AKI

• Department of Transplantology, Nephrology and Internal

Diseases
 KIDNEYS

• paired organ
• retroperitoneal
• consist of cortex and medulla
• nephron is a functional part of the kidney
 NEPHRON

• glomeruli
• proximal tubule
• loop of henle
• kidney distal tubule
• kidney collecting duct
• interstitium
• renal arteries and their branches
 GLOMERULUS

• glomerular parietal cell

• podocytes
• mesangium
 KIDNEY TUBULES

• proximal tubule- readsorption

• henle loop- urine concentration
• distal tubule- H+ and K+ secretion and Na+
readsorption
 KIDNEY FUNCTION

• Waste products excretion

• Homeostasis
1. water
2. Ions
3. acid/ base

• Hormone secretion
1. erythropoetin
2. renin
3. active (post hydroxylation) Vitamin D
AZOTEMIA:
a pathologic increase in urea and other nitrogenous substances in the blood

UREMIA:
systemic manifestation of severe persistent decrease in renal function
 AKI vs ARF
The term AKI has largely replaced acute renal failure (ARF), reflecting the
recognition that smaller decrements in kidney function that do not result in
overt organ failure are of substantial clinical relevance and are associated with
increased morbidity and mortality.

AKI: acute kidney injury ARF: acute renal failure

Covers the entire spectrum
from mild to severe
decrease in function
Defined as abrupt change
in serum creatinine and/or
urine output,
classified according to
RIFLE criteria
Defined as significant decrease in
renal sufficiency to excrete
waste products, and to regulate
water and electrolytes
homeostasis
manifested by:
• nausea, vomiting
• drowsiness,
• fatigue and weakness
• itching
• metabolic acidosis, Na+↓, K+↑
 AKI
•sudden decline in GFR (hours to days)
•retention of nitrogenous wastes
•disturbances in extracellular fluid volume
•disturbance in electrolyte and acid base homeostasis
 AKI DEFINITION
• Rapid impairment in renal function resulting in raised
plasma urea/creatinine, fluid and/or acid-base
imbalance which is reversible.

• AKIN Criteria for diagnosis of AKI

1. time course – rapid (<48hours)
2. reduction in Kidney function
1. ↑serum creatinine (absolute increase of >0.3mg/dl or
percentage increase of > 50%)
2. ↓urine output (<0.5ml/kg/hr for >6hours)

• RIFLE criteria for staging of AKI:

Risk, Injury, Failure, Loss, End stage kidney disease
 Staging RIFLE Criteria
• SEVERITY (Stage 1-3)

– Risk: GFR decrease >25%, serum creatinine increased 1.5

times OR urine production of <0.5 ml/kg/hr for >6 hours

– Injury: GFR decrease >50%, doubling of creatinine OR urine

production <0.5 ml/kg/hr for 12 hours

– Failure: GFR decrease >75%, >tripling of creatinine or

creatinine >355 μmol/l (>4 mg/dl) OR urine output below 0.3
ml/kg/hr for 24 hours

• OUTCOME
– Loss: persistent AKI or complete loss of kidney function for
more than 4 weeks

– End-stage renal disease: need for renal replacement

therapy (RRT) for more than 3 months
 Serum creatinine concentration vs GFR

Age 70
Age 25

Cr serum concentration: 0.8 mg/dL 0.8 mg/dL

eGFR (MDRD): 75 mL/min/1.73 m2 125 mL/min/1.73 m2

SERUM CREATININE DOES NOT ACCURATELY REFLECT THE GFR

 RIFLE Criteria: URINE OUTPUT

ANURIA: <100 mL/24 h

OLIGURIA: 100-400 mL/24h
NONOLIGURIA: : > 400 mL/24h

50-60% of AKI cases are nonoliguric

 ARF/AKI
PRERENAL AKI
• MOST COMMON (55%)
• Pre-Renal • A PHYSIOLOGIC RESPONSE TO MILD-MODERATE
RENAL HYPOPERFUSION
• IS RAPIDLY REVERSIBLE UPON RESTORATION OF
– hypoperfusion RENAL BLOOD FLOW AND GLOMEURLAR
FILTRATION PRESSURE

• hypovolaemia
– dehydration, burns, trauma, post-surgery, sepsis, hemorrhage, GI-fluid loss (diarrhea, vomiting)

• drugs side effects

– ACEIs and ARBS (reduce efferent vasoconstriction), NSAIDS (reduce afferent vasodilation),
diuretics, beta blockers

– low cardiac output

– thromboembolism
– renal artery stenosis
– cardiogenic shock
– hepatorenal syndrome
 ARF/AKI
RENAL AKI ACCOUNTS FOR NEARLY 40% OF ALL AKI

• Renal

– ischemic (part of the spectrum of renal hypoperfusion effects,

evolves in case of more severe hypoperfusion)
– nephrotoxic tubular necrosis
• drugs (NSAIDS, ACE-I, aminoglycosides)
• Organic solvents (e.g. ethylene glycol)
– toxins
• exogenous:Radio contrast, cyclosporine, antibiotics, chemotherapy (e.g.
cisplatin)
• endogenous: myoglobin, uric acid, oxalate,
– glomerulonephritis
– paraproteinemia: myeloma
– vasculitis
– renal artery and vein obstruction
 ARF/AKI
RENAL AKI ACCOUNTS FOR UP TO 5% OF ALL AKI

• Post Renal
– prostatic hypertrophy,
– urethra: stricture, congenital valve
– stones
– tumour (pelvic, bladder, prostate incl. BPH)
– obstructed catheter
– neurogenic bladder
– external compression (retroperitoneal fibrosis, malignancy)
 ARF/AKI
• taking history is essential……
– exposure to nephrotoxins and drugs
– limbs ischemia or trauma may indicate rhabdomyolysis
– diarrhea, bleeding may speak for volume depletion
– recent surgical or radiologic procedures
– a history of prostatic disease, nephrolithiasis

• physical examination
– prerenal AKI: is suggested by clinical signs of intravascular volume depletion
(e.g. orthostatic hypotension , rapid pulse and poor skin turgor)

– acute allergic interstitial nephritis: is suggested by signs of allergy (e.g. periorbital

edema, esosinophilia, maculopapular rash , and wheezing )

– lower urinary tract obstruction: is suggested by suprapubic or flank mass or

symptoms of bladder dysfunction (e.g. urgency, hesitancy)
 ARF/AKI

•Urinalysis:
– RBCs may suggest calculi, trauma, infection or tumor
– RBCs and RBC casts in glomerular diseases
– crystals, RBCs and WBCs in post-renal ARF
– pigmented casts without erythrocytes in the sediment from urine but with positive
dipstick for occult blood indicates hemoglobinuria or myoglobinuria
– brownish pigmented cellular casts and many renal epithelia cells are seen in
patients with acute tubular necrosis (ATN )
– dipstick test: trace or no proteinuria with pre- renal and post-renal AKI;
– moderate to severe proteinuria with glomerular diseases.
 ARF/AKI
URINE AND BLOOD CHEMISTRY
MOST OF THESE TESTS HELP TO DIFFERENTIATE PRERENAL AZOTEMIA, IN WHICH
TUBULAR REABSORPTION FUNCTION IS PRESERVED
FROM ACUTE TUBULAR NECROSIS WHERE TUBULAR REABSORPTION IS SEVERELY
DISTURBED.

– osmolality or specific gravity: decreased in ATN and post-renal AKI (urine is

diluted) , while increased in pre-renal AKI (urine is concentrated)
– BUN/plasma creatinine ratio:
normal at 10-15:1 in ATN, but greater than 20:1 in prerenal disease (due to the
increase in the passive reabsorption of urea that follows the enhanced proximal
transport of sodium and water).
A high BUN/plasma creatinine ratio ratio is highly suggestive of prerenal disease
as long as some other cause is not present.
– Renal failure index: ratio of urine Na+ to urine to plasma creatinine ratio:
UNa/Ucr/Pc <1 % indicates prerenal AKI,
UNa/Ucr/Pc >1% indicates ATN
– Fractional excretion of Na+:
ratio of urine-to-plasma Na ratio to urine-to-plasma creatinine (%)
(UNa/PNa)/(Ucr/Pcr )X 100 < 1% suggests prerenal failure
(UNa/PNa)/(Ucr/Pcr )X 100 < 1% suggests ATN
 ARF/AKI
BLOOD CHEMISTRY

– RBC, WBC, platelets, CK,

– myeloma screen (proteinogram, free light chains concentration
and ratio),
– ANA, ANCA, anti-GBM, C3, C4
 ARF/AKI
RADIOGRAPHY/ULTRASONOGRAPHY

• confirms the presence of two kidneys (or reveals the presence of

one kidney)
• allows for evaluating kidneys size and shape,
• allows for detection of hydronephrosis or hydroureter.
• helpful in detection of renal calculi, and renal vein thrombosis.
 ARF/AKI

RENAL BIOPSY
• allows for the differentiation between glomerular, vascular and
interstitial disorders,
• allows for the differentiation between inflammatory and non-
inflammatory ones
• allows for defining of the extent/intensity/ advancement of acute and
chronic lesions
• hepls to establish prognosis and treatment
 ARF/AKI
COMPLICATIONS
• Intravascular overload
– weight gain , hypertension ,elevated central venous pressure pulmonary edema
• electrolyte disturbance
– hyperkalemia: serum K+ >5.5 mEq/L:
• decreased renal excretion combined with tissue necrosis or hemolysis.
– hyponatremia : serum Na+ concentration < 135 mEq/L
• excessive water intake in the face of excretory failure
– hyperphosphatemia : serum Phosphate concentration of > 5.5 mg /dl
• failure of excretion or tissue necrosis
– hypocalcemia: serum Ca++< 8.5 mg/dl
• results from decreased Active Vit-D, hyperposhphatemia, or hypoalbuminemia
– hypercalcemia: serum Ca++ > 10.5 mg /dl
• may occur during the recovery phase following rhabdomyolysis induced acute renal failure

• metabolic acidosis: arterial blood PH < 7.35

– associated with sepsis or severe heart failure
• hyperuricemia: due to decreased uric acid excretion
 ARF/AKI
MANAGEMENT
Prevention:
•many cases of ischemic AKI can be avoided by close attention to
cardiovascular function and intravascular volume in high-risk patients, such as
the elderly and those with preexisting renal insufficiency.
•in patients with preexisting renal impairment the incidence of nephrotoxic ARF
can be limited by the reduction of the drugs dosages or frequency of
administration.
 ARF/AKI
MANAGEMENT

Treatment:
• exclusion of reversible causes: obstruction, infection
• correction of prerenal factors: intravascular volume and cardiac
performance should be optimized
hypervolemia:
• restriction of salt and water intake and diuretics.
metabolic acidosis:
• is not treated unless serum bicarbonate concentration falls below 15 mmol/L
or arterial pH falls below 7.2. More severe acidosis is corrected by oral or
intravenous sodium bicarbonate.
hyperkalemia:
• in all patients with AKI, K+ in infusions and medications should be avoided
as much as possible
• dietary potassium intake should be restricted to approximately 2 grams daily
 HYPERKALEMIA
• Potassium range is 3.5 – 5mmol/L
• Rise in serum K+ >5mmol/l
• Signs/symptoms: muscle weakness

• ECG changes:
– Flattened P waves
– Broad QRS complex
– Slurring of ST segment
– Tall tented T waves

http://www.aafp.org/afp/2006/0115/p283.html
 HYPERKALEMIA

• Potassium >6.0 mmol/L

– calcium resonium 15g QDS PO
– If septic or rising quickly treat as though K+ 6.5

• Potassium >6.5 mmol/L

– dextrose-insulin (50ml 50% Dextrose with 10units
Actrapid insulin, IV over 5mins) Monitor BM
– calcium resonium 15g QDS PO
 HYPERKALEMIA
• Potassium >7 mmol/L
– Calcium gluconate (10ml of 10% solution into central
vein or diluted into 40ml 0.9% saline into peripheral
vein over 10mins, with cardiac monitor)
– Dextrose insulin
– Nebulised salbutamol 5mg
– IV sodium bicarbonate (50ml 8.4% over 5mins
centrally or 500mls 1.26% over 30mins peripherally
– Calcium resonium
 TREATMENT APPROACH
TO HYPERKALEMIC EMERGENCIES
 DIALYSIS

• Dialysis replaces renal function until regeneration and

repair restore renal function.
• Hemodialysis and peritoneal dialysis appear equally
effective for management of ARF.
 DIALYSIS INDICATIONS

• hyperkalaemia
(persistent >7mmol/L)
• metabolic Acidosis (if
pH<7.2, bicarbonate <12)
• pulmonary oedema
(refractory)
• pericarditis
• symptomatic ureamia -
encephalopathy

http://homeopathyexpert.blogspot.co.uk/2011/05/chronic-renal-failure.html