PPT ON AKI IN A SEMINAR OF GOVERNMENT MEDICAL COLLEGE AS 2ND YEAR PG RESIDENT IN YEAR 2022

1. DIAGNOSTIC APPROACH
AND MANAGEMENT OF
ACUTE KIDNEY INJURY
DR SUBHAYAN BATABYAL
2ND YEAR PG RESIDENT
DEPARTMENT OF MEDICINE

2. ACUTE KIDNEY INJURY(AKI) is ABRUPT impairment of
filtration and excretory function of kidneys over
days to weeks (usually with in 7 days) resulting in
retention of nitrogenous waste products with in
blood.
AKI is not a single entity rather it is a heterogenous
group of disease that share common characteristics
like reduction of URINE VOLUME and increase in
serum CREATININE and UREA.

3. AKI is diagnosed if ONE of the following
criteria is met:
Increase in serum creatinine (SCr) at
least 0.3mg/dl within 48hours .
A 50% increase in baseline SCr with in 7
days .
Urine output less than 0.5mg/kg /hr for
atleast 6hours .

4. EPIDEMIOLOGY
• AKI comprises of 5-7 percent of all hospital
admission and 30 percent of ICU admission.
• Large studies have shown that increase in
serum creatinine by 0.3mg/dl may increase
mortality by FOUR folds .
• Mortality rate of about 50 percent is prevalent
among ICU admitted patients despite
improvement in medical infrastructure.

5. COMMUNITY
ACQUIRED AKI
HOSPITAL
ACQUIRED AKI
ICU ACQUIRED AKI
INCIDENCE LOW <1% MODERATE(2-20%) HIGH (20-60%)
CAUSE SINGLE SINGLE/MULTIPLE MULTIFACTORIAL
MORTALITY RATE 15% 15-40% 30-50%
RISK FACTORS CHF
DRUG ADVERSE
EFFECT
URINARY TRACT
OBSTRUCTION
MALIGNANCY
SEPSIS
SURGERY
NEPHROTOXIC
DRUG REACTION
VOLUME
DEPLETION DURING
SURGICAL
PROCEDURE
MODS
NEPHROTOXIC
DRUG REACTION
SEPTIC SHOCK

6. TOP FIVE CAUSES OF AKI IN INDIA
• DIARRHEAL DISEASES
• SEPSIS
• ACUTE FALCIPARUM MALARIA
• DRUG INDUCED
• HOSPITAL ACQUIRED

8. CLASSIFICATION OF AKI
• RIFLE CRITERIA: RISK- INURY -
FAILURE LOSS OF KIDNEY FUNCTION- END
STAGE RENAL DISEASE
• AKIN CRITERIA :ACUTE KIDNEY INJURY
NETWORK
• KDIGO CRITERIA :KIDNEY DISEASE
IMPROVING GLOBAL OUTCOME

9. RIFLE CRITERIA

10. AKIN CRITERIA

11. KDIGO CRITERIA

12. PATHOPHYSIOLOGY
• AKI is broadly classified into 3 categories :
• PRERENAL
• RENAL or INTRINSIC
• POSTRENAL

15. INTRINSIC AKI
GLOMERULAR TUBULAR AND INTERSTITIUM VASCULAR
ACUTE
GLOMERULO
NEPHRITIS
ISCHEMIA SEPSIS /INFECTON NEPHROTOXINS VASCULITIS
RENAL ARTERY
STENOSIS
,B/L RENAL VEIN
THROMBOSIS
OPERATIVE
ARTERIAL CROSS
CLAMPING
MALIGNANT
HYPERTENSION
TTP-HUS
POST
OPERATIVE
SIRS
BURNS
PANCREATITIS
Due to
microvascular
and
endothelial
Damage by
leucocytes and
ROS
Exogenous:
Contrast agents
Aminoglycoside
Cisplatin
Amphotericin B
PPI
NSAIDS
Endogenous
Rhabdomyolosis,
hemolysis,
myeloma,
intratubular
crystals
ACUTE INTERSTITIAL NEPHRITIS :
Drug HSN :Antibiotic uses ,Diuretics ,
NSAIDS ,Anticonvulsant drugs ,Allopurinol
Infective: Bacterial(staph strepto,)viral ( CMV
EBV),Tubercular,fungal(candida)

17. POST RENAL AKI
• BLADDER OUTLET
OBSTRUCTION(BPH,Neurogenic bladder
anticholingeric drug blood clots calculi
urethral strictures )
• BILATERAL PELVIURETERAL
OBSTRUCTION(neoplasia retropetritoneal
fibrosis abscess )
• SOLITARY FUNCTION KIDNEY

18. PATHOPHYSIOLOGY OF PRERENAL AND INTRINSIC AKI

20. CLINICAL PRESENTATIONS OF AKI
DECREASED URINE OUTPUT
NAUSEA /VOMITING/ DIARRHEA/ ANOREXIA
WEIGHT GAIN
PERIPHERAL EDEMA
ALTERED MENTAL STATUS
FATIGUE
DYSPNEA
PRURITIS

21. DIAGNOSTIC ALGORITHM TO AKI
 HISTORY TAKING AND PHYSICAL EVALUATION
 URINE FINDINGS
 BLOOD PARAMETERS
 RENAL FAILURE INDICES
 RADIOLOGICAL FINDINGS
 NOVEL BIOMARKERS
 RENAL BIOPSY

22. HISTORY AND PHYSICAL FINDINGS
H/O of vomiting diarrhea
Use of medications like NSAIDS, ACEI ,ARB and their doses
H/O of prostatic disease, Nephrolithiasis , pelvic malignancy
H/O of Autoimmune disease like SLE
H/O of Pregnancy
PHYSICAL SIGNS :
Orthostatic hypotension, tachycardia , reduced JVP, decreased skin
turgour ,dry tongue indicative of PRERENAL AZOTEMIA
Supra pubic pain hints to Bladder outlet obstruction
Atheroembolic disease leads to livedo reticularis and other emboli signs
in leg
Fever arthalgia and rashes may accompany in Allergic Interstitial Nephritis
Palpable purpura raises the possibility of any vasculitis
Tense abdomen may be considered as COMPARTMENT SYNDROME
Signs of Limb ischemia opts for Rhabdomylosis

23. URINE ANALYSIS
URINE ANALYSIS gives good interpretation towards
cause of AKI but lacks sensitivity and specificity.
Oliguria (urine output <400ml in 24 hrs denotes poor
prognosis in AKI .
Anuria is uncommon in AKI but usually associated
with complete Urinary tract obstruction ,profound
septic shock, severe ischemic necrosis ,vasculitis .

24. • CAUSES OF NORMAL URINARY FINDINGS OR
FEW HYALINE CAST :
1) PRERENAL AZOTEMIA
2) POST RENAL AKI
3) TTP/HUS
4) PREGLOMEERULAR VASCULITIS
5) SCLERODERMA CRISIS
6) ATHERO EMBOLISM

25. ABNORMAL URINE FINDINGS
RBC CAST WBC CAST RENAL
TUBULAR CELLS
/ PIGMENT
CAST
GRANULAR
CASTS
EOSINOPHILS CRYSTALURIA
GLOMERULO
NEPHRITIS
(GN)
VASCULITIS
MALIGNANT
HYPERTNSION
THROMBOTIC
MICRO
ANGIOPATHY
PYELO
NEPHRITIS
INTERSTITIAL
NEPHRITIS
ALLOGRAFT
REJECTION
TUBULO
INTERSTITIAL
NEPHRITIS
MYO –
GLOBINURIA
HEMO -
GLOBINURIAA
ATN
GLOMERULO
NEPHRITIS
(GN)
VASCULITIS
ALLEGIC
INTERSTTIAL
NEPHRITIS
GN
PYELO
NEPHRITIS
CYSTITIS
URIC ACID
NEPHROPATHY
CALCIUM
GLUCONATE
INGESTION
DRUGS
(SULFADIAZINE
,ACYCLOVIR ,
INDINAVIR )

26. BLOOD INVESTIGATIONS
COMPLETE BLOOD COUNT
PERIPHERAL BLOOD SMEAR
RENAL FUNCTION TEST
SERUM ELECTROLYTES
SERUM URIC ACID /PHOSPHATES
CPK /LDH
SERUM ELECTROPHORESIS
ANA/ANCA/ANTI GBM /ANTI
PHOSPHOLIPASE A2 Antibodies
COMPLEMENTS

27. BLOOD PARAMETERS
 ELEVATED serum CREATININE above baseline
Associated findings In different clinical settings:
 LOW Haemoglobin(Hb)
 PERIPHERAL EOSINOPHILIA
 THROMBOCYTOPENIA
 HYPERKALEMIA
 HEPERPHOSPHATEMIA
 HYPERURICEMIA
 HYPOCALCEMIA
 ALTERED ANION GAP
 FREE LIGHT CHAINS IN SERUM ELECTROPHORESIS

28. RENAL FAILURE INDICES
Several indices have been used to distinguish
prerenal azotemia from intrinsic AKI .
The FeNa (fractional excretion of filtered sodium
load ) is one such indicator which justify the ability of
kidneys to carry out proper tubular reabsorption .
It has high sensitivity but low specificity.

32. RADIOLOGICAL ASSESSMENT
UTRASOUND
CTSCAN
MRI
ANTEGRADE /RETROGRADE
PYELOGRAPHY

33. • IN CKD kidneys are shruken except for Diabetic
nephropathy ,HIV associated nephropathy
,Infiltrative diseases .
• Kidneys are normal sized in AKI .
CONTRAST AGENTS SHOULD BE USUALLY
AVOIDED IN SEVERE AKI LIKE IODINATED
AGENTS AND TYPE 1 GADOLINIUM BASED
AGENTS.

34. NOVEL BIOMARKERS
BUN and SCr are functional markers of
glomerular filtration but not indicative
of Tissue injury .
BUN and Scr are slow to rise after AKI as
a result accurate diagnosis gets belated .
Several Protein Biomarkers have been
discovered by research work and are
used to confirm AKI faster .

35. NOVEL BIOMARKERS

36. APPROACH TO AKI
TYPE HISTORY FEATURES
PRERENAL
AZOTEMIA
H/O of poor fluid intake, fluid loss,
diarrhea
Vomiting ,
NSAIDS ,ARB ,ACEI
Decreased circulatory volume
(cirrhosis, heart failure )
BUN/Cr>20%
FeNa<1%
HYALINE CAST
URINE
OSMOLALITY >500
URINE SGPECIFIC GRAVITY
>1.08
SEPSIS a/w AKI Septic shock or overt infection POSITIVE CULTURE FROM
SITES ,URINE SEDIMENT
GRANULAR CAST ,TUBULO
EPITHELIAL CAST
FeNa>1%
ISHEMIA a/wAKI Systemic hypotension a/w sepsis
CKD ,Old age
URINE SEDIMENT GRANULAR
CAST ,TUBULO EPITHELIAL
CAST
FeNa>1%

37. TYPE HISTORY FEATURES
RHABDOMYLOSIS TRAUMATIC CRUSH
INJURIES
SEIZURE
IMMOBILIZATION
ELEVTED MYOGLOBIN,
CREATINE KINASE, URIC
ACID ,URINE HEME
POSITIVE BUT FEW RBC
HEMOLYSIS TRANSFUTION REACTION ANAEMIA ,ELEVATED LDH
LOW HAPTOGLOBIN
TUMOUR LYSIS
SYNDROME
RECENT CHEMO THERAPY HYPERKALEMIA
HYPERPHOAPHATEMIA
HYPOCALCEMIA NORMAL
TO MARGINALLY INCREASED
URIC ACID AND CREATINE
KINASE
MULTIPLE MYELOMA AGE >65 BONE PAIN
CONSTITUTIONAL
SYMPTOMS
MONOCLONAL M SPIKE IN
ELECTROPHORESIS LOW
ANION GAP ANAEMIA

38. TYPE HISTORY FEATURES
CONTRAST NEPHROPATHY EXPOSURE TO IODINATED
COMPOUNDS
RISE IN SCr WITH IN 2-3
DAYS PEAK IN 3-5 DAYS
RECOVERY IN 7 DAYS
ANTIBIOTICS :
AMINOGLYCOSIDE,CISPLATIN
,VANCOMYCIN ,TENOFOVIR
ETHELYNE GLYCOL MELAMINE
SUGGESTIVE DRUG
HISTORY
URINE SEDIMENT
GRANULAR CAST ,TUBULO
EPITHELIAL CAST
FeNa>1%

39. TYPE HISTORY FEATURES
GLOMERULO NEPHRITIS,
VASCULITIS
SUGGESTIVE SYMPTOMS ANA,ANCA AGBM POSITIVE
KIDNEY BIOPSY SUGGESTIVE
INTERSTITIAL NEPHRITIS LEIGONELLA INFECTION
TUBULOINTERSTITIAL NEPHRITIS-
UVEITIS
STERILE PYURIA ,EOSINOPHILURIA
NONOLIGURIC
TTP/HUS RECENT DIARRHEA ,
NEUROLOGICAL ANOMALIES
,CALCINEURIN INHIBITORS ,
PREGNANCY POST PARTUM
SCHISTOCYTES IN PBS
ELEVATED LDH ,ANAEMIA
THROMBOCYTOPENIA
TYPICAL HUS IS DIARRHEAL
DISEASE DUE TO SHIGA TOXIN
ATYPICAL HUS IS DUE TO
ACQUIRED COMPLEMENT
DYSREGULATION
ADAMTS13 ACTIVITY REQUIRED

40. TYPE HISTORY FEATURES
POST RENAL AKI
H/O KIDNEY STONES
PROSTRATE DISEASE
OBSTRUCTED BLADDER
RETROPERITONEAL PELVIC
NEOPLASM
MAY BE ASSOCIATED WITH
PYURIA ,HEMATURIA
USG ,CT SUGGESTIVE

41. INDICATION OF RENAL BIOPSY
ARF of unknown etiology
Suspicion of glomerulonephritis,systemic
diseases (eg. Vasculitis )or AIN (acute
interstitial nephritis).
ATN not recovering after 4-6 weeks of
dialysis with no more recurrent insults

42. COMPLICATIONS OF AKI
HYPERVOLEMIA /HYPOVOLEMIA
HYPONATREMIA
HYPERKALEMIA
ACIDOSIS
HYPERPHOSPHATEMIA
HYPOCALCEMIA
BLEEDING
INFECTIONS
CARDIAC
COMPLICATIONS(arrythmias,pericarditis,pericardial
effusion )
MALNUTRITION

43. MANAGEMENT OF AKI
 MEDICAL MANAGEMENT
 DIALYSIS
 TREATMENT OF COMPLICATIONS

44. CONSERVATIVE MANAGEMENT
• COMPLETE FLUID INTAKE AND OUTPUT
• DAILY WEIGHT RECORD
• INTRAVASCULAR VOLUME ASSESSMENT
CLINICALLY DAILY. CV line for measure CVP
• SERUM Na /K /Ur/Cr /Calcium/Phosphate

45. :
PRENAL AKI MANAGEMENT
a) Correct volume depletion
 When Prerenal AKI is due to deficits in ECF volume FLUID
THERAPY is indicated.
 In severe hemorrhage PRBC is indicated .
 BUFFERED CRYSTALLOIDS SOLUTIONS (RINGER LACTATE
,PLASMALYTE,HARTMAN SOLUTION)
 In Severe Hypovolemia with hypochloremia 0.9% NORMAL
SALINE is used.

46. FLUID CHALLENGE
In young patients 500-1000ml of bolus should be
given .In old patients 250 ml bolus given
irrespective of cardiac status.
ASSESS VOLUME STATUS
If EUVOLEMIA achieved SERUM ELECTROLYTES are
monitored.
Total fluid requirment =Total output of kidney and
GI tract in previuos 24hr with additional 500-
1000ml for inacessible losses.

47. b)Ineffective arterial blood volume with edema:

48. In case of Cardiac failure :
DIURETIC AGENTS in combinatins
with Digitalis therapy may increase
Cardiac output and improve renal
perfusion and lessen azotemia
.CARDIAC AFTER LOAD REDUCERS
like ACEI, nitrates ,hydralazine may
improve the outcome.

49. 2.). Cirrhosis and Hepato renal failure:
Fluid management in individulals with
cirrhosis & ascites AKI Is challeging due to
difficulty in assessing intravascular volume
status.
Administration of IV fluids in wrong pattern
may lead to worsening of ascites and
pulmonary compromise.

50. • ALBUMIN may prevent AKI in those treated
with antibiotics for sponteneous bacterial
peritonitis.
• Definiive treatment for HEPATORENAL FAILURE
Is LIVER TRANSPLANTATION.
• Bridge therapy include
terlipressin(vasopressin analogue)
combination therapy with octreotide
(somatostatin analogue)and midodrine(alfa
adrenergic analogue)and noradrenaline along
with albumin (1g/kgbody wt max to 100g)

51. MONITORING OF THERAPY
• Assessment of JUGULARVENOUS PRESSURE
ORTHOSTATIC CHANGES IN BLOOD PRESSURE
AND PULSE.
• ULTRASOUND GUIDED MEASUREMENT OF
DIAMETER OF IVC WITH RESPIRATORY
CHANGES is most reliable.
• Presence of basal crepts and third heart
sound indicates vigorous fluid administration
with resultant pulmonary congesion.

52. • The patients in whom vigorous resusitation is
required and cardiovascular tolerance to
sudden fluid challenges ,monitoring should be
done with CENTRAL VENOUS CATHETER.
• It is a satisfactory guide to measure CVP which
ranges between 8-12 cm of water.
• In volume depleted states CVP ranges low to
zero.
• A CVP rise more than 5 cm of water suggests
cardiac failure & indication to stop fluid
transfusion.

53. MANAGEMENT OF INTRINSIC AKI
There is no specific treatment of ATN.
First of all VOLUME STATUS of patient is
assessed.
If VOLUME DEFICIT :it should be corrected with
adequate fluid therapy.
If EUVOLEMIC :Fluid challenge & Diuretic
challenge.
If VOLUME OVERLOAD :Diuretic challenge to
convert oliguric AKI to nonoliguric AKI.

54. DIURETIC CHALLENGE: may be given in oliguric
patients with volume overlod.
Initially iv furosemide 40-120 mg given as
bolus if urine output improves then continous
infusion 20mg/hr should be given.
Diuretics only convert oliguric renal failure to
non oliguric renal failure but not improves
renal complications like hyperkalemia.

55. RENAL DOSE OF DOPAMINE:
DOPAMINE is a selective renal vasodilator
acting in a dose range of 1-3 microgram
/kg/per minute.
In several studies it had been shown risk
benefit ratio of dopamine is high leading to
very rare use in ARF unless cardiovascular
compromise is evident.
Complications like BOWEL ISCHEMIA &
ARRYTHMIAS may occur.

56. C.)AVOIDANCE OF NEPHROTOXIC DRUG:
Potential nephrotoxic drugs like NSAIDS ,ACEI
CYCLOSPORINE ,TACROLIMUS CONTRAST
AGENTS AMPHOTERICIN B,AMINOGLYCOSIDE
should not be used as they can agravate ARF.
D.)ADJUSTMENT OF DRUG DOSES:
Drug doses are adjusted on CREATININE
CLEARANCE not on serum creatinine.

57. 3.) AKI DUE TO GLOMERULONEPHRITIS /VASCULITIS: May
respond to immunosuppressants or plasmapheresis.
4.)ALLERGIC INTERSTITIAL NEPHRITIS :Tapering dose of
glucocorticoids are used.
5.)AKI DUE TO SCLERODERMA: Should be treated with ACEI

58. SUPPORTIVE MANAGEMENT OF INTRINIC AKI
INTRAVASCULAR VOLUME OVERLOAD:
Restriction of salt<1g/day and water(<1Lt)
DIURETICS :Usually furosemide as bolus or
infusion .If no response opt for
ULTRAFILTRATIION.
HYPERKALEMIA :
• Restriction of dietary potassium
• Discontinue potassium sparing diuretics
• CALCIUM GLUCONATE 10ml10% over 3mins
• GLUCOSE +INSULIN
• INHALED B2 AGONIST
• K+ BINDING RESINS
• SODIUM BICARBONATE

59. METABOLIC ACIDOSIS :
• RESTRICTION OF DIETARY PROTEIN
• SODIUM BICARBONATE
• DIALYSIS
HYPERPHOSPHATEMIA:
• RESTRICTION OF DIETARY PHOSPHATE
• PHOSPHATE BINDING AGENTS (CALCIUM CARBONATE /SEVELAMER)
HYPOCALCEMIA:
• CALCIUM CARBONATE (IV)
HYPONATREMIA :
RESTRICTION OF ORAL AND IV FLUIDS
HYPERMAGNESEMIA:
• DISCONTINUE MAGNESIUM CONTAINING ANTIACIDS
NUTRITION :
• RESTRICTION OF DIETARY PROTEIN
• 0.8 G/KG/DAY UPTO 1.5 G/KG/DAY AND 25-30KCAL /DAY BY ENTERAL ROUTE

60. MANAGEMENT OF POST RENAL AKI
• The site of obstruction defines the treatment
approch .Transuretheral or suprapubic bladder
catheterization is needed for urethral
strictures bladder neck obstruction .
• Ureteric obstruction is treated by
percutaneous nephrostomy or ureteral stent .

62. MODES OF DIALYSIS
• INTERMITTENT HEMODIALYSIS:Standard
• INTERMITTENT PERITONEAL DIALYSIS: If hemodialysis
not available.
• CONTINUOUS RENAL REPLACEMENT THERAPY:
1.hemodyanamic instability 2.active bleeding

63. KEY PARAMETERS FOR MONITORING PATIENTS WITH AKI

64. CAUSES OF DIURETIC RESISTANCE IN PATIENTS OF AKI

65. REFERENCES
• HARRISONS PRINCIPLES OF INTERNAL
MEDICINE 21st EDITION
• JAYPEE MANUAL OF NEPHROLOGY 2nd
EDITION
• BRENNER &RECTORS THE KIDNEY