ILE X - Acute Kidney Injury

Stage of AKI:

SCr increased by > 0.3 mg/dL

1.5-2 fold from baseline

UOP < 0.5 mL/kg/hour for SIX to twelve hours

I

Stage of AKI:

SCr increases 2-3 fold from baseline

UOP < 0.5 mL/kg/hour for TWELVE hours or more

II

Stage of AKI:

SCr increase of more than 3 times from baseline;

Anuria for TWELVE hours or more

SCr > 4 with an acute increase of 0.5

Need for RRT

III

AKI Risk Factors

CKD, diabetes, heart/liver disease, albuminuria, major surgery (especially cardiac), acute decompensated heart failure, sepsis, hypotension, volume depletion, medications, advanced age, male gender, AA race

Define Nonoliguric

Normal UOP (> 500 mL/day)

Define Oliguric

Decreased UOP (< 500 mL/day)

Define anuric

Absent UOP (< 50 mL/day)

What is the GFR of a person who produced 32 mL of urine in past 24 hours?

0; this is Andria

What causes pre renal AKI?

Decreased renal perfusion in the setting of undamaged tissues as a result of volume depletion, decreased blood volume, use of NSAIDs/ACEi/ARB, sepsis

What tests/labs should we look at to confirm pre renal AKI?

Urine Na < 20, FENa < 1%

Pre renal AKI treatment

Hemodynamic support, volume replacement

What causes intrinsic AKI?

Structural damage to the kidney, most commonly the tubule, from an ischemic or toxic insult; could be drugs, infection, occlusion of vessels

What tests/labs should we look at to confirm intrinsic AKI?

Urine Na > 40, FENa > 2%

Intrinsic AKI Treatment

remove offending agent

What causes post-renal AKI?

Obstruction; could be bladder outlet, urethra, renal/pelvic tubular

What tests/labs should we look at to confirm post-renal AKI?

Mostly look for severely decreased UOP

Post-renal AKI treatment

remove obstruction

What does FENa tell us? How do we interpret this?

The percentage of sodium in the body that is coming out of the urine; Na is usually completely reabsorbed in the kidney, so if the kidney is working properly, this number should be < 1%. If the kidney is damaged, it won't reabsorb Na as well and this number will be elevated.

Why do we use IV fluids in AKI?

To maintain or restore effective intravascular volume to ensure adequate renal profusion

What is the most common electrolyte disorder in patients with AKI?

Hyperkalemia

AKI Monitoring Parameters

Fluid Ins/Outs

Weight

Hemodynamics

Blood Chemistries

Na/K/Cl/Bicarb/Ca/Phos/Mg

BUN/SCr

Drugs/Dosing

Nutritional Regimen

Blood Glucose

UOP

What is the problem with ACE-I/ARBs in AKI?

STOP THESE

These agents prevent the auto regulation of kidney function

What is the problem with diuretics in AKI?

They can make hypovolemia worse

Contrast induced nephrotoxicity prevention

Minimize contrast dye dose, use non-iodinated contrast studies, avoid use of nephrotoxic drugs, NS infusion 3-12 hours prior and 6-24 hours after

Fluid Requirements in Normal Pts

30-35 ml/kg/day

Fluid requirement in edema forming conditions

20-25 ml/kg/day

Fluid requirements in anuric patients with AKI

Fluid restrict to 1000-1200 ml/day

Fluid requirements in oliguric pts with AKI

Patients may tolerate larger volumes of fluids

Fluid requirements in nonoliguric patients with AKI

Do not restrict sodium or water

Which pump is the key in the regulation of K? What is the cofactor?

Na/K/ATPase; Magnesium

Which potassium extreme do we see commonly in AKI?

Hyperkalemia

What is the rule for IV K depletion in Hyperkalemia?

Max infusion rate of 10 mEq/hour

When do we use IV K repletion in hypokalemia?

Symptomatic patients or patients with a nonfunctional GI tract

When using oral K repletion therapy to treat hypokalemia, what is the dose?

20-40 mEq PO every 2-4 hours

When should hyperkalemia be treated emergently?

Symptomatic pts (peaked T waves), K > 6

What are the steps for treatment of hyperkalemia in AKI?

1. Antagonize cardiac effects with IV _ _ or calcium chloride

2. Shift K intracellularly with _ + _ , _, or _

3. Remove K from the body with _, _, _, or _

1. calcium gluconate

2. insulin + dextrose, bicarb, albuterol

3. diuretics, Kayexalate, Lokelma, or dialysis

MOA = exchanges Na for K ions in the GI tract at a 1:1 ratio

SPS (kayexalate)

SPS (kayexalate) pD/pK

1 hour onset

Not absorbed

Excreted in the feces

SPS (kayexalate) dosing

15-60 g repeated Q4H PRN

SPS (kayexalate) ADRs

Risk of colonic necrosis with sorbitol-containing formulations

MOA = preferentially exchanges K in exchange for Na and H

SZC (Lokelma)

SZC (Lokelma) pD/pK

1 hour onset

Not absorbed

Fecal elimination

SZC (Lokelma) dosing

10 g PO TID for up to 48 hours

SZC (Lokelma) ADRs

Edema

Which electrolyte is the most prevalent cation?

Calcium

What are serum Ca levels controlled by?

PTH, vitamin D, calcitonin

Which electrolyte has to be corrected and why?

Calcium because it is highly bound to albumin; if albumin is low, you need to correct

Which calcium extreme is more common in AKI?

Hypokalemia

How to do treat hypocalcemia?

IF on RRT, can manipulate dialysate fluid and/or the anticoagulant

If not, IV calcium

What is the primary intracellular ion?

Phosphorus

Which phosphorus should be used to replete if the patient has low K levels?

KPhos

Which phosphorus extreme is commonly seen in AKI?

Hyperphosphatemia

How do we treat hyperphosphatemia?

Phosphate binders or restriction

What might hypomagnesemia cause?

Tornadoes

How to we treat hypomagnesemia?

IV infusion; do not exceed 1 g/hour (may take several days)

How to we treat hypermagnesemia?

1. D/c magnesium products

2. IV calcium gluconate to stabilize membranes

3. Diuretics to increase renal elimination

Could also do dialysis

What metabolic disorder is common in AKI

Metabolic acidosis

At what pH do we start using bicarbonate to treat metabolic acidosis?

7.2

When do we stop giving HCO3?

When levels reach 18-20 mEfq

What three lab values are assessed to determine if a patient is experiencing AKI, according to KDIGO?

SCr, UOP, BUN

What is the most sensitive indicator of renal dysfunction due to being a byproduct of skeletal muscle metabolism that is filtrate at the glomerulus via passive diffusion?

SCr

What is considered the first indicator for AKI, but it is non-specific and may vary due to volume status, diuretic administration or obstruction

UOP

How long after AKI onset may SCr become elevated?

1-2 days

What lab value indicates renal dysfunction by assessing elevations in nitrogenous waste products

BUN

How can corticosteroids, tetracyclines, GI bleeds, or a high protein diet affect BUN levels?

Elevate

What medication may lead to AKI due to its update into proximal tubular epithelial cells of the nephron, leading to tubular cell death (ATN)

Displaying

What medications may lead to AKI due to decreased renal blood flow (ischemia) and increased concentration in tubule epithelial cells fo the nephron, leading you tuburnal cell death (ATN)

Contrast dye

What medications may lead to AKI due to decreased renal blood flow (ischemia) and increased concentration in tubule epithelial cells fo the nephron, leading you tuburnal cell death (ATN)

Amphotericin B

What medication may lead to AKI due to high concentrations accumulating in the proximal tubular epithelial cells of nephrons, creating a reactive oxygen species that leads to tubular cell necrosis (ATN)?

Aminoglycosides

What AKI classification is evident when compensatory mechanisms are overwhelmed and typically presents with hypotension, dehydration, and ascites?

Pre-renal

What AKI classification is evident with direct damage to the kidneys and is further categorized based on the area that the kidney is damaged?

Intrinsic

What category of intrinsic AKI is due to endogenous or exogenous toxins, like aminoglycosides, contrast dye, amphotericin B, and cisplatin?

Acute Tubular Necrosis (ATN)

What category of intrinsic AKI is typically a idiosyncratic, delayed hypersensitivity immune reactions that is most commonly due to medications like antibiotics or NSAIDs?

Acute Allergic Interstitial Nephritis (AIN)

How long may intrinsic AIN AKI be delayed after initiation of penicillin, ciprofloxacin, or PPIs?

14 days

How long may intrinsic AIN AKI be delayed after initiation of NSAIDs?

6 months

What AKI classification is due to unrelieved obstruction causing continued elevated intraluminal pressure that results in damage and may present with distended bladder or an enlarged prostate?

Post-renal

What may present in post renal drug-induced obstructive nephropathy due to precipitation in the renal tubules or collection system?

Crystalluria

What AKI classification is typically associated with the following lab values?

Urine Na: < 20

Urine Sediment: normal, hyaline casts

FENa: <1%

Pre-renal

What AKI classification is typically associated with the following lab values?

Urine Na: >40

Urine Sediment: granular casts, cellular debris

FENa: > 2%

Intrinsic

T/F: even mild, reversible AKI has important clinical consequence including a risk of death

True

What is the goal of treatment for patients with AKI in terms of renal function, in addition to reducing complications related to decreased kidney function and adverse effects from accumulation of medications cleared by the kidneys?

Pre-AKI baseline

What amp B formulation is the better alternative to minimize nephrotoxicuty

Liposomal

What medication should not be utilized in patients without volume overload, but may be used to achieve euvolemia in patients with AKI?

Loop Diuretics

What therapy is indicated in AKI patients with the following conditions?

Metabolic acidosis

Hyperkalemia +/- Hypermagnesemia

Intoxications

Fluid overload

BUN > 100 and symptomatic

RRT

What RRT mortality is done via diffusion over 3-4

Loved it!

What RRT modality is done at diffusion for 6-12 hours?

SLED/PIRRT

What RRT modality is done via convention for 24 hours/day?

CVVHD

What RRT modality is done via convection AND diffusion for 24 hours/day

CVVHDF

IN which patient populations may CVVH, CVVHD, or CVVHDF be beneficial

Hemodynamic instability

What is required with the use of continuous RRT modalities that is NOT required in the office.

Anticoagulation

Roles of the kidneys

vitamin d regulation, control blood pressure, filter, elimination, reabsorption, regulation of pH, RBC production, regulate bone mineralization (ca, p)

Medications that cause AKI

nsaids: ibuprofen, toradol, celecoxib

vancomycin, AGs, FQs,

sglt2i

diuretics

How much resting cardiac output the kidneys receive

25%

Kidney disease less than 7 days

AKI

Kidney disease greater than 3 months

AKD

abrupt decrease in kidney function as evidenced by changes in SCr, UOP, BUN

one of the following:

-increase in SCr by > 0.3 mg/dL within 48 hours

-increase in SCr to >1.5 times baseline within 7 days

-UOP <0.5 ml/kg/hr for > 6 hours

AKI

AKI usually associated/...

Accumulation of waste products and volume

Renal dysfunction can cause elevation of nitrogenous products such as ___

Urea (BUN)

Things that increase BUN separate from AKI

corticosteroids, tetracyclines, gi bleed, high protein diet

Type of AKI:

glomerular injury, tubulointerstitial, tubular obstruction

-vascular damage

-glomerular damage

-acute tubular necrosis

-acute interstitial nephritis

Intrinsic