Lec AKI.ppt

Acute Kidney Injury
Saba .B MD. INTERNIST
Date June 6,2017

Out line of presentation
• Introduction
• Epidemiology
• Etiology
• Diagnostic criteria's
• Evaluation of patient
• Treatment and prognosis

Acute Kidney Injury: Introduction
 AKI, previously known as acute renal failure
 Is characterized by the sudden impairment of kidney
function resulting in the retention of nitrogenous & other
waste products normally cleared by the kidneys.

Epidemiology - AKI
 AKI complicates 5–7% of acute care hospital
admissions and up to 30% of admissions to the ICU.
 AKI is also a major medical complication in the
developing world, particularly in the setting of diarrheal
illnesses & infections like malaria
 Markedly increase risk of death in hospitalized
individuals

Etiology and Pathophysiology - AKI
 The causes of AKI have traditionally been divided into
three broad categories:
 Prerenal azotemia
 Intrinsic renal parenchymal disease
 Post renal obstruction

Prerenal Azotemia
 Prerenal azotemia is the most common form of AKI
 It is a rise in serum Cr or BUN due to inadequate renal
plasma flow and intraglomerular hydrostatic pressure
 The most common clinical conditions associated with
prerenal azotemia are:
 Hypovolemia,
 Decreased cardiac output, and
 Medications that interfere with renal autoregulatory
responses such as NSAIDs & inhibitors of angiotensin II

Disturbances of normal autoregulation of GFR
Abuelo JG, N Engl J Med 2007;357:797-805

Prerenal Azotemia…
 Drugs can affect the compensatory changes evoked to
maintain GFR.
 NSAIDs inhibit renal prostaglandin production, limiting
renal afferent vasodilation.
 ACEI & ARBs limit renal efferent vasoconstriction
 This effect is particularly pronounced in patients with
bilateral renal artery stenosis

Prerenal Azotemia…
 Prolonged periods of prerenal azotemia may lead to
ischemic injury, often termed ATN
 By definition, prerenal azotemia involves no parenchymal
damage to the kidney & is rapidly reversible once
intraglomerular hemodynamics are restored

Intrinsic AKI
The most common causes of intrinsic AKI are
 Sepsis,
 Ischemia, and
 Nephrotoxins
Other causes of intrinsic AKI are less common and can
involve damage to
 Glomeruli,
 Tubulointerstitium, and
 Vessels.

Contrast Agents & AKI
 Iodinated contrast agents are a leading cause of AKI
 The risk of "contrast nephropathy," increases markedly
in the setting of CKD , particularly diabetic nephropathy
 The most common clinical course is rise in Cr within
24–48 hrs , peaking within 3–5 days, & resolving in a
week
 Pts with multiple myeloma and renal disease are
particularly susceptible to severe disease

Antibiotics & AKI
 Aminoglycosides & Amphotericin B cause tubular necrosis
 Nonoliguric AKI may occur even when plasma levels are
in therapeutic range
 AKI typically manifests after 5–7 days of Rx & can
present even after drug discontinuation
 Nephrotoxicity from amphotericin B is dose and duration
dependent

Endogenous Toxins & AKI
 A number of endogenous compounds: Myoglobin, hemoglobin,
uric acid, and myeloma light chains.
 Myoglobin can be released by injured muscle cells
 Hemoglobin can be released during massive hemolysis
 Rhabdomyolysis may result from traumatic crush injuries,
compression during coma /immobilization, prolonged seizure
 Pathogenic factors for AKI: intrarenal vasoconstriction, direct
proximal tubular toxicity, & mechanical obstruction of distal
nephron lumen

Endogenous Toxins & AKI…
 TLS may follow initiation of Chemotheraphy in pts with high-
grade lymphomas & ALL
 Massive release of UA (often >15 mg/dL) leads to precipitation
of UA in the renal tubules and AKI
 Myeloma light chains can also cause AKI by direct tubular
toxicity and by obstructing intratubular lumen

Post renal Acute Kidney Injury
 Obstruction to urinary flow may be caused by functional or
structural derangements anywhere from the renal pelvis to the
tip of the urethra
 For AKI to occur in healthy individuals, obstruction must
affect both kidneys unless only one kidney is functional
 Bladder neck obstruction can be due to prostate ds (BPH or
prostate Ca), neurogenic bladder, or Rx with anticholinergics

Post renal Acute Kidney Injury…
 Other causes of lower tract obstruction are blood clots,
calculi, and urethral strictures
 Ureteric obstruction can occur from:
 Intraluminal obstruction (calculi, blood clots)
 Infiltration of the ureteric wall (neoplasia), or
 External compression (retroperitoneal fibrosis, neoplasia
or abscess)

Diagnostic Evaluation - AKI
 AKI is currently defined by a rise in SCr 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

AKIN and RIFLE stratification of AKI
(Endre, Adv Chron Kidney Dis,
15: : 213-221, 2008)
(Within 48 hrs)
Abrupt:within 1 -7 days )
Sustained:> 1 day
Definitions of AKI (AKIN-RIFLE)

KDIGO definition /classification of AKI
It is recommended that acute kidney injury/impairment (AKI)
be defined as any of the following :
• Increase in Scr by >0.3 mg/dl within 48 hours, or
• Increase in Scr by >1.5-fold above baseline which is
known or presumed to have occurred within 7 days or
• Urine volume <0.5 ml/kg/h for 6 hours

!!! WATCH OUT !!!!
1.The rise/fall in serum creatinine always lags
behind changes in GFR
2. Estimated GFR formulas do NOT work in
AKI TRY TO TAKE LOWEST GFR

Diagnostic Evaluation - AKI…
 Clues suggestive of CKD
 Radiologic studies: Small, shrunken kidneys with cortical thinning
on U/S, or evidence of renal osteodystrophy or
 Laboratory tests: normocytic anemia or 20 hyperparathyroidism with
hyperphosphatemia and hypocalcemia
 No set of tests, however, can rule out AKI superimposed on
CKD since AKI is a frequent complication in patients with CKD
 Once the dx of AKI is established, its cause needs to be
determined

History and Physical Examination - AKI
 Prerenal azotemia should be suspected in the setting of
vomiting, diarrhea, glycosuria causing polyuria, &
medications including diuretics, NSAIDs, ACEIs & ARBs
 Signs of orthostatic hypotension, tachycardia, ↓ ed skin
turgor, & dry mucous membranes are often present in
prerenal azotemia
 A Hx of prostatic ds, nephrolithiasis, or pelvic or paraaortic
malignancy would suggest the possibility of postrenal AKI

Urine Findings - AKI
 Complete anuria in early AKI is uncommon except in the
following situations:
 Complete urinary tract obstruction
 Renal artery occlusion
 Overwhelming septic shock or
 Severe ischemia (often with cortical necrosis)

 A reduction in UOP (oliguria, defined as <400 ml /24 h)
 Oliguria is associated with worse clinical outcomes
 Red or brown urine may be seen +/- gross hematuria
 If the color persists in the supernatant after centrifugation,
then pigment nephropathy from rhabdomyolysis or
hemolysis should be suspected
Urine Findings - AKI

Urine Findings - AKI …
 AKI from ischemia or nephrotoxins - mild proteinuria (<1
g/d).
 Greater proteinuria in AKI suggests damage to the
glomeruli or excretion of myeloma light chains
 Light chains are not detected on urine dipstick
 Dipstick positive for hemoglobin but few RBCs in the
urine sediment - rhabdomyolysis or hemolysis.

Hyaline
cast
Coarse granular cast

Blood Laboratory Findings - AKI
 Elevated Serum Cr
 CBC may provide diagnostic clues
 Anemia is common & is usually multifactorial in origin
 Severe anemia in the absence of bleeding may reflect
hemolysis, MM, or thrombotic microangiopathy (e.g., HUS or
TTP)
 Peripheral eosinophilia can accompany interstitial nephritis,
atheroembolic disease, and Churg-Strauss vasculitis.

Blood Laboratory Findings – AKI…
 AKI often leads to hyperkalemia, hyperphosphatemia,
and hypocalcemia
 Marked hyperphosphatemia with accompanying
hypocalcemia - Rhabdomyolysis or TLS
 CPK & UA levels are elevated in rhabdomyolysis
 TLS shows normal or marginally ↑ed CK and markedly
↑ ed UA

Blood Laboratory Findings – AKI…
 The anion gap may be increased due to retention of
anions such as phosphate, sulfate, and urate
 GN & Vasculitis - depressed complement levels and
high titers of ANAs, ANCAs, & anti GBM antibodies

Radiologic Evaluation AKI
 Simple bladder catheterization can R/o urethral obstruction
 Imaging of the urinary tract with renal ultrasound or CT
 Findings of obstruction include dilation of the collecting
system and hydroureteronephrosis
 Obstruction can be present without radiologic
abnormalities in the setting of volume depletion, RPF &
encasement with tumor

Radiologic Evaluation AKI…
 Antegrade or retrograde pyelography
 Large kidneys - Diabetic nephropathy, HIVAN, infiltrative
diseases, or occasionally acute interstitial nephritis
 Vascular imaging may be useful if venous or arterial
obstruction is suspected - risks of contrast administration

Renal Failure Indices
 Can help differentiate prerenal azotemia from intrinsic AKI
 The low tubular flow rate &↑ed recycling of urea seen in
prerenal azotemia may cause a disproportionate ↑ of the
BUN compared to Cr
 FeNa is the fraction of the filtered Na load that is excreted
in the urine
 With prerenal azotemia, the FeNa may be below 1%,
suggesting avid tubular sodium reabsorption

Renal Failure Indices…
 The response of UOP to fluid administration may be
both Dxic & therapeutic in prerenal azotemia
 In ischemic AKI, the FeNa is frequently above 1%
because of tubular injury
 In the pt with good baseline kidney function, urine
osmolality may be above 500 mOsm/kg in prerenal
azotemia, consistent with an elevated vasopressin

Kidney Biopsy
 If the cause of AKI is not apparent based on the clinical
context, P/E, & laboratory , 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

Complications AKI
 Uremia
 Hypervolemia and Hypovolemia
 HypoNa+, HyperK+, HyperPo4- & HypoCa+2
 Acidosis
 Bleeding
 Infections
 Cardiac Complic (arrhythmias, pericarditis / pericardial effusion)
 Malnutrition

Treatment: Acute Kidney Injury
 Varies according to the underlying cause
 Optimization of hemodynamics, correction of Fluid &
electrolytes, D/C of nephrotoxic medications, & dose
adjustment of medications are all critical
 The kidney may recover remarkably after even severe,
dialysis-requiring AKI
 However, some pts with AKI do not recover fully and may
remain dialysis dependent.

Rx of Ischemia & Nephrotoxin-Associated AKI
General Issues
1. Optimization of systemic & renal hemodynamics through
volume resuscitation & use of vasopressors
2. Elimination of nephrotoxic agents (ACEIs, ARBs,
NSAIDs, aminoglycosides) if possible
3. Initiation of renal replacement therapy when indicated

Specific Issues
1. Nephrotoxin-specific
Rx: a. Rhabdomyolysis: consider forced alkaline diuresis
b. Tumor lysis syndrome: Allopurinol or rasburicase
2. Volume overload
Rx: a. Salt and water restriction
b. Diuretics
Rx of Ischemia & Nephrotoxin-Ass AKI …

3. Hyponatremia
Rx: Restriction of free H2O intake, minimization of
hypotonic IV solutions including those containing dextrose
4.Hyperkalemia
Rx:
 Restriction of dietary K+ intake
 D/C potassium-sparing diuretics, ACEIs, ARBs
 Loop diuretics to promote urinary K+ loss
 Insulin & glucose to promote entry of K + intracellularly
 Calcium gluconate or calcium chloride to stabilize the
myocardium
Rx of Specific Issues …

5. Metabolic acidosis
Rx: Sodium bicarbonate (if pH <7.2 to keep HCo3->15 mmol /L)
Renal replacement therapy
6. Hyperphosphatemia
Rx: Restriction of dietary phosphate intake
Phosphate binding agents (calcium acetate, sevelamer,
Al(OH)3)

7. Hypocalcemia
RX:
Calcium carbonate or calcium gluconate if symptomatic
8. Nutrition
Rx: Sufficient protein & calorie intake to avoid negative
nitrogen balance
9. Drug dosing
Rx: Careful attention to dosages & frequency drugs,
adjustment for degree of renal failure

Rx - Prerenal Azotemia
 Replacement fluids targeted to the type of fluid lost
 Severe acute blood loss should be treated with PRBCs
 Crystalloid &/or colloid should be used for less severe
hemorrhage or plasma loss (in burns & pancreatitis)
 Renal hypoperfusion from poor cardiac output may require
use of inotropic agents, preload- and afterload-reducing
agents & antiarrhythmic drugs

Rx - Postrenal AKI
 The site of obstruction defines the treatment approach
 Urethral strictures or functional bladder impairment
Rx: Transurethral or suprapubic bladder catheterization
 Ureteric obstruction
Rx: Percutaneous nephrostomy tube or ureteral stent
 Relief of obstruction is usually followed by an appropriate
diuresis for several days

Supportive Measures AKI
Volume Management
 Hypervolemia in oliguric or anuric AKI may be life threatening
due to acute pulmonary edema
 Fluid & Na should be restricted, and diuretics may be used to
increase the urinary flow rate
… There is no evidence that ↑ing UOP itself improves the natural history of AKI
 In severe cases of volume overload - furosemide as a bolus
(200 mg) followed by an IV drip (10–40 mg/h), with or with a
thiazide diuretic
 Diuretic therapy should be stopped if there is no response

Dialysis Indications in AKI
 When medical management fails to control volume
overload, hyperkalemia, acidosis
 When there are severe complications of uremia (astrexis,
pericardial rub/effusion, encephalopathy, uremic
bleeding)
 The initiation of dialysis should not await the
development of a life-threatening complication of renal
failure

Outcome and Prognosis
 AKI is ass with a significantly ↑ed risk of in-hospital &
long-term mortality, longer length of stay & ↑ed costs
 Prerenal azotemia (with the exception of the cardiorenal and
hepatorenal syndromes) and postrenal azotemia carry a better
prognosis than most cases of intrinsic AKI
 Survivors of an episode of AKI requiring temporary
dialysis, are at extremely high risk for progressive CKD,
and up to 10% may develop ESRD

Summary
• AKI is one complication specially in critically ill
patient
• In general there are 3 causes
– Prerenal
– Renal
– Post renal
• KIDGO criteria is used for Dx of AKI

• Cr lag behind decrement in GFR
• Can use FeNa >1% and urine osmolality to differentiate
between pre-renal and renal
• Urine microscopic features helps to Dx causes of intrinsic
AKI
• Treatment is supportive and if indicated dialysis

Lec AKI.ppt

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