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Acute Kidney Injury - Mini Lecture: Updated 02/2013

This document provides an overview of acute kidney injury (AKI), including its incidence, presentation, evaluation, and causes. It discusses the AKIN criteria for staging AKI and outlines the approach to determining if the cause is prerenal, intrinsic renal, or postrenal. Common intrinsic renal diseases like acute tubular necrosis, acute interstitial nephritis, and contrast-induced nephropathy are reviewed along with their typical lab and microscopy findings. The take-home points emphasize early identification of AKI, differentiating the cause, initiating appropriate treatment, and monitoring patients at risk.

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Asmalina Azizan
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150 views11 pages

Acute Kidney Injury - Mini Lecture: Updated 02/2013

This document provides an overview of acute kidney injury (AKI), including its incidence, presentation, evaluation, and causes. It discusses the AKIN criteria for staging AKI and outlines the approach to determining if the cause is prerenal, intrinsic renal, or postrenal. Common intrinsic renal diseases like acute tubular necrosis, acute interstitial nephritis, and contrast-induced nephropathy are reviewed along with their typical lab and microscopy findings. The take-home points emphasize early identification of AKI, differentiating the cause, initiating appropriate treatment, and monitoring patients at risk.

Uploaded by

Asmalina Azizan
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPT, PDF, TXT or read online on Scribd
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TEACHING RESEARCH PUBLIC SERVICE

Acute Kidney Injury - Mini Lecture


Updated 02/2013
Objectives
Quickly and easily identify and workup acute
kidney injury.
Background
The incidence of AKI is estimated at 1% of patients that
present to the hospital and 7-50% of patients in the ICU.
Part of the initial history should be determining every
patients baseline Cr.
May present as Uremia (malaise, anorexia, nausea,
vomiting), but is usually asymptomatic.
Acute Kidney Injury Network (AKIN) Criteria
Stage Cr Criteria UOP Criteria
1 Crby 1.5-2x baseline or < 0.5 ml/kg/hr for 6hr
Crby 0.3 mg/dl
2 Crby 2-3x < 0.5 ml/kg/hr for 12hr
3 Crby more than 3x or Crby < 0.3 ml/kg/hr for 24hr
0.5 if baseline >4mg/dl Or anuria for 12h
AKI can be Prerenal, Intrinsic or Postrenal

Acute Kideny Injury

Prerenal
Postrenal
Uosm > 5000 mosm/kg
Uosm: variable
Una < 20meq/L
FEna < 1% Intrinsic Renal Diseases Una: low early, high late
FEna: variable
Microscopy - bland
Microscopy - bland

Acute Interstitial Nephritis Acute Glomerulonephritis


Ischemic / Toxic ATN
Uosm: variable, ~300 mosm.kg Uosm: variable (>400 in early GN)
Uosm ~ 300 mosm/kg
Una > 40 meq/L Una: variable (<20meq/l in early GN)
Una > 40meq/L FEna: variable, <1% in early GN
FEna > 2%
FEna > 2% Microscopy hematuria, proteinuria
Microscopy leukocytes,
Microscopy dark pigment cast Erythrocyte casts (dysmorphic)
erythrocyts, leukocyte casts
Prerenal Azotemia
Prerenal azotemia is the most common cause of
acute kidney injury in the outpatient setting
Look for patients with decreased PO, diarrhea,
vomiting, tachycardia, orthostasis.
Order: UA, Uosm, Una, Ucr, BMP, Uurea (if on
diuretics)
The kidney functions properly in patients with
prerenal azotemia.
True volume depletion can be treated with normal
saline.
Decreased effective arterial blood volume can be
present in CHF, Cirrhosis or nephrotic syndrome.
Treatment should focus on the underlying disease.
Intrinsic Kidney Diseases
ATN - Acute Tubular Necrosis
Usually occurs after an ischemic event or exposure to
nephrotoxic agents.
Look for muddy brown casts and FeNa>2%
AIN - Acute Interstitial Nephritis
Classic presentation is fever, rash, eosinophilia and Cr bump 7-
10 days after drug exposure.
Urine may show leukocytes, leukocyte casts and erythrocytes,
cultures will be negative.
CIN - Contrast Induced Nephropathy
Increased Cr of 0.5mg/dl or 25% 48hrs after contrast
administration.
Prevent with NS or isotonic fluid+sodium bicarb, hold NSAIDs,
metformin and diuretics (in patients without fluid overload).
Others Glomerular Disease, Pigmented Nephropathy,
Thrombotic Microangiopathy
Postrenal Disease
Obstruction anywhere in the urinary tract
Bladder outlet obstruction can be seen with bladder
scan and relieved with catheterization
Ureteral obstruction and hydronephrosis may be seen
on ultrasound and noncontrast CT
Order: Order: UA, Uosm, Una, Ucr, BMP, Uurea (if on
diuretics)
Patients often have a history of pelvic tumors,
irradiation, congential abnormalities, kidney
stones, genitourinary, procedures or surgeries,
and prostatic enlargement.
AKI can be Prerenal, Intrinsic or Postrenal

Acute Kideny Injury

Prerenal
Postrenal
Uosm > 5000 mosm/kg
Uosm: variable
Una < 20meq/L
FEna < 1% Intrinsic Renal Diseases Una: low early, high late
FEna: variable
Microscopy - bland
Microscopy - bland

Acute Interstitial Nephritis Acute Glomerulonephritis


Ischemic / Toxic ATN
Uosm: variable, ~300 mosm.kg Uosm: variable (>400 in early GN)
Uosm ~ 300 mosm/kg
Una > 40 meq/L Una: variable (<20meq/l in early GN)
Una > 40meq/L FEna: variable, <1% in early GN
FEna > 2%
FEna > 2% Microscopy hematuria, proteinuria
Microscopy leukocytes,
Microscopy dark pigment cast Erythrocyte casts (dysmorphic)
erythrocyts, leukocyte casts
Practice Question
A 74 year old man was hospitalized 3 days ago with
cellulitis. He has a history of HTN, HLD, PVD and has
been non-compliant with his medications. At presentation,
his vitals were T-37, BP-170/90, HR-90, RR-20 and Cr was
1.5. He was started on Cefazolin and his home meds
(Lisinopril, Metoprolol, HCTZ, Amolodipine, Pravastatin and
ASA) were restarted.
Today, his vitals are T-37, BP-110/55, HR-60, RR-16
and his Cr is 2.7, FeNa-2.3%, FeUrea-51%, UA shows
trace protein and occasional Granular casts. UOP has been
stable.
What is the most likely cause of his AKI?
A. Acute Interstitial Nephritis
B. Benign Prostate Hypertrophy
C. Acute Tubular Necrosis
D. Prerenal Azotemia
Take Home Points
Identify AKI early on
Monitor serum Cr for at risk patients
Make sure I/Os are recorded correctly
Diagnose as Prerenal, Intrinsic or Postrenal
Detailed history
Order routine labs including BMP, UA, Uosm, Ucr,
Una (Urine Urea if on diuretics)
Imaging studies as necessary
Begin appropriate treatment
Stop offending agent
Fluids if appropriate
Relieve obstruction
Renal dosing of meds
Thank You

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