The document discusses acute kidney injury (AKI), its incidence, causes, and definitions, highlighting the significant morbidity and mortality associated with it, especially in ICU settings. It reviews various criteria for diagnosing and staging AKI, including RIFLE, AKIN, and KDIGO, while discussing their limitations and the importance of early detection and management. The text also emphasizes the critical role of fluid resuscitation, vasopressors, glycemic control, and nutritional support in preventing and managing AKI effectively.

1. By
Dr. Ankit Purohit
Senior Resident,
DNBSS CCM,
MODERATOR
Dr. Ajay Kumar Goila
CMO HAG,
Deptt Of CCM
ABVIMS, Dr. RML Hospital,
New Delhi.

2. Anatomy and Physiology PG dilate Afferent
ANGIOTENSIN
constrict efferent
cortex
medulla

3. Tubuloglomerular feedback

4. Renal blood flow
 RBF accounts for 20% of total cardiac output
 10% of total oxygen consumption
 Autoregulation is hampered at SBP< 80 mmHg, mean BP of 65 mmHg
 Renal medulla is more prone to hypoxic ischaemic injury.
 Atherosclerosis, long standing HTN → impaired relaxation of afferent
arteriole.

5. Acute Kidney Injury: History
 Eknoyan gave first description of ARF,
 Termed ischuria renalis, by William Heberden in 1802.
 At the beginning of the twentieth century, ARF, named Acute Bright’s
disease, was well described in William Osler’s Textbook for Medicine
(1909).
 During the First World War the syndrome was named, war nephritis.
 Homer W. Smith is credited for the introduction of the term ‘‘acute renal
failure’’ in his textbook The kidney-structure and function in health and
disease (1951).
REF – KDIGO AKI 2012 guidelines

6. Incidence
 Recent trials indicate 57% incidence in ICU.
 41% caused by sepsis.
 Independent factor for increased in hospital mortality and long term
mortality.
 AKI associated with increased risk of death, particularly ICU where
mortality rate exceeds 50%.

7. Definition
 Impairment of kidney filtration and excretory function over days to week,
resulting in retention of nitrogenous waste products.
 Cluster of heterogeneous group of conditions that share common
diagnostic features.
 Reduction in urine output and raised serum creatinine.
 term ‘‘acute kidney injury/impairment’’ has been proposed to encompass
the entire spectrum of the syndrome from minor changes in markers of
renal function to requirement for renal replacement therapy (RRT).

9. Differential Algorithm

10. RIFLE Criteria
• Acute Dialysis
Quality Initiative
(ADQI) group
developed it.
•RIFLE stands for the
increasing severity
classes Risk, Injury,
and Failure; and the
two outcome classes,
Loss and End-Stage
Renal Disease (ESRD).
•Severity grade – SCr
and UOP
•Outcome criteria –
duration of loss of
kidney function

11. Shortcomings of RIFLE
 Hoste et al, only 14% of patients
reaching RIFLE ‘‘F’’ received RRT.
 These patients experienced a
hospital mortality rate more than
five times compared to patients
without AKI.
 Levy et al.
1) examined outcomes for over
1000 patients enrolled in the
control arms of two large sepsis
trials.
2) Early improvement (within 24
hours) in cardiovascular
(P<0.0010), renal (P=0.0001), or
respiratory (P<0.0469) function
was significantly related to
survival.
3) outcomes for patients with severe
sepsis in the ICU are closely
related to early resolution of AKI.
4) Early resolution have better
outcomes.
 RIFLE criteria caused late initiation
of RRT, more mortality.

12. Shortcomings of RIFLE
 AKI defined by RIFLE is associated with decreased survival and increased severity
of AKI. Lead to increased mortality.
 Uchino et al - RIFLE was independent predictor of hospital mortality
 Ali et al – RIFLE predictor of renal recovery, but no correlation with mortality

13. AKIN
• Acute Kidney Injury
Network(AKIN)
•Thakar et al. found
that increased severity
of AKI was associated
with an increased risk
of death independent
of comorbidity
•Pediatric patient
additional modification
was done for
creatinine clearence.

14. KDIGO
 Kidney Disease: Improving Global Outcomes (KDIGO),
 a nonprofit foundation, established in 2003
 MOTO - ‘‘to improve the care and outcomes of kidney disease patients
worldwide through promoting coordination, collaboration, and integration
of initiatives to develop and implement clinical practice guidelines’’.

15. KDIGO criteria
 AKI is common.
 AKI imposes a heavy burden of illness (morbidity and mortality).
 The cost per person of managing AKI is high.
 AKI is amenable to early detection and potential prevention.
 There is considerable variability in practice to prevent, diagnose,
treat, and achieve outcomes of AKI.
 Clinical practice guidelines in the field have the potential to reduce
variations, improve outcomes, and reduce costs.
 Formal guidelines do not exist on this topic.

16. Level of evidence

17. KDIGO criteria
•AKI is defined as
increase in SCr >
0.3mg/dl within 48
hours
•Increase in serum
creatinine.1.5 times
baseline, which is
presumed to have
occurred within the
prior 7 days.
•Urine volume
<0.5ml/kg/hr for 6
hours
•Staging of AKI
•Determining the
cause

18. Conceptual model for AKI

22. Intrinsic renal failure

23. Post renal AKI
 GFR is decreased due
to obstruction of
urine flow.
 Increased intratubular
pressure leading to
increased hydrostatic
pressure.
 Absence of
hydronephrosis
doesn't always rule
out obstruction, like in
cases of severe
volume depletion,
retroperitoneal
fibrosis.
 Post void urine >100
ml is indicative of
Bladder outlet
obstruction.
 Post obstruction relief
diuresis – marked
polyuria

24. Evaluation

25. Relevant diagnostic test
 FENa – Fractional sodium extraction.
 Helps to differentiate between pre renal and renal AKI
 Pre renal AKI, Sodium Excretion in urine less, FENa<1%
 Renal Sodium Excretion in urine more, FENa>1%
 CKD, diuretic use, severe oligouria, glucosuria, FENa not reliable.
 FEurea – Fractional Excretion of urea
 <35% pre renal
 Feurea>35% severe tubular damage
 Reliable in conditions where FENa not reliable

26. Urinary sediments

27. Radiological findings
 In a study of normal volunteers, median renal lengths were 11.2 cm on the
left side and 10.9 cm on the right side.
 Renal size decreased with age, almost entirely because of parenchymal
reduction.(Emamiam et al)
 Increased cortical echogenecity, Decreased corticomedullary
differentiation indicate CKD.

28. Prevention and management of AKI
 Evaluate patients suspected having AKI promptly.
 Determine the cause, specially reversible causes.
 Monitor patients with AKI with measurements of SCr and urine output to
stage the severity.
 Manage patients with AKI according to the stage and cause.
 Evaluate patients 3 months after AKI for resolution or worsening of pre-
existing CKD.
 Treat accordingly.

29. Stage based AKI management

30. Prevention of AKI: fluid
resuscitation
 Hypotension
cause decreased
renal perfusion .
 sustained period
lead to tubular
injury
 FLUIDS
 In the absence of
hemorrhagic
shock, isotonic
crystalloids rather
than colloids
(albumin or
starches) as initial
for expansion of
intravascular
volume in patients
at risk for AKI or
with AKI.

31. Fluid resuscitation
 large multicenter studies - a positive fluid balance is an important factor associated
with increased 60-day mortality.(REF – Prowle et al, Bouchard J et al, Payen d et al)
 SAFE STUDY –
 Saline vs Albumin Fluid evaluation
 RCT comparing 4% Albumin to 0.9 % NS.
 Showed no difference in need and duration of RRT in AKI patients.
 Albumin group required less fluid and were less positive than saline group.
 Work group concluded, crystalloids are initial choice, but colloids are required for
later fluid balance.

32. Fluid resuscitation
 HES vs Saline –
 tetrastarches (HES 130/0.4 and HES
130/0.42) have also been introduced,
previous were pentastarch and
hexastarch.
 Affect factor VIII,VIIIc and von
willebrand factor by reducing
concentrations
 Block platelet fibrinogen receptors GP
IIb/IIIa.
 Tetrastarch have negligible effects on
coagulation.
 Hypertonic HES has osmotic nephrosis
effect.
 So avoided in ICU and perioperative
period.
 In the Efficacy of Volume Substitution
and Insulin Therapy in Severe Sepsis
(VISEP)study,
 patients with hypertonic HES had
increased incidence of AKI and 90 days
mortality.
 Comprehensive Cochrane review – no
evidence that colloids instead of
crytalloids decrease risk of death in
patients of trauma, burns surgery.

33. Fluid resuscitation
 Lower molecular weight tetrastarch isotonic-
 Magder et al – compared 10% 250 /0.45 HES to NS
 no evidence of AKI, nephrotoxicity, raised creatinine, increased need for RRT.
 Patient in the HES group required 60% less volume.
 Wiedermann CJ et al, recent meta analysis showed that hyperoncotic albumin was
renoprotective ,while hyperoncotic HES was renotoxic.
 Normal saline – proof from hyperchloremia direct toxicity is lacking.
 NS is preffered resuscitation agent.
 Buffered salt solution have found to cause lesser acid base disturbance, less
chloride load, but efficacy is not proven.

34. Fluid resuscitation

35. Fluid resuscitation
 STAR TRIAL – standardization of care for AKI recovery.
 They discussed end points of study MAKE(major adverse kidney events) at 30, 60
and 90 days.
 HES increased AKI incidence in sepsis.
 HES has no advantage in 28 day mortality in AKI or improvement in hemodynamic
parameters
 NS should be replaced with buffered solutions carrying normal chloride load.
 Better outcomes in AKI patients.

36. Vasopressors
 Recommend the use of vasopressors in
conjunction with fluids in patients with
vasomotor shock with, or at risk for, AKI
 Septic shock is high output low
resistance condition.
 Severe pancreatitis, liver failure, burns,
anaphylaxis are similar.
 After proper volume resuscitation,
vasopressors help improve renal
perfusion.
 Improvement in creatinine clearance
(CrCl) following a 6- to 8-hour infusion
of norepinephrine. (Redl-Wenzl Emet
al).
 Dopamine with NE increased incidence
of arrhythmias, increased mortality in
cardiogenic shock but not in septic or
hypovolemic shock.
 Use of dopamine was associated with
more adverse events(De becker D et al)
 Vasopressin reduced the need for
norepinephrine increased urine output
and CrCl. (Lauzier F et al).
 Vasopressin in comparison to NE,
treatment of shock refractory to NE
increase perfusion pressure, dieresis.
 No improvement in survival or need of
RRT.
 Vasopressin associated with lower rate
of progression of AKI.

37. Hemodynamic management
 Protocol-based management of
hemodynamic and oxygenation
parameters to prevent development or
worsening of AKI in high-risk patients in
the perioperative setting (2C) or in
patients with septic shock (2C).
 Early Goal-Directed Therapy (EGDT) –
achieving hemodynamic goals within 6
hours of admission
 consists of fluids, vasopressors and
blood transfusions ,targeting
physiological parameters.
 Rivers et al – EGDT improved outcome
and prevented end organ failure in
septic patients.
 The physiologic goals are:
1) return of mean arterial blood pressure
to 65-90 mm Hg.
2) central venous pressure between 8–
12mm Hg.
3) improvement in blood lactate levels.
4) central venous oxygen saturation
(ScvO2) >70%;
5) a urine output of >0.5 ml/kg/hr.
6) in-hospital mortality rate in the control
group was 46.5% vs. 30.5% in the EGDT
group (P<0.01).

38. Glycemic control and nutritional support
 In critically ill patients, insulin therapy
targeting plasma glucose 110–149
mg/dl (6.1–8.3 mmol/l). (2C)
 Stress hyperglycemia -- exogenous
insulin administration normalizes blood
glucose levels in this setting.
 Kosiborod et al.- in MI population,
hypoglycemia was associated with
increased mortality.
 Iatrogenic hypoglycemia after insulin
therapy was not associated with higher
mortality risk.
 vanderBerghe et al and Schetz et al -
found intensive insulin control
decreased AKI progression but no
decrease in requirement of RRT.
 Gandhi GY et al , Mangano et al –
Intensive insulin control led to decrease
in AKI post cardiac surgery.
 Stroke incidence increased in intensive
control group.
 VISEP trial – intensive sugar control
never provide benefit, rather more
episode of hypoglycemia.
 Wienner et al- no significant benefit in
mortality of AKI with intense control,
increased mortality.

39. Nutritional Aspect
 Total energy intake of 20–30 kcal/kg/d in patients with any stage of AKI. (2C)
 Hyperglycemia –
 due to insulin resistance,.
 hepatic neoglucogenesis.
 protein catabolism.
 Hypertriglyceridemia, due to inhibition of lipid metabolism.
 30 to 40 kcal of energy was associated with hyperglycemia and
hypertriglyceridemia rather than positive nitrogen balance in AKI patients.
 Energy provision should be composed of 3–5 (maximum 7) g per kilogram body
weight carbohydrates and 0.8–1.0 g per kilogram body weight fat.

40. Nutritional Aspect
 Avoid restriction of protein intake with
the aim of preventing or delaying
initiation of RRT. (2D)
 Administering 0.8–1.0 g/kg/d of protein
in noncatabolic AKI patients without
need for dialysis (2D),
 1.0–1.5 g/kg/d in patients with AKI on
RRT (2D), and up to a maximum of 1.7
g/kg/d in patients on continuous renal
replacement therapy (CRRT) and in
hypercatabolic patients. (2D).
 Nutritional protein administration
should not be restricted as a means to
attenuate the rise in BUN associated
with declining GFR.
 CRRT techniques can better control
azotemia.
 In CRRT, about 0.2 g amino acids are lost
per litre of filtrate, total daily loss of 10–
15 g amino acids.
 5–10 g of protein are lost per day,
depending on the type of therapy and
dialyzer membrane.

41. Nutritional Aspect
 suggest providing nutrition preferentially via the enteral route in patients with AKI.
(2C).
 PROBLEMS – AKI leads to impaired gut motility, bowel edema
 ADVANTAGE - maintains gut integrity, decrease gut atrophy, prevent endotoxemia
via gut flora.
 critically ill children, like adults, should receive 100–130% of the basal energy
expenditure.
 estimated with acceptable precision and accuracy by the Caldwell-Kennedy
equation.
 (resting energy expenditure [kcal/kg/d]= 22+31.5 X weight [kg]+ 1.16 X age [years]).

42. Diuretics
 Recommend not using diuretics to
prevent AKI. (1B)
 Not using diuretics to treat AKI, except
in the management of volume overload.
(2C).
 HYPOTHESIS
1) LOOP DIURETICS may decrease oxygen
consumption in the loop of Henle by
inhibiting sodium transport, thus
potentially lessening ischemic injury.
2) Hasten recovery of AKI by washing out
necrotic debris blocking tubules and by
inhibiting prostaglandin
dehydrogenase, which reduces
renovascular resistance and increases
renal blood flow.
 Minimal data to support above theory.
 Post cardiac surgery, harmful,
ineffective to prevent AKI.
 Increased mortality in patients with AKI
and critical illness.
 Ho et al - Loop diuretic not effective in
preventing AKI.
 no reduction in hospital mortality or
need for RRT.
 Van DerVoot et al – furosemide lead to
early discontinuation of RRT.
 PROGNOSTICATION- urine flow in
response to bolus furosemide. 1 – 1.5
mg/kg dose bolus. Less than 200 ml
over 2 hours of urine, higher risk of
progression to AKI.

43. Diuretic Resistance

44. Mannitol
 Weisberg et al - Mannitol, Dopamine and ANP aggravated ARF.
 Loop diuretics and mannitol worsened contrast induced nephropathy.
 The sparse controlled data available have shown that 250 ml of mannitol 20% given
immediately before vessel clamp removal reduces the incidence of post-transplant
AKI.
 Under study to Prevent AKI by Rhabdomyolysis.

45. Vasodilator therapies
 DOPAMINE - Low-dose dopamine
administration (1–3 mg/kg/min) to
healthy individuals causes renal
vasodilation, natriuresis, and increased
GFR.
1) Prophylaxis for AKI associated with
radiocontrast administration.
2) repair of aortic aneurysms.
3) orthotopic liver transplantation.
4) unilateral nephrectomy.
5) renal transplantation.
6) chemotherapy with interferon.
 Lauschke et al., found that dopamine
significantly increased renal vascular
resistance in AKI patients.
 Kellum and Decker, found no benefit of
dopamine for prevention or therapy of
AKI in an adequately-powered meta-
analysis.
 Marik et al found no benefit in a
systematic review.
 recommend not using low-dose
dopamine to prevent or treat AKI. (1A)

46. Vasodilator therapies
 Fenoldopam mesylate is a pure dopamine type-1 receptor agonist that has similar
hemodynamic renal effects as low-dose dopamine, without systemic alpha- or
beta-adrenergic stimulation.
 suggest not using fenoldopam to prevent or treat AKI. (2C).
 Cogilati et al - 24-hour infusion of 0.1 mg/kg/min of fenoldopam prevented AKI in a
high-risk population undergoing cardiac surgery.
 Morelli et al and Tumlin et al – found no additional benefit in prevention of AKI.

47. Vasodilator therapy
 NATRIURETIC PEPTIDE – Atrial Natriuretric Peptide decreases preglomerular
vascular resistance and increases postglomerular vascular resistance, leading to
increased GFR.
 suggest not using atrial natriuretic peptide (ANP) to prevent (2C) or treat (2B) AKI.
 RCT - ANP at dose of 0.2 mcg/kg/min had no advantage in reducing dialysis free
trial
 Nigweker et al – no advantage of fenoldopam in oligouric kidney to prevent dialysis.
 URODILANTIN – released from renal tubules
 Few studies have shown it improves course of established post operative AKI.
 NESIRITIDE – no benefit in 21 day dialysis or death in patients undergoing CTVS
surgery.

48. Growth Factors
 recommend not using recombinant human (rh)IGF-1 to prevent or treat AKI. (1B).
 IGF 1 showed benefit in animals in post AKI recovery.
 No benefits noted in humans.
 ERYTHROPOETIN
 Not useful due to longer onset time of action.
 Relative state of bone marrow resistance in AKI patient.

49. Adenosine receptor Antagonist
 Adenosine released as part of the
tubuloglomerular feedback loop
 binds to glomerular adenosine A1
receptor.
1) vasoconstriction of the afferent
arteriole.
2) decreased renal blood flow and GFR
3) sodium and water retention.
 Prevent or treat AKI in perinatal
asphyxia, radiocontrast exposure, and
cardiorenal syndrome.
 suggest that a single dose of
theophylline may be given in neonates
with severe perinatal asphyxia, who are
at high risk of AKI. (2B)
 60% of infants suffer from perinatal
asphyxia, leads to adenosine induced
vasoconstriction in kidneys from
normocapneic hypoxia.
 Theophylline single dose (5 mg/kg or
8mg/kg ) have found to benefit such
neonates.
 ROLOFYLLINE – dose dependent
attenuation of rise of SCr in adult acute
decompensated heart failure patients
 PROTECT TRIAL – no benefit in cardiac
patients for AKI. Rather one group had
seizures as known side effect.

50. Prevention of AKI in Aminoglycoside
 AMINOGLYCOSIDE - suggest not using
aminoglycosides for the treatment of
infections unless no suitable, less
nephrotoxic, therapeutic alternatives
are available. (2A).
 Risk of AKI attributable is upto 25% in
some studies.
 AKI occurs 5 to 7 days after
administration.
 Recovery takes several weeks after
withdrawal.
 Older patients, DM, Septic patients,
prolonged use are risk factors
 in patients with normal kidney function
in steady state, aminoglycosides are
administered as a single dose daily
rather than multiple-dose daily
treatment regimens. (2B).
 concentration-dependent bactericidal
activity, with a prolonged
‘‘postantibiotic effect’’,
 .
 permitting extended interval dosing in
an effort to optimize efficacy and
minimize toxicity.
 Nephrotoxicity is primarily by uptake of
drug via MEGALIN receptor in PCT.
 Toxicity is potentiated by Neuromuscular
blocking agents.
 Inhaled route showed renal
toxicity.(Zampieri et al, critical care
2015)

51. Aminoglycosides
 Recommend monitoring aminoglycoside
drug levels on treatment with multiple
daily dosing is used for more than 24
hours. (1A).
 Dosing strategy for once-daily
aminoglycosides is 5 mg/kg/d for
gentamicin and tobramycin (with
normal renal function); 6 mg/kg/d for
netilmicin; and 15 mg/kg/d for
amikacin.
 suggest monitoring aminoglycoside
drug levels when treatment with single-
daily dosing is used for more than 48
hours. (2C).
 Suggest using topical or local
applications of aminoglycosides (e.g.,
respiratory aerosols, instilled antibiotic
beads), rather than i.v. application,
when feasible and suitable. (2B)
 IHD and High flux CRRT can be used for
prolonged aminoglycoside toxicity.

52. Amphotericin B
 Side effects
1) Thrombophlebitis.
2) Electrolyte disturbances.
3) Hypoplastic anemia.
 Systemic toxicity –
 fever, chills, hypotension, and cytokine
release.
 Suggest using lipid formulations of
Amphotericin B (2A).
 Mechanisms
1) ischemic injury – due to
vasoconstriction of afferent arteriole
2) direct tubular- and glomerular-cell
membrane toxicity.
 To sublime toxicity
1) continues infusion approach.
2) alternate day regime
 Liposomal Amphotericin consists of
Amphotericin B complexed with
hydrogenated soy phosphatidylcholine,
distearoylphosphatidylcholine, and
cholesterol.
 Treatment of systemic mycoses or
parasitic infections.
 azole antifungal agents and/or the
echinocandins rather than conventional
amphotericin B, if equal therapeutic
efficacy can be assumed. (1A)

53. Other Drugs
 INTRAVENOUS ACYCLOVIR –
 cause renal tubular obstruction.
 Form needle shaped crystals blocking tubules.
 hydration. For treatment
 CISPLATIN –
 Dose related cumulative effect
 Profound renal magnesium wasting
 Vigorous hydration and monitoring of serum potassium and magnesium.
 ETHYLENE GLYCOL/METHANOL-
 elevated osmol gap.
 Anion gap metabolic acidosis.
 Oxalate crystals block tubules.
 FOMEPIZOLE -15 mg/kg over 30 min and hydration protective,15 mg/kg every 12
hourly.

54. Pigments
 RHABDOMYOLYSIS –
 Crush injury, prolonged immobility, Status epilepticus, hyperthermia, statin
induced.
 Muscle enzyme levels doesn't correlate with severity of AKI.
 Renal vasoconstriction, tubular occlusion, proximal tubule injury.
 Hyperkalemia, hyperphosphaetemia, hypocalcaemia.
 FENa<1%
 Require vigorous hydration.
 HEMOGLOBINURIA-
 Hemolysis leads to ATN
 LDH elevated, Haptoglobin decreased.
 Urine dipstick shows heme pigment in absence of RBC.

55. Tumor lysis syndrome
 Post treatment of tumor after chemotherapy
 Due massive killing of neoplastic cells.
 48 to 72 hours after killing of cells.
 Hyperkalemia, hyperphosphetemia, hyperuricemia.
 Hyperuricemia is main cause for tubule obstruction in acidic environment.
 Calcium phosphate crystals deposit due to hyperphosphetemia
 Aggressive hydration, allopurinol and rasburicase as treatment.

56. Glomerular Autoimmune diseases
 Steroids are main line and shows improvement in AKI.
 i.v. Methylprednisolone 7 – 15 mg/kg/day.
 Followed by oral 1 mg/kg/day.
 Cyclophosphamide 15 mg/kg or 750 mg/metre square.
 HUS/TTP(hemolytic uremic syndrome/thrombotic thrombocytopenic purpura) –
 HIV, malignancy, calceineurin inhibitors, ticloidine, clopidegrol, shiga like toxin
 Daily plasma exchange
 ECULIZUMAB C5 complement inhibitor.

57. Atheroembolic and interstital nephritis
 ATHEROEMBOLIC –
 Invasive cardiovascular procedures result in it.
 Renal dysfunction days to week after procedure
 Peripheral eosinophillia
 Eosinophiluria
 Hypocomplementia
 High mortality
 ACE inhibitors, nutritional support , judicious control of BP have better prognosis.
 INTERSTITAL NEPHRITIS –
 Sterile pyuria with eosinophillia.
 Methicillin, NSAIDS, sulfonamides, allopurinol,leptospira.
 Symptomatic plus treating root cause.


58. Hepatorenal Syndrome
 DIAGNOSTIC CRITERIA-
 Cirrhosis with ascites.
 Worsening of renal function over days
to weeks, with SCr >1.5 mg/dl.
 Absence of intrinsic renal disease(no
proteinuria >500mg/day, no
microscopic hematuria >50 RBC /hpf).
 absence of structural kidney disease.
 Absence of shock
 No improvement in renal function after
diuretic withdrawal and volume
expansion with albumin for at least 2
days.
 SUBTYPES –
 TYPE I – rapidly progressive , creatinine
getting doubled to level of 2.5 mg.dl in
<2 weeks
 TYPE II – moderate- slow progressive
course/ creatinine 1.5 – 2.5 mg/dl
associated with refractory ascites.

59. Hepatorenal syndrome
 PATHOPHYSIOLOGY –
 Severe vasoconstriction in view of splanchnic vasodilation.
 ESLD spontaneous development.
 SBP is another cause.
 Diagnosis of exclusion, poor prognosis(type I more than II)
 Few therapeutic options
 MANAGEMENT –
 Vasoconstrictors(terlipressin, midodrine)
 Octreotide(inhibitor of vasodilator response).
 TIPS (transjugular intrahepatic portosystemic shunt), more obsolute now
 RRT bridge to liver transplant.

60. Special situations
 ON-PUMP VS. OFF-PUMP CORONARY
ARTERY BYPASS SURGERY.-
 Off pump reduced incidence of AKI,
perioperative mortality, risk of
neurological incidences.
 Off pump is associated with more
hemodynamic variations
 suggest that off-pump coronary artery
bypass graft surgery not be selected
solely for the purpose of reducing
perioperative AKI or need for RRT. (2C).
 N ACETYL CYSTEINE-
 suggest not using NAC to prevent AKI in
critically ill patients with hypotension.
(2D)
 NAC regenerate Glutathione stores,
potent antioxidant.
 NAC is usually recommended for eGFR <
60ml/min/metre square in CKD
 Hasse et al, Rehman et al, Mainra et al
didnt find any advantage of NAC post
surgically to improve SCr levels.
 recommend not using oral or i.v. NAC
for prevention of postsurgical AKI. (1A)

61. Contrast induced AKI
 Define and stage AKI after administration of intravascular contrast media
 evaluate for CI-AKI as well as for other possible causes of AKI.
 defined as a rise in SCr of >0.5 mg/dl (>44 mmol/l) or a 25% increase from baseline
value, assessed at 48 hours after a radiological procedure.
 cystatin C as an early marker for AKI,
 a cut-off cystatin C increase concentration of >10% at 24 hours after contrast-media
exposure.
 have 100% negative predictive value.
 CI-AKI have high progressive mortatlity (McCullough et al).
 CI-AKI Consensus Working Panel also supported the use of dipstick testing for urine
protein as a rapid screen.

62. CI-AKI

63. CI-AKI
 RISK FACTORS –
1) diabetes
2) hypertension
3) CHF
4) advanced age,
5) volume depletion
6) hemodynamic instability
7) use of concurrent nephrotoxic
medications
8) large volume or high osmolality of the
contrast agent
9) metabolic syndrome
10) hyperuricemia
 GADOLINIUM CHELATE-
 Perazella et al. , Gd-induced
nephrotoxic AKI compared to CI-AKI.
 risk of developing Nephrogenic systemic
fibrosis.
 Use of macrocyclic chelate, use lowest
possible dose

64. CI-AKI
 NONPHARMALOGICAL PREVENTION –
 Use the lowest possible dose of contrast medium in patients at risk for CI-AKI. (Not
Graded)
 CI-AKI appears more after arterial than venous injection.
 recommend using either iso-osmolar or lowosmolar iodinated contrast media,
rather than high-osmolar iodinated contrast media in patients at increased risk of
CI-AKI. (1B)

65. CI-AKI
 PHARMACOLOGICAL INTERVENTION-
 Recommend i.v. volume expansion with
either isotonic sodium chloride or
sodium bicarbonate solutions, (1A).
 A ‘‘good’’ urine output in the 6 hours
after the radiological procedure has
been associated with reduced rates of
AKI.
 Oral NAC, together with i.v. Isotonic
crystalloids, in patients at increased risk
of CI-AKI. (2D).
 Statins have also shown improved
kidney funstions in AKI (PRAVASTATIN)
 A daily dose greater than 1200 mg or a
single periprocedural dose greater than
600 mg (periprocedural being described
as immediately or within 4 hours of the
planned contrast exposure) as
preventive.
 suggest not using theophylline to
prevent CI-AKI. (2C).
 Recommend not to use Fenoldopam to
prevent CI-AKI.(1B)

69. New markers
 NGAL – neutrophil gelatinase associated lipocalin
 IL-18
 KIM 1 – Kidney injury molecule
 TIMP II – tissue inhibitor of metalloproteinases.
 IGFBP7 – insulin like growth factor binding protein 7
 Cystatin C
 NEPHROCHECK-
 TIMP/IGFBP7 combination.
 Used in ICU patients with age>21 years with cardiac and respiratory compromise.
 Value >0.3 means high risk of having AKI within 12 hours.
 Prognostication .

70. THANK YOU