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Acute kidney injury
1. Acute Kidney
Injury
Dr. P. M. Jha
Senior Resident
Nephrology Department
PGIMER & Dr. RML Hospital,
New Delhi-110001.
2. Acute kidney injury (AKI) is rapid and usually reversible
decline in renal function as evident by rapid decline in
GFR over a period of hours to days .
It may occur in patient with previously normal renal
function or patient with chronic kidney disease.
In 2002 Acute Dialysis Quality Initiative(ADQI) developed
new definition/classification i.e. RIFLE -Risk, Injury,
Failure, Loss & ESKD.
In 2007 Acute Kidney Injury Network (AKIN) had given
new criteria :
3. RIFLE criteria
For RIFLE increase in Serum creatinine should be both
abrupt (with in 1-7 days) and sustained (>24 hours)
Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P. Crit Care. 2004;8(4):R204-R212.
4. AKIN criteria
• the increase in serum creatinine must occur in less than 48 hours
Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network (AKIN): report of an
initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31.
5. The term acute kidney injury(AKI) now replaces the
term ARF ; the term ARF should now be restricted
to the patient who have AKI and needs renal
replacement therapy .
Advantage of RIFLE/AKIN criteria
High sensitivity for early diagnosis of AKI
Allow detection of patient at risk to develop AKI
Allow detection of patient with established AKI
Manual of Nephrology: Diagnosis and Therapy 7th edition: By Robert W Schrier
MD By Lippincott Williams & Wilkins Publishers
6. Calculation of GFR
1) Cockcroft – Gault Formula
[ (140-Age) x Lean body wt. (kg)]
72 x S. creatinine
2) MDRD Equation (modification of diet for renal disease)-
More accurate, but cumbersome
GFR (ml/min/1.73m2)= 1.86 × (PCr)-1.154×(age)-0.203
Multiplied by 0.742 for women
Multiplied by 1.21 for African Americans
X (0.85 If female)GFR =
(ml/min)
Harrison's Principles of Internal Medicine 18th ed.
7. 1. Prerenal AKI (55%)
2 . Intrinsic AKI (40%)
3.Postrenal AKI (5%)
Classification acute Kidney Injury
Brenner: Brenner & Rector's The Kidney, 7th ed.
8. Causes of Prerenal AKI
1:-Intravascular
volume depletion,
2:-Effective volume depletion
from arterial underfilling
a. Hemorrhage
b. Renal fluid losses.
c. Gastrointestinal fluid loss
d. Skin loss of sweat
e. Third-space losses
• Burns
• Traumatized tissue
• Peritonitis
• Pancreatitis
1 )Reduced cardiac output,
a. Congestive heart failure
b. Cardiogenic shock (e.g., acute MI)
c. Pericardial effusion with tapenade
d. Massive pulmonary embolism
2) Peripheral vasodilation,
a. Gram-negative sepsis
b. Antihypertensive medications
c. Anaphylaxis
D .Anesthesia
e Cirrhosis & other liver diseases
10. Causes of intrinsic AKI
2 Vascular—large vessels
Vascular—small vessels
3. Glomerular
1. Tubular
4. Interstitial.
Manual of Nephrology: Diagnosis and Therapy 7th edition :
By Robert W Schrier MD By Lippincott Williams & Wilkins Publishers
12. Vascular—large vessels: Renal artery stenosis, thrombosis,
or embolism
a. Operative arterial cross-clamping
b. Bilateral renal vein thrombosis
Diseases of glomeruli and renal microvasculature
Glomerulonephritis and vasculitis
Hemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
DIC
Toxemia of pregnancy
13. a. Antibiotics,
beta-lactam antibiotics
rifampicin, sulfonamides,
erythromycin, and
ciprofloxacin
B .Diuretics (e.g., furosemide,
thiazides, chlorthalidone)
c. NSAIDs
d. Anticonvulsant drugs (e.g.,
phenytoin, carbamazepine)
e. Allopurinol
Acute interstitial nephritis(AIN)
1-Drug hypersensitivity 2-Infection associated-AIN
a. Bacterial
(i.e. Staphylococcus &
Streptococcus)
b. Viral
(i.e. CMV &EBV)
c. Tuberculosis
d. fungal
(i.e. candidiasis)
14. Causes Of Postrenal AKI
B/L Ureteral obstruction- Intraureteral
Extraureteral
Bladder neck obstruction – BPH
prostatic cancer
Urethral obstruction
15. Decrease in Effective circulatory volume
Activation of central baroreceptor
Angiotensin-II Norepinephrine AVP/ADH
Vasoconstriction of non
essential vascular beds1. Preferential
constriction of
efferent arterioles
2. Prostaglandin
synthesis
3. Auto regulation
If hypotension sufficient to overwhelm
renal autoregulatory defense
Ischemic injury to renal parenchyma
Maintain renal blood flow & GFR
PATHOPHYSIOLOGY OF PRE RENAL AKI & ISCHEMIC INTRINSIC AKI
17. Clinical features
Prerenal AKI-
H/O
1) Excessive Fluid Losses from vomiting or diarrhea; third-
space losses in burn and pancreatitis.
2) Compromised cardiac function in patients with congestive
heart failure; recent myocardial infarction.
3) Liver cirrhosis and failure (hepatorenal syndrome);
4) Drugs- cyclosporine, NSAID, or ACE inhibitor use.
Symptoms related to hypovolemia- increased thirst ,
decrease urine output, postural hypotension, dizziness,
fatigue, Muscle cramp.
Manual of Nephrology: Diagnosis and Therapy 7th edition
18. 1) Reduction in ECF volume
a. Tachycardia
b. Orthostatic hypotension
c. Dry mucus membrane
d. Absence of axillary sweat
e. A recent reduction in body weight
f. “Tenting” of upper thorax skin when pinched between the fingers
g. Jugular venous pulse not visible
2)Arterial underfilling with expanded ECF
a. Elevated jugular venous pressure,
b. Ascites,
c. Peripheral edema
d. CHF may be identified by Pulmonary crackles & S3 gallop
e .Liver failure may be identified by Jaundice, palmer erythema, spider
angiomas, decrease liver size.
Manual of Nephrology: Diagnosis and Therapy 7th edition
Physical findings
19. Intrinsic/Intrarenal AKI:
H/O -
1) Use of Nephrotoxic agents, Current medications ,
Contrast agent.
2) Glomerular disease- Nephrotic / Nephritic syndrome with
hematuria, edema and hypertension .
3) Tubular disease: ATN should be suspected in any patient
presenting after a period of hypotension secondary to cardiac
arrest, hemorrhage or sepsis.
Physical finding:
• Peripheral edema
• Raised JVP
• Pulmonary rales
• Signs of uremia- Asterixis, myoclonus, pericardial rub.
20. POST RENAL FAILURE
Usually occur in elderly male with prostatic obstruction.
H/O – Urinary Frequency, urgency & Hesitancy
PHYSICAL FINDINGS –
a. Costovertebral Angle Tenderness
b. Pelvic & Rectal Masses
c. Prostatic Hypertrophy
d. Distended Bladder
Manual of Nephrology: Diagnosis and Therapy 7th edition
21. DIAGNOSTIC INDEX
PRERENAL
AKI
ATN
UNa+/PNa+
Ucr / PCr
<1 >1
Urinary Na+ concentration(mEq/L) <10 >20
Urinary creatinine/plasma
creatinine ratio
>40 <20
Urinary urea nitrogen/blood urea
nitrogen ratio
>8 <3
Urine specific gravity >1.018 <1.012
Urine osmolality (mOsm/kg H2O) >500 <250
B. Urea nitrogen/Creatinine ratio >20 <10–15
Renal failure index (UNa+/Ucr/Pcr) <1 >1
Urine sediment Hyaline casts
Muddy brown
granular casts
Brenner: Brenner & Rector's The Kidney, 7th ed.
×100FENa (%) =
23. Urine Sediment in the Differential Diagnosis of AKI
Normal or Few Red Blood Cells or White Blood Cells
Prerenal AKI
Arterial thrombosis or embolism
Preglomerular vasculitis
HUS or TTP
Scleroderma crisis
Postrenal AKI
Granular Casts
Acute tubule necrosis (muddy brown)
Glomerulonephritis or vasculitis
Interstitial nephritis
Red Blood Cell Casts
Glomerulonephritis or vasculitis
Malignant hypertension
Rarely interstitial nephritis
25. Indications of renal biopsy
1. ARF of unknown etiology.
2. Suspicion of glomerulonephritis, systemic disease (e.g.,
vasculitis), or AIN as the cause of ARF.
A renal biopsy in such circumstances may provide the
basis and justification for aggressive and lifesaving therapy (e.g.,
high-dose steroids, cytotoxic agents, plasmapheresis).
3. ATN not recovering after 4 to 6 weeks of dialysis with no
more recurrent insults.
A renal biopsy may determine that a less favorable condition, such
as diffuse cortical necrosis, has developed and that chronic
hemodialysis may need to be instituted.
Manual of Nephrology: Diagnosis and Therapy 7th edition
26. Management of ARF
A)MEDICAL MANAGEMENT
B)DIALYSIS
C) Tt. OF COMPLICATIONS
1:Conservative medical management of ARF requires
a. Complete fluid intake &output record
b. Daily wt record
c. Intravascular volume should be assessed clinically daily
d. Frequent(3 times / week) measurement of serum Na/K,
Bld. Urea ,s. creatinine ,calcium &phosphate.
Put CVP line to measure CVP (10 - 12)cm of water.
Washington Manual Of Medical Therapeutics 32 Ed.
27. A. Pre-renal AKI
1. Correction of underlying disorder
(a) Pure volume depletion
When pre-renal AKI is due to deficits in ECF volume, therapy is
directed to restoring fluids that are similar to those lost.
In severe acute hemorrhage, packed RBC is indicated.
In less severe acute blood loss or plasma loss i.e. burn and
pancreatitis isotonic normal saline indicated.
Gastrointestinal fluid losses vary widely in electrolyte content and
tonicity, and laboratory analysis for sodium, potassium, and
chloride concentrations is the most precise way to determine the
type of replacement fluid.
28. Crystalloid solution are less expensive and equally effective as
colloid.
In severe hypovolemia 0.9% saline should be used.
In less severe hypovolemia 0.45% saline should be used.
FLUID CHALLENGE-
In young stable patient 500 ml – 1000 ml bolus should be given in
1 hr.
In elderly patient in whom cardiac status is unknown, bolus of
250 ml over 1 hr. should be given.
After that patient should be monitored for hypo or hypervolemia.
Once euvolemia is achieved S. electrolytes should be monitored
and replaced.
Total Fluid requirement = total output of kidney &GI tract in
previous 24 hr. with additional 500 ml -1000 ml for inaccessible
loss.
29. (b) Ineffective arterial blood volume with edema:
Prerenal AKI occurring in this setting usually represents
a secondary problem overshadowed by a primary cardiac &
hepatic disease.
1. In case of cardiac failure-
Diuretic agents in combination with digitalis therapy may
increase the cardiac output and improve renal perfusion,
thus lessen the azotemia. Cardiac unloading agents such as
ACE inhibitors, nitrates, and hydralazine may also improve
Cardiac function.
Manual of Nephrology: Diagnosis and Therapy 7th edition
30. 2 .Cirrhosis and Hepatorenal Syndrome
Fluid management in individuals with cirrhosis, ascites, and AKI
is challenging because of the frequent difficulty in ascertaining
intravascular volume status.
Administration of intravenous fluids as a volume challenge may
be required diagnostically as well as therapeutically. Excessive
volume administration may result in worsening of ascites and
pulmonary compromise .
Manual of Nephrology: Diagnosis and Therapy 7th edition
31. Albumin may prevent AKI in those treated with
antibiotics for spontaneous bacterial peritonitis.
The definitive treatment of the hepatorenal syndrome is
liver transplantation.
Bridge therapies that have shown promise include
terlipressin (a vasopressin analog), combination therapy
with octreotide (a somatostatin analog) and midodrine
(an α-adrenergic agonist), and norepinephrine, all in
combination with intravenous albumin (1 gm/kg body wt,
maximum 100 g/d)
Manual of Nephrology: Diagnosis and Therapy 7th edition
Harrison's Principles of Internal Medicine 18th ed.
32. MONITORING OF THERAPY
Patient's response to replacement therapy is frequently
monitored by jugular venous pulsation, orthostatic changes in
blood pressure and pulse.
In a normovolemic patient, jugular venous pulsations are
visible when the patient is supine but disappear when the patient
assumes the sitting position. Jugular venous pulsations are not
visible in the volume-depleted patient.
Thus, their reappearance following fluid administration suggests
that the central venous pressure (CVP) has returned to normal.
The presence of basilar crackles or a third heart sound implies
too-vigorous fluid replacement, with resultant pulmonary
congestion.
Manual of Nephrology: Diagnosis and Therapy 7th edition
33. The patients in whom vigorous resuscitation efforts are required,
and cardiovascular tolerance to sudden fluid challenges is in
doubt, monitoring should be done by Central venous catheter .
Central venous catheter Central venous catheter is a satisfactory
guide to the speed of fluid administration. The CVP normally ranges
between 8 and 12 cm of water.
In volume-depleted states, CVP may be zero or below . Before
vigorous volume repletion is begun, a fluid challenge of 200 to
300 mL of normal saline should be attempted over a 10- to 20-
minute period.
In uncomplicated volume-depleted patient, this amount of saline
has little effect on the CVP reading.
A CVP rise of more than 5 cm of water suggests cardiac failure,
and the infusion should be immediately discontinued.
Manual of Nephrology: Diagnosis and Therapy 7th edition
34. MANAGEMENT OF INTRARENAL OR INTRINSIC AKI
1)ACUTE TUBULAR NECROSIS
There is no specific treatment for ATN.
First of all, volume status of pt. should be assessed.
Pt. may be in state of hypovolemia , euvolemia or
hypervolemia .
If volume deficit -it should be corrected with adequate fluid
therapy.
In euvolemic Pt. fluid challenge & diuretic challenge may
be tried.
In case of volume overload diuretic challenge is given which
may convert oliguric AKI to nonoliguric AKI.
35. A.Diuretics challenge –may be given in oliguric pt with volume
overload .
Initially I.V. Furosemide (40-120 mg) given as a bolus , if urine out
put improves then continuous infusion of 10 to 20 mg/hour
should be given.
Diuretic therapy only converts oliguric AKI to non oliguric AKI,
may simplify fluid management but does not improves renal
outcome & complication like hyperkalemia.
So, routine use of diuretics is not recommended in established
AKI.
Washington Manual Of Medical Therapeutics 32 Ed
36. B. Renal-dose dopamine.
Dopamine is a selective renal vasodilator. It elicits
profound natriuresis and increases urine output. The
renal selective dose is 1 to 3μg per kg per minute.
No evidence suggests that renal-dose dopamine is
beneficial in ARF.
In fact, several studies have identified a deleterious
effect such as bowel ischemia and arrhythmias.
Unless dopamine is required for circulatory support, it
should not be used for acute renal failure.
Manual of Nephrology: Diagnosis and Therapy 7th edition
37. C. Avoidance of nephrotoxic drugs. Potentially
nephrotoxic drugs and agents should be completely
avoided in ARF—they perpetuate the renal injury.
These include NSAIDs, ACE inhibitors, cyclosporine,
tacrolimus, aminoglycosides, radiocontrast agents,
amphotericin B, and chemotherapeutic agents.
D. Adjustment of drug dosages. Drug dosages should
be based on the creatinine clearance, not merely on
the serum creatinine.
Manual of Nephrology: Diagnosis and Therapy 7th edition
38. MANAGEMENT OF INTRARENAL OR INTRINSIC AKI……
2)AKI due to acute glomerulonephritis or vasculitis
may respond to immunosuppressive agents and/or
plasmapheresis .
3)Allergic interstitial nephritis due to medications
requires discontinuation of the offending agent.
Glucocorticoids (High dose short term prednisone-60
mg/day for 3-4 weeks) may be used in cases where AKI
persists or worsens despite discontinuation of the
suspected medication.
4)AKI due to scleroderma (scleroderma renal crisis)
should be treated with ACE inhibitors.
Manual of Nephrology: Diagnosis and Therapy 7th edition
39. POSTRENAL AKI
The site of obstruction defines the treatment approach.
Transurethral or suprapubic bladder catheterization is
needed initially for urethral strictures, bladder neck
obstruction or functional bladder impairment.
Ureteric obstruction may be treated by percutaneous
nephrostomy tube placement or ureteral stent placement.
Relief of obstruction is usually followed by an appropriate
diuresis for several days.
In rare cases, severe polyuria persists due to tubular
dysfunction and may require continued administration of
intravenous fluids and electrolytes for a period of time.
40. Supportive Management of Intrinsic AKI
1)Intravascular volume overload
• Restriction of salt (<1–1.5 g/day) and water (<1 L/day)
• Diuretics - furosemide may be given as a bolus (200 mg)
followed by an intravenous drip (10–40 mg/hour), with or
without a thiazide diuretic.
• Diuretic therapy should be stopped if there is no response &
Ultrafiltration should be considered.
Brenner & Rector's The Kidney, 7th ed.
41. 2)HYPERKALEMIA
1. Restriction of dietary potassium.
2. Discontinue K+ supplements or K+-sparing diuretics.
3. Calcium gluconate (10 mL of 10% solution over 3 min).
4. Glucose (50 mL of 50% dextrose) + insulin (10 U regular
insulin) IV.
5. Inhaled beta-2 agonist therapy (10-20 mg of nebulized
albuterol in 4 ml of normal saline over 10 min )
6. K+-binding resin (SPS 15-30gm with 33% sorbitol)
7. Loop diuretics
8. Sodium bicarbonate (150 mEq in 1L of D5W) IV infusion,
if concmitant metabolic acidosis is present.
9. Dialysis/hemofiltration
Harrison's Principles of Internal Medicine, 18th ed.
42. 3)Metabolic acidosis
Restriction of dietary protein
Sodium bicarbonate (if HCO3
-
<15 mEq/L)
Dialysis/hemofiltration
4)Hyperphosphatemia
Restriction of dietary phosphate intake
Phosphate-binding agents (calcium carbonate,
calcium acetate, sevelamer)
Brenner & Rector's The Kidney, 7th ed.
43. 5) Hypocalcemia
Calcium carbonate (if symptomatic or sodium
bicarbonate is to be administered).
6) Hypermagnesemia
Discontinue magnesium-containing antacids.
7) Hyponatremia
Restriction of oral and intravenous free water.
Brenner & Rector's The Kidney, 7th ed.
44. 8)Nutrition
Restriction of dietary protein (<0.8 g/kg/day up to 1.5
g/kg/day on continuous venovenous hemodialysis)
25–30 kcal/day. Enteral route of nutrition preferred.
Brenner & Rector's The Kidney, 7th ed.
45. Dialysis therapy
The indications to start dialysis
CLINICAL
• Anuria (< 50 mL/day)
more than 3 days
• Uremic encephalopathy,
• Uremic pericarditis
• Uremic bleeding
• Volume overload
• Pulmonary edema
BIOCHEMICAL
• S.Cr more than 6.7/dl
• BUN more than 100
mg/dl
• Metabolic Acidosis
• Hyperkalemia
Brenner & Rector's The Kidney, 7th ed.
46. MODES OF DIALYSIS:
1) Intermittent hemodialysis – Standard
2) Intermittent peritoneal dialysis - If hemodialysis is
not available
3) Continuous renal replacement therapy -
- Hemodynamic instability
- Active bleeding
47. ACUTE KIDNEY
INJURY
PRE RENAL RENAL POST
RENAL
SURGICAL
TREATMENT
INTRINSIC ATN
(glomerulonephritis,
AIN or vascular)
