by Dr.Ghufran A. Hariri Family medicine department 22.4.2020

1. Dr. Ghufran A. Hariri
Supervised by:
Dr.Abeer Al-mohammadi

2. Objectives:
• Introduction
• Staging
• Causes
• History & Exam
• Investigation
• Management
• Prognosis
• Follow up ( post AKI )
• Summery

3. Introduction
• Acute kidney injury (AKI)
• previously called acute renal failure (ARF)
• is an abrupt and usually reversible decline in the glomerular filtration rate (GFR).
This results in an elevation of serum blood urea nitrogen (BUN), creatinine, and
other metabolic waste products that are normally excreted by the kidney.

4. Introduction
• Acute kidney injury (AKI) has been observed in 9 % of
hospitalized patients and in more than 50 % of patients in
the intensive care unit.
• The two major causes of AKI that occur in the hospital are
prerenal disease and acute tubular necrosis (ATN).
Together, they account for approximately 65 to 75 % of
cases of AKI.

5. KDIGO
• The Kidney Disease: Improving Global Outcomes
• Before diagnosing and classifying AKI, one should assess and optimize volume
status and exclude obstruction
• The KDIGO guidelines define AKI as follows :
• Increase in serum creatinine by ≥0.3 mg/dL (≥26.5 micromol/L) within 48 hours, OR
• Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to
have occurred within the prior seven days, OR
• Urine volume <0.5 mL/kg/hour for six hours.

6. Staging criteria (KDIGO)
AKI
Stage 1
Increase in serum creatinine to 1.5 to 1.9 times
baseline
increase in serum creatinine by ≥0.3 mg/dL (≥26.5
micromol/L)
reduction in urine output to <0.5 mL/kg/hour for 6 to
12 hours
Stage 2
Increase in serum creatinine to 2.0 to 2.9 times
baseline
reduction in urine output to <0.5 mL/kg/hour for ≥12
hours.
Stage 3
Increase in serum creatinine to 3.0 times baseline
increase in serum creatinine to ≥4.0 mg/dL (≥353.6
micromol/L)
reduction in urine output to <0.3 mL/kg/hour for ≥24
hours
anuria for ≥12 hours
the initiation of renal replacement therapy
in pt. <18 years, decrease in estimated glomerular
filtration rate (eGFR) to <35 mL/min/1.73 m2.
OR OR
OR
OR
OR
OR
OR
OR

7. Causes
AKI
Pre-renal
Intrinsic
Post-renal

8. Pre-renal
Systemic
Vasodilation
Sepsis,
shock
Volume Depletion
Renal loss
Diuretic Overuse,
Osmotic Diuresis (e.g,
DKA )
Extrarenal loss
•Vomiting, Diarrhea,
Burns,
•Ex. Sweating, Blood
Loss
Intrarenal
vasoconstriction
Drugs
•NSAID, ACEI/ARBS,
Cyclosporine,
Tacrolimus, Contrast.
Cardiorenal
Syndrome
Hepatorenal
Syndrome
Abdominal
Compartment
Syndrome
Hypercalcemia
1. Pre-renal AKI

9. 2. Intrinsic AKI
Intrinsic
Tubular
Acute Tubular
Necrosis (ATN)
Interstitial
Acute Interstitial
Nephritis (AIN)
Glomerular
glomerulonephritis
Vascular
Small-med vessels

10. Post-renal
Extrarenal
Bladder neck
BPH, prostate CA, neurogenic
bladder, anticholinergic drugs.
Ureteral (bilateral or unilateral in
single kidney)
pelvic mass/malignancy ,
lymphadenopathy,
retroperitoneal fibrosis.
Intrarenal
Nephrolithiasis, crystals (e.g,
acyclovir, indinavir), clots, tumors
3. Post-renal AKI

11. 1. Pre-renal AKI History
• Medical conditions : liver cirrhosis , fulminant hepatitis , CHF , primary
hyperparathyroidism, malignancy, uncontrolled diabetes.
• Drug intoxication ( vitamin D, NSAID, ACEI/ARBS, Diuretics, laxatives)
• h/o of fluid loss (vomiting , diarrhea, bleeding, burns).
• h/o reduced fluid intake.

12. • Signs of dehydration ( tachycardia,
tachypnea , orthostatic hypotension, delay
capillary refill, pale/mottled skin, Poor skin
turgor)
• Signs of chronic liver disease
• Dilated neck veins, S3 heart sound,
pulmonary rales, peripheral edema.
1. Pre-renal AKI Exam

13. 2. Intrinsic AKI

14. 2.A. AcuteTubular Necrosis
ATN
Ischemic
Same as
pre-renal
Nephrotoxic
Exogenous
Endogenous

15. Nephrotoxic
Exogenous
Radiographic contrast, Amphotericin B, Aminoglycoside, Cyclosporine
and tacrolimus (calcineurin inhibitors), Cisplatin, Ifosfamide, Foscarnet,
Sulfa drugs, Pentamidine, Mammalian target of rapamycin (mTOR)
inhibitors (eg, everolimus, temsirolimus), Oral Sodium phosphate.
crystal-induced :
ethylene glycol , vitamin C, Acyclovir and indinavir
Endogenous
2.A. AcuteTubular Necrosis

16. 2.A. AcuteTubular Necrosis
Nephrotoxic
Exogenous
Endogenous
•Crystal-induced :
•high cellular turnover (ie, uric acid, calcium phosphate), in certain
malignancies or the treatment of malignancies
Pigments :
-Myoglobinuria (heme protein found in muscle) e.g Rhabdomyolysis.
-Hemoglobinuria most often is associated with transfusion reactions.
Monoclonal :
Multiple Myloma ( Ig light chains )

17. • Recent surgery, hypotension, sepsis, muscle necrosis, or volume depletion, as well as exposure
to nephrotoxic agents.
• Myalgias,Generalized weakness, Darkened urine H/O recent trauma or infection
(Rhabdomyolysis)
• Several of those may be present Simultaneously, which increases the risk and severity of ATN.
• pre-existing medical conditions or medication use (eg, diabetes mellitus, multiple myeloma,
nonsteroidal anti-inflammatory drugs)
2.A. AcuteTubular Necrosis History

18. • Muscle tenderness due to rhabdomyolysis
• Abdominal distension may raise the concern of intra-abdominal hypertension and
compartment syndrome
• Hypovolemia (eg, low jugular venous pressure, loss of skin turgor, orthostatic
hypotension, dry mucous membranes, tachycardia).
2.A. AcuteTubular Necrosis Exam

19. 2.B. Acute Interstitial Nephritis
AIN
Drugs (70 - 75%)
Systemic diseases (10 -20%)
Infections (4 – 10%)
Tubulointerstitial nephritis and uveitis (TINU)
syndrome (5 – 10%)

20. Drugs
Diuretics Furosemide (Lasix), thiazides, triamterene (Dyrenium)
NSAID Almost all agents
Antibiotic
Cephalosporins, penicillin , rifampin, sulfonamides ciprofloxacin6,
ethambutol (Myambutol), isoniazid (INH), macrolides, tetracycline,
vancomycin7.
Miscellaneous
Acyclovir, Allopurinol, amlodipine8 ,azathioprine, captopril,
carbamazepine, clofibrate, cocaine, creatine9, diltiazem10 , famotidine ,
indinavir11, mesalazine12 , omeprazole13 (Prilosec), phenteramine14,
phenytoin , pranlukast 15, propylthioruacil16, quinine, ranitidine.
2.B. Acute Interstitial Nephritis

21. Infection
Viral
Cytomegalovirus, Epstein-Barr Virus,
Hantaviruses, Hepatitis C, Herpes Simplex Virus,
HIV, Mumps4, Polyoma Virus.
Bacterial Infections Corynebacterium Diphtheriae, Legionella3,
Staphylococci, Streptococci, Yersinia.
2.B. Acute Interstitial Nephritis

22. Systemic diseases SLE, sarcoidosis, and Sjögren's syndrome.
2.B. Acute Interstitial Nephritis
Tubulointerstitial nephritis and
uveitis (TINU) syndrome
interstitial nephritis + uveitis
& occasionally systemic findings: fever, weight loss,
fatigue, malaise, anorexia, asthenia, abdominal and
flank pain, arthralgias, myalgias, headache, polyuria,
and/or nocturia.

23. • Medication use, rash, arthralgias, fever, infectious illness.
• Rifampin, PPI and NSAIDs less commonly associated with fever, rash, and eosinophilia.
• Nonspecific signs and symptoms.
• Symptoms of nephrotic syndrome :
• Face / body swelling ( started around eyes and legs , then generalized) , foamy urine , fatigue
, loss of appetite.
• Mostly seen in pt.AIN induced by NSAID.
2.B. Acute Interstitial Nephritis History :

24. • In most patients, no characteristic findings exist.
• Fever , Rash
• Nephrotic Syndrome: In AIN induced by NSAID
• Edema, Ascites
• Pleural effusions.
• Hematuria and hypertension manifest in a minority of patients.
• Some patients present with hypertension, although others may be normotensive or
hypotensive.
2.B. Acute Interstitial Nephritis Exam :

25. 2.C. Glomerulus diseases History
• Hematuria, Oliguria
• Triad of sinusitis, pulmonary infiltrates, and nephritis (Wegener granulomatosis)
• Nausea and vomiting, abdominal pain, and purpura (Henoch-Schönlein purpura)
• Rash , Arthralgias (SLE)
• Hemoptysis (Goodpasture syndrome)
• arthritis, uveitis, sinusitis
• Constitutional symptoms : weight loss, fatigue, loss of appetite.
• Infection : hepatitis C virus infection, HIV.
• Edema ( peripheral or periorbital ).

26. • Hypertension
• Altered level of consciousness (malignant hypertension or hypertensive encephalopathy)
• Edema ( peripheral or periorbital ).
• Crackles (ie, if pulmonary edema)
• Elevated jugular venous pressure
• Arthritis , rash , pallor
• Others : pharyngitis, impetigo, weight gain, oral ulcers
2.C. Glomerulus Diseases Exam

27. 2.D.VascularAKI History
• The presence of a condition requiring anticoagulation
• History of polyarthritis nodosa PAN
• Medical history: (thrombotic thrombocytopenic purpura, hemolytic uremic syndrome,
malignant hypertension, disseminated intravascular coagulation, HELLP , scleroderma
renal crises ) can lead to TMA then this can lead to AKI.
• History of vascular surgery
• Recent history of arterial catheterization

28. • Funduscopic examination retinal hemorrhages, exudates, and
papilledema (showing severe hypertension).
• Progressive skin tightness and induration, tightening of the skin
in the face, hyperpigmentation and
hypopigmentation (scleroderma).
• Livedo reticularis (e.g PAN ,TTP ).
• Abdominal bruit (e.g PAN).
2.D.VascularAKI Exam
Livedo reticularis

29. 3. Post- renal AKI History
• Obstructive Symptoms (BPH):Hesitancy , intermittency ,
weak urine stream, straining, sensation of incomplete
bladder.
• Irritative Symptoms (BPH): Nocturia , urgency ,
frequency.
• Urinary Stones: Hematuria, abdominal pain, dysuria.
• Malignancy : Smoking , male , FHx of bladder cancer h/o
irritative or obstructive symptoms.
• Medications

30. 3.Post-renal AKI Exam
• Bladder distention
• pelvic mass
• prostate enlargement

31. MCQ 1
• A 65-year-old female patient suffering from diabetes mellitus presents with complaints of
decreased urination, nausea, fatigue, and swelling in her legs. One week ago, she was
started on medication for the treatment of her urinary tract infection.Today, her blood tests
show elevated blood urea nitrogen (BUN) and serum creatinine levels.Which of the
following medications most likely precipitated her current symptoms?
A. Insulin
B. Amoxicillin
C. Ceftriaxone
D.Trimethoprim/sulfamethoxazole

32. Answer is D
• The patient’s symptoms indicate renal dysfunction. Sulfamethoxazole is a nephrotoxic drug that
can result in acute kidney injury (AKI).
• Sulfonamide containing medications, such as trimethoprim/sulfamethoxazole, are nephrotoxic
and can cause intrinsic renal impairment that decreases creatinine clearance.
• Sulfonamide containing medication can result in the buildup of crystals that block renal tubules.
• This leads to the mechanical blocking of tubules and ureters. Hematuria, oliguria, and anuria
may follow.Ceftriaxone and amoxicillin are unlikely to cause damage to renal function.

33. A PATIENT HISTORY AND PHYSICAL
EXAMINATION, WITH AN EMPHASIS ON
ASSESSINGTHE PATIENT’SVOLUME STATUS,
ARE CRUCIAL

34. Investigation
Work up
Lab
CBC & diff
Fractional
excretion
of NA
Renal
function
test
Urine
output
Urine
analysis
dipstick
Microscopic
exam
Serology
Urine
osmolality
Imaging
CT scan
U/S
others
Renal
biopsy

35. Laboratory findings
• PRE-RENAL
• ↓Urine volume (Oliguric)
• Except in diuretic s use , which will acutely raise
the urine volume while the diuretic is acting.
• Fraction excretion of NA is < 1%
• Fractional excretion of urea ≤ 35%
• this is helpful incase the pre-renal AKI is due to
diuretics use.
• BUN/CR >20
• urine osmolality > 500 mosmol/kg
• Urinalysis
• Bland sediments , Transparent Hyaline casts

36. Cont.
• INTRINSIC
1. AcuteTubular Necrosis
• Urine volume : either oliguric or non-oliguric.
• Fraction excretion of NA is > 2%
• Fractional excretion of urea > 50%
• BUN/CR < 20
• urine osmolality <450 mosmol/kg (almost all cases) & usually < 350
mosmol/kg
• Urinalysis
• Bland sediments
• Pigmented granular muddy brown casts
• ± RBCs & protein (from the tubular damage)

37. Cont.
Pre-renal ATN
Urine analysis Generally Normal RBC , pigmented
granular casts
Urinary Na <20 >20 mEq/L
Urinary Na/Cr <20 >20
Urine osmolality >500 <350 mOsm/KgH2O
BUN/Cr >20 <20
FeNa < 1% > 1%

38. Cont.
2. Acute interstitial nephritis
• Urinalysis
• WBCs
• WBC casts
• ± RBCs
• Negative Urine culture.
• Urine Eosinophil
• In case of Antibiotic induced AIN
• Lymphocytes
• In case of NSAID induced AIN

39. Cont.
3. Glomerulus diseases
• Urinalysis
• Hematuria
• Dysmorphic RBCs
• RBCs Casts
4.Vascular (small-med vessels)
• Urinalysis
• ± RBCs
• Urine Eosinophil
• In case of Cholesterol emboli

40. Cont.
• POST RENAL
• Urine volume : anuria (urine output <50 to 100 mL/day) is
rare.
• Anuria is most often seen in two conditions: shock and
complete bilateral urinary tract obstruction.
• Urinalysis
• Normal urine analysis.
• ± Non dysmorphic RBCs,WBCs , crystals.
• RBCs Casts.

41. Imaging
• Imaging is generally performed in patients with AKI when the underlying cause is not clear.
• Assess For Urinary Tract Obstruction.
• Patients who have an obvious cause of AKI do not require imaging, at least initially.
• (U/S) most commonly used.
• safe, easy to perform, and sensitive for obstruction.
• (CT) scan without contrast is generally preferred among patients with possible urolithiasis.
• (MRI) with gadolinium should be avoided.

42. Other
• RENAL BIOPSY
1. Is reserved for patients whom prerenal and postrenal causes ofAKI have been excluded
and the cause of intrinsic renal injury is unclear.
2. When clinical assessment and labs suggest a diagnosis that requires confirmation before
starting disease specific therapy (e.g., Immunosuppressive medications).
3. Need to be performed urgently in patients with (oliguria who have rapidly worseningAKI ,
hematuria, and red blood cell casts, anemia, hymoptysis ). In this setting the biopsy may
support the initiation of special therapies, such as plasmapheresis if goodpasture
syndrome is present.

43. Cont.
• RENAL BIOPSY
4. Renal biopsy may need to be performed urgently in patients with oliguria who
have rapidly worsening acute kidney injury, hematuria, and red blood cell casts.
5. Patients who have a characteristic urinalysis for AIN but are not being treated
with a drug known to cause AIN.
6. Patients who are being treated with a drug known to cause AIN but do not have a
characteristic urinalysis.
7. Diagnosis of AIN to be uncertain.

44. Management
• collaboration among primary care physicians,
nephrologists, hospitalists, and other subspecialists
participating in the care of the patient.
• management is primarily SUPPORTIVE.
• Patients with acute kidney injury generally should be
hospitalized unless the condition is mild and clearly
resulting from an easily reversible cause.

45. General management
• Volume depletion in pre-renal AKI
• IV fluids isotonic solutions (e.g., Normal saline) are preferred over hyper
oncotic solutions.
• MAP goal greater than 65 mm hg is reasonable.
• May require the use of vasopressors in patients with persistent hypotension.
• Renal-dose dopamine is associated with poorer outcomes & it is no longer
recommended.

46. Cont.
• Correction of electrolyte imbalances (e.g Severe hyperkalemia):
• 5 to 10 units of regular insulin.
• Dextrose 50% given intravenously.
• Calcium gluconate (10 mL of 10% solution infused intravenously over five minutes)
to stabilize the membrane and reduce the risk of arrhythmias.
• In patients without ECG evidence of hyperkalemia, calcium gluconate is not necessary.
• Dietary intake of potassium should be restricted.

47. Cont.
• Diuretics:
• The main indication for use of diuretics is management of volume overload.
• diuretics do not improve morbidity, mortality, or renal outcomes, and should
not be used to prevent or treat acute kidney injury in the absence of volume
overload.

48. Cont.
• Medications:
• All medications that may potentially affect renal function by direct toxicity or by
hemodynamic mechanisms should be discontinued, if possible.
• Avoidance of iodinated contrast media and gadolinium is important and, if imaging
is needed, noncontract studies are recommended.
• The dosages of essential medications should be adjusted.

49. Cont.
• Corticosteroids :
• Some studies show a benefit to kidney function recovery after AIN with using corticosteroids,
particularly if started within 1 to 2 weeks of diagnosis.
• So, short course of prednisolone should be considered in most patients whose kidney function does
not improve rapidly after drug withdrawal, unless corticosteroid therapy is contraindicated.
• This should be undertaken with the results of a kidney biopsy confirming the diagnosis of AIN and
excluding other possible diagnoses.
• Corticosteroids should be continued for 1 to 1.5 months as much of the recovery of kidney function is
expected in this period.

50. • Indications (when conditions are refractory to conservative management):
• Acid base disturbance : refractory acidemia
• Certain poisonings and intoxications: (metformin, valproic acid, methanol, ethylene glycol, lithium,
salicylates, barbiturates, thallium, theophylline).
• Electrolyte disorder: ↑K, ↑Ca, ↑PO4, tumor lysis syndrome.
• Overload: refractory hypervolemia ( e.g CHF, Pulmonary edema )
• Uremic: pericarditis or pleuritis, uremic encephalopathy
• No mortality benefit to early initiation of RRT
Renal ReplacementTherapy (RRT)

51. • A 65-year-old woman who lives in a nursing home is brought to the emergency department due to a day of
lethargy and confusion. She is febrile and disoriented. Past medical history includes diabetes mellitus and
hypertension. During the hospitalization, she received gentamicin sulfate 3 mg/kg every 8 hours to treat a life-
threatening infection. Following the administration of this drug, the patient became more irritable and vomited
several times. Fluid balance indicates a blood urea nitrogen of 46 mg/dL, creatinine of 2.6 mg/dL, sodium of 148
mEq/L, and potassium of 4.8 mEq/L. Which of the following is the most appropriate next step in the management
of this patient?
A. Discontinue gentamicin and initiate volume repletion
B. Continue current care with close observation
C. Add IV cephalosporin
D. Repeat urine analysis
MCQ 2

52. • Kidney damage is a problem in 10-25% of people who receive aminoglycosides,
and gentamicin is one of the most nephrotoxic drugs of this class.
• Oftentimes, acute nephrotoxicity is reversible, but it may be fatal.
• Fluid resuscitation is vital in the treatment of acute kidney injury due to
nephrotoxic agents.
Answer is A

53. Management Key Recommendations
• Adequate fluid balance should be maintained in patients with acute kidney injury by using
isotonic solutions (e.g., normal saline) instead of hyperoncotic solutions (e.g., dextrans,
hydroxyethyl starch, albumin). (C)
• Balanced crystalloids are preferred over 0.9% sodium chloride for fluid resuscitation in
critically and non-critically ill patients. (B)

54. Management Key Recommendations
• There is no difference in 90-day mortality between early initiation of renal
replacement therapy and delayed initiation. (B)
• High-dose statins lower the risk of contrast media induced acute kidney
injury in patients undergoing coronary angiography or percutaneous
intervention compared with lower-dose statins. (A)

55. Management Key Recommendations
• KIDO recommends not using diuretics to preventAKI. (1B)
• KIDO suggests not using diuretics to treat AKI, except in the management
of volume overload. (2C)

56. Management Key Recommendations
• KIDO recommends not using low-dose dopamine to prevent or treat AKI.
(1A)
• KIDO suggests not using fenoldopam to prevent or treat AKI. (2C)

57. Management Key Recommendations
• KIDO suggests not using atrial natriuretic peptide (ANP) to prevent AKI.
(2C)
• KIDO suggests not using atrial natriuretic peptide (ANP) to treat AKI. (2B)

58. Diagnosis andTreatment of AKI

59. Cont.

60. Referral
To Emergency
department
To Non-Emergency
department
URGENT NEPHROLOGY
REFERRAL
Referral

61. Non-Emergency
department
URGENT
NEPHROLOGY
REFERRAL
Initial interventions fail to substantially improve the kidney injury.
•AKI occurs as a complication of treatment of an unrelated
condition and future treatment depends upon nephrology input
(such as AKI occurring as a complication of chemotherapy)
Glomerulonephritis (GN) is strongly suspected (such as in a patient
withAKI, hematuria, and proteinuria).
Referral

62. To Emergency
department
Patients with stage 2 or 3 AKI as per the KDIGO criteria.
Patients with AKI of any stage seen in a resource-limited
outpatient setting where the initial diagnostic evaluation
(eg, renal ultrasound to rule out urinary tract obstruction)
or interventions (eg, intravenous fluid administration)
Patients with stage 1 AKI
Unclear etiology
Unknown duration or trajectory of elevated
creatinine
Here is concern that the condition may not
be rapidly reversible with simple
interventions
If they have a concomitant, uncontrolled
comorbid condition
Referral

63. • Patients with acute kidney injury are more
likely to develop:
• Chronic kidney disease in the future
• Higher risk of end-stage renal disease
• Higher risk for premature death.
Prognosis

64. Follow up ( post AKI )
• It Is Important For Primary Care PhysiciansTo Identify PatientsWhoAre At High Risk Of
DevelopingAKI.
• ThoseAt Highest Risk Include:
• Adults OlderThan 75Years.
• PersonsWith Diabetes.
• Preexisting Chronic Kidney Disease.
• PersonsWith Medical Problems Such As Cardiac Failure, Liver Failure.
• Sepsis.
• ThoseWhoAre ExposedTo Contrast Agents.
• Who Are Undergoing Cardiac Surgery.

65. Cont.
• F/U 3 months after hospitalization is reasonable if renal function is recovered (90% or
greater from baseline).
• F/U at 3 weeks and then again at 3 months for patients with a slower recovery.
• Blood pressure, weight, serum creatinine level, and GFR should be measured at each
visit.
• Nephrology consultation is recommended if the estimated GFR remains less than 60
mL per minute per 1.73 m2.
• The optimal duration of monitoring after acute kidney injury is unclear

66. Follow up (Post AKI )

67. • A 62-year-old man with hypertension, hypercholesterolemia, and benign prostatic hypertrophy (BPH)
presents to his physician with increasing muscle aches in his thighs and shoulders and complains of
tea-colored urine.These symptoms started about 10 days ago. He has been drinking plenty of fluids as
a new diet, specifically grapefruit juice. On routine laboratory evaluation, his serum transaminases are
elevated to nearly three times the normal limit, serum creatinine is 1.4 mg/dL (baseline 1.2 mg/dL),
urinalysis reveals 1+ proteinuria. His only medications are lisinopril, simvastatin, and a baby aspirin.
of the following is the most likely diagnosis in this patient?
A. Drug-induced hepatitis from long-term simvastatin
B. Postrenal azotemia and proteinuria due to BPH
C. Acute kidney injury secondary to aspirin and lisinopril
D. Hepatic enzyme inhibition leading to elevated circulating drug levels
MCQ 3

68. • Grapefruit juice inhibits the cytochrome P450 3A4 system that metabolizes simvastatin.
• This patient has rhabdomyolysis from increased circulating levels of simvastatin. Simvastatin
may increase transaminases, but associated cases of hepatitis and liver failure are very rare.
• The combination of aspirin and lisinopril has not been shown to cause acute kidney injury; a
creatinine level of 0.2 mg/dL above baseline levels does not confer acute kidney injury.
• Moderate proteinuria and a mild elevation in serum creatinine do not constitute postrenal
azotemia and proteinuria due to BPH in this patient.
Answer is D

69. COVID19 & AKI

70. COVID19 & AKI

71. Summary
1-The two major causes of acute kidney injury (AKI) developing in the hospital are prerenal disease and acute
tubular necrosis (ATN).
2- Causes of AKI can be divided to ( pre-renal, intrinsic and post renal) .
3- KDIGO system staging AKI into three stages using SCR and urine output.
4-The FeNa is typically less than 1 % in prerenal disease and above 2 % in ATN.
5- A patient history and physical examination, with an emphasis on assessing the patient’s volume status, are
crucial.
6- Not recommended to use low dose dopamine to treat or prevent AKI.
7- Not recommended to use diuretics to prevent or treat AKI unless there is volume overload.

72. 8- Management of acute kidney injury involves fluid resuscitation, avoidance of nephrotoxic
medications and contrast media exposure, and correction of electrolyte imbalances
9- F/U 3 months after hospitalization is reasonable if renal function is recovered (90% or greater
from baseline).
10- F/U at 3 weeks and then again at 3 months for patients with a slower recovery.
11- Recognition of risk factors (e.g., older age, sepsis, hypovolemia/shock, cardiac surgery, infusion
of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver
failure) is important.
Summary

73. References:
• KDIGO Clinical PracticeGuidelines for Acute Kidney Injury.
• AmericanAcademyOf Family Physicians.
• Royal Collage of General Practitioners.
• Toronto Notes Book 34th Edition.
• Pocket Medicine 7th Edition.
• Case files 4th edition.
• BMJ Best Practice.
• Medscape.
• Uptodate.
• Statpearls.