AKI

Blunt trauma or acceleration-deceleration injury

Atheroembolic AKI-from instrumentation and __

NSAIDs inhibits prostaglandin production, afferent arteriole constrict, ACEIs inhibit Ang II synthesis, efferent arteriole dilate

NSAIDs, ACEIs effect on arteriole

Antibiotic-associated AIN

Fever, rash, eosinophilia

IgG4-related TIN and renal allografts infected with polyoma virus

AIN with plasma cells as dominant infiltrate

24-48 hrs

3-5 days

1 week

Radiocontrast media induced nephropathy acute decline in GFR, peak and return to baseline

Neomycin

Tobramycin, Amikacin, Gentamicin

Neomycin

Aminoglycoside most, intermediate, least nephrotoxic

Cilastatin

Antibiotic that blocks megalin to reduce aminoglycoside nephrotoxicity

>7-15 days

>4g

Antipseudomal beta lactam (piptaz)

Vancomycin Nephrotoxicity- increased risk bec of duration of tx, dose, antibiotic

Copper transport protein 1 (Ctr1)

Organic cation transporter 2 (OCT2)

Two primary transporters involved in cisplatin toxicity

Multidrug and toxin extrusion 1 (MATE1)

Found on apical membrane of PT responsible for efflux of cisplatin, contribute to nephrotoxicity

Bluish-purplish crystals that are nonpolarizable

Renal biopsy of calcium phosphate precipitation in renal tubules

Deferoxamine and glutathione

NO supplementation

Volume expansion

Urine alkalization

Treatment principles of myoglobulinuria (4)

Proximal Tubule

Distal tubule

What part of kidney Ig LC

-Direct tubule toxicity

-Cast Nephropathy

Structural or functional obstruction of bladder neck due to prostatic conditions, anticholinergic agents, neurogenic bladder

Most common cause of postrenal azotemia

Volume depleted patients and patients with severe reduction in GFR

Imaging not reliable in postrenal AKI in what types of patients

S3 segment of the proximal tubule in the outer stripe of the medulla

Bec limited capacity to do anaerobic glycolysis and primarily venous capillary regional blood flow

Part most susceptible to ischemic injury and why? (2)

Reduction in GFR <60 ml/min/1.73 m2

Decrease in GFR >35%

Increase in crea >50%

Structural kidney damage <3 mos

AKD definition (4)

Serum cystatin C

More sensitive and specific than serum creatinine for changes in the GFR

Urinary Cystatin C

Proposed marker of tubular injury

Acute tubular necrosis

Most common form of intrinsic AKI

Diabetic Nephropathy

HIV-associated Nephropathy

Amyloidosis and other infiltrative disease

Polycystic Kidney Disease

Enlarged kidneys but does not rule out CKD (4)

>10-20%

Decrease in ECFV for signs and symptoms of hypovolemia to manifest

Prompt resolution of AKI after restoration of renal perfusion

Definitive diagnosis of prerenal AKI

Hypercalcemia, hyperoxalemia

What electrolye imbalance-band keratopathy and flecked retina?

Necrotizing granulomatous vasculitis

Aminoglycoside toxicity

What causes conductive deafness and neural deafness (2)

Sg > 1.015-1.020, sg 1.010

Specific gravity of prerenal AKI and isosthenuria (ATN)

Phase contrast microscopy

What type of microscope can dysmorphic RBC best seen?

Oxalate crystalluria (needle or dumbbell shaped monohydrate and enveloped-shaped dihydrate)

Ethylene glycol toxicity crystals (2)

Pink, clear

Color of PLASMA in hemolysis and rhabdomyolysis

Contrast administration

Rhabdomyolysis

Sepsis

Ischemia

Burns

Selected nephrotoxins

Fena <1% but observed in the setting of ATN (6)

AKI-ATN

<1, >2

<20, >40

>20, <10-15

<1, >1

Hyaline, muddy brown granular

<35, -

Prerenal AKI vs ATN

FeNa, UNa, BCR, RFI, urine sediment, FeUrea

UNa / (Ucr/Pcr)

Renal failure index formula

Ethylene glycol toxicity

Widening of both serum anion and osmolal gap

Thrombotic microangiopathy

Low plt

Dysmorphic RBCs

Low haptoglobin

High LDH

KIM-1 (kidney injury molecule 1)

Novel biomarker of AKI with decreased specificity since also in CKD and renal cell carcinoma

NGAL (neutrophil gelatinase-associated lipocalin)

Novel biomarkers for ischemic and nephrotoxic kidney injury, children undergoing cardiac surgery

>100-150 ml

Bladder outlet obstruction post void residual volume

Ischemic ATN

Severe toxemia of pregnancy

Postpartum HUS and TTP

Most common causes of AKI in later term pregnancy (3)

-Initiation of chemotherapy of poorly differentiated, rapidly growing lymphoproliferative malignancies

-Spontaneously

-Solid tumors that are highly sensitive to radiation/chemotherapy

Patients at risk for TLS (3)

Hepatic venooclusive disease (VOD)

Profound jaundice, avid salt retention, edema and ascites, oliguric AKI after myeloablative allogeneic transplant

Tubular atrophy and fibrosis

Lymphocytic infiltration

Intranuclear BK virus inclusion bodies

BK nephropathy renal biopsy (3)

At least you in 24 hours from 3 days before to 7 days after chemotherapy initiation

UA >/= 8.0 mg/dL or >/= 25% increase

K 6 or 25

Phos >4.6 (6.5) or 25

Ca </= 7 or >/= 25% decrease

Laboratory TLS + 1 of the ff

Crea >/=1.5x adjusted upper limit

Cardiac arrhythmia or sudden death

Seizure

Cairo-Bishop Laboratory and Clinical TLS definition

Cirrhosis with ascites

AKI

Failure of improvement of kidney function after 2 days of diuretic withdrawal and volume expansion with albumin

Absence of shock or nephrotoxic drugs

Absence of parenchymal renal disease

HRS criteria (5)

Proteinuria > 500 mg/day

Hematuria >50 RBCs/HPF

Abnormal renal sonography

Definition of absence of parenchymal kidney disease

Within 1 month

Within 6 months

Death after how long in HRS 1 and 2

Aminoglycosides, cisplatin, amphotericin B

Hypokalemia in AKI due to impaired K reabsorption from epithelial cell injury in the thick ascending loop

Resistance to PTH

Reduced 1.25 dihydroxyvitamin D

Ca sequestration in injured tissues

Metastatic deposition of calcium phosphate salts

Contributes to hypocalcemia in AKI (4)

Rhabdomyolysis

Acute Pancreatitis

Treatment of metabolic acidosis with HCO3

Hypocalcemia in AKI (4)

Infection

Most common and serious complications in AKI

Delayed resolution or secondary hyperparathyroidism

Cause of mild transient hypercalcemia in recovery of AKI

Critically ill patients with sepsis

Non-critically ill patients with baseline crea >1.5 mg/dL or hyperchloremia >110 mmol/L

SALT-ED trial-use of balanced crystalloid compared to isotonic saline greatest benefit in what patients (2)

Decreasing ventricular distention-shift in starling curve from descending limb to ascending limb

Decreasing venous congestion

Diminishing intraabdominal pressure

Diuretic therapy exacerbate prerenal AKI how? (3)

Albumin 1g/kg per day

6-8 g of albumin/L exceeding 5L

1.5 g/kg of albumin at start and additional 1g/kg on the third day of tx

Albumin dose in

HRS

Large volume paracentesis

Tx of SBP

Crea >1 mg/dL

BUN >30 mg/dL

Total bili >4 mg/dL

albumin tx in SBP will benefit who? (3)

Intraabdominql pressure 20 mmHg or higher associated with dysfunction of one or more organ systems

Abdominal compartment syndrome definition

MAP > 65 nmHg

CVP 10-12 mmHg

UO >0.5 ml/kg/hr

ScVO2 >70%

Hemodynamic targets in early goal-directed therapy (4)

Absolute >0.5 mg/dL and/or relative >25% increase in serum crea that occur within 2-4 days ff iodinated contrast administration

Contrast-associated AKI (CA-AKI) definition

Isotonic intravenous fluids

Low or iso-osmolal contrast media

Beneficial in CA-AKI prevention (2)

low risk 1 ml/kg/hr for 6-12 hours then 6-12 hous after

High risk 3 ml/kg over 1 hr prior then 6 ml/kg over 2-6 hours after

rate and duration of IV saline for prevention of CA-AKI (PRESERVE trial) low risk and high risk

Allopurinol 100 mg/m every 8 hours max 800 mg/day

Rasburicase 0.2 mg/kg

prevention or uric acid generation in AKI (2 with dose)

Amifostine

NAC and dimercaprol

Ethanol and fomepizole

prevention of AKI

Cisplatin nephrotoxicity

Acetaminophen (2)

Ethylene glycol (2)

<2mg/kg/min

renal dose of dopamine

Triggering afferent arteriolar vasodilation and constriction of efferent arteriole

Inhibits sodium transport

Lowers oxygen requirements

How does ANP augment GFR (3)

1.0-1.5 mg/kg

UO <200 mL in 2 hrs

Dose of loop diuretics and goal UO to demonstrate progression to AKI Stage 3

ACEis

Treatment for HPN and AKI associated with scleroderma

Within 7-15 days of discontinuation of offending meds

Methylprenisolone 250-500 mg/day for 3-4 days then oral prednisone 1 mg/kg over 8-12 weeks

Corticosteroids in AIN

-when to give and dose

Furosemide 200 mg, 20 mg/hr

Dose of high dose loop diuretics as IV bolus and continuous infusion

IV regular insulun 10-20 units + 25-50g over 30-60 mins

Albuterol 10-20 mg neb

Dose of IV insulin and dextrose, inhaler albuterol

HCO3 below 15 mmol/l

pH beliw 7.15 to 7.20

when to give emergent treatment for metabolic acidosis

0.8-1 g/kg per day

1-1.5 g/kg if AKI prolonger, hypercatabolif, receiving RRT

dietary protein in AKI

When to give higher? 1-1.5 g/kg body wt per day (3)

20-30 kcal/kg/day, not to exceed 25

Water-soluble vitamins, trace element

Total caloric intake in AKI

What supplements to give if on RRT

< 7g/dl

What hgb level to transfuse

Absolute-volume overload unresponsive to diuretic, persistent hyperk despite medical tx, severe metab acidosis, overt uremic symptoms

Relative-progressive azotemia without uremia, persistent oliguria

Indications for RRT in AKI

Absolute (4)

Relative (2)

Continue crcl <12 ml/min

Stop crcl >20 ml/min

Between up to physician

In acute renal failure network study, when to continue or stop RRT in AKI

3.9/week

KDIGO weekly Kt/v in IHD for AKI

Regional citrate

Nafamostat

Direct thrombin inhibitors hirudin, lepirudin, argatroban

Prostanoids espolrostenol and iloprosy

Alternative anticoagulation during IHD aside from UFH and LMWH (4)

CVVH-convection

CVVHF-diffusion

CVVHDF

Types of CRRT (3)

= ultrafiltrate + dialysate flow rates

=effluent volume indexed to body weight

Clearance of urea = total effluent rate

Dose of therapy

20-25 ml/kg/hr

KDIGO effluent volume during CRRT in AKI

SLEF

EDD

SLEDD-f

Types of PIRRT (3)