ACUTE KIDNEY INJURY

MD3
Presenter;Dr .Francisca
B.Komanya(MMED2)
Facilitator;Dr. Alfred
Meremo(MD,MMED,Nephrologist)
 Definition
• Acute kidney injury (AKI) denotes to a sudden
decrease in kidney function, causing retention of
urea and other nitrogenous waste products and in
the dysregulation of extracellular volume and
electrolytes.
• The term AKI has largely replaced acute renal
failure (ARF), indicating that smaller decrease in
kidney function that do not result in obvious organ
failure are of significant clinical importance and are
associated with increased morbidity and mortality.
 Diagnostic criteria
According to KIDIGO,2012
• 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 seven days, or
• Urine volume <0.5 mL/kg/hour for six hours
 Etiology of AKI
• Clinically, AKI can be conveniently grouped
into three primary etiologies:
Prerenal AKI,
 Renal/Intrinsic AKI and
 Post renal AKI.
Pre renal AKI(approximately 60% of cases)

• Refers to any condition which leads to a decrease

in renal perfusion pressure without damage to the
renal parenchyma .
• Its most common and rapidly reversible upon
restoration of Blood Volume.
• The kidneys receive up to 25% of the cardiac
output and thus any failure of the general
circulation or isolated failure of the intra renal
circulation can have a profound impact on renal
perfusion.
 Pre renal AKI cont..
Causes of Pre renal ARF includes;
1.Hypovolemia resulting from conditions such as
hemorrhage, vomiting, diarrhea ,poor oral intake, burns,
excessive sweating, renal losses (e.g. diuresis).
2. Impaired cardiac output resulting from congestive
heart failure or decreased cardiac output states (e.g.
pericardial tamponade, severe pulmonary hypertension).
3.Decreased vascular resistance (peripheral vasodilation)
resulting from conditions such as sepsis, vasodilator
medications, autonomic neuropathy, or anaphylaxis; and
renal vasoconstriction from vasoconstrictive medications
or conditions such as hypercalcemia
 PRE RENAL ARF PATHOPHYSIOLOGY AND
AUTOREGULATION
• A decreased renal blood flow is usually
accompanied by decreased GFR and decreased
urine output of water and solutes.
• Hence conditions that acutely diminish blood flow
to the kidneys cause Oliguria.
• If renal blood flow is markedly reduced, total
cessation of urine output can occur -Anuria.
• Hypovolemia -> reduced arterial pressure ->
reduced stretch by arterial & cardiac baroreceptors -
> neuro hormonal response activation
 Pre renal Pathophysiology cont..
• SNS, RAAS, ADH- restores Blood volume & arterial
pressure
• In mild hypo perfusion -> GFR is maintained through
Afferent arteriolar vasodilation (local myogenic
response) and selective efferent constriction through
Ag2
• Severe hypo perfusion-compensation overwhelmed -
>GFR falls ->prerenal ARF
• Lesser hypotension provoke prerenal ARF in elderly
with diseases of afferent arterioles(HTN, DM ). This is
due to reduction of nephron function by 10% per
every 10yrs and further defective arterioles
contributed by HTN, DM as complications
 2.INTRINSIC OR INTRARENAL
CAUSES(approximately 35% of cases)
• Direct damage to kidney parenchyma, hence its
integrity is compromised.
• Causes includes;
(i)Conditions that damage renal tubular
epithelium, such as ischemic ATN, Nephrotoxic ATN
(ii)Conditions that damage Glomerular
capillaries ,such as Glomerulonephritis
(iii)Conditions that damage Renal interstitium,such
as Drugs, myeloma, sarcoidosis
 Renal tubular epithelial damage
pathophysiology
• Is the most common cause of intra renal ARF, is
triggered by ischemic or nephrotoxic resulting
in ATN.
Ischemic ARF -renal hypo perfusion causes
ischemic injury to tubular epithelium.
Nephrotoxic ARF- Is damage to kidneys by
nephrotoxic pharmacologic agents:
 Radio contrast agents & cyclosporine, causes
intra renal vasoconstriction – decrease GFR
 Pathophysiology in ATN
• Severe ischemia of the kidney can result from
circulatory shock or any other disturbance that
severely impairs blood supply to the kidney.
• If the ischemia is severe enough to seriously impair the
delivery of nutrients and oxygen to the renal tubular
epithelial cells, + if the insult is prolonged, damage or
eventual destruction of the epithelial cells can occur.
• Tubular cells “slough off” and plug many of the
nephrons, so that there is no urine output from the
blocked nephrons
 Glomerular vascular damage
pathophysiology
• Is caused by an abnormal immune reaction that
damages the glomeruli.
• In about 95 %of the pts, damage to the glomeruli
occurs 1 to 3 weeks after an infection elsewhere
in the body, usually caused by group A beta
streptococci.
• Antibodies develop against the streptococcal
antigen -> Ag-Ab – immune complexes which get
deposited onto glomerular basement membrane
Glomerular pathophysiology cont..
• The acute inflammation of the glomeruli
usually subsides in abt 2 weeks, and in most
patients, kidneys return to almost normal
function within the next few weeks to few
months.
• Sometimes, many of the glomeruli are
destroyed beyond repair, and in a small
percentage of patients, progressive renal
deterioration continues -> chronic renal failure
 3.POST RENAL (approximately 5% of cases)

• Postrenal causes of AKI are characterized by acute

obstruction to urinary flow. Urinary tract obstruction
increases intratubular pressure and thus decreases
GFR.
• Obstruction of the urinary tract at any level may
produce AKI.
• In general, obstruction must involve both kidneys or a
solitary kidney to produce significant renal failure.
However, a patient with pre-existing renal insufficiency
may develop AKI with obstruction of only one kidney.
 Post renal AKI cont..
• Causes of obstructions includes;
 Benign prostatic hyperplasia and prostate cancer in
men,
 Gynecologic cancers especially cervical cancer in
women,
Retroperitoneal fibrosis, ureteral stones, papillary
necrosis, neurogenic bladder, and intratubular
obstruction due to precipitation of various
substances such as acyclovir or indinavir
medications.
 Pathophysiology of post renal AKI
• Abnormalities in the lower urinary tract can block or partially block
urine flow and therefore lead to ARF even when the kidneys’ blood
supply and other functions are initially normal.
• If the urine output of only one kidney is diminished, no major
change in body fluid composition will occur because the
contralateral kidney can increase its urine output sufficiently to
maintain relatively normal levels of extracellular electrolytes and
solutes as well as normal extracellular fluid volume
• But chronic obstruction of the urinary tract, lasting for several days
or weeks, can lead to irreversible kidney damage
• During early stages, continued GFR leads to increased intraluminal
pressure upstream -> distension of proximal ureter, pelvis, calyces
-> fall in GFR eventually
 Physiologic effects of AKI
• Major effect is retention in the blood and ECF of water, waste
products of metabolism, and electrolytes.
• Water and salt overload, lead to edema and hypertension.
• Excessive retention of potassium, to more than about 8 mEq/L
(only twice normal) can be fatal.
• Kidneys are also unable to excrete sufficient hydrogen ions, pts
develop metabolic acidosis, which in itself can be lethal or can
aggravate the hyperkalemia.
• In the most severe cases, complete anuria occurs. The patient
will die in 8 to 14 days unless kidney function is restored or
unless an artificial kidney is used to rid the body of the excessive
retained water, electrolytes, and waste products of metabolism
 Presentation
• Symptoms
-Malaise
-Anorexia, Nausea and Vomiting
-Pruritus
-Dehydration
-Confusion, convulsions
• Signs
-Hypertension
-Fluid overload: peripheral edema, SOB/ bibasilar crackles/raised JVP
-Dehydration: postural hypotension, poor urine output (palpable
bladder)
 Investigations for AKI
• Serum Creatinine ,BUN (increased)
• Serum Potassium(Increased)
• Serum Sodium(decreased)
• Examination of the urine is very important in the diagnosis of
AKI!(General Appearance, Urine Dipstick,
Centrifugation/Microscopy)
• The absence of cells (“bland sediment”) indicates a pre-renal
diagnosis
• The presence of cells (“active sediment”) indicates an intrinsic
renal diagnosis-Granular casts - Acute Tubular Necrosis (ATN)
-Dysmorphic RBCs/casts - Glomerulonephritis
-Eosinophils - Acute Interstitial Nephritis
 Investigations cont..
• Abdominal ultrasound should be done in all
patients with severe acute renal failure to
exclude a post-renal cause and, if present, to
determine the site of obstruction
 Treatment of AKI
Prerenal ARF
• Volume restoration
• Treat underlying cardiac disease (arrhythmia,
MI, tamponade)
• Inotropes as necessary to increase cardiac
output or support systemic BP in distributive
shock
• Stop NSAIDs and ACEIs
 Treatment cont…
Renal/intrinsic failure mgt;
• ATN
-Volume restoration
-Remove any offending agent
-Most pts return to baseline Cr in 7-21 days
• AGN / vasculitis
-May respond to glucocorticoids, alkylating agents,
and/or plasmapheresis, depending on primary
pathology
 Treatment cont..
Post-renal
• Foley catheter
• May need to consult urology for placement of
percutaneous nephrostomy tubes for upper
tract obstruction
 Indications for dialysis
• Clinical evidence of uremia
• Intractable intravascular volume overload
• Hyperkalemia or severe acidosis resistance to
conservative measures
• Prophylaxis dialysis when
-Urea > 100-150 mg/dL
-Creatinine > 8-10 mg/dL