nephrology 2 Flashcards
who should be tested
ppl >60 CKD HTN or DM blacks, native americans, hispanics and asians fx of kidney disease polycystic kidney disease
first sign of diabetic neuropathy
microalbuinuria
tx recommendations for state 3 and 4
decrese phosphorus intake and use phosphorus binder therapy
treat elevated PTH w/ vitamin D
normalize serum calcium
how to help prevent CKD from getting worst
alcohol awarness tobacco awarness (wellbutrin and patch) control lipids (niacin or statins) control BP (ACEI or ARBS) tight control of diabetes stay away from nephrotoxic meds (NSAIDS, be careful w/ abc)
what is leading cause of death in CKD pts
cardiovascular disease
most important predictors of poor outcome in ESRD
increasing age
CVD
diabetes
poor nutrition
KUB
looking for stones (has to be pretty big stones)
US
Ultrasound is very non invasive and is good to use to check the anatomy safe for pregnant women tell if mass is a cyst or solid detects obstruction Polycystic kidney disease Chronic renal failure maybe see stones
Intravenous pyelogram
suspect an obstruction to flow of urine
CT
CT is still the gold standard for: Renal stones Stage renal cell carcinoma Diagnose renal vein thrombosis Polycystic kidney disease
MRI
usually done on pts w/ CT contraindications
renal arteriography
Gold standard for renal artery stenosis
Renal arteriography used with suspected Polyarteritis nodosa… aneurysms
Renal venography
to determine if renal vein thrombosis
nuclear imaging
can predict GFR
good to evaluate for nephrectom
evaluates function
what detects vescouretal refulx
Voiding Cystourethrogram
Voiding Cystourethrogram
usually done in children w/ uti
in males evaluate for renal abnormalities
most accurate test for kidney stone
CT
A 64 year old man has a Cr of 2.3 and has been diagnosed with chronic renal failure. What is the best initial imaging test?
US
A 56 yo woman presents with flank pain and bloating. What would be your initial imaging test?
KUB (looking for stone)
Your patient has had 6-10 RBC’s on his UA x 3. All other labs are WNL. You decide to consult to nephrology. What would be the best initial study to do prior to him being seen by the specialist?
US
Along with renal venography and CT, MRI is reliable for the diagnosis of renal vein thrombosis. MRA is playing an increasing role in suspected renovascular hypertension
true
what is lost in nephrotic syndrome
albumin
Clotting proteins (antithrombin 3)
immunoglobulins
binding proteins ( stuff that bind vit D)
what is most common thrombosis in nephrotic syndrome
renal vein thrombosis
etiology of nephrotic syndrome
Adults:
systemic disease (lupus, DM, amyloidosis)
NSAIDS
minimal change disease, focal glomerulosclerosis, membranous nephropathy
Children:
minimal change disease
what happens in minimal change disease
fusion of podocytes
focal and segmental glomeruloscelrosis
Hard to treat so give prednisone for 6 months
Characterized by the presence in some of the glomeruli of segmental areas of mesangial collapse and sclerosis
Idiopathic syndrome or may be associated with issues such as HIV infection or massive obesity
since its only focal can do biopsy and might be negative
membranous glomerulopathy
Characterized by basement membrane thickening with little or no cellular proliferation or infiltration, presence of electron dense deposits across the basement membrane
Idiopathic but can be associated with processes such as hepatitis B, autoimmune diseases, cancer, or use of certain drugs
If do biopsy and come back positive for this need to do some other tests to check for cancer, etc
post strep glomerulnephritis
SUDDEN onset of gross hematuria edema HTN back pain oliguria renal insufficiency heart failure from volume overload azotemia
tetrad for henoch scholein purpura
palpable purpura w/out thrombocytopenia
arthralgias
abdominal pain
renal disease
HSP characterized by tissue deposition of IgA-containing immune complexes. its basically the same thing except IgA is only in kidney and HSP is systemic
IgA nephropathy
aka verger’s disease
Most common lesion to cause primary GN in the developed world
GROSS HEMATURIA (usually after URI)
protinuria
flank pain
diagnosis is confirmed w/ Prominent IgA deposits in the mesangium and along glomerular capillary walls
rapidly progressive glomerulonephritis
Crescent formation nonspecific response to severe injury to glomerular capillary wall
Development of fibrous crescents represent disease stage resistant to therapy**
principal signs are oliguria edema hematuria anemia
cause of rapidly progressive glomeurlonephritis
good pastures (anti GBM) Immune complex (ig A or post infectious strep) Pauci immune (few or no immune deposits)-ANCA (P and C)/Wegener’s Granulomatosis
presentation of rpg
Insidious onset: Fatigue Edema More acute onset: Macroscopic hematuria Oliguria Edema Renal insufficiency
tx or RPG
pulse methylprednisone
then daily prednisone
Oral or IV cyclophophamide
goodpastures
antibodies against GBM
pulmonary hemorrhage and RPGN with circulating antibodies against basement membrane antigens.
It has a course of rapidly progressive renal failure with hemoptysis, pulmonary infiltrates, dyspnea and renal failure.
Associated with cigarette exposure
ANCA disease
Anti neutrophil cytoplasmic antibody
Wegener’s granulomatosis
Biopsy shows no immunofluorescense: pauci-immune crescentic GN
C anka
cytoplasmic antibody
proteinase 3 antigen (PR3)
often w/ respiratory tract involvement
p anka
perinuclear staining
myeloperoxidase 3 (MP3)
only in kidney
membranoproliferative glomerulonephritis
accounts for 10% of all nephrotic syndrome in adults Thickening of GBM due to immune complex deposition presentation: decrease GFR acute glomerulonephritis nephrotic syndrome hematuria HTN
interstitial nephritis
Interstitial inflammatory response with edema and possible tubular cell damage
drugs account for 70% of cases, also infectious disease and systemic illnesses
sxs-fever, rash, arthralgias, peripheral blood esoniphilia, red and white cells in urine, oliguria, azotemia
risk factors for renal cell carcinoma
smoking obesity HTN acquired cystic disease occupational exposure analgesics genetic factors hepatitis C
what are clear cell carcinoma associated w/
von hippel lindau disease
papillary (chromophillic) carcinoma
usually multi focal and bilateral
triad for renal cell carcioma
flank pain hematuria palpable mass also non specific sxs (fatigue and weight loss) can have scrotal variocele paraneoplasic syndromes
major criteria for cyst
sharply demarcated
non echoic
strong exterior wall echo meaning good presentation (black)
assessing for mets in RCC
CT scan
bone scan
MRI of IVC and right atrium
pet scan
staging and prognosis of RCC
stage 1 confined in cortex 7cm
stage 3 tumor has got to adrenal gland, major vein, gerota fascia (1 lymph node involvement)
stage 4 beyond gerota fascia or >1 lymph node
tx of choice for RCC
surgery, nephrectomy
nephron sparing surgery
usually do this for small mass <4 cm or bilateral masses or kidney failure or systemic disease (diabetes)
wilms tumor
nephroblastoma pediatric tumor mean age 3.5 years present- palpable mass abdominal pain HTN hematuria
transitional cell carcinoma
starts in renal pelvis and then erodes out (whereas RCC starts in cortex and erodes in)
renal papillary adenoma
tx as cancer
arrise in renal tubules
renal fibroma/hamartoma
nodules in renal pyramids
colloid fluid
albumin
Fresh frozen plasma
hydroethyl starch (hetastarch)
dextran
crystalloids
hypotonic, hypertonic, and isotonic
hypotonic
fluid flows out of vascular into cell
.45% NaCl
Isotonic
D5W
.9 NaCl
lactated ringer
hypertonic
7-7.5% NaCl D5 in ½ NS Dextrose 5% in NS Dextrose 10% D50
when determining fluid status it is important to note
urine output
serum sodium
urine osmolality
what are adults obligate fluid loss
1600 mL
ideal maintence fluid
0.45% NaCl + 20 mEq KCl (the kidney will regulate Na, K and H20 retention)
how much do water requirements increase w/ fever
Water requirement increases 100-150ml/day for each degree fever > 37C
Hypovolemia due to decreased intake or excess excretion
0.45% NaCl until labs are back
If serum Na > 145 change to 0.25% NaCl
If serum Na < 138 change to 0.9% NaCl (NS)
Initially run at 125 ml/hr unless hemodynamically unstable
Monitor electrolytes and vitals
Gross estimate of renal perfusion is to make 30cc/hr (minimum) urine
hypovolemia due to vomitting or diarrhea
0.9% NaCl (NS) until labs are back
If serum Na > 145 change to 0.45% NaCl
Initially run at 125 ml/hr unless hemodynamically unstable
Monitor electrolytes and vitals
Gross estimate of renal perfusion is to make 30cc/hr (minimum) urine
hypovolemia due to hemorrhage
Bolus 1-2 LITERS 0.9% NaCl (NS) or LR through large bore IVs until labs are back
Continue fluid resuscitation based on vital signs and urine output
Packed Red Blood Cells (PRBC) as soon as available
Monitor electrolytes, ABGs and vitals
Gross estimate of renal perfusion is to make 30cc/hr (minimum) urine
hypovolemia due to burns
Bolus 1-2 LITERS 0.9% NaCl (NS) or LR through large bore IVs until labs are back
Continue fluid resuscitation based on vital signs and urine output
Consider Albumin early to maintain pressure and limit edema
Monitor electrolytes, ABGs and vitals
Gross estimate of renal perfusion is to make 30cc/hr (minimum) urine
pt fluid needs
Patient fluid needs are 1600ml/day plus any urine output over 500 ml plus any measured or quantified loss (diarrhea, vomiting, NG suction, drains, or bleeding) [Don’t forget increased need with fever = 150ml per degree C over 37]
if pt comes in and needs fluid
get CBC, CMP, UA
then start 1L NS or LR for approx 1 hr until labs get back
do not stop fluids until pt can urinate
different types of stones
calcium oxylate uric acid calcium phosphate struvite cystine
most common stone and what causes
calcium oxalate from RTA (decrease Ca reabsorption or primary parathyroid0
imaging for stones
non contrast CT (gold standard)
US (gold standard for pregnant ppl)
KUB
IVP
workup for first time presenting kidney stone
UA- consider straining for composition
minimal labs (UA, BMP, PTH if Ca is elvated)
imaging to confirm diagnosis
top tx for stones
increase water input so have ATLEAST 2 liters of fluid per day
calcium oxylate stones
hypercalcuria (primary hyperparathyroid, idiopathic, increased absorption) tx w/ thiazide diuretics and decerase sodium intake
hyperoxaluria (decrease oxylate intake and increse Ca intake)
hypocitraturia (RTA and idiopathic) tx w/ potassium citrate
uric acid stones
hyperurocosuria (gout, low urinary pH, malignancy)
tx allopropinol for hyperuricemia and potassium citrate to increase pH of urine
struvite stones
recurrent UTI w/ urea splitting organisms: proteus and ureaplasma
proteus is most common
cystine stones
Autosomal recessive disorder leading to decreased cystine resorption in the kidney- acidic urine
often presents in childhood
tx-Hydration, urine alkalization, Low Na/protein diet cystine binders
