By: Dr. Muhammad Asim Fazal Meeqat General Hospital (ICU) Al-Madinah Al-Munawwara

1. Acute Renal Failure
By: Dr. Muhammad Asim Fazal
Meeqat General Hospital (ICU)
Al-Madinah Al-Munawwara

2. Objective
• Definition
• Classification
• Epidemiology
• Etiology
• Management
– Diagnosis
– Treatment

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

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

5. 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.

6. Acute Kidney Injury
PRERENAL
AKI
INTRINSIC POSTRENAL

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

8. 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

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

10. 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

11. • 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
Postrenal azotemia

12. 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

13. Epidemiology
• 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.

14. 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.

15. Etiology
• 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

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

17. Diagnosis
• 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)

18. • 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

19. AKI: Diagnostic studies-urine
• Urinalysis for sediment, casts
• Response to volume repletion with return to
baseline SCr 24-72 hr in 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

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

21. 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

22. 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

23. 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.

24. • 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

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

26. 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.

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

28. 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.

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

30. 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

31. 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.

32. Acute : 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

33. THANKYOU