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Acute Kidney Injury
1. Dr. Ratan Jha (consultant nephrologist)
Dr. Mohd Viquas Uddin Saim (DNB medicine
resident)
Medwin hospital
2. introduction
Previously known as acute renal failure
Sudden impairment of kidney function
Retention of nitrogenous waste products
Not a single disease
Designation for conditions sharing common
diagnostic features
Increase in blood urea and serum creatinine
Severity ranges from asymptomatic to fatal
3. Why term AKI preferred over ARF ?
failure reflects only part of the spectrum of damage to the
kidney
In most cases damage is modest
Modest damage is not nearly as omnious as frank kidney
failure
Frank kidney failure often requires acute dialysis therapies
term renal is not well understood in the general population
Hence kidney has replaced renal
4. epidemiology
5–7% of acute care hospital admissions
30% of admissions to the intensive care unit
Major complication of diarrheal illnesses, malaria and
leptospirosis
markedly increased risk of death in hospitalized
individuals
mortality rates may exceed 50% in ICU patients
6. Pre renal azotemia
"azo," meaning nitrogen, and "-emia“
most common form of AKI
rise in SCr or BUN concentration due to inadequate renal
plasma flow and intraglomerular hydrostatic pressure to
support normal glomerular filtration
may coexist with other forms of intrinsic AKI
When prolonged may lead to ischemic injury called Acute
tubular necrosis
prerenal azotemia involves no parenchymal damage to the
kidney
rapidly reversible once intraglomerular hemodynamics are
restored.
8. Renal autoregulation
Normal GFR is maintained by the relative resistances of the
afferent and efferent renal arterioles
Renal blood flow accounts for 20% of cardiac output
renal vasoconstriction and salt and water reabsorption
occur as a homeostatic response to decreased effective
circulating volume or cardiac output
to maintain blood pressure and increase intravascular
volume to sustain perfusion to the cerebral and coronary
vessels
Mediators of this response include angiotensin II,
norepinephrine, and vasopressin
9. Renal autoregulation
Glomerular filtration can be maintained despite
reduced renal blood flow by angiotensin II–mediated
renal efferent vasoconstriction
Intrarenal biosynthesis of vasodilator prostaglandins
(prostacyclin, prostaglandin E2 also increase in
response to low renal perfusion pressure
also accomplished by tubuloglomerular feedback
decreases in solute delivery to the macula densa
(specialized cells within the proximal tubule) elicit
dilation of the juxtaposed afferent arteriole
10. Failure of autoregulation
There is a limit to autoregulation
in healthy adults, renal autoregulation usually fails once
the systolic blood pressure falls below 80 mmHg
Atherosclerosis, long-standing hypertension, and older age
cause impaired capacity for renal afferent vasodilation
NSAIDs inhibit renal prostaglandin production, limiting
renal afferent vasodilation
ACE inhibitors and angiotensin receptor blockers (ARBs)
limit renal efferent vasoconstriction
NSAID’s and ARBs should not be given together.
11. Intrinsic AKI
most common causes of intrinsic AKI are sepsis,
ischemia, and nephrotoxins
In many cases, prerenal azotemia advances to tubular
injury
classically termed "acute tubular necrosis
Other causes of intrinsic AKI are less common
12. Intrinsic AKI - Glomerular causes
Post-infectious
SLE
ANCA associated
Henoch schnolen purpura
Cryoglobulinaemia
TTP
HUS
Accounts for 5 % of cases
13. Intrinsic AKI - tubular causes (ATN)
Ischemic (50%)
kidneys are the site of one of the most hypoxic regions in the
body, the renal medulla
outer medulla is particularly vulnerable to ischemic damage
AKI more commonly develops when ischemia occurs in the
context of limited renal reserve or coexisting insults such as
sepsis,
Toxins (35%)
kidney has very high susceptibility to nephrotoxins due to
extremely high blood perfusion
Endogenous nephrotoxins : hemoglobin, myoglobin
Exogenous nephrotoxins : contrast agents, antibiotics, etc,.
15. Post renal AKI
occurs when the unidirectional flow of urine is acutely
blocked either partially or totally
leads to increased retrograde hydrostatic pressure and
interference with glomerular filtration
For AKI to occur in healthy individuals, obstruction must
affect both kidneys unless
Unilateral obstruction may cause AKI in the setting of
significant underlying CKD
Bladder neck obstruction is a common cause of postrenal
AKI and can be due to prostate disease ,neurogenic
bladder, or therapy with anticholinergic drugs
Other causes of lower tract obstruction are blood clots,
calculi, and urethral strictures
16. Post renal AKI- ureteric obstruction
intraluminal obstruction (e.g., calculi, blood clots,
sloughed renal papillae)
infiltration of the ureteric wall (e.g., neoplasia)
external compression (e.g., retroperitoneal fibrosis,
neoplasia, abscess, or inadvertent surgical damage)
pathophysiology of postrenal AKI involves
hemodynamic alterations triggered by an abrupt
increase in intratubular pressures
Reduced GFR is due to underperfusion of glomeruli
17. Diagnostic evaluation
presence of AKI is usually inferred by an elevation in
the SCr concentration
AKI is currently defined by a rise of at least 0.3 mg/dL
or 50% higher than baseline within a 24–48-hours
period or a reduction in urine output to 0.5 mL/kg per
hour for longer than 6 hours
The distinction between AKI and chronic kidney
disease is important for proper diagnosis and
treatment
18. Diagnostic evaluation
Features suggestive of CKD than AKI
from radiologic studies (e.g., small, shrunken kidneys
with cortical thinning on renal ultrasound, or evidence
of renal osteodystrophy)
laboratory tests such as normocytic anemia or
secondary hyperparathyroidism with
hyperphosphatemia and hypocalcemia, consistent
with CKD
distinction is straightforward when a recent baseline
SCr concentration is available
19. Diagnostic evaluation : history &
physical evaluation
Prerenal azotemia : in the setting of vomiting,
diarrhea, glycosuria causing polyuria, and several
medications including diuretics, NSAIDs, ACE
inhibitors, and ARBs
Postrenal AKI : history of prostatic disease,
nephrolithiasis, or pelvic or paraaortic malignancy .
Abdominal fullness and suprapubic pain can
accompany massive bladder enlargement
A careful review of all medications is imperative in the
evaluation of an individual with AKI
20. Diagnostic evaluation : Urine
findings
Anuria is seen in complete urinary tract obstruction, renal
artery occlusion, overwhelming septic shock, severe
ischemia, or severe proliferative glomerulonephritis or
vasculitis
oliguria, defined as <400 mL/24 husually denotes more
significant AKI than when urine output is preserved
Preserved urine output can be seen in longstanding urinary
tract obstruction, tubulointerstitial disease, or
nephrotoxicity from cisplatin or aminoglycosides
In the absence of preexisting proteinuria from CKD, AKI
from ischemia or nephrotoxins leads to mild proteinuria
(<1 g/d)
21.
22. Diagnostic evaluation : blood lab
findings
Certain forms of AKI are associated with characteristic
patterns in the rise and fall of SCr
Prerenal azotemia typically leads to modest rises in
SCr that return to baseline with improvement in
hemodynamic status
Contrast nephropathy leads to a rise in SCr within 24–
48 hours, peak within 3–5 days, and resolution within
5–7 days
With aminoglycoside antibiotics and cisplatin ,the rise
in SCr is characteristically delayed for 4–5 days to 2
weeks after initial exposure.
23. Diagnostic evaluation : blood lab
findings
Severe anemia in the absence of bleeding may reflect
hemolysis, multiple myeloma, or thrombotic
microangiopathy
Peripheral eosinophilia can accompany interstitial
nephritis, atheroembolic disease, polyarteritis nodosa,
and Churg-Strauss vasculitis
AKI often leads to hyperkalemia, hyperphosphatemia,
and hypocalcemia
The anion gap may be increased with any cause of
uremia due to retention of anions such as phosphate,
hippurate, sulfate, and urate
25. Diagnostic evaluation : renal failure
indices
The fractional excretion of sodium (FeNa) is the fraction of the filtered sodium load that
is reabsorbed by the tubules and is a measure of both the kidney's ability to reabsorb
sodium
26. Diagnostic evaluation : novel
biomarkers
BUN and creatinine are functional biomarkers of
glomerular filtration and not tissue injury biomarkers
suboptimal for the diagnosis of actual parenchymal
kidney damage
Kidney injury molecule-1 (KIM-1) : for ischemic /
nephrotoxic ATN
Neutrophil gelatinase associated lipocalin (NGAL), also
known as lipocalin-2 or siderocalin
28. treatment
General issues
Optimization of systemic and renal hemodynamics
through volume resuscitation and judicious use of
vasopressors
Elimination of nephrotoxic agents (e.g., ACE
inhibitors, ARBs, NSAIDs, aminoglycosides)
Initiation of renal replacement therapy when
indicated
29. Treatment : specific issues
Nephrotoxin-specific
a. Rhabdomyolysis: consider forced alkaline diuresis
b. Tumor lysis syndrome: allopurinol or rasburicase
Volume overload
a. Salt and water restriction
b. Diuretics
c. Ultrafiltration
Hyperkalemia
a. Restriction of dietary potassium intake
b. Discontinuation of potassium-sparing diuretics, ACE inhibitors, ARBs, 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
30. Treatment : specific issues
Metabolic acidosis
a. Sodium bicarbonate (if pH <7.2 to keep serum
bicarbonate >15 mmol/L)
b. Administration of other bases e.g., THAM
(tromeThamine injection)
c. Renal replacement therapy
Hyperphosphatemia
a. Restriction of dietary phosphate intake
b. Phosphate binding agents (calcium acetate, sevelamer
hydrochloride, aluminum hydroxide—taken with meals)
Hypocalcemia
a. Calcium carbonate or calcium gluconate if symptomatic
31. Indications of dialysis
indicated when medical management fails to
control
volume overload
hyperkalemia
Acidosis
in some toxic ingestions
severe complications of uremia
Many nephrologists initiate dialysis for AKI empirically when the
BUN exceeds 100 mg/dL
32. Outcome and prognosis
associated with a significantly increased risk of in-
hospital and long-term mortality
Prerenal azotemia and postrenal azotemia carry a
better prognosis than most cases of intrinsic AKI
kidneys may recover even after severe, dialysis-
requiring AKI
up to 10% may develop end-stage renal disease
Postdischarge care under the supervision of a
nephrologist for aggressive secondary prevention of
kidney disease is prudent