Renal Approach to AKI and CKD Flashcards
how is AKI defined?
one of the following: increase in serum creatinine by >.3 mg/dL within 48 hours; increase in serum creatinine to >1.5 times baseline within 7 days; urine volume
how is anuria defined?
urine output less than 50-100 mL/day
how is oliguria defined?
urine output <400-500 mL/day
what is pre-renal azotemia?
elevation in serum BUN out of proportion to elevation in serum creatinine, specifically due to poor renal perfusion
what are two physical exam findings seen in patients with uremia?
asterixis and uremic frost
what are the 4 broad causes of pre-renal AKI?
hypovolemia, hypervolemia, systemic vasodilation, or drugs causing impaired renal autoregulation
what could cause systemic vasodilation leading to pre-renal AKI?
sepsis, SIRS, cirrhosis
what drugs could cause impaired renal autoregulation leading to pre-renal AKI?
NSAIDs or ACEi
what is the most common cause of pre-renal AKI?
hypovolemia
what could cause hypovolemia leading to pre-renal AKI?
bleeding, vomiting/diarrhea, or overdiuresis
how do they kidneys respond to seeing a decreased blood flow?
they activate the RAAS, which then signals the adrenal glands to release aldosterone. The aldosterone then tells the kidneys to reabsorb Na+ and water follows
what are the three lab values to know for pre-renal AKI?
there is going to be a urine Na <20 mEq/L; the BUN/Cr ratio is going to be >20:1; the urine osmolality is going to be > 500 mosm/kg
why is the urine osmolality >500 mosm/kg in cases of pre-renal AKI?
the kidneys are holding onto water, so they are going to create a concentrated urine
when renal blood flow increases, what is another way the body responds besides the RAAS?
dilation of the afferent arterioles and constriction of the efferent arterioles
how is the dilation of the afferent arteriole seen in cases of pre-renal AKI blunted by medications?
NSAIDs inhibit prostaglandin production (so you don’t get that vasodilation)
how is the constriction of the efferent arteriole blunted by medications?
ACEi/ARBs inhibit angiotensin II production (angiotensin II preferentially constricts the efferent arteriole)
what are 4 broad things that could lead to intrarenal AKI?
acute tubular necrosis, acute interstitial nephritis, glomerular disease, or vascular issues
what could cause acute tubular necrosis (ATN) leading to intrarenal AKI?
prolonged prerenal AKI (sepsis is common cause) or toxins
what are some toxins that lead to ATN?
myoglobin, uric acid, myeloma light chains, IV contrast
what things could lead to acute interstitial nephritis?
PPIs, NSAIDs, certain antibiotics
what vascular issues could lead to intrarenal AKI?
vasculitis, malignant HTN, or TTP/HUS
what is the most common cause of intrarenal AKI?
acute tubular necrosis
what is the pathophysiology of ATN?
prolonged prerenal state or toxin leads to ischemia, which then leads to tubular necrosis; the tubular necrosis leads to debris obstructing the tubular flow, which ultimately leads to to decreased GFR
what happens if pre-renal AKI is present long enough?
acute tubular necrosis will develop
what is acute interstitial nephritis caused by?
type I and type IV hypersensitivity due to nonsteroidal anti-inflammatory drugs (NSAIDs)/penicillins, diuretics
what are the pain problems associated with intrinsic renal AKI?
1) problems with filtration 2) problems with reabsorption and secretion
what are the lab values you need to know for intrinsic renal AKI?
urine Na > 40, BUN/Cr ratio is going to be <15:1, urine osm< 350 mosm/kg
what are the two main causes of post-renal AKI?
bladder outlet obstruction and ureteral obstruction
what could cause bladder outlet obstruction?
BPH and blood clots
what could cause ureteral obstruction?
stones or external compression from malignancy
what is important to remember about post-renal AKI?
you need either bilateral ureteral obstruction or bladder outlet obstruction to cause post-renal AKI
what is the most common cause of post-renal AKI?
BPH
what should all patients with an AKI get for their workup?
at least a basic metabolic panel and a UA
what things could be included in the initial workup for AKI?
BMP, UA with microscopy, urine electrolytes, urine microalbumin/Cr ratio or urine protein/Cr ratio
if you see a urinary pattern of hylaine casts, which kidney disease is suggested?
non-specific; pre-renal azotemia
if you see a urinary pattern of renal tubular epithelial cells, granular casts (“muddy brown”), which kidney disease is suggested?
acute tubular necrosis
if you see WBCs, WBC casts, or urine eosinophils on urinary pattern, which kidney disease is suggested?
acute interstitial nephritis
if the urinary pattern shows proteinuria (less than 3.5 g/day), hematuria, dysmorphic RBC, and RBC casts, what kidney disease is suggested?
nephritic syndrome
if you see a urinary pattern of heavy proteinuria (>3.5 g/ day), fatty casts, oval fat bodies, and minimal hematuria?
nephrotic syndrome
What is the FENa? and what is it used for?
the fractional excretion of sodium; often used to differentiate between pre-renal AKI and ATN
what does the FENa tell you?
if it is less than 1% it suggests pre-renal; if it is greater than 2% is suggests ATN
when can you not rely on FENa? and what should you use in these cases?
FENa is less accurate in patients on diuretics; use FEUrea instead
what does the FEUrea tell you?
if it is less than 35% then it is prerenal; if it is greater than 50% then it suggests ATN
what are 4 additional tests you can order for someone with AKI?
post-void residual, renal ultrasound, urine eosinophils, and renal biopsy
when should you order a post-void residual if you suspect AKI?
if you have concerns for bladder outlet obstruction
when should you order a renal ultrasound if you are diagnosing AKI?
if you have concerns for ureteral obstruction or other post-renal process
when do you order a urine eosinophils when diagnosing AKI?
it has historically been used to assess for AIN, but sensitivity and specificity are poor
when do you order a renal biopsy when diagnosing AKI?
it is reserved for severe AKI of unclear etiology
in all patients with AKI, what should you consider when treating the patient?
avoid nephrotoxins, renally dose all meds, dialysis if needed
how do you treat pre-renal AKI?
correct hemodynamics; if low preload–> fluids; if high preload–> diuretics
how do you treat intrinsic renal AKI?
treat the underlying disease: ATN–> supportive care; AIN–> stop offending med, consider steroids; glomerular disease–> depends on cause
how do you treat post-renal AKI?
relieve the obstruction; ureteral obstruction: nephrostomy tube or stent; BPH with obstruction–> foley catheter
the likelihood of recovery depends on what two things?
severity of renal injury and baseline renal function
What are the indications for dialysis?
AEIOU
A: acidosis (ph<7.1-7.2)
E: electrolytes (life threatening hyperkalemia)
I: Intoxication (methanol, ethylene glycol, lithium)
O: overload
U: Uremia (if encephalopathy or pericarditis)
what is the text book difference between AKI and CKD?
if it is less than 3 months with GFR less than 60 ml/min and/or markers of kidney damage present, then the patient has AKI; after three months, then the patient can be labeled with CKD
what are the stages of CKD?
1,2,3a,3b,4, and 5
what also effects the severity of the CKD stages?
albuminuria
what is the vast majority of CKD cases caused by?
diabetes and hypertension
what is the pathophysiology of CKD?
there is damage to nephrons from underlying disease (eg DM or HTN)–> nephrons die–> hyperfiltration and hypertrophy of remaining nephrons–> glomerular damage from increased pressure and flow
what are the symptoms specific to CKD if the patient is not asymptomatic?
anemia (the kidneys normally produce EPO); bone pain and fragility (secondary to secondary hyperparathyroidism)
besides decreased EPO, how else can CKD lead to anemia?
CKD can lead to iron deficiency due to chronic blood loss from hemodialysis and from a decrease in GI iron absorption
how does CKD lead to bone disease?
in cases of CKD, there is phosphate retention leading to increased serum phosphorus, which leads to hypocalcemia. The hypocalcemia leads to secondary hyperparathyroidism; also, in cases of CKD, there is decreased active vitamin D, leading to decreased gut Ca reabsorption, leading to hypocalcemia
what is the pathophysiology of secondary hyperparathyroidism?
there is low serum calcium–> increased PTH production by the parathyroid gland–> leading to increased bony turnover
what do the labs look like in cases of secondary hyperparathyroidism?
calcium is low, PTH is high, and phosphorus is high
what is the pathophysiology of tertiary hyperparathyroidism?
prolonged secondary hyperparathyroidism–> parathyroid gland hyperplasia–> autonomously functioning parathyroid gland + loss of function of Ca2+ sensing receptors
what do the labs look like for tertiary hyperparathyroidism?
calcium is high, PTH is high, and phosphorus is high
which bone disease is associated with CKD?
osteitis fibrosis cystica
what is osteitis fibrosis cystica?
theres excess PTH–> osteoclast activation–> bony breakdown
what pathologic findings are associated with osteitis fibrosis cystica?
subperiosteal bony reabsorption, bone cyst formation, “brown tumors”
why are pathologic fractures common in patients with advanced CKD?
due to renal osteodystrophy
what can renal ultrasound be used for in cases of CKD?
you may be able to see small atrophic kidneys in CKD; to assess for hydronephrosis
