Defination

-increase in serum creatinine by ≥0.3 mg within 48 hours or

- an increase to ≥1.5 times the presumed baseline value that is known or presumed to
have occurred within the prior seven days, or
- a decrease in urine volume to <0.5 mL/kg/hour over six hours

Presentation:
Patients with AKI may present with symptoms and signs resulting directly from
diminished kidney function. These typically include edema,
hypertension, and/or decreased urine output or, in severe AKI, anuria. However, many
patients have no clinical symptoms, and an increase in creatinine is detected by
laboratory tests that are routinely obtained among hospitalized patients.

AKI catagories based on etiology

Pre-renal (decreased renal perfusion pressure) – either from intravascular volume

depletion, low cardiac output, or disordered vasodilation (hepatic cirrhosis)

Renal Hypoperfusion / reduced GFR

1. True Hypovolemia – excessive fluid loss (diarrhea, vomiting, acute hemorrhage)

or reduced intake – no replenishing kidneys
On physical exam: dry mucous membrane, poor skin turgor, orthostatic vital signs (drop
in BP by 20/10 or inc in HR by 10bpm when standing from supine), CVP < 8

2. low cardiac output: effective circulating volume is low despite volume overload
RAAS system stimulated and ADH released both lead to inc salt + water retention – inc
urea nitrogen absorption so BUN to Cr ratio is high
Diuretics can help

3. similarly hepatic failure leads to splanchnic vasodilation – RAAS/ADH – salt and water
retention
Hepatorenal syndrome: diagnosis of exclusion
Criteria: rise in serum creatinine of >1.5 mg/dL that is not reduced with
administration of albumin (1 g/kg of body weight) and after a minimum of 2
days off diuretics. The diagnosis of HRS should be in the absence of shock,
nephrotoxic agents, or findings of renal parenchymal disease
Precipitating factors: SBP, GI bleed, over diuresis, large volume paracentesis

4.NSAIDS, Iodine Contrast – afferent constriction

Ace and Arb efferent vasodilation and drop in gfr

5. Abdominal Compartment Syndrome: from intestinal obstruction, massive ascites,

or obstruction can decrease flow through renal vasculature

Post renal (obstruction of urinary flow)

Flow of urine is obstructed anywhere w/in urinary collecting system
Back up of flow- inc intratubular hydrostatic pressure – diminished gfr

Common causes prostate enlragement, b/l kindey stones, malignancy

Tx placement of bladder catheter - postvoid residual urine volume > 300 is
diagnostic

Imp: relief of obstruction usually followed by post obst diuresis – if polyuria monitor
lytes closely and replace with ½ normal saline

Micro-obstructive uropathy in tubules from crystals : IV acyclovir or protease

inhibitor indavir

intrinsic renal (pathology of the vessels, glomeruli, or tubules-interstitium),

TUBULAR
1. ischemic acute tubular necrosis - sepsis, hemorrhage, or prolonged pre renal
insult leads to ATN
-muddy brown cast, FeNA>1%, FeUrea > 35%

2. Toxic ATN: from hemoglobin or myoglobin (rhabdomyolysis) or exogenous

chemicals: iodinated contrast, aminoglycoside

Iodine contrast is potent vasoconstrictor and causes tubular injury causing

Cr to rise in 24 to 48 hrs, Cr will peak in 3-5 days and plateau off
Fluids – isotonic saline at 1-2 ml/kg/hr 3 to 12 hrs prior with goal of
150ml/hr post procedure diuresis, sodium bicarb

Aminoglycosides and cisplastin: require exposure for atleast 5 days

Direct toxicity to proximal tubules leads to wasting of potassium and
magnesium
 Pigment nephropathy: rhabdomyolysis: CK level elevated 10x upper limit, inc
in Cr phos, potassium,

Tumor lysis syndrome: uric acid nephropathy use ppx allopurinol 600mg or
rasburicase - is a recombinantversion of urate oxidase, an enzyme that metabolizes uric
acid to allantoin.

3. Atheroembolic disease:after invasive cardiac procedure rise in Cr or and

physica signs like LE livedo reticularis, arteriolar plaque in retina, digital
necrosis

Interstitial
AIN involves inflammation of the renal parenchyma, typically caused by
medications or infections.

The classic triad of fever, rash, and eosinophilia - seen in less than one-third
Pyuria, WBC casts, and eosinophiluria are also suggestive of AIN.

β-Lactam antibiotics are the most frequently cited causative agents, but nearly
all antibiotics can be implicated. The time course typically requires exposure for
at least 5-10 days before renal impairment occurs.
Fasting lipid panel

Obtain after 8 to 12 hr fasting –

Serum total and HDL cholesterol are measured directly, and there are only small,
clinically insignificant differences in these values when measured in the fasting or non-
fasting state.

Triglyceride levels may vary after a recent meal. Thus, we generally advise that the lipid
profile be measured in the fasting state. Fasting is imp when you are trying to diagnose
triglyceride disorder otherwise non fasting is ok

Panel Gives you: Total Cholesterol, LDL, HDL, TG

Use ASCVD app to calculate risk

Who to screen?
Screening
Screening for hypercholesterolemia should be done in all adults age 20 years or older
(Circulation 2014;129:S49).

Screening is best performed with a lipid profile (total cholesterol, LDL cholesterol, HDL
cholesterol, and triglycerides) obtained after a
12-hour fast.

If a fasting lipid panel cannot be obtained, total and HDL cholesterol should be measured. Non-
HDL cholesterol ≥220 mg/dL may indicate a genetic or secondary cause. A fasting lipid panel is
required if non-HDL cholesterol is ≥220 mg/dL or triglycerides are ≥500 mg/dL.

If the patient does not have an indication for LDL-lowering therapy, screening can be performed
every 4-6 years between ages 40-75
(Circulation 2014;129:S49).

Patients hospitalized for an acute coronary syndrome or coronary revascularization should have
a lipid panel obtained within 24 hours of admission if lipid levels are unknown.

Individuals with hyperlipidemia should be evaluated for potential secondary causes, including
hypothyroidism, DM, obstructive liver disease, chronic renal disease such as nephrotic
syndrome, and medications such as estrogens, progestins, anabolic steroids/androgens,
corticosteroids, cyclosporine, retinoids, atypical antipsychotics, and antiretrovirals (particularly
protease inhibitors).
Treatment

Lifestyle modification and diet first

Diet: adopt a diet that is high in fruits and vegetables, whole grains, fish, lean meat, low-fat dairy,
legumes, and nuts, with lower intake of red meat, saturated and trans fats, sweets, and sugary
beverages

Exercise: Aerobic or resistance- weight reduction of 3 to 5 percent beneficial in reducing ASCVD risk

Who is considered to have ASCVD:

coronary syndromes, history of MI, stable angina, arterial revascularization (coronary or otherwise),
stroke, transient ischemic attack, or atherosclerotic peripheral arterial disease
or pt with LDL 190 or above

start on high intensity – if cant tolerate then switch to moderate intensity and always try to give max
tolerated dose- try to reduce LDL by 50% atleast on high intensity before switching
Treatment