Chronic Renal Failure CIS Flashcards
stage 1 CKD
GFR > 90
*diabetics
stage 2 CKD
GFR 60-89
stage 3 CKD
GFR 30-59
chronic kidney disease**
stage 3 for 3 months
70% of CKD**
HTN or DM
then GN and cystic disease
then prostate and tubulointerstitial disease
important signs of CKD
bone disease anemia broad waxy casts paresthesias bilateral small kidneys
decreased GFR causing HTN
decreased sodium > turns on sympathetics > turns on RAAS
therefore - get sodium and water retention
bone disease and CKD
PTH
- normally inhibits P reabsorption and increases Ca reabsorption
- CKD - no 1,25 hydrox of Vit D
- decreased PTH and no Ca reabsorption
phosphate vs. calcium
decreased GFR
- PTH can’t get rid of P
- P goes up, and Ca goes down
decreased GFR and P/Ca
increased P and decreased Ca
Vit D metabolism
1 hydrox - liver
25 hydrox - kidney (prox tub)
- therefore don’t get Vit D
- calcium low
low Ca
activates PTH release
- increased osteoclast bone resorption
- get osteitis fibrosia cystica
anemia and CKD
no erythropoietin
isosthenuria
same concentrated urine
-with CKD
waxy broad casts
chronic renal disease
subepithelial deposit humps
IgG and C3
hematuria and RBC casts
complement low
immune complex disorder
-post-infectious GN
shunt -staph
synpharyngitic hematuria
same time as infection
post-strep week later**
mesangium
IgA nephropathy
-most common in world
prognosis with proteinuria?
more proteinuria - gets worse
bergers disease
IgA nephropathy
-IgA1 - galactose deficiency in O-linked glycans
diseases with altered IgA - hepatic cirrhosis, HIV, CMV, celiac disease
IgA nephropathy with arthralgia, nausea, colic, melena, rash
henoch-schonlein
heamturia, rash, P-ANCA, RBC casts
microscopic polyangitis
P-ANCA
microscopic polyangitis (churg strauss) -no granulomatous inflammation and no upper resp involvement**
C-ANCA
granulomatosis with polyangitis
-wegeners
pauci immune
not immune complex
-but instead neutrophil activation
ANCA type**
formation of ANCAs
MPO - antibodies to strong cations - pANCA
PR3 - antibodies to neutral/weak cations - cANCA
pANCA
anti-MPO - strong cations
cANCA
anti-PR3 - neutral/weak cations
anti-GMB disease
alpha 3 chain of type IV collagen
linear antibody deposition
goodpasture
or anti-GMB GN
hematuria, hepatosplenomegaly, cold night purpura, RBC casts, hep C positive
essential mixed cryoglobulinemia
cryoglobulinemia
hep C
-antibodies against antibodies
cold aggultinin
mycoplasm
type 1 cryoglobulinemia
cancers of blood and immune system
type 2 and 3 cryoglobulinemia
autoimmune diseases and viruses (Hep C)
ultimate causes of lots of disorders
malignancy
autoimmune
infection
drugs
best initial treatment for most CKD patients
ACE inhibitors
-unless Cr over 3**
type I MPGN
subendo and subepi
- complement low (C3 and C4)***
- tram-tracking
typically with Hep C virus
type II MPGN
- complement normal
- dense deposit disease
Hep C virus**
1 type I MPGN (nephritic
2 mixed cryoglobulinemia (nephritic)
3 membranous nephropathy (nephrotic)
type II MPGN
dense deposit disease
- alternate complement
- C3 low, C4 normal***
- ribbon like deposits
low C3
type II MPGN
low C3 and C4
type I MPGN
Tx for nephritic
ACE (-)** - for proteinuria
methylpredisolone for proteinuria > 1 g/day and GFR >70
cyclophosphamide for GFR <70 and prediction to ESRD within 5 years
black, HIV, heroin, HTN, periorbital edema, oval fat bodies
likely FSGS
FSGS
focal and segmental
- polymorphisms in APOL1 gene (blacks)
- C1q nephropathy
HIV, heroin, obesity, UV reflux
lymphoma, edema, weight gain, recurrent infections, dyspnea, thickened GBM with spike and dome of subepithelial deposits
membranous GN
membranous GN
cause - lymphoma, carcinoma, PCN, gold, SLE, MCTD, thyroiditis, Hep B/C, endocarditis, syphilis
IgG and C3 spike and dome subepithelial deposits
PLA2
hereditary membranous GN
alpha-1 antithrombin***
gets through the glomerulus
- get clotting
- nephrotic syndrome
nephrotic
loss of antithrombin III
protein C
protein S
increased lipoprotein, fibrinogen, and platelet aggregation
causes of chronic tubulointerstitial disease**
proud american veterans love GM
prostate analgesics VUR lead gout myeloma
back pain and increased sed rate
multiple myeloma
non-anion gap acidosis**
hyperchloremic acidosis**
myeloma
can give you low anion gap
RTA type I
distal tubules
-failure of H secretion by alpha intercalated cells
urine pH >5.5 (cannot secrete protons to acidify urine)
basic urine**
RTA type II
proximal
-failure of HCO3 reabsorption in prox tub
RTA type IV
adrenal
-aldosterone deficiency
get high potassium**
multiple myeloma
damage prox tubule
-RTA type II
causes of type I RTA**
ampoteracin B
hyper PTH
sjogrens
distal tubule H secretion problems
causes of type II RTA**
myeloma protein, tenovofir, toluene, acetazolamide, toperimate, zonisamide
Cl/HCO3 relationship
Cl high - bicarb low
> metabolic alkalosis
fanconi syndrome
bence jones proteins damaged prox tub and caused to leak HCO3
myeloma kidney
high Ca high uric amyloidosis B cell infiltrates hyperviscosity
