ACUTE KIDNEY INJURY
(AKI)
Dr. Tamar khutchua
ATMU
Definition (AKI)
Previously known as acute renal failure, is characterized by the sudden
impairment of kidney function resulting in the retention of
nitrogenous and other waste products normally cleared by the kidneys.
an increase in the blood urea nitrogen (BUN) concentration
and/or an increase in the plasma or serurn creatinine (SCr)
concentration
often associated with a reduction in urine volume
rapidly derangements in electrolite and acid-base composition of
the plasma
EPIDEMIOLOGY
AKI complicates 5-7% of acute care hospital admissions and up to 30% of
admissions to the intensive care unit, particularly in the setting of diarrheal
illnesses, infectious diseases like malaria and leptospirosis, and natural
disasters such as earthquakes
AKI is also a major medical complication in the developing world
ETIOLOGY AND PATHOPHYSIOLOGY
Prerenal azotemia
Intrinsic renal parenchymal disease
Postrenal obstruction
PRERENAL AZOTEMIA
The most common form of AKI
To rise in SCr or BUN concentration due to inadequate renal plasma flow and
intraglomerular hydrostatic pressure:
* hypovolemia,
* decreased cardiac output
* medications that interfere with renal autoregulatory responses such as nonsteroidal
anti-inflammatory drugs (NSAIDs) and inhibitors of angiotensin II
Prolonged periods of prerenal azotemia may lead to ischemic injury, often termed
acute tubular necrosis (ATN)
Because renal blood flow accounts for 20% of the cardiac output, renal
vasoconstriction and salt and water reabsorption occur as homeostatic responses
to decreased effective circulating volume or cardiac output in order to maintain
blood pressure and increase intravascular volume to sustain perfusion to the
cerebral and coronary vessels. Mediators of this response include angiotensin 11,
norepinephrine, and vasopressin (alsotermed antidiuretic hormone) .
INTRINSIC AKI
The most common causes of intrinsic AKI are sepsis, ischemia, and nephrotoxins, both
endogenous and exogenous
In many cases, prerenal azotemia advances to tubular injury
Postoperative aki (blood loss and intraoperative hypotension)
Burns and Acute Pancreatitis
Allergic Acute Tubulointerstitial Disease
NEPHROTOXIN-ASSOCIATED AKI
Other Causes of Intrinsic AKI
NEPHROTOXIN-ASSOCIATED AKI
* Iodinated contrast agents (hypoxia, cytotoxic damage, transient tubule
obstruction with precipitated contrast material)
* Antibiotics (Aminoglycosides and amphotericin B…)
* Chemotherapeutic Agents (Cisplatin and carboplatin are accumulated by proximal
tubular cells and cause necrosis and apoptosis
* Toxic Ingestions Ethylene glycol, present in automobile antifreeze, is metabolized to oxalic acid,
glycolaldehyde, and glyoxylate, which may cause AKI through direct tubular injury
* Endogenous Toxins AKI may be caused by a number of endogenous compounds, including
myoglobin, hemoglobin, uric acid, and myeloma light chains
*The tumor Iysis syndrome
POSTRENAL AKI
occurs when the normally unidirectional flow of urine is acutely blocked
either partially or totally, leading to increased retrograde hydrostatic
pressure and interference with glomerular filtration
Unilateral obstruction may cause AKI in the setting of significant underlying
CKD or, in rare cases, from reflex vasospasm of the contralateral kidney
Bladder neck obstruction can be due to prostate disease (benign prostatic
hypertrophy or prostate cancer) , neurogenic bladder, or therapy with
anticholinergic drugs
lower tract obstruction are blood clots,calculi, and urethral strictures
infiltration of the ureteric wall (e.g, neoplasia)
external compression (e.g, retroperitoneal fibrosis, neoplasia, abscess, or
inadvertent surgical damage)
DIAGNOSTIC EVALUATION
An elevation in the SCr concentration rapidly
Reduction in urine output to less than 0.5 mL/kg per hour for longer than 6 h.
In such cases, clues suggestive of CKD can come from radiologic studies (e.g.,
small, shrunken kidneys with cortical thinning on renal ultrasound)
laboratory tests such as normocytic anemia in the absence of blood loss or
secondary hyperparathyroidism wi 出 hyperphosphatemia and hypocalcemia,
consistent with CKD
HISTORY AND PHYSICAL EXAMINATION
Once the diagnosis of AKI is established, its cause
needs to be determined
HISTORY AND PHYSICAL EXAMINATION
vomiting, diarrhea,
glyιosuria causing polyuria
oliguria, defined as <400 mL/24 h or anuria
several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs
Orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased
skin turgor, and dry mucous membranes are often present in prerenal azotemia
flank pain radiating to the groin suggests acute ureteric obstruction
allergic interstitial nephritis, which may be accompanied by fever, arthralgias, and
a pruritic erythematous rash
AKI accompanied by palpable purpura, pulmonary hemorrhage, or sinusitis raises
the possibility of systemic vasculitis with glomerulonephritis
URINE FINDINGS
Complete anuria early in the course of AKI is uncommon except in the
following situations: complete urinary tract obstruction, renal artery
eocclusion, overwhelming septic shock, severe ischemia (often with cortical
necrosis), or severe proliferative glomerulonephritis or vasculitis
Hematuria
mild proteinuria (< 1 g/d)
Eosinophiluria
Extremely heavy proteinuria ("nephrotic range,">3.5 g/d)
Glomerulonephritis may lead to dysmorphic red blood cells or red blood cell
casts
Interstitial nephritis may lead to white blood cell casts
BLOOD LABORATORY FINDINGS
Certain fo rms of AKI are associated with characteristic patterns in the rise
and fall of SCr.
Peripheral eosinophilia can accompany interstitial nephritis, atheroembolic
disease, polyarteritis nodosa, and Churg-Strauss vasculitis
Severe anemia in the absence of bleeding may reflect hemolysis, multiple
myeloma, or thrombotic microangiopathy (e.g., HUS or TTP)
Marked hyperphosphatemia with accompanying hypocalcemia, however,
suggests rhabdomyolysis or the tumor Iysis syndrome
Depressed complement levels and high titers of antinuclear antibodies
(ANAs), antineutrophilic cytoplasmic antibodies (ANCAs) , antiglomerular
basement membrane(AGBM) antibodies, and cryoglobulins (g.n)
KIDNEY BIOPSY
If the cause of AKI is not apparent based on the clinical context, physical
examination, laboratory studies, and radiologic evaluation, kidney biopsy
should be considered
The procedure is most often used in AKI when prerenal azotemia, postrenal
AKI, and ischemic or nephrotoxic AKI have been deemed unlikely, and other
possible diagnoses are being considered such as glomerulonephritis, vasculitis,
interstitial nephritis, myeloma kidney, HUS and TTP, and allograft dysfunction
COMPLlCATIONS
UREMIA: BUN itself poses little direct toxicity at levels below 100 mg/dl.
mental status changes and bleeding complications can arise
HYPERVOLEMIA: The result can be weight gain, dependent edema, increased
jugular venous pressure, and pulmonary edema
HYPOVOLEMIA: Recovery from AKI can sometimes be accompanied by
polyuria, which, if untreated, can lead to significant volume depletion
HYPONATREMIA: can cause neurologic abnormalities, including seizures
HYPERKALEMIA: The more serious compliιation of hyperkalemia is due to
effects on cardiac conduιction, leading to potentially fatal arrhythmias
ACIDOSIS : sepsis, diabetic ketoaadosis, or respiratory acidosis.
ANEMIA AND BLEEDING: decreased erythropoiesis and platelet dysfunction
CA RDIAC COMPUCATIONS: The major cardiac complications of AKI are
arrhythmias, pericarditis, and pericardial effusion
MALNUTRITION : AKI is often a severely hypercatabolic state
PREVENTION AND TREATMENT
1. Nephrotoxin-specific
a. Rhabdomyolysis: aggressive intravenous fiuids; consider forced alkaline diuresis
b. T umor Iysis syndrome: aggressive intravenous fluids and allopurinol or rasburicase
2. Volume overload
a. Salt and water restriction
b. Diuretics
c. Ultrafiltration
3. Hyponatremia
a. Restriction of enteral free water intake, minimization of hypotonic intravenous solutions
including those containing dextrose
b. Hypertonic saline is rarely necessary in A Vasopressin antagonists are generally not needed
4. Hyperkalemia
a. Restriction of dietary potassium intake
b. Discontinuation of potassium-sparing diuretics, ACE inhibitors, ARßs, NSAIDs
c. Loop diuretics to promote urinary potassium loss
d. Potassium binding ion-exchange resin (sodium polystyrene sulfonate)
e. Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote
entry of potassium intracellularly
f. Inhaled beta-agonist therapy to promote entry of potassium intracellularly
g. Calcium gluconate or calcium chloride (1 g) to stabilize the myocardium
5. Metabolic acidosis
a. Sodium bicarbonate (if pH <7.2 to keep serum bicarbonate > 15 mmol/U
b. Administration of other bases
c. Renal replacement therapy
6. Hyperphosphatemia
a. Restriction of dietary phosphate intake
b. Phosphate binding agents (calcium acetate, sevelamer hydrochloride,
aluminum hydroxide-taken with meals)
7. Hypocalcemia
a.Calcium carbonate or calciumgluconate if symptomatic
8. Hypermagnesemia
a. Discontinue Mg2+ containing antacids
9. Hyperuricemia
a. Acute treatment is usually not required except in the setting of tumor
Iysis syndrome (see above)
10. Nutrition
a. Sufficient protein and calorie intake (20-30 kcal/kg per day) to avoid negative
nitrogen balance. Nutrition should be provided via the enteral route if possible
11. Drug dosing
Thank you
