AKI part 1 Flashcards
AKI results in sudden decrease in what kidney functions
deceased ability to manage:
* fluid
* electrolytes
* acid base balance
* excretion of waste products (decreased excretion of urea and creatinine)
what labs result from AKI
deceased GFR
increased BUN and/or serum Cr
deceased Urine volume
what should you keep in mind when observing AKI
that by the time serum Cr rises, GFR usually has already fallen significantly!
What is the criteria for diagnosing AKI
KDIGO - Most recent, most preferred
RIFLE Criteria - Risk, Injury, Failure, Loss, ESRD
AKIN (Acute Kidney Injury Network) Criteria
All correlate with prognosis in AKI patients
dont think we need this
what is the KDIGO staging criteria for AKI
she said not testable so basically skip this
what is considered anuria and what does anuria indicate
<50mL/24 hrs
* Ominous finding!
* indicates Acute obstruction, cortical necrosis, aortic dissection, etc.
what is considered oliguria. what is oliguria indicative of
<400mL/24 hrs of urine output
* indicated poor prognosis in AKI
* Higher mortality and poorer recovery than non-oliguric AKI
what is considered polyuria
excessive urine (2500 - 3000 mL/day +)
what is azotemia
increased nitrogenous wastes in the blood
what is uremia and what are the symptoms
nonspecific symptoms caused by elevated nitrogenous waste (especially urea) in the blood
symptoms could include:
General - weakness, fatigue
Neuro - tremors, seizures, encephalopathy, confusion, coma
Skin - itching, dryness
Cardiovascular - pericardial effusion, pericarditis, HTN
GI - anorexia, nausea, vomiting
Other - shallow breaths/tachypnea, metabolic acidosis
risk factors for AKI
does not expect us to know but says that by the end of class this may be intuitive to us
Know the difference between prerenal, intrarenal and post renal (pic)
what are the three categories of AKI
prerenal azotemia
intrinsic kidney injury
postrenal obstruction
what is the MCC of AKI
prerenal azotemia
what is the least common cause of AKI
postrenal obstruction
what is prerenal azotemia
caused by inadequate renal perfusion due to:
* hypovolemia
* decreased cardiac output
* changed vascular resistance
what lab findings are present with prerenal azotemia
- decreased GFR and increased BUN:Cr ratio (>20:1 usually)
- if oliguric there should be low fractional excretion of sodium (FENa+) in the urine - <1%
- normal Urinary sediment - may see hyaline casts
what are the signs and symptoms associated with prerenal azotemia
- uremia
- signs of cause (dehydration, sepsis, cardiomegaly ect)
- diffuse abdominal pain and ileus
- decreased urine output
what are the hyaline casts in urinary sediment caused by in prerenal azotemia
formed from Tamm-Horsfall mucoprotein secreted by the tubule
what is the treatment for prerenal azotemia
resolve underlying cause!
usually by:
* maintaining euvolemia
* correcting electrolytes
* avoid nephrotoxic drugs. (NSAIDS, ACEi, ARBs ect)
what is postrenal obstruction
obstruction of urinary outflow that is affecting one or both kidneys
what is the pathophysiology of postrenal obstruction
the obstruction causes elevated intraluminal pressure which leads to damaged renal parenchyma
what areas are common in postrenal obstruction
obstruction of urethra, bladder, ureters, or renal pelvises
what are common causes of postrenal obstruction
- benign prostatic hyperplasia (MCC in men)
- devices (foley cath)
- medications (anticholinergics)
- cancer
- retroperitoneal fibrosis
- neurogenic bladder
other rare causes can include:
* blood clots
* stones
* benign papillary necrosis
what are signs and symptoms of postrenal obstruction
- anuria or polyuria
- lower abdominal pain
- large prostate, distended bladder, pelvic/abdominal mass
what is used to look for hydroureter and obstruction
bladder catheterization
or
abdominopelvic US
what are lab findings in postrenal obstruction
- decreased GFR
- increased BUN:Cr (>20:1)
- urine sodium (varies)
- urine osmolality of 400 or less
- normal urine sediment (may see RBCs, WBCs or crystals)
What are intrinsic kidney injuries
direct damage to the kidney as a result of:
infections
sepsis
nephrotoxins
ischemia
what are the most common sites of instrinsic kidney injury
- tubules
- glomeruli
- interstitium
- vasculature
what can prerenal azotemia progress to
tubular injury (intrinsic kidney injury)
what are the major forms of intrinsic kidney injury
- acute tubular necrosis
- acute glomerulonephritis
- acute interstitial nephritis
what is the most common intrinsic AKI
acute tubular necrosis (ATN)
what are the 3 major causes of ATN
ischemia (prerenal turning into intrinsic problem)
nephrotoxins
sepsis
what are the MC antimicrobial exogenous nephrotoxins?
- Aminoglycosides - up to 30% of patients at therapeutic levels (typically begins 5-7 days after tx started)
- Amphotericin B - nephrotoxic after 2-3 grams
what is the least nephrotoxic aminoglycoside?
streptomycin
what other antimicrobials are known to be exogenous nephrotoxins
ABX - vanc, sulfonamides, cephs, tetracycline
Antivirals - acyclovir, foscarnet
what non-antimicrobial things are known to be nephrotoxic
- Radiographic contrast
- chemo/immunosuppressant - MTX, cyclosporine, cisplatin
- environmental toxins (heavy metals, ethylene glycol, insecticides/herbicides)
what is the endogenous nephrotoxins
Myoglobinuria
hemoglobinuria
hyperuricemia
Bence Jones Protein
what is myoglobinuria a result of
rhabdomyolysis and muscle necrosis
How is myoglobinuria nephrotoxic
it is directly damaging to tubules and can cause tubule obstruction.
what lab values often indicates presence of myoglobinuria
- CK>20,000-50,000 IU/L
- false + hemoglobin in urine dipstick
- urine will appear dark brown but no RBCs are present on microscopy
what is the mainstay of treatment for myoglobinuria
rehydration.
what are possible complications of myoglobinuria
- hypocalcemia (usually resolves on its own)
- hyperkalemia
- hyperphosphatemia
- hyperuricemia
when is hemoglobinuria seen
- transfusion reaction
- hemolytic anemia
when is hyperuriciemia common
- rapid cell turnover and lysis such as during chemo
what lab value is seen with hyperuricemia
- serum uric acid of >15-20mg/dL
intratubular deposition of uric acid crystals may also be seen
how do you treat hyperuricemia
medications to lower uric acid may help
how is Bence Jones Protein harmful
it is directly toxic to the kidneys and obstructs the tubules.
when is Bence Jones Protein seen
Multiple myeloma
what are signs and symptoms of ATN
- signs of underlying cause
- arrhythmias
- abdominal pain
- uremia
- oliguria or nonoliguria (wow thats just great)
what are labs associated with ATN
- hyperkalemia and hyperphosphatemia
- decreased GFR, increased BUN:Cr (<20:1)
- elevated urine sodium
- urinary sediment shows pigmented granular casts or “muddy brown” casts, renal tubular cells and epithelial cell casts
what is the treatment for ATN
- remove the cause and avoid complications
- avoid volume overload and hyperkalemia
- diet changes
what should be done if a patient is at risk of volume overload with ATN
start loop diuretics or dialysis
what dietary changes should be done in ATN
- protein restriction to prevent metabolic acidosis
- increase or decrease dietary phosphate, calcium and magnesium accordingly
what is the prognosis for ATN
20-50% mortality rate
70% mortality rate in ICU
may never fully return to baseline renal function
what suggests better long-term outcome for ATN
nonoliguric ATN
what is acute glomerulonephritis
intrinsic glomerular AKI mostly involving inflammation of the glomerulus
what are the two types of intrinsic glomerular AKI
nephritic - involving inflammation
nephrotic - minimal inflammation but with proteinuria present
acute glomerular AKI (acute glomerularnephritis) is accountable for what percent of intrinsic AKI cases?
5%
what is developed in almost all acute glomerulonephritis cases
- inflammatory glomerular lesions
- crescent lesions (severe breaks in glomerular walls)
what is the classic presentation of acute glomerulonephritis
HTN
edema
urine containing protein, WBCs, RBCs and RBC casts.
what are the different types of acute glomerulonephritis
immune complex deposition
Anti-GBM-associated
C3 Glomerulopathy
Monoclonal Ig-Mediated
Pauci-Immune glomerulonephritis
what is immune complex deposition type acute glomerulonephritis
when antigen excess over antibody production occurs and antigen-antibody complexes get lodged in glomerular basement membrane.
what are the causes of immune complex deposition
- IgA nephropathy (Berger disease)
- Post-infectious (especially seen with endocarditis and streptococcus)
- Autoimmune disease (especially lupus)
- Membranoproliferative (MPGN)
- Cryoglobulinemic glomerulonephritis (HCV)
what is Anti-GBM-associated acute glomerulonephritis
autoantibodies against glomerular basement membrane (GBM). This can be confined to the kidney or involve lungs as well
what is Goodpastures syndrome
Anti-GBM-associated acute glomerulonephritis with pulmonary involvement
what is C3 Glomerulopathy
C3 deposition in the glomerulus, +/- Ig deposition
what causes C3 glomerulopathy
abnormalities in the alternative complement pathway
what are labs that can indicate C3 Glomerulopathy
Low serum C3 levels can help identify, but normal C3 does not rule out
What is monoclonal Ig-Mediated Glomerulonephritis
Monoclonal Ig deposited in GBM and/or tubular basement membrane.
no excess antigens as seen in immune complex GN
(so many antibodies floating around in blood stream that they just get stuck and cause destruction. )
what labs can help identify monoclonal Ig-Mediated glomerulonephritis
- Serum protein electrophoresis
can also use:
immunofixation
free light chain analysis
what is Pauci-Immune Glomerulonephritis
small-vessel vasculitis associated with Antineutrophil cytoplasmic antibodies (ANCAs)
what is the pathophysiology of pauci-immune glomerulonephritis
- No immune complexes or direct Ig or complement deposition or binding
- Tissue injury secondary to cell-mediated immune processes
- Can see manifestations in other areas of the body (lungs, skin, upper airway)
pathophysiology probs isnt the right word here. Im doing my best lol
what are other known causes of acute glomerulonephritis
- hypertensive emergencies
- thrombotic microangiopathies
what are signs and symptoms of acute glomerulonephritis
HTN and edema.
edema usually begins with in body parts with low tissue tension such as scrotal edema or periorbital edema
(Edema caused because 1. na is being reabsorbed because kidneys sense damage. 2. protein is being lost in the urine. protein is responsible for keeping water in the vessels/cells and so without protein, water is moved out of the vessels and into the tissues) said in class
what are lab findings in acute glomerulonephritis
Serum Cr (high)
Urinalysis - hematuria, moderate proteinuria
Urine sediment - RBCs, WBCs, RBC casts
complement levels - C3/C4 low in Gn, only C3 low in C# glomerulonephropathy
ASO titers - evaluate for recent strep infection
ANti-GBM antibodies
SPEP
P-ANCA and C-ANCA levels
Other general autoimmune labs - CRP, ESR, ANA
(in class - “ if you ask professor jensen which should I order first? just be like me and order all of them at once as soon as you are suspicious” )
how do you treat acute glomerulonephritis
- treat underlying disease
- high dose corticosteroids
- cytotoxic agents
- plasma exchange for goodpasture disease and pauci-immune glomerulonephritis
what is acute interstitial nephritis
interstitial inflammatory response causing inflammation of the area surrounding the tubules of the nephron (the interstitium)
what percent of intrinsic AKI does acute interstitial nephritis account for
10-15%
what are the causes of acute interstitial nephritis
- medications (70%)
- infections
- immunologic
- other
what medications are known to cause acute interstitial nephritis
antimicrobials such as:
PCN, cephs, rifampin, sulfonamides, HIV drugs
Other meds: diuretics, NSAIDS, anticonvulsants, allopurinol, PPIs, H2 blockers
what infections are potential causes of acute interstitial nephritis
bacterial - strep, staph, diptheria, legionella, rickettsia
viral - CMV, EBV
fungal - histoplasmosis
what immunologic diseases could potentially cause acute interstitial nephritis
SLE
Sjogrens
Sarcoidosis
what are the “other” causes of acute interstitial nephritis
allergic reaction
collagen vascular disease
what are the signs and symptoms of acute interstitial nephritis
the classic triad:
* fever
* rash
* arthralgia
it says all three only present in 10% of patients which is so dumb, like why is it called the “classic triad” then
what lab values are found in acute interstitial nephritis
- eosinophilia
- urine sediment with WBCs, RBCs, WBC casts, eosinophiluria.
minimal proteinuria unless it is NSAID related
what labs/studies are ordered for Acute interstitial nephritis
CBC
Urine sediment
Renal biopsy
what would a renal biopsy of acute interstitial nephritis show
inflammatory cells within renal interstitium
what is the treatment for acute interstitial nephritis
removal of cause and supportive care
If you remove the cause of acute interstitial nephritis and your patient is still suffering from renal injury what could you do
start oral or IV corticosteroids
urgent dialysis may be necessary in 1/3 of patients
what is the prognosis of acute interstitial nephritis
recover over weeks to months
may have slightly better outcomes than other AKI causes
How does a Abdominal/Pelvic US present in most AKI
normal-sized kidneys
How does a Abdominal/Pelvic US present in acute interstitial nephritis
enlarged kidneys
How does a Abdominal/Pelvic US present in patients with hx of CKD
normal, may have polycystic kidneys
How does a Abdominal/Pelvic US present in postrenal AKI
may see dilated urine collecting system proximal to point of obstruction
what diagnostic studies are used to rule out urethral obstruction when evaluating an AKI
urethral catheter
bladder scan
when is a kidney biopsy used in AKI diagnosis
- Primarily when prerenal, postrenal, and ischemic/nephrotoxic AKI etiologies have been ruled out
- Can help dx glomerulonephritis, vasculitis, interstitial nephritis, etc.
