eLecture By Dr.Moh'd Asim ICU specialist- Meqat Qeneral Hospital Medinah-KSA

2. Acute Kidney Injury in Critical
Care
By: Dr. Muhammad Asim Fazal
Meeqat General Hospital (ICU)

3. Objective
• Definition of AKI
• Classification of AKI
• Epidemiology
• Etiology of AKI
• Management of AKI
– Diagnosis of AKI
– Treatment of AKI

4. Definition of AKI
• There are more than 35 definitions of AKI
(formerly acute renal failure) in literature! -
shows the complexity of the problem.
• Deterioration of renal function over a period of
hours to days, resulting in
• the failure of the kidney to excrete nitrogenous
waste products and
• to maintain fluid and electrolyte homeostasis

5. Classification of AKI
• Can be Classified into 3 ways
• 1* Oliguric / Non-Oliguric
• 2* Pre-Renal / Renal / Post-Renal
• 3* RIFLE Criteria

6. Oliguric / Non-Oliguric
• Oliguric : AKI associated with decrease urine
output (<400ml/24 hours)
• Non-Oligguric: AKI associated with normal
urine output (>400ml/24 hours)
• Very simple classification but not much helpful
except that non-oliguric AKI has better
prognosis.

7. Acute Kidney Injury
AKI
PRERENAL INTRINSIC POSTRENAL

8. Acute Kidney Injury
• PRERENAL: 40-80%
– Volume loss/Sequestration
– Impaired Cardiac Output
– Hypotension (and potentially hypo-oncotic states)
• Net result: glomerular hypoperfusion

9. Acute Kidney Injury
• Prerenal Azotemia: fall in GFR secondary to
renal hypoperfusion that potentially has rapid
reversible component
• Restoration of effective intravascular
volume, perfusion pressure
• By current detectable methods, AKI reverses
with minimal evidence of tubular ischemia

10. Acute Kidney Injury
• RENAL/INTRINSIC: 10-30%
– Vascular disorders:
– small vessel
– large vessel
– Glomerulonephritis
– Interstitial disorders:
– Inflammation
– Tubular necrosis:
– Ischemia
– Toxin
– Pigmenturia

11. Acute Kidney Injury
• Prerenal and ATN encountered most often in
the hospital setting: 70-75% in many studies
• Most common diagnostic consideration is
therefore between these two conditions
• Prerenal:
1. Intravascular volume depletion
2. Hypotension
3. Edematous states
4. Localized renal ischemia
• ATN:
1. All causes for prerenal, leading to post-ischemic ATN
2. Toxins

12. Postrenal azotemia
• Stones
• Blood clots
• Papillary necrotic tissue
• Urethral disease
anatomic: posterior valve
functional: anticholinergics, L-DOPA
• Prostate disease
• Bladder disease
anatomic: cancer, schistosomiasis
functional: neurogenic bladder

13. RIFLE Criteria
– Risk
• 1.5X increase in creatinine or UO < 0.5 ml/kg for 6 hours
– Injury
• 2X increase in creatinine or UO < 0.5 ml/kg for 12 hours
– Failure
• 3X increase in creatinine or UO < 0.3 ml/kg for 24 hours or anuria
for 12 hours
– Loss
• Complete loss of function for more than 4 weeks
– ESRD
• Complete loss of function for more than 3 months

14. Epidemiology of AKI
• AKI occurs in
 ≈ 7% of hospitalized patients.
 36 – 67% of critically ill patients (depending
on the definition).
 5-6% of ICU patients with AKI require Renal
Replacement Therapy.

15. Mortality
• Dialysis requiring 40-90%
• Increased mortality even in patients not requiring dialysis
• 25% increase in creatinine associated with a mortality
rate of 31% compared with 8% for matched patients
without renal failure.

16. Etiology of AKI
• Categorize the different causes of acute renal
insufficiency.
– Prerenal: volume depletion and relative hypotension
– Vascular: Consider vasculitis, TTP, nephrosclerosis, renal
artery stenosis
– Glomerular: Consider the nephritic and nephrotic
syndromes
– Tubular/interstitial: Consider
ATN, drugs, PCKD, myeloma, autoimmune disorders
– Obstructive: Consider prostate disease, stones, metastatic
cancer

17. • What are the most likely causes in hospitalized
patients?
– ATN (45%)
– Prerenal (21%)
– Acute on chronic kidney disease (13%)
– Obstruction (10%)
– Glomerulonephritis or vasculitis (4%)
– Acute interstitial nephritis (2%)
– Atheroemboli (1%)

18. Management of AKI
• Consists of 2 Parts:
• 1* Diagnosis of AKI
• 2* Treatment of AKI
History and Physical exam
Detailed review of the chart, drugs
administered, procedures
done, hemodynamics during the procedures.

19. Diagnosis of AKI
• The following tests can aid in the diagnosis
and assessment of AKI:
• Kidney function studies: Increased levels of
blood urea nitrogen (BUN) and creatinine are
the hallmarks of renal failure; the ratio of BUN
to creatinine can exceed 20:1 in conditions
that favor the enhanced reabsorption of
urea, such as volume contraction (this
suggests prerenal AKI)

20. • Complete blood count
• Peripheral smear
• Serologic tests: These may show evidence of
conditions associated with AKI, such as
schistocytes in disorders such as hemolytic-
uremic syndrome and thrombotic
thrombocytopenic purpura
• Fractional excretion of sodium and urea

21. AKI: Diagnostic studies-urine
• Urinalysis for sediment, casts
• Response to volume repletion with return to
baseline SCr 24-72 hr c/w prerenal event
• Urine Na; FENa
FENa (%) = UNa x SCr x 100
SNa x UCr
– FENa < 1%: Prerenal
– FENa 1-2%: Mixed
– FENa > 2%: ATN
• Hansel’s stain

22. Acute Kidney Injury
OTHER LABORATORY DATA
• HCO3ˉ: anion gap, lactic acid, ketones
• Serun Electrolytes especially serum K level
• CPK/LDH/Uric acid/liver panel
• Serologies:
– Complement
– ESR, RF, ANA, ANCA, AntiGBM
– Electrophoresis
• Toxicology studies

23. Acute Kidney Injury
IMAGING STUDIES
• Ultrasound: evaluates renal size, able to
detect masses, obstruction, stones.
• Renal biopsy: Can be useful in identifying
intrarenal causes of AKI

24. AKI: Acute Tubular Necrosis
• Non-oliguric vs. Oliguric
• Prognosis worse with oliguric ATN in most series
• Ischemic insult: medulla most susceptible to
hypoxic event, cellular ATP depletion, oxidative
injury
• AKI/ARF phase of ATN: 7-21 days on average
• Recovery phase of ATN: also known as diuretic
phase
• High urine output (>3-4 L)
• K, Mg, PO4 wasting
• Associated with high FENa

25. Treatment of AKI
• It cannot be overstated that the current
treatment for AKI is mainly supportive in
nature; no therapeutic modalities to date have
shown efficacy in treating the condition.

26. • Maintenance of volume homeostasis and
correction of biochemical abnormalities
remain the primary goals of AKI treatment and
may include the following measures:
• Correction of fluid overload with furosemide
• Correction of severe acidosis with bicarbonate
administration, which can be important as a
bridge to dialysis

27. • Correction of hyperkalemia
• Correction of hematologic abnormalities
(eg, anemia, uremic platelet dysfunction) with
measures such as transfusions and
administration of desmopressin as needed.

28. Dietary Modification
• Dietary changes are an important facet of AKI
treatment. Restriction of salt and fluid
becomes crucial in the management of
oliguric renal failure, wherein the kidneys do
not adequately excrete either toxins or fluids.

29. • Because potassium and phosphorus are not
excreted optimally in patients with AKI, blood
levels of these electrolytes tend to be high.
• Restriction of these elements in the diet may
be necessary, with guidance from frequent
measurements.

30. • In the polyuric phase of AKI, potassium and
phosphorus may be depleted, so that patients
may require dietary supplementation and IV
replacement.

31. • Calculation of the nitrogen balance can be
challenging, especially in the presence of
volume contraction, hypercatabolic states, GI
bleeding, and diarrheal disease.

32. • Critically ill patients should receive at least 1
g/kg/day protein but should avoid
hyperalimentation, which can lead to an
elevated blood urea nitrogen (BUN) level and
water loss resulting in hypernatremia.

33. • Pharmacologic treatment of AKI has been
attempted on an empiric basis, with varying
success rates.

34. Avoid Nephrotoxic agents
• In AKI, the kidneys are especially vulnerable to
the toxic effects of various chemicals. All
nephrotoxic agents (eg, radiocontrast
agents, antibiotics with nephrotoxic
potential, heavy metal preparations, cancer
chemotherapeutic agents, nonsteroidal anti-
inflammatory drugs [NSAIDs]) should be
avoided or used with extreme caution.

35. • Similarly, all medications cleared by renal
excretion should be avoided, or their doses
should be adjusted appropriately.

36. Acute Kidney Injury
INDICATIONS FOR RENAL REPLACEMENT THERAPY
• Consensus generally includes:
1. Refractory volume overload
2. Severe metabolic acidosis; HCO3 may be variable,
but declining level of factor; also falling pH to 7.1-
7.2
3. Hyperkalemia, with levels > 6.5, or documented
rapid rise refractory to medical therapy
4. Major uremic target organ manifestations i.e.
pericarditis, progressive neuropathy, seizure
5. Platelet dysfunction, bleeding diasthesis
6. AKI in setting of dialyzable drug/toxin

37. Acute Kidney Injury
INDICATIONS FOR RENAL REPLACEMENT THERAPY
• Despite modalities available (IHD, CRRT) mortality remains 50% for AKI in
critically ill patients
• Clinicians will generally opt for RRT induction prior to development of the
above symptoms; BUN of 80-100 in absence of other sx’s sometimes is a
indication, but practices vary
• While concept of prophylactic RRT has been around since 1950-60’s, its
benefit remains uncertain, whether due to dose, timing, modality
– Studies based on BUN criteria
– Studies based on volume removal/ultrafiltration in cardiac patients rather
than high-dose diuretics
• No benefit proven of IHD vs CRRT

38. CRRT
• CRRT may have a role in patients who are
hemodynamically unstable and who have had
prolonged renal failure after a stroke or liver
failure.
• Such patients may not tolerate the rapid shift
of fluid and electrolytes caused during
conventional hemodialysis.

39. Acute Kidney Injury: conclusions
• Major advances in understanding AKI, but no clear
definition that guides research on prophylaxis, prognosis
• AKI still carries high M/M risk, especially in ICU setting
• Improving volume status, hemodynamics rapidly aids in
minimizing ischemic AKI risk; volume resuscitation, relief
of urinary obstruction can be done concurrently
• Patient history, hosp chart review, PEx coupled with
routine labs, UA may establish cause in 40-60% of AKI
• Serologies and consideration of Bx are also adjuncts

40. THANKYOU