Artifacts in Nuclear Medicine with Identifying and resolving artifacts.
AKI.pptx
1. TEACHING · RESEARCH · PUBLIC SERVICE
Acute Kidney Injury - Mini Lecture
Updated 02/2013
2. • Quickly and easily identify and workup acute
kidney injury.
Objectives
3. • 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
Background
Stage Cr Criteria UOP Criteria
1 Cr↑by 1.5-2x baseline or
Cr↑by 0.3 mg/dl
< 0.5 ml/kg/hr for 6hr
2 Cr↑by 2-3x < 0.5 ml/kg/hr for 12hr
3 Cr↑by more than 3x or Cr↑by
0.5 if baseline >4mg/dl
< 0.3 ml/kg/hr for 24hr
Or anuria for 12h
4. AKI can be Prerenal, Intrinsic or Postrenal
Acute Kideny Injury
Prerenal
Uosm > 5000 mosm/kg
Una < 20meq/L
FEna < 1%
Microscopy - bland
Intrinsic Renal Diseases
Postrenal
Uosm: variable
Una: low early, high late
FEna: variable
Microscopy - bland
Ischemic / Toxic ATN
Uosm ~ 300 mosm/kg
Una > 40meq/L
FEna > 2%
Microscopy – dark pigment cast
Acute Interstitial Nephritis
Uosm: variable, ~300 mosm.kg
Una > 40 meq/L
FEna > 2%
Microscopy – leukocytes,
erythrocyts, leukocyte casts
Acute Glomerulonephritis
Uosm: variable (>400 in early GN)
Una: variable (<20meq/l in early GN)
FEna: variable, <1% in early GN
Microscopy – hematuria, proteinuria
Erythrocyte casts (dysmorphic)
5. • 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.
Prerenal Azotemia
6. • 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
Intrinsic Kidney Diseases
7. • 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.
Postrenal Disease
8. AKI can be Prerenal, Intrinsic or Postrenal
Acute Kideny Injury
Prerenal
Uosm > 5000 mosm/kg
Una < 20meq/L
FEna < 1%
Microscopy - bland
Intrinsic Renal Diseases
Postrenal
Uosm: variable
Una: low early, high late
FEna: variable
Microscopy - bland
Ischemic / Toxic ATN
Uosm ~ 300 mosm/kg
Una > 40meq/L
FEna > 2%
Microscopy – dark pigment cast
Acute Interstitial Nephritis
Uosm: variable, ~300 mosm.kg
Una > 40 meq/L
FEna > 2%
Microscopy – leukocytes,
erythrocyts, leukocyte casts
Acute Glomerulonephritis
Uosm: variable (>400 in early GN)
Una: variable (<20meq/l in early GN)
FEna: variable, <1% in early GN
Microscopy – hematuria, proteinuria
Erythrocyte casts (dysmorphic)
9. 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
Practice Question
10. • 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
Take Home Points
Other points to consider:
1) Can occur over hours to weeks (presence for >3 months meets definition of CKD)
2)While we typically measure the serum Cr to determine kidney function, it is not a great marker as some individuals can lose ~50% of their GFR before the level becomes abnormal. It is important to be aware that the rise in Cr lags behind the time of injury.
3) A patient’s Cr going for 0.6 to 0.9 can potentially be much more concerning that going from 3 to 4
4) A rise in Cr is not always pathogenic (ex. Bactrim and H2-blockers decrease tubular secretion of creatinine)
The whole talk can be given from this slide, so take time to go over each box
Audience Participation:
Sodium is not a good marker of kidney function in patients on diurectics. What test should you use?
- FeUrea (replace sodium with urea in the equation above). FeUrea<35% suggests prerenal AKI
Audience Participation:
Why do you get an elevated BUN-creatinine ratio?
In patients with prerenal azotemia, both BUN and Creatinine can increase, but BUN often increases disproportionately more than creatinine. In the setting of decreased effective blood volume, slow flow through the tubules allows more time for BUN to be reabsorbed and creatinine to be secreted. In other words, BUN clearance goes down lower than Cr.
If you don’t identify Prerenal Azotemia, it will progress to ATN
Other types of disease to consider are:
Pigmented Nephropathy from hemoglobin or myoglobin
Thrombotic Microangiopathy- TTP/HUS
And the whole topic of glomerular disease
This is a repeat of the earlier slide to review
Correct answer is C. The patient is suffering from iatrogenic ATN. His history suggests CKD and vascular disease. If he is chronically hypertensive and has his BP dropped to the normal range, he becomes effectively hypotensive if his kidneys cannot compensate to increase renal blood flow.
A – AIN usually manifests a week after starting the offending agent
B – There is nothing in the question stem to indicate that this patient without a history of BPH is suffering from it acutely
D – His FeNa and FeUrea are elevated making ATN more likely