2 Rapid loss of renal function leading to abnormal water, electrolyte and solute balance. Occurs over a period of hours to days. Usually associated with oliguria. Some patients develop non oliguric ARF eg. After radiocontrast media. It can be reversed with treatment of the cause. Acute-on top of chronic renal failure may occur.
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Rapid loss of renal function leading to abnormal water, electrolyte and solute balance.
Occurs over a period of hours to days. Usually associated with oliguria. Some
patients develop non oliguric ARF eg. After radiocontrast media.
1) Prerenal ARF was defined as ARF to renal hypoperfusion with recovery after correction of hemodynamic disturbances.
2) Ischemic Acute tubular necrosis (IATN) was diagnosed when renal function did not improve after correction of possible prerenal causes, and when hepatorenal syndrome, vascular, interstitial, glomerular and obstructive aetiologies were excluded.
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Any documented decline in blood pressure to less than 90/60 mmHg.
Overt volume contraction on physical examination (postural hypotension, decreased skin turgor, …), and central venous pressure (CVP) less than 5 cm H2O.
Clinically evident congestive heart failure with improvement in renal function following appropriate treatment of heart failure.
• Decreased renal perfusion was identified by the following observations :
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3) Nephrotoxic ARF (either AIN or ATN)
Nephrotoxic Acute Interstitial Nephritis
(AIN): history of drug ingestion, fever, rash, or
arthralgias. Urinary increase in WBCs (frequently
eosirophiluria), WBC casts RBCs, and
proteinuria, with systemic eosinophilia, if
histologically demonstrated by renal biopsy or
when there was a high grade of clinical
suspicion.
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Nephrotoxic Acute Tubular Necrosis (ATN): was defined as ARF occurring after administration of drugs known to cause ATN (e.g. aminoglycosides, amphotericin, contrast media etc …).
Concurrent administration of vancomycin & aminoglycosides to critically ill septic patients with normal renal function of baseline induces mainly slight and transient toxic tubular effects.
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Radiographic contrast media, were determined to
be the cause of renal insufficiency when the
serum creatinine concentration increased – as
defined – within 72 hours following a radiologic
procedure employing these agents (e.g.
intravenous pyelogram – angiography – computed
tomography scan).
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4) Sepsis induced ARF was diagnosed if ARF is associated with at least one of the following three conditions:
Documented bacteremia. A known focus of infection Immunosuppression with neutropenia,
and at least two additional findings: rigors – unexplained hyperventilation unexplained sudden fall in blood pressure – abrupt rise in temperature to more than 38C not due to transfusion reaction – unexplained leukocytosis of more than 15.000 mm3.
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5) Hepatorenal syndrome was assigned as the
cause of renal failure if the patient had severe liver
failure (e.g. ascites – jaundice, hepatic
encephalopathy) – and a urine sodium concentration
less than 10 mEq/Liter, and the renal function did not
respond to a volume expansion.
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6) Other causes:
Obstruction was determined to be the cause of
renal failure if obstruction was present by
physical examination (as enlarged bladder) or by
radiological evaluation and if improvement in
renal function followed relief of obstruction.
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Pigment induced-ARF, history suggestive of
rhabdomyolysis, urine dispstick positive for blood
(heme) without microscopic haematuria
hyperkalemia, hyperphosphatemia, hypocalcemia,
increased creatine kinase-MM fraction and serum
uric acid.
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Associated with emboli of fragments of atherosclerotic plaque from aorta and other large arteries.
Diagnose by history, physical findings (evidence of other embolic phenomena, ischemic digits, “blue toe” syndrome, etc), low serum C3 and C4, peripheral eosinophiluria, rarely WBC casts.
Commonly occur after intravasculer procedures or cannulation (cardiac catheter, CABG).
Atheroembolic ARF:
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Number of patients admitted in different
ICUs with acquired ARF in each ICU
ICUNo. of admitted patients
No. & % of patients with ICU acquired ARF in each ICU
* The initiation of RRT in patients with AKI prevents uremia and immediate death from the adverse complications of renal failure.
* It is possible that variations in the timing of initiation, modalities, and/or dosing may affect clinical outcomes.
* Multiple modalities of RRT are currently available. These include intermittent hemodialysis (IHD), continuous renal replacement therapies (CRRTs), and hybrid therapies, such as sustained low-efficiency dialysis (SLED). Despite these varied techniques mortality in patients with ARF remains high greater than 50% in severely ill patients.
6.5 meq/L) or rapidly rising potassium levels.3) Metabolic acidosis (pH less than 7.1).4) Signs of uremia e.g. pericarditis and decline in
mental state.5) Certain alcohol and drug intoxications.
* The likelihood of requiring RRT is increased in
patients with underlying CKD (Acute on top of
chronic).
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Studies published during the 1960s and 1970s
suggested that improved outcomes were associated
with the initiation of hemodialysis when BUN reached
exceeded 150 to 200 mg/dL.
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More recent studies have evaluated the relationship
between the timing of RRT initiation and clinical
outcomes. Several non-randomized studies have
reported that improved outcomes, including survival,
are associated with early versus late initiation of RRT.
It has been suggested that initiation of RRT dialysis
prior to the development of overt symptoms and
signs of renal failure due to AKI improves the
outcome.
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There is at least theoretical concern that dialysis might have detrimental effects on renal function.
Three factors may be important in this regard:
Can dialysis delay recovery of renal function ?
1) A reduction in urine output; Both removal of excess volume and of urea contribute to a reduction in or even cessation of the urine output. The fall in urine output should not delay the regeneration of tubules.
2) Induction of hypotension; Autoregulation is impaired in ATN, because vascular endothelial injury reduces the release of vasodilating substances so recurrent ischemic tubular injury is more likely to occur, thereby delaying the restoration of function.
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3) Complement activation resulting from a blood-dialysis membrane interaction, can lead to neutrophilic infiltration into the kidney (and other tissues) and prolonged acute kidney injury.
4) High flux membranes can enhance removal of putative toxins and improve outcome, but may also allow the back transport (from dialysate to blood).
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1) Intermittent hemodialysis (IHD).
2) Continuous renal replacement therapy (CRRT).
3) Peritoneal dialysis.
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Dialysis = diffusion = passive movement of solutes across a semi-permeable membrane down concentration gradient.
Principles of dialysis
Figure (1): Principles of dialysis (top panel) and filtration
(lower panel).
* Good for small molecules.
(Ultra) filtration = convection = solute + fluid removal across semi permeable membrane down a pressure gradient (solvent drag).* Better for removal of fluid
and medium-size molecules.
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Hemodialysis = solute passively diffuses down concentration gradient.
Principles of dialysis
Dialysate flows countercurrent to blood flow. Urea, creatinine, K move from blood to dialysate. Ca and bicarb move from dialysate to blood.
Ultrafiltration = This is the convective flow of water and dissolved solutes down a pressure gradient caused by hydrostatic or osmotic forces.
Hemodiafiltration = combination of dialysis and ultrafiltration
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Oldest and most common technique. Primarily diffusive treatment: blood and
dialysate are circulated in countercurrent manner.
Intermittent hemodialysis (IHD)
Also some fluid removal by ultrafiltration due to pressure driving through circuit.
Best for removal of small molecules.
Typically performed 4 hours 3x / wk or daily.
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CRRT strategies are particularly useful in haemo-dynamically compromised patients with ARF.
They allow slow and gentle removal of solutes and fluid, avoiding major intravascular fluid shifts and minimizing electrolyte disturbances, hypotension and arrhythmias.
Inflammatory mediators may also be continuously removed by CRRT, so it may be useful in sepsis syndrome.
Continuous Renal Replacement Therapy (CRRT)
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Types of Continuous Renal Replacement Therapies (CRRT)
Provides solute clearance by convection as solutes are dragged down pressure gradient with water.
It provides better removal of large MW solutes e.g. B2-microglobulin, improved clearance of low MW uraemic toxins and better cardiovascular stability and Bp control than HD.
Inflammatory markers are improved.
Haemofiltration
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Uses conventional dialysis machines but blood flow of 100-200 ml/M and dialysate flow of only 100 ml/M for 8-24 hr/D.
Major advantages: Flexibility of duration and intensity, reduced costs.
Excellent tolerability, cardiovascular stability and solute removal.
Sustained low-efficiency daily dialysis(SLED):
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Used for fluid removal in overloaded CHF patients with refractory edema without severe renal failure.
Blood is driven through a highly permeable filter in a venovenous mode to primarily remove water, not solute.
The ultrafiltrate produced during membrane transit is not replaced.
Slow continuous ultrafiltration ((SCUF):
Simultaneous use of HD and UF. It is good with CVS instability. It can remove the inflammatory mediators.
Haemodiafiltration (HDF):
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* Current data suggest that survival and recovery of renal function are similar with both CRRT and IHD.
* Advocates for CRRT have claimed that CRRT is associated with the following advantages compared with IHD:
1) Enhanced hemodynamic stability, in hemodynamically
unstable patients.
2) Increased net salt and water removal, thereby
permitting superior management of volume overload
and nutritional requirements.
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3) Enhanced clearance of inflammatory mediators, which
may provide benefit in septic patients, particularly
using convective modes of continuous therapy.
4) Among patients with acute brain injury or fulminant
hepatic failure, continuous therapy may be associated
with better preservation of cerebral perfusion.
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Least useful form of CRRT in the ICU.
Diffusive treatment: Blood in capillaries of peritoneal membrane exposed to dialysate in abdomen.
Continuous or intermittent.
Inefficient solute/ volume clearance if unstable or poor intestinal blood flow.
Can’t use if intra-abdominal pathology – risk of peritonitis.
Respiratory burden.
Peritoneal dialysis:
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* Intermittent hemodialysis – Dosing in IHD is based upon the dose delivered per session plus the frequency of sessions.
* Improved survival was observed with a higher Kt/V (greater than 1), which was particlarly evident among patients with intermediate levels of illness severity.
* Compared with every other day dialysis, daily therapy was associated with a significant reduction in mortality, fewer hypotensive episodes during hemodialysis, and more rapid resolution of acute renal failure.
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* In contrast, the Acute Renal Failure Trial Network (ATN) Study did NOT find a difference in mortality associated with a more intensive dosing strategy for renal replacement therapy.
* The Hanover Dialysis Outcome study compared extended duration dialysis, provided for approximately 8 hours per day, to a more intensive regimen where additional 8-hour treatment sessions were provided to maintain the BUN < 42 mg/dL. No difference in survival or recovery of kidney function was observed with more intensive treatment.
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• The Randomized Evaluation of Normal versus Augmented Legal of RRT study and two meta-analyses were performed. All studies found that, compared with standard intensity dialysis, higher intensity dialysis did not result in improved survival or clinical benefits.
• It is recommended that IHD be provided 3 times/week with monitoring of the delivered dose of therapy to ensure a minimum delivered Kt/V of 1.2 per treatment.
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RRT is usually continued until the patient manifests evidence of recovery of kidney function.
1. Increase in urine output.2. A progressive decline in serum creatinine
concentration after initial attainment of stable values (assessed daily during CRRT or predialysis in patients managed with IHD) despite a constant dose of renal support.
3. Measurement of creatinine clearance e.g. on six- hour timed urine collections obtained when the urine output exceeded 30 mL/hour based on an average serum creatinine at the beginning and end of the timed collection.
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A precise level of kidney function needed to
allow discontinuation of renal support has not
been established; however,
Creatinine clearance < 12 mL/min no discontinuation.
Creatinine clearance > 20 mL/min discontinue.
Creatinine clearance 12 to 20 mL/min optional.
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1) No drugs are currently available to enhance or hasten renal recovery once ARF occurs.
2) There is now clear evidence that ARF is associated with excess mortality, irrespective of whether the patient requires renal replacement therapy.
3) Hense prevention is the only powerful tool to improve outcome of AKI.
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Identification of patients at high risk to develop AKI-Elderly, DM, HT. Sepsis etc ....
Non PharmacologicalPharmacological Ensuring adequate
hydration (reversing dehydration,
Maintenance of adequate mean arterial pressure,
Minimizing exposure to nephrotoxins.
Loop diuretics, Mannitol, Dopamine &
Fenoldopam. Natriuretic Peptides.
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NS, albumin, plasma …. CVP = 8-12 cm H2O, MAP > 65 mmHg. Optimal rate of infusion remain unclear and
should be individualized.
Target MAP 65 mmHg. Which vasopressors to be used. Role of low dose dopamine..
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Noradrenaline is the drug of choice in AKI in
sepsis. Norepinephrine has been demonstrated to
preserve splanchnic blood flow better than
dopamine. Optimise fluid before starting vasopressors. Low dose dopamine should not be used for
renal protection in severe sepsis.
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Meta-analysis: Low-Dose Dopamine Increases Urine Output but Does Not Prevent Renal Dysfunction or Death
Low-dose dopamine offers transient improvements in renal physiology, but no good evidence shows that it offers important clinical benefits to patients with or at risk for acute renal failure.
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In animal studies the use of mannitol and loop
diuretic minimize the degree of renal injury if
given at the time of ischemic injury.
Loop diuretics decrease the active Na
transport in the thick ascending loop
decreasing the energy requirement.
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Increasing the urine output by loop diuretic
make the management easier but does not
affect cell injury or the severity of the renal
damage.
Loop diuretic increase the urine output in the
remaining nephrons and therefore huge
doses are required that may cause deafness.
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ANP had been tried in experimental models without any benefit despite their ability to increase renal blood flow and Na excretion.
Calcium channel blockers decrease Ca influx to the cells that lead to cell injury.