Case: Acute Kidney Injury and Drug-induced AKI

Category of AKI:

AKI is classified into three categories.

 Prerenal AKI is secondary to reduced blood delivery to the kidney, such as with

hypotension or severe heart failure.

 Intrinsic AKI is a result of damage (eg, nephrotoxic drugs) to the structural tissues of the

kidney and

 postrenal AKI is caused by obstruction of the urinary outflow, such as with prostatic

hypertrophy.

There are additional laboratory tests that can aid in the differential diagnosis of AKI:

Estimation of creatinine clearance: As an estimate of kidney function is necessary to

determine dosages of medications in kidney disease, creatinine clearance (CLcr) is routinely

calculated to estimate GFR. Refer to the textbook chapter on quantifying kidney function for

equations to estimate kidney function.

1
The Cockcroft–Gault equation for estimation of Clcr was derived in steady-state conditions

(e.g., creatinine production/elimination is constant) and can provide a quick bedside estimate of

GFR in individuals whose kidney function is relatively constant. However, SCr is a relatively

insensitive marker for AKI as a rise in SCr may lag 48–72 hours from the time of kidney injury.

Thus, factoring in a single creatinine value in the Cockcroft–Gault equation may overestimate

GFR in AKI, thus limiting its use in patients with unstable kidney function (i.e., fluctuating by

more than 20% per day). In addition, equations to estimate GFR, such as the Modification of

Diet in Renal Disease (MDRD) equation and the Chronic Kidney Disease-Epidemiology

Collaboration (CKD-EPI) equation, are not useful in AKI since they are also based on steady-

state SCr concentrations. Several equations have been developed to assess unstable kidney

function, such as the Jelliffe equation,3, which factors in a 3 change in SCr over 24 hours.

Further research is needed to validate these equations before their routine use.

Measuring Clcr using urinary creatinine elimination data may also overestimate GFR,

particularly in critically ill patients. Thus, it is important to acknowledge that estimated Clcr

values derived in AKI patients using equations that assume steady state are likely to overestimate

kidney functioning in patients whose kidney function is worsening. New biomarkers are needed

to detect early evidence of AKI.• In this case, the patient’s SCr concentration on admission was

stable at 1.5 mg/dL. His admission Clcr is estimated as:

2
 Where weight is ideal body weight (IBW) in the instance where the patient does not weigh less

than their IBW or is not overweight; see the textbook chapter discussion on appropriate weights

to factor into the calculations. Using Cockcroft–Gault equation with his most current SCr data is

as follows:

 Stage of AKI:• AKI can be classified into stages based on changes in SCr from baseline,

changes in urine output, or need for renal replacement therapy (RRT).

 Stage 1: AKI includes a modest increase in SCr from baseline (SCr of at least 0.3 mg/dL from

baseline or 1.5- to 1.9-fold increase from baseline) or urine output of <0.5 mL/kg/ hr for 6–12

hours. There is no need for RRT.

 Stage 2 is defined as a 2- to 2.9-fold increase in SCr from baseline or urine output of <0.5

mL/kg/hr for 12 hours or greater, with no need for RRT.

 Stage 3:It represents the most severe stage and includes a threefold increase in SCr from

baseline or an increase inSCr to at least 4 mg/dL. It is also defined as a urine output of <0.3

mL/kg/hr for at least 24 hours or anuria for 12 hours or more. If RRT is needed, this indicates

stage 3 regardless of SCr or urine output. In patients <18 years of age, a decrease in estimated

glomerular filtration rate (GFR) to <35 mL/min per 1.73 m2 also represents stage 3

Case:

3
A 72-year-old man with a history of hypertension (HTN), CAD, heart failure (HF),uncontrol DM

dyslipidemia and Osteoarthritis is admitted to the hospital with an acute UGI bleed resulting in

prerenal acute kidney injury (AKI) from hypovolemia and hypotension and uncontrol diabetes.

After an unsuccessful attempt to stop the bleeding during an EGD, the patient is taken for

emergent surgery where hypotension continues requiring the start of norepinephrine.

Postoperatively, the patient remains hypotensive and experiences oliguric acute tubular necrosis

(ATN) that fails to respond to IV hydration and furosemide. Subsequently, he experiences acute

pulmonary oedema from volume overload and worseningHF and is started on dobutamine and

continuous venovenous hemodiafiltration (CVVH-DF).Then, Patients were found to have an

infection due to Serratia Marcescens mediastinitis (a gram-negative bacillus that is an

opportunistic agent in respiratory tract infections, urinary tract infections, and septicemia) and

start treatment of gentamicin plus cefepime for 6 weeks.

A. Patient Description
Name : UCE Age: 72 years old
Reg. No. : Gender: male
Admission : 8/3/2019 Weight: ~ 45kg
Race : Arab Height: ~ 160cm
BMI: ~17.58kg/m2(underweight)

B. Chief Complaint (CC)

Acute UGI bleed

4
History of Present Illness (HPI)
Patient was admitted before 1 year and discharged after 1 week of admission due to a
hypertension crisis and severe pain due to astoeothritis

Past Medical History (PMHx)

 Diabetes Mellitus 10 years ago
 Hypertension
 Dyslipidemia
 History of heart failure (HF), and
 Osteoarthritis
 Uncontrol DM

Family History
Patient is living with her wife and a caregiver who are taking care of her.

 Medication History Interview

1. What medicines (prescribed medicine) are you having at home or prior to
the current hospitalization/admission?

DRUGS INDICATION RECORD HERE WHAT THE PATIENT

SAYS, NOTING ANY ANOMALIES WITH
THE DRUGS

enalapril Hypertension

Ibuprofen Painkiller

T. Simvastatin 20mg ON Hyperlipidemia

T. Bisoprolol 5mg OD HF

S/C Mixtard 14U BD Diabetes Mellitus

5
G. Review of System (ROS)/physical examination
Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7
8/3/19 9/3/19 10/3/19 11/3/19 12/3/19 13/3/19 14/3/19

GENERAL STATUS Lethargic Lethargic Lethargic Lethargic Lethargic Lethargic Lethargic

Giddiness Giddiness Giddiness Giddiness Giddiness Giddiness Giddiness
Confused Confused Confused Confused Confused Confused Confused
GENITOURINARY vomit vomit vomit vomit vomit vomit vomit
Poor appetite Poor Poor Poor Poor Poor Poor
GI Bleeding appetite appetite appetite appetite appetite appetite
GI GI Bleeding GI GI Bleeding GI Bleeding GI
Bleeding Bleeding Bleeding
HEPATIC - - - - - - -

RESPIRATORY No No No No Pulmonary Pulmonary Pulmonary

tachypnea tachypnea tachypnea tachypnea Edema Edema Edema
No bilateral No No bilateral No tachypnea tachypnea tachypnea
crackles bilateral crackles bilateral bilateral bilateral bilateral
Lungs clear crackles Lungs clear crackles crackles crackles crackles
Lungs Lungs clear
clear clear
CARDIOVASCULAR DRNM, DRNM, DRNM, DRNM, DRNM, DRNM, DRNM,
normal S1,S2 normal normal normal normal normal normal
S1,S2 S1,S2 S1,S2 S1,S2 S1,S2 S1,S2
ABDOMEN tender tender tender tender tender tender tender

SKIN/MUSCLE No skin No skin No skin No skin No skin No skin No skin

lesions, lesions, lesions, lesions, lesions, lesions, lesions,
warm, dry warm, dry warm, dry warm, dry warm, dry warm, dry warm, dry
HEENT PERRLA, PERRLA, PERRLA, PERRLA, PERRLA, PERRLA, PERRLA,
EOMI EOMI EOMI EOMI EOMI EOMI EOMI
HEMATOLOGIC Bleeding Bleeding Bleeding Bleeding Bleeding Bleeding Bleeding
tendency in tendency tendency in tendency tendency in tendency in tendency in
GI in GI GI in GI GI GI GI
ALLERGIC AND NKDA NKDA NKDA NKDA NKDA NKDA NKDA
IMMUNOLOGIC

6
 LABORATORY/OBJECTIVE DATA Please make a plot (data vs day) in excel sheets for each of
the available data to see the trend throughout the
hospitalization*refer to clinical practice guideline
REFLO CHART

HbA1c last month: 7.0%

D1 8/3/19: 11.30pm 26mmol/L

D2 D3 D4 D5 D6 D7
9/3/2019 10/3/2019 11/3/2019 12/3/2019 13/3/2019 14/3/2019
Time Readin Time Readin Tim Readin Time Readin Time Readin Time Readin
gs gs e gs gs gs gs
(mmol (mmol (mmol (mmol (mmol (mmol
/L) /L) /L) /L) /L) /L)
7am 10.0 7am 9.3 7am 8.3 8am 14.0 7 am 13.4 7am 14.4

11.30p 5.3 11am 13.0 11p 10.5 10.30a 16.0 11.30a 14.5 11.30a 9.4
m m m m m
3pm 8.4 4.30p 18.0 5pm 16.0 5pm 21.6 5pm 14.0 5pm 16.2
m
5.30p 13.5 10pm 17.7 10p 16.4 10pm 19.9 10 pm 11.3 10pm 9.4
m m
10pm 12.2

D8 D9 D10 D11 D12 D13

15/3/2019 16/3/2019 17/3/2019 18/3/2019 19/3/2019 20/3/2019
Time Reading Tim Reading Tim Reading Tim Reading Tim Reading Tim Reading
s e s e s e s e s e s
(mmol/ (mmol/ (mmol/ (mmol/ (mmol/ (mmol/
L) L) L) L) L) L)
7am 9.5 7am 17.1 7am 10.0 7am 11.2 7am 11.6 7am 10.2

10.30a 10.8 11a 18.3 11p 13.5 11a 14.3 11a 12.3 11a 9.2
m m m m m m
5pm 16.8 5pm 21.8 5pm 18.6 5pm 17.0 5pm 15.6

10pm 13.8 10p 18.1 10p 13.7 10p 13.1 10p 10.5
m m m m

7
BLOOD PRESSURE, HEART RATE AND SPO2 CHART

8/3/2019
Time BP (mmHg) HR (beats/min) SPO2 (%) Comments
11PM 100/50 80 98

9/3/2019
Time BP (mmHg) HR (beats/min) SPO2 (%) Comments
7AM 95/45 68 95
12PM 90/44 65 95
3PM 95/45 85 96
10PM 100/50 75 95

10/3/2019
Time BP (mmHg) HR (beats/min) SPO2 (%) Comments
4AM 95/45 70 95
7AM 90/44 75 95
11AM 95/45 80 95
3.15PM 100/50 67 95
3.35PM 90/44 70 97

8
 4.15PM 95/45 66 97
6.20PM 100/50 61 96
11PM 98/44 54 99

11/3/2019
Time BP (mmHg) HR (beats/min) SPO2 (%) Comments
7AM 90/44 56 100
2.15PM 95/45 72 95
7PM 100/50 88 95
11PM 95/45 92 95

12/3/2019
Time BP (mmHg) HR (beats/min) SPO2 (%) Comments
7AM 90/44 89 99
2.15PM 95/45 104 99
10PM 100/50 100 99
2AM 95/45 98 99

13/3/2019
Time BP (mmHg) HR (beats/min) SPO2 (%) Comments
7AM 90/44 89 98
12PM 95/45 70 98
2.30PM 100/50 68 98
9.50PM 95/45 74 98

14/3/2019
Time BP (mmHg) HR (beats/min) SPO2 (%) Comments
7AM 90/44 68 100
2.45PM 95/45 70 98
10.40PM 100/50 64 98

15/3/2019
Time BP (mmHg) HR (beats/min) SPO2 (%) Comments
7AM 100/50 63 98
1PM 95/45 87 95
4PM 100/50 72 96
10.35PM 95/45 67 98

16/3/2019
Time BP (mmHg) HR (beats/min) SPO2 (%) Comments
7AM 90/44 62 97
12PM 90/44 68 97
2.30PM 95/45 69 98
11PM 100/50 74 97

9
 DAY DAY DAY 3 DAY 4 DAY5 DAY6 DAY7 DAY8 DAY9 DAY10 DAY11 DAY12 DAY13
1 2 10/3/1 11/3/1 12/3/1 13/3/1 14/3/1 15/3/1 16/3/1 17/3/1 18/3/1 19/3/1 20/3/1
8/3/1 9/3/1 9 9 9 9 9 9 9 9 9 9 9
NORMAL 9 9
VITAL SIGNS
140/90
mmHg
BP -Ave AM (JNC8)
140/90
mmHg
BP -Ave PM (JNC8)
60-100
HR -Ave beats/min
60-100
HR -Ave beats/min
TEMP (0C) 37.7 37.7 37.3 37 37.1 37.1 37.1 38 37.5 37.1 38.5 37.3 37.1
BLOOD
CHEMISTRY
135-145
Na+ mmol/L 123 126 124 126 124 129 127 130
3.5-5.0
8 8 8 8 8 8 8 8 8 8 8
K+ mmol/L
1.7-8.3
BUN mg/dL 15 50
Serum
Creatinine 1.2 mg/dL 1.5 1.8 1.9 1.9 2.00 2.2 2.3 2.3 2.3 2.4 2.5
2.1-2.55
Ca2+ mol/L
0.66-
Mg2+ 0.99mmol/L
0.87-
Phosphate 1.45mmol/L
<
RBS 10mmol/L
210-
240umol/
Uric acid L
AM (6-
10am) 33-
537nmol/L
PM (4-8am)
68-327 600
Cortisol nmol/L (AM)
FLUID
Input 1450 1450 1450 1450 1450 1450 1450 1450 1450 1450 1450 1450
Output 1500 1500 1500 1500 1500 1500 1500 1500 1500 1500 1550 1550
800-
Balance 1200ml -50 -50 -50 -50 -50 -50 -50 -50 -50 -50 -100 -100

10
HEMATOLOG
Y
Hct 36 - 46 I 26.3 21.8 22.2 29.4
HgB 12-16g/dl 8.9 7.4 7.5 7
4.5-11
WBC x109/L 17.4 25.7 22.7 20.3
4.7-6.1 x
RBC 1012/L
MCV 80-100 fL
32-36
MCHC g/dL

130-400
PLT x103/ ml
CRP <3mg/L 60.8
LIVER
FUNCTION
Total Protein 66-87g/L
Albumin 38-51g/L
Globulin 20-36
Tot bilirubin 0-24 mol/L
ALT 0-42U/L 29 51 59
ALP 34-104U/L 173 283 244
AST 5 – 40 U/l
COAGULATION PROFILE
NORMAL
10.7-13.7
PT sec
INR 0.9 – 1.2
27.6 – 38.8
APPT sec
D - dimer < 0.5Ng/ml
BLOOD GASES
pH 7.36-7.44 7.47
32-45
pCO2 mmHg 40.3
83-
pO2 108mmHg 20.7
23-29
HCO3- mmol/L 28.4
CARDIAC
CK 24-195U/L
LDH
Lipid profile

11
 LDL 190mg/DL
Total cholesterol 300mg/DL

Drug treatment in the ward-Medication record

12
 Drug Dose/ Indication D1 D2 D3 D4 D5 D6 D7 D8 D9 D1 D11
Name/Route Frequency 8/3 9/3 10/ 11/ 12/ 13/ 14/ 15/ 16/ 0 18/3
3 3 3 3 3 3 3 17/
3
T. 20mg ON Dyslipide
Simvastatin mia
T. 40mg OD Gastritis
Pantoprazol
e
S/C Mixtard *adjusted Diabetes 14 14 14 16 20 20 20 22 22 24 28U(7a
based on Mellitus U U U U U U U U U U m)
Reflo 24U(5p
m)
Gentamicin
Cefepime
Furosemide 40 mg IV 80
MG IV 160
MG IV 4-6
HOURS
IV hydration
Dobutamine
Norepineph Vasopressor
rine
naproxen
Dual
anitplatlete
therapy

1.a. What subjective and objective information indicates the presence of AKI?

1.b. What additional information is needed to assess this patient’s AKI postoperatively

fully?

2.a. Assess the severity of AKI based on the subjective and objective information available

13
2.b. Create a list of the patient’s drug therapy problems and prioritize them. Include an

assessment of medication appropriateness, effectiveness, safety, and patient adherence.•

Problem #1:

• Problem #2:

• Problem #3:

Problem #5: cells

Problem #6:

Develop a Care Plan

3.a. What are the goals of pharmacotherapy in this case?

• Correct anaemia:

).

3.b. What non drug therapies might be useful for this patient?

14
.

• Renal replacement therapy (RRT):

• Nutritional support:

What feasible pharmacotherapeutic alternatives are available for treating the disease or

drug therapy problem?

• Furosemide: overloaded.

• Low-dose dopamine (=3 mcg/kg/min):

.• Natriuretic peptides:

• Mannitol:

3.d. Create an individualized, patient-centered, team-based care plan to optimize

medication therapy for this patient’s AKI and other drug therapy problems. Include

specific drugs, dosage forms, doses, schedules, and durations of therapy:

Problem #1:

AKI requires nonpharmacologic and pharmacologic management and modification of drugs that

may contribute to AKI.

15
• Initiate loop diuretic therapy:.

• Continue to hold metoprolol, furosemide, enalapril, and amlodipine

Problem #2:

Acute UGI bleed is likely caused by the combination of NSAID and DAPT use.

Utilize vasopressor therapy (norepinephrine) to maintain an adequate BP to maintain renal

blood flow and perfusion.

Implement the Care Plan

4.a. What information should be provided to the patient to enhance compliance, ensure

successful therapy, and minimize adverse effects?

Problem #1:.

Problem #3:

Ciprofloxacin•

4.b. Describe how care should be coordinated with other healthcareproviders.• Treatment of

16
.

Clinical parameters:

17