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Krishna Institute of Medical Sciences (KIMS)
PERIOPERATIVE
RENAL
PROTECTION :
WHAT IS THE EVIDENCE?
Dr. JAYASHREE PATKI
MBBS, MD, PGDHHM
Sr. Consultant
Krishna Institute of Medical Sciences
Hyderabad
Introduction :
• Perioperative AKI - common complication with high
morbidity and mortality
• Mostly after cardiac and vascular surgery
• Incidence - 18 to 47% with mortality of 1-30% 1,2
• Mostly acute and hence prevention is better than cure in this
setup.
• Ischaemia- or toxin mediated acute tubular necrosis is the
primary cause.
• Anesthesia and renal function are connected and can interfere
with each other. Induced hypotension anesthesia and the toxic
effects of anesthetic drugs can further deteriorate renal
function.
• Appropriate perioperative strategies are required to protect
renal function to optimize patient outcome
1 .Carmichael P, Carmichael AR. Acute renal failure in the surgical setting. ANZ JSurg 2003; 73:144–
153.
2. Shusterman N, Strom BL, Murray TG, et al. Risk factors and outcome of hospital-acquired acute renal
failure. Clinical epidemiologic study. Am J Med1987; 83:65–71
•AKI - consequence of
reduced cardiac output,
systemic hypotension and
triggered neuroendocrine
reflexes.
•Surgery - leading cause of
AKI in hospitalized Patients
ESKD
> 3 months
Persistent ARF = Complete
loss of kidney function
> 4 weeks
↑ SCr x 3
↓ GFR 75%
Or sCr ≥ 4mg/dl
Acute rise ≥0.5mg/dll
Urine < 0.3ml/kg/hr
X 24 hr or
Anuria x 12 hr
↑ SCr x 2 or
↓ GFR > 50%
Urine < 0.5ml/kg/hr
x 12 hr
Urine < 0.5ml/kg/hr
x 6 hr
↑ SCr x 1.5 or
↓ GFR > 25%
Oliguria
R:Risk of renal dysfunction
I: Injury to the kidney
F: Failure of kidney function
L: Loss of kidney function
E: End Stage Kidney Disease (ESKD)
High
Sensitivity
High
Specificity
GFR Criteria Urine Output Criteria
The most recent definition arises from The Kidney
Disease: Improving Global Outcomes (KDIGO)
workgroup that merged RIFLE and Acute Kidney Injury
Network criteria and published the new KDIGO definition
for use in both research and clinical practice .
According to this most recent definition, for the diagnosis
of AKI, at least one of the following criteria must be met:
• an increase in serum creatinine above 0.3mg/dl in 48h,
•an increase in serum creatinine by 50% in 7 days, or
•Urine output less than 0.5 mL/kg/h for 6 hours
/oliguria
(Piper Julie Hughes, MD, MS; Chief Editor: Vecihi Batuman, MD, FASN. Classification Systems for
Acute Kidney InjuryDrugs & Diseases > Nephrology
Updated: Apr 27, 2017 )
Pre-op Risk
•↑ SCr/BUN
•↓ cardiac performance
•Past history renal dysfunction
•Other
•Advance age
•Active bacterial endocarditis
•↓ serum albumin
•Malignancy
•Emergency
•Vascualr disease
Perioperative
AKI
Patients at Risk :
Mortality > 50%
Causes of AKI :
Pre-renal
• reversible absolute or
relative renal hypoperfusion
• ischemic acute tubular
necrosis (ATN)
Intrinsic renal
• glomerular
• tubular
• vascular
• interstitial
Post-renal
• obstruction
Lameire N, et al. Lancet 2005; 365: 417-30
Pre-operative factors Intra-operative factors Post-operative factors
•Chronic disease
•Advanced age Female
Sex
•Chronic renal disease
•Diabetes mellitus
•Chronic cardiac
failure
•Aortic and peripheral
vascular disease
•Chronic liver disease
•Genetic
Predisposition
•Acute conditions
•Hypovolaemia
•Sepsis
Type of surgery
•Cardiac
•Aortic
• Peripheral vascular
Non-renal solid organ
transplantation
•Cardiac surgery
•Prolonged CPB time
•Combined procedures
•Emergency surgery
•Previous cardiac
surgery
•Aortic surgery
•Aortic clamp
placement Intra-
Acute conditions
•Acute
cardiacDysfunction
•Haemorrhage
•Hypovolaemia
•Sepsis
•Rhabdomyolysis
•Intra-abdominal
hypertension
•MODS Drug
nephrotoxicity
Risk Factors
Pathophysiology :
The majority of cases of AKI in surgical and critically ill
patients are because of intrinsic renal causes; acute
tubular necrosis is the most common.
Acute tubular necrosis:
A combination of microvascular and tubular injury
Intra-renal vasoconstriction because of local vasoactive
mediators, activation of tubuloglomerular feedback,
structural endothelial damage,and leucocyte activation all
lead to microvascular damage
Perioperative Nephrotoxins :
Nephrotoxic agents commonly used in perioperative patients
include :
•non-steroidal antiinflammatory drugs,
• angiotensin-converting enzyme inhibitors,
•aldosterone-receptor antagonists,
•i.v. radio-contrast agents,
•aminoglycoside and betalactam antibiotics,
•amphotericin B,
•Cyclosporin
Perioperative Renal Protection :
The identification of high-risk patients
and implementation of prophylactic measures
are the main goals
•Non-pharmacological strategies :
•maintenance of renal blood flow and renal perfusion
pressure,
•intravascular volume expansion
• avoidance of nephrotoxic agents,
• strict glycaemic control,
•Pharmacotherapeutic intervention
Renal Perfusion :Autoregulation (MAP 80-160
mmHg)
•The optimal therapeutic target for systemic arterial
pressure for renal protection has not been established.
•A minimum mean arterial pressure of 65–75 mm Hg is
often targeted in clinical practice.
•Hypotensive anesthesia contraindicated in CRF
•A higher target may be necessary in patients with pre-
existing hypertension.
•Thus, optimization of hemodynamic status and renal
perfusion pressure may decrease AKI in surgical patients.
 Walsh M, Devereaux PJ,
Garg AX, et al.
Relationship between
intraoperative mean
arterial pressure and
clinical outcomes after
noncardiac surgery:
toward an empirical
definition of hypotension.
Anesthesiology 2013;
119:507–515
• Any MAP of less than
55mmHg was associated with
adverse outcomes.
• For AKI, there was a strong
correlation between the
duration of such hypotension
– starting with periods of less
than 5min – and reaching a
maximum if hypotension
lasted more than 20min
Adequate renal blood flow and perfusion pressure
•cardiac output
•and systemic arterial pressure.
•Inotropic and vasopressor therapy .
•. norepinephrine is an excellent first-line vasopressor agent
.
• no firm evidence to suggest that the drug compromises
renal, hepatic, or gastrointestinal blood flow `ˆwhen used to
treat arterial hypotension.
•2.Vasopressin and terlipressin
•post-operative catecholamine-resistant vasodilatory shock.
1.Bersten AD, Rutten AJ.
Renovascular interaction of
epinephrine, dopamine and
intraperitoneal sepsis. Crit
Care Med. 1995;23:537-544
2.Duke GJ, Bersten AD.
Dopamine and renal salvage
in the critically ill patient.
Anaesth Intensive Care
1992;20: 277-302.
 Adrenaline has been shown
to produce a sustained
increase in RBF even in the
presence of systemic
vasoconstriction and
hypertension.
 Low-dose dobutamine have
also been shown to be
effective in improving
creatinine clearance,
presumably due to the result
of improved systemic
haemodynamics.
Intravascular volume expansion:
Colloids and Renal Dysfunction:
•The role of crystalloids compared with colloids for
intravascular volume expansion remains unclear.
• Albumin and gelatin appear to be safe in patients with
normal renal function.
•The safety of hydroxyethyl starch solutions in the setting
of established renal impairment has not been clarified.
•The dehydrated patient who receives considerable amounts
of (hyperoncotic) colloids is especially at risk for developing
ARF. It may be advisable to administer colloid in addition
to, rather than in lieu of, crystalloids.
•(DysfunctionBoldt Priebe, A and A 2003 )
•Recent evidence suggests that hydroxyethyl starch
is associated with a higher incidence of ARF than
Ringer’s lactate in critically ill patients with severe
sepsis.
( Stephen T, Webb J, Stephen D, Allen Perioperative renal protection. Contin Educ Anaesth
Crit Care Pain.2008;8:176–80.)
Normal saline
• Saline contains unphysiologically high amounts of
chloride (154mmol/l) compared with human serum (112–
116mmol/l).
• The infusion of such solutions may cause hyperchloremic
acidosis and renal vasoconstriction with concomitantly
reduced glomerular filtration rate.
(Bullivant EM, Wilcox CS, Welch WJ. Intrarenal vasoconstriction during hyperchloremia: role of
thromboxane. Am J Physiol 1989; )
• Balanced crystalloids are probably superior to normal
saline, especially in the case of large intravenous fluid
administration.
(Zaccaria Ricci, MDa,*, Stefano Romagnoli, MDb, Claudio Ronco, MDc,d Perioperative intravascular
volume replacement and kidney insufficiencyBest Practice & Research Clinical Anaesthesiology
26 (2012) 463–474)
Meta-analysis of high versus low-chloride content in
perioperative and critical care fluid resuscitation.
( Krajewski ML, Raghunathan K, Paluszkiewicz SM, et al. Br J Surg 2015; 102:24–36.)
•These observations were very recently confirmed in a
metaanalysis with data from 6253 patients from 21 studies.
Infusion therapy with fluids containing a high chloride
content was associated with a significantly higher rate of
hyperchloremia and metabolic acidosis and AKI.
•The study demonstrated a weak but significant association
between higher chloride content fluids and unfavorable
outcomes, but with no effect on the mortality.
Remote ischemic preconditioning :
Published evidence suggests that RIPC is
beneficial in patients at intermediate or high risk
of AKI, whereas no protective effect on the
kidney is detectable in patients at low risk.
However,a large multicenter trial is required to
prove whether RIPC has a therapeutic value in
the clinical setting
Circulation 2007; 116:98-105
Avoidance or Minimizing perioperative exposure of
nephrotoxic drugs :
• The use of once-daily aminoglycoside dosing
• the use of lipid formulations of amphotericin B
There are concerns regarding the risk of renal injury
associated with the antifibrinolytic agent aprotinin.
Recent controversial evidence suggests that the use of
aprotinin during coronary artery bypass graft (CABG)
surgery may be associated with an increased risk of
ARF requiring dialysis.
Continuing Education in Anaesthesia, Critical Care & Pain j Volume 8 Number 5
2008
Strict glycaemic control :
•Perioperative hyperglycemia during cardiac
and vascular surgery is associated with increased
renal morbidity and overall mortality.
•Strict glycemic control using intensive insulin
therapy improved survival and reduced the
incidence of ARF requiring RRT.
•But adequate scientific data are not available
to show rigorous intra-operative glycemic control
reduces this.
( Continuing Education in Anaesthesia, Critical Care & Pain j Volume 8 Number 5
2008)
Pharmacotherapeutic intervention :
•Dopamine (renal dose) ?
• Diuretics
•Anaritide
•Fenoldopam mesylate
Dopamine :
•Renal dose
•Dopamie infusion has not been shown to prevent ARF,
avert the need for RRT , or reduce mortality, and should not
be administered solely for renal protection.
(Stephen T Webb FRCA J Stephen D Allen FCARCSI MD .Perioperative renal protection )
•More recent studies, have thrown considerable doubt over
the clinical role of low-dose dopamine.
•Renal vasodilatation does not necessarily occur in the
compromised kidney
•(Duke GJ, Bersten AD. Dopamine and renal salvage in the critically ill patient. Anaesth Intensive Care
1992;20: 277-302.
•Bersten AD, Rutten AJ. Renovascular interaction of epinephrine, dopamine and intraperitoneal sepsis. Crit
Care Med.1995.)
•Its diuretic action increases urine output but not
creatinine clearance. (Duke GJ, Briedis JH, Weaver RA. Renal support in critically ill
patients: low dose dopamine or low-dose dobutamine? Crit Care Med 1994;22:1919-1925. 50,52 )
Diuretics
Loop diuretics inhibit tubular re-absorption
in the loop of Henle´ whereas mannitol
acts primarily as an osmotic diuretic.
The available evidence for the use
of diuretics in surgical and critically
ill patients is scarce.
The perioperative use of neither loop
diuretics nor mannitol demonstrates
significant renal protection in patients undergoing
cardiac surgery
(Bagshaw SM, Delaney A, Haase M, et al. Loop diuretics in the management of acute
renal failure: a systematic review and meta-analysis. Crit Care Resusc 2007; 9: 60– 8)
Dexmetedomedine
1,Lempiainen J, Finckenberg P,
Mervaala EE, et
al .Dexmedetomidine
preconditioning ameliorates kidney
ischemia-reperfusion injury.
Pharmacol Res Perspect
2014; 2:e00045
2.Luo C, Yuanf D, Yao W, et al.
Dexmedetomidine protects
against apoptosis induced by
hypoxia/reoxygenation t
hrough the inhibition of gap
junctions in NRK-52E cells.
Life Sci 2015; 122:72–77.
 In animal studies,
Dexmetedomedine was shown to
ameliorate reperfusion injury and
inflammatory response [1]
as well as
hypoxemia-induced apoptosis in
kidney proximal tubular cells [2].
 Number of patients investigated up
to date is small
 So too early to give a general
recommendation, yet.
Sevoflurane and kidney protection :
Controversial results:
Formation of compoundA–nephrotoxic
 Lee TH, Am J Physiol Renal Physiol
2006; 291: F67-F78
 Kharash ED, Hankins DC, Thummel
KE: Human kidney methoxyflurane and
sevoflurane metabolism. Intrarenal
fluoride production as a possible
mechanism of methoxyflurane
nephrotoxicity. Anesthesiology. 1995
• Sevoflurane has direct anti-
inflammatory and antinecrotic
effects in vitro in a renal cell
type particularly sensitive to
injury following IR injury
• Only mild dysfunction
Marini F, Bellugi I, Gambi D, et al. :
Compound A, formaldehyde and methanol
concentrations during low-flow sevoflurane
anaesthesia: comparison of three carbon
dioxide absorbers. Acta Anaesthesiol Scand.
2007
Xin Weil,Yanzi Chang :
Effects of low-flow sevofluran eanesthesia
on renal function in low birth weight infants
BMC Anesthesiology 2015
Jin Ha Park , Jae Hoon Lee :
Korean J Anesthesiol 2012 June 62
(6): 529-535
 Precausions:
 avoid low flow –min 1-2 lit
 Prevent rise in temp
 Smaller canisters
 Modern absorbents like
DrägerSorb Free and Amsorb
Plus
 Low-flow sevoflurane semi-
closed inhalation anesthesia has
no significant effect on the renal
function of low birth weight
infants.
 Compared to desflurane,
sevoflurane had no adverse
effects on grafted renal function
or on the shortterm outcome of
renal transplantation.
In the last decade, a variety of pharmacological
approaches to prevent AKI have been tested.
•aspirin,
•statins,
• sodium bicarbonate for akalinization of urine,
• insulin infusion for tight glycemic control,
• atrial natriuretic peptide,
• dopamine
•fenoldapam.
As a common feature, none of these interventions
proved to be effective in larger human studies.
(Martensson J, Bellomo R. Prevention of renal dysfunction in postoperative
elderly patients. Curr Opin Crit Care 2014; 20:451–459.)
The most recent study investigated
the perioperative application of aspirin and
clonidine in almost 7000 patients after noncardiac
Surgery.
Neither aspirin nor clonidine altered the risk of
AKI.
(Garg AX, Kurz A, Sessler DI, et al.
Perioperative aspirin and clonidine and risk ofacute kidney injury: a randomized clinical
trial. J AmMed Assoc 2014; 312:2254 )
KEY POINTS :
• There are no pharmacological agents yet with proven
benefits in the management of AKI.
• Avoiding hyperchloremic fluid solution is effective in
preventing AKI.
• Most other treatments remain preventive, aiming to keep
patients optimally hydrated and maintain renal perfusion
pressure while avoiding nephrotoxic agents.
• Clinical evidence suggests that RIPC can attenuate AKI
after surgical procedures.
•At present, there is no firm evidence to suggest that the use
of any specific pharmacological intervention is clinically
beneficial.
PERIOPERATIVE  RENAL PROTECTION : WHAT IS THE EVIDENCE?

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PERIOPERATIVE RENAL PROTECTION : WHAT IS THE EVIDENCE?

  • 1. Krishna Institute of Medical Sciences (KIMS)
  • 2. PERIOPERATIVE RENAL PROTECTION : WHAT IS THE EVIDENCE? Dr. JAYASHREE PATKI MBBS, MD, PGDHHM Sr. Consultant Krishna Institute of Medical Sciences Hyderabad
  • 3. Introduction : • Perioperative AKI - common complication with high morbidity and mortality • Mostly after cardiac and vascular surgery • Incidence - 18 to 47% with mortality of 1-30% 1,2 • Mostly acute and hence prevention is better than cure in this setup. • Ischaemia- or toxin mediated acute tubular necrosis is the primary cause. • Anesthesia and renal function are connected and can interfere with each other. Induced hypotension anesthesia and the toxic effects of anesthetic drugs can further deteriorate renal function. • Appropriate perioperative strategies are required to protect renal function to optimize patient outcome 1 .Carmichael P, Carmichael AR. Acute renal failure in the surgical setting. ANZ JSurg 2003; 73:144– 153. 2. Shusterman N, Strom BL, Murray TG, et al. Risk factors and outcome of hospital-acquired acute renal failure. Clinical epidemiologic study. Am J Med1987; 83:65–71
  • 4. •AKI - consequence of reduced cardiac output, systemic hypotension and triggered neuroendocrine reflexes. •Surgery - leading cause of AKI in hospitalized Patients
  • 5. ESKD > 3 months Persistent ARF = Complete loss of kidney function > 4 weeks ↑ SCr x 3 ↓ GFR 75% Or sCr ≥ 4mg/dl Acute rise ≥0.5mg/dll Urine < 0.3ml/kg/hr X 24 hr or Anuria x 12 hr ↑ SCr x 2 or ↓ GFR > 50% Urine < 0.5ml/kg/hr x 12 hr Urine < 0.5ml/kg/hr x 6 hr ↑ SCr x 1.5 or ↓ GFR > 25% Oliguria R:Risk of renal dysfunction I: Injury to the kidney F: Failure of kidney function L: Loss of kidney function E: End Stage Kidney Disease (ESKD) High Sensitivity High Specificity GFR Criteria Urine Output Criteria
  • 6. The most recent definition arises from The Kidney Disease: Improving Global Outcomes (KDIGO) workgroup that merged RIFLE and Acute Kidney Injury Network criteria and published the new KDIGO definition for use in both research and clinical practice . According to this most recent definition, for the diagnosis of AKI, at least one of the following criteria must be met: • an increase in serum creatinine above 0.3mg/dl in 48h, •an increase in serum creatinine by 50% in 7 days, or •Urine output less than 0.5 mL/kg/h for 6 hours /oliguria (Piper Julie Hughes, MD, MS; Chief Editor: Vecihi Batuman, MD, FASN. Classification Systems for Acute Kidney InjuryDrugs & Diseases > Nephrology Updated: Apr 27, 2017 )
  • 7. Pre-op Risk •↑ SCr/BUN •↓ cardiac performance •Past history renal dysfunction •Other •Advance age •Active bacterial endocarditis •↓ serum albumin •Malignancy •Emergency •Vascualr disease Perioperative AKI Patients at Risk : Mortality > 50%
  • 8. Causes of AKI : Pre-renal • reversible absolute or relative renal hypoperfusion • ischemic acute tubular necrosis (ATN) Intrinsic renal • glomerular • tubular • vascular • interstitial Post-renal • obstruction Lameire N, et al. Lancet 2005; 365: 417-30
  • 9. Pre-operative factors Intra-operative factors Post-operative factors •Chronic disease •Advanced age Female Sex •Chronic renal disease •Diabetes mellitus •Chronic cardiac failure •Aortic and peripheral vascular disease •Chronic liver disease •Genetic Predisposition •Acute conditions •Hypovolaemia •Sepsis Type of surgery •Cardiac •Aortic • Peripheral vascular Non-renal solid organ transplantation •Cardiac surgery •Prolonged CPB time •Combined procedures •Emergency surgery •Previous cardiac surgery •Aortic surgery •Aortic clamp placement Intra- Acute conditions •Acute cardiacDysfunction •Haemorrhage •Hypovolaemia •Sepsis •Rhabdomyolysis •Intra-abdominal hypertension •MODS Drug nephrotoxicity Risk Factors
  • 10. Pathophysiology : The majority of cases of AKI in surgical and critically ill patients are because of intrinsic renal causes; acute tubular necrosis is the most common. Acute tubular necrosis: A combination of microvascular and tubular injury Intra-renal vasoconstriction because of local vasoactive mediators, activation of tubuloglomerular feedback, structural endothelial damage,and leucocyte activation all lead to microvascular damage
  • 11. Perioperative Nephrotoxins : Nephrotoxic agents commonly used in perioperative patients include : •non-steroidal antiinflammatory drugs, • angiotensin-converting enzyme inhibitors, •aldosterone-receptor antagonists, •i.v. radio-contrast agents, •aminoglycoside and betalactam antibiotics, •amphotericin B, •Cyclosporin
  • 12. Perioperative Renal Protection : The identification of high-risk patients and implementation of prophylactic measures are the main goals •Non-pharmacological strategies : •maintenance of renal blood flow and renal perfusion pressure, •intravascular volume expansion • avoidance of nephrotoxic agents, • strict glycaemic control, •Pharmacotherapeutic intervention
  • 13. Renal Perfusion :Autoregulation (MAP 80-160 mmHg) •The optimal therapeutic target for systemic arterial pressure for renal protection has not been established. •A minimum mean arterial pressure of 65–75 mm Hg is often targeted in clinical practice. •Hypotensive anesthesia contraindicated in CRF •A higher target may be necessary in patients with pre- existing hypertension. •Thus, optimization of hemodynamic status and renal perfusion pressure may decrease AKI in surgical patients.
  • 14.  Walsh M, Devereaux PJ, Garg AX, et al. Relationship between intraoperative mean arterial pressure and clinical outcomes after noncardiac surgery: toward an empirical definition of hypotension. Anesthesiology 2013; 119:507–515 • Any MAP of less than 55mmHg was associated with adverse outcomes. • For AKI, there was a strong correlation between the duration of such hypotension – starting with periods of less than 5min – and reaching a maximum if hypotension lasted more than 20min
  • 15. Adequate renal blood flow and perfusion pressure •cardiac output •and systemic arterial pressure. •Inotropic and vasopressor therapy . •. norepinephrine is an excellent first-line vasopressor agent . • no firm evidence to suggest that the drug compromises renal, hepatic, or gastrointestinal blood flow `ˆwhen used to treat arterial hypotension. •2.Vasopressin and terlipressin •post-operative catecholamine-resistant vasodilatory shock.
  • 16. 1.Bersten AD, Rutten AJ. Renovascular interaction of epinephrine, dopamine and intraperitoneal sepsis. Crit Care Med. 1995;23:537-544 2.Duke GJ, Bersten AD. Dopamine and renal salvage in the critically ill patient. Anaesth Intensive Care 1992;20: 277-302.  Adrenaline has been shown to produce a sustained increase in RBF even in the presence of systemic vasoconstriction and hypertension.  Low-dose dobutamine have also been shown to be effective in improving creatinine clearance, presumably due to the result of improved systemic haemodynamics.
  • 17. Intravascular volume expansion: Colloids and Renal Dysfunction: •The role of crystalloids compared with colloids for intravascular volume expansion remains unclear. • Albumin and gelatin appear to be safe in patients with normal renal function. •The safety of hydroxyethyl starch solutions in the setting of established renal impairment has not been clarified.
  • 18. •The dehydrated patient who receives considerable amounts of (hyperoncotic) colloids is especially at risk for developing ARF. It may be advisable to administer colloid in addition to, rather than in lieu of, crystalloids. •(DysfunctionBoldt Priebe, A and A 2003 ) •Recent evidence suggests that hydroxyethyl starch is associated with a higher incidence of ARF than Ringer’s lactate in critically ill patients with severe sepsis. ( Stephen T, Webb J, Stephen D, Allen Perioperative renal protection. Contin Educ Anaesth Crit Care Pain.2008;8:176–80.)
  • 19. Normal saline • Saline contains unphysiologically high amounts of chloride (154mmol/l) compared with human serum (112– 116mmol/l). • The infusion of such solutions may cause hyperchloremic acidosis and renal vasoconstriction with concomitantly reduced glomerular filtration rate. (Bullivant EM, Wilcox CS, Welch WJ. Intrarenal vasoconstriction during hyperchloremia: role of thromboxane. Am J Physiol 1989; ) • Balanced crystalloids are probably superior to normal saline, especially in the case of large intravenous fluid administration. (Zaccaria Ricci, MDa,*, Stefano Romagnoli, MDb, Claudio Ronco, MDc,d Perioperative intravascular volume replacement and kidney insufficiencyBest Practice & Research Clinical Anaesthesiology 26 (2012) 463–474)
  • 20. Meta-analysis of high versus low-chloride content in perioperative and critical care fluid resuscitation. ( Krajewski ML, Raghunathan K, Paluszkiewicz SM, et al. Br J Surg 2015; 102:24–36.) •These observations were very recently confirmed in a metaanalysis with data from 6253 patients from 21 studies. Infusion therapy with fluids containing a high chloride content was associated with a significantly higher rate of hyperchloremia and metabolic acidosis and AKI. •The study demonstrated a weak but significant association between higher chloride content fluids and unfavorable outcomes, but with no effect on the mortality.
  • 21. Remote ischemic preconditioning : Published evidence suggests that RIPC is beneficial in patients at intermediate or high risk of AKI, whereas no protective effect on the kidney is detectable in patients at low risk. However,a large multicenter trial is required to prove whether RIPC has a therapeutic value in the clinical setting
  • 23. Avoidance or Minimizing perioperative exposure of nephrotoxic drugs : • The use of once-daily aminoglycoside dosing • the use of lipid formulations of amphotericin B There are concerns regarding the risk of renal injury associated with the antifibrinolytic agent aprotinin. Recent controversial evidence suggests that the use of aprotinin during coronary artery bypass graft (CABG) surgery may be associated with an increased risk of ARF requiring dialysis. Continuing Education in Anaesthesia, Critical Care & Pain j Volume 8 Number 5 2008
  • 24. Strict glycaemic control : •Perioperative hyperglycemia during cardiac and vascular surgery is associated with increased renal morbidity and overall mortality. •Strict glycemic control using intensive insulin therapy improved survival and reduced the incidence of ARF requiring RRT. •But adequate scientific data are not available to show rigorous intra-operative glycemic control reduces this. ( Continuing Education in Anaesthesia, Critical Care & Pain j Volume 8 Number 5 2008)
  • 25. Pharmacotherapeutic intervention : •Dopamine (renal dose) ? • Diuretics •Anaritide •Fenoldopam mesylate
  • 26. Dopamine : •Renal dose •Dopamie infusion has not been shown to prevent ARF, avert the need for RRT , or reduce mortality, and should not be administered solely for renal protection. (Stephen T Webb FRCA J Stephen D Allen FCARCSI MD .Perioperative renal protection ) •More recent studies, have thrown considerable doubt over the clinical role of low-dose dopamine. •Renal vasodilatation does not necessarily occur in the compromised kidney •(Duke GJ, Bersten AD. Dopamine and renal salvage in the critically ill patient. Anaesth Intensive Care 1992;20: 277-302. •Bersten AD, Rutten AJ. Renovascular interaction of epinephrine, dopamine and intraperitoneal sepsis. Crit Care Med.1995.) •Its diuretic action increases urine output but not creatinine clearance. (Duke GJ, Briedis JH, Weaver RA. Renal support in critically ill patients: low dose dopamine or low-dose dobutamine? Crit Care Med 1994;22:1919-1925. 50,52 )
  • 27. Diuretics Loop diuretics inhibit tubular re-absorption in the loop of Henle´ whereas mannitol acts primarily as an osmotic diuretic. The available evidence for the use of diuretics in surgical and critically ill patients is scarce. The perioperative use of neither loop diuretics nor mannitol demonstrates significant renal protection in patients undergoing cardiac surgery (Bagshaw SM, Delaney A, Haase M, et al. Loop diuretics in the management of acute renal failure: a systematic review and meta-analysis. Crit Care Resusc 2007; 9: 60– 8)
  • 28. Dexmetedomedine 1,Lempiainen J, Finckenberg P, Mervaala EE, et al .Dexmedetomidine preconditioning ameliorates kidney ischemia-reperfusion injury. Pharmacol Res Perspect 2014; 2:e00045 2.Luo C, Yuanf D, Yao W, et al. Dexmedetomidine protects against apoptosis induced by hypoxia/reoxygenation t hrough the inhibition of gap junctions in NRK-52E cells. Life Sci 2015; 122:72–77.  In animal studies, Dexmetedomedine was shown to ameliorate reperfusion injury and inflammatory response [1] as well as hypoxemia-induced apoptosis in kidney proximal tubular cells [2].  Number of patients investigated up to date is small  So too early to give a general recommendation, yet.
  • 29. Sevoflurane and kidney protection : Controversial results: Formation of compoundA–nephrotoxic  Lee TH, Am J Physiol Renal Physiol 2006; 291: F67-F78  Kharash ED, Hankins DC, Thummel KE: Human kidney methoxyflurane and sevoflurane metabolism. Intrarenal fluoride production as a possible mechanism of methoxyflurane nephrotoxicity. Anesthesiology. 1995 • Sevoflurane has direct anti- inflammatory and antinecrotic effects in vitro in a renal cell type particularly sensitive to injury following IR injury • Only mild dysfunction
  • 30. Marini F, Bellugi I, Gambi D, et al. : Compound A, formaldehyde and methanol concentrations during low-flow sevoflurane anaesthesia: comparison of three carbon dioxide absorbers. Acta Anaesthesiol Scand. 2007 Xin Weil,Yanzi Chang : Effects of low-flow sevofluran eanesthesia on renal function in low birth weight infants BMC Anesthesiology 2015 Jin Ha Park , Jae Hoon Lee : Korean J Anesthesiol 2012 June 62 (6): 529-535  Precausions:  avoid low flow –min 1-2 lit  Prevent rise in temp  Smaller canisters  Modern absorbents like DrägerSorb Free and Amsorb Plus  Low-flow sevoflurane semi- closed inhalation anesthesia has no significant effect on the renal function of low birth weight infants.  Compared to desflurane, sevoflurane had no adverse effects on grafted renal function or on the shortterm outcome of renal transplantation.
  • 31. In the last decade, a variety of pharmacological approaches to prevent AKI have been tested. •aspirin, •statins, • sodium bicarbonate for akalinization of urine, • insulin infusion for tight glycemic control, • atrial natriuretic peptide, • dopamine •fenoldapam. As a common feature, none of these interventions proved to be effective in larger human studies. (Martensson J, Bellomo R. Prevention of renal dysfunction in postoperative elderly patients. Curr Opin Crit Care 2014; 20:451–459.)
  • 32. The most recent study investigated the perioperative application of aspirin and clonidine in almost 7000 patients after noncardiac Surgery. Neither aspirin nor clonidine altered the risk of AKI. (Garg AX, Kurz A, Sessler DI, et al. Perioperative aspirin and clonidine and risk ofacute kidney injury: a randomized clinical trial. J AmMed Assoc 2014; 312:2254 )
  • 33. KEY POINTS : • There are no pharmacological agents yet with proven benefits in the management of AKI. • Avoiding hyperchloremic fluid solution is effective in preventing AKI. • Most other treatments remain preventive, aiming to keep patients optimally hydrated and maintain renal perfusion pressure while avoiding nephrotoxic agents. • Clinical evidence suggests that RIPC can attenuate AKI after surgical procedures. •At present, there is no firm evidence to suggest that the use of any specific pharmacological intervention is clinically beneficial.

Editor's Notes