linear immune complex deposits
endothelial cell and podocyte injury
ckd proteinuria and haematuria
antigbm disease
73
subepithelial immune complex deposits
```
podocyte injury
large proteinuria
membranous nephropathy
primary (pla2R)
secondary (lupus nephritis class V)
```
74
A 68 y/o male presents with polyuriaalternating with oliguriaand
1g/d proteinuria. History is positive for working with leadbase paint.
The patient recently finished a course of tetracyclinefor a UTI. BP is
164/90 and the patient has a suprapubicmass. Labs are as follows:
Na+138 meq/L, K+ 5.6 meq/L, HCO3-18 meq/L, Cl-110 meq/L
Urine: no eosinophils, no crystals, SG 1.010, casts as shown. broad and waxy
BUN 52 mg/dL, Creatinine2.2 mg/dL
Calcium 7.5 mg/dL, Phosphorus 5 mg/dL
Uric acid 4.5 mg/dL(3.5-7.7)
This man is most likely suffering from:
prostatic obsturction
75
Chronic TubulointerstitialDisease
characterized by
```
isosthenuriawith polyuria
moderate proteinuria
very few cells
type I, II or IV RTA
broad waxy casts
small kidneys
```
76
Chronic TubulointerstitialDisease
Causes
Proud American Veterans Love GM
```
Prostate(obstructive uropathy)
Analgesics (NSAIDs)
VU reflux
Lead (heavy metals)
Gout
Myeloma
```
77
A 55 y/o male presents with back pain and weight loss. He takes hydrochlorthiazidefor hypertension. Lab reports reveal a hemoglobin of 8 grams and a sedrate of 90 compatible with multiple myeloma. Further lab tests show:
Na+138 meq/L, K-3.2 meq/L
Cl-121 meq/L, HCO3-16 meq/L
BUN 20 mg/dL, Creatinine1.8 mg/dL
Urine pH is 5.0.
This patient has which type of acid base problem?
Type II RTA
78
type 1 rta
impaired dista acidification
nephrocalcinosis
plasma bicarb may be below 10
urin ph is greater than 5.3
plasma potassium is usually reduced but hyperkalemic fomrs exist, hypokalemia largely corrects with alkali therapy
causes:AmphoteracinB,
HyperparaT,
Sjogrenssyndrome,
Medullary sponge kidney
79
type 2rta
reduced proxima bicar reabsorption
plasma bicarb is usually 12 to 20
urine ph can acidiy to
80
type 4 rta
decreased aldosterone secretion or effect
plasma bicarb is greater than 17
urine ph is less than 5.3
plasma potassium is increased
```
Causes:
Diabetics, ACE inhibitors,
K sparing diuretics,
Obstruction, Interstitial
Nephritis, HIV, NSAIDs.
```
81
A 55 y/o male presents with back pain and weight loss. He takes hydrochlorthiazidefor hypertension. Lab reports reveal a hemoglobin of 8 grams and a sedrate of 90 compatible with multiple myeloma.Further lab tests show:
Na+138 meq/L, K-3.2 meq/L
Cl-121 meq/L, HCO3-16 meq/L
BUN 20 mg/dL, Creatinine1.8 mg/dL
Urine pH is 5.1.
What is true of the CL/HCO3 relationship in this patient?
Na+138 meq/L, K-3.2 meq/L
Cl-121 meq/L, HCO3-16 meq/L
The Cl-is increased by 21 meq/L, while the HCO3-is decreased by 9 meq/L indicating that the HCO3-is 12 meq/L higher than it should be or in other words there is in addition to the metabolic acidosis, a metabolic alkalosis.
82
in other words there is in addition to the metabolic acidosis, a metabolic alkalosis.
What is the cause of the low anion gap hyperchloremicmetabolic acidosisand the occult metabolic alkalosis?
patient was taking a thiazide which creates hypokalemic alkalosis
The light chains of MM (multiple myeloma) (BenceJones protein) have damaged the proximal tubule causing it to leak HCO3 as in the Fanconisyndrome.
83
Renal Disease of Myeloma
* “Myeloma kidney”
* Hypercalcemia
* Hyperuricemia
* Amyloidosis
* B cell infiltration
* Hyperviscosity
myeloma cells produce osteoclast activating (il1) factor, that causes bones to release calcium
84
Thiazide effect =
| Gitelman’ssyn
it produces the same syndrome as what is listed below
hypkalemic alkalosis with hypomganesemia and hypocalciuria
Diuretics cause hypokalemic alkalosis both by decreased plasma volume (contraction alkalosis)
and, even in the formers absence, by presenting increased luminal Na to the collecting duct
principle cells.
