Acute Renal Failure (ARF)Acute Kidney Injury (AKI)

Mitra BasiratniaPed Nephrologist

SUMS

AKI• Formerly referred to as acute renal failure• Abrupt reduction in kidney function

measured by decline in GFR• Results in disturbances

– Impaired nitrogenous waste excretion– Loss of H2O & electrolyte regulation– Loss of acid-base regulation

• Contributing factor in morbidity & mortality of critically ill

The pRifle Criteria

End-stage kidney disease

Persistant AKI = complete loss of renal function > 4 weeks

Increased creatinine × 3 or GFR decrease >75% or creatinine > 4 mg/dL

(acute rise >0.5 mg/dL)

UO < 0.3 ml/kg/hr × 24 hours or anuria × 12 hours

Increased creatinine × 2or GFR decrease > 50%

UO <0.5 ml/kg/hr × 16 hours

Increased creatinine × 1.5or GFR decrease > 25%

UO<0.5 ml/kg/hr × 8 hours

Bellomo et al. Crit Care 2004;8:R204-R212.

Oliguri

a

Speci

fici

ty

Sensi

tivit

y

Risk

Injury

Failur

e

Loss End-stage

Azotemia is a consistent feature of acute renal failure (ARF), oliguria is not.

anuria ::: urine output < 0.5 ml/kg/h

Oliguria ::: urine output< 1 ml/kg/h

acute renal failure: common clinical features

• azotemia

• hypervolemia

• electrolytes abnormalities:

K+ phosphate

Na+ calcium

• metabolic acidosis

• hypertension

• oliguria - anuria

acute renal failure: classification

• Prerenal (hypoperfusion)

• Renal (intrinsic)

• Postrenal (obstructive)

prerenal

• decreased perfusion without cellular injury• renal tubular and glomerular functions are

intact• reversible if underlying cause is corrected

prerenal

• common etiologies: – dehydration– hypovolemia– hemodynamic factors that can compromise

renal perfusion (CHF, shock)

Sustained prerenal azotemia is the main factor

that predisposes patients to ischemia- induced acute tubular necrosis (ATN)

postrenal

• obstruction of urinary tract• important to rule out quickly:

– potential for recovery of renal function is often inversely related to the duration of the obstruction

renal

• classified according primary site of injury:– tubular– interstitium– vessels– glomerulus

Clinical Approach to AKI: Pre-, Intra-, and Post-Renal

HistoryVolume status

UltrasoundUrinalysis US shows

Hydronephrosis

Post-Renal

Urinalysis Normal

UrinalysisAbnormal

Tubulointerstial Disorders

Glomerular and Vascular Disorders

Pre-renal

Nephrologists Clinical Approach to AKIHistory

Volume StatusUltrasoundUrinalysis

Hydronephrosis

Post-Renal

Prostate disease BPH

CancerPelvic malignancy

StonesStricture

Retroperitoneal fibrosis

Normal Urinalysis

Pre-Renal

Low ECF Volume GI losses

Hemorrhage Diuretics

Osmotic diuresis

Altered renal blood flowor hemodynamics

Sepsis Heart failure

Cirrhosis/Hepatorenal syndrome Hypercalcemia

Medications NSAIDs/Cox-2 inhibitors

ACE inhibitors Angiotensin II receptor blockers

Vascular disease

Vascular Disorders

TubulointerstitialDisorders

Glomerular Disorders

Tubular obstruction Crystals

Calcium oxalate (Ethylene glycol,

orlistat) Indinivir Acyclovir

Methotrexate Tumor lysis syndrome

Myeloma cast nephropathy

Acute tubular necrosis Ischemic

Nephrotoxic Contrast-induced Rhabdomyolysis

Acute interstitial nephritis Medication-induced

Autoimmune Sjogren syndrome

Sarcoidosis Infection-related

Arterial Renal artery stenosis

Renal artery thromboembolism Fibromuscular dysplasia

Takayasu arteritisMedium vessel

Polyarteritis nodosa Kawasaki disease

Small vessel Glomerulonephritis

Thrombotic microangiopathies Cholesterol emboli

Renal vein Renal vein thrombosis

Abdominal compartment syndrome

Renal parenchymal disorders

Abnormal urinalysis

acute renal failure: diagnosis

• History and Physical examination

• Blood tests : CBC, BUN/creatinine, electrolytes, uric acid, CK

• Urine analysis

• Renal Indices

• Renal ultrasound (useful for obstructive forms)

• Doppler (to assess renal blood flow)

• Nuclear Medicine Scans DMSA: anatomy DTPA and MAG3: renal function, urinary excretion and upper tract outflow

Presentation: Children• History:

– AGE, hemorrhage, sepsis, decreased oral intake– Bloody diarrhea w/ oliguria (<500ml/1.73m2/day) or

anuria – HUS– Pharyngitis or impetigo – PIGN– Hemoptysis and renal impairment – Pulm-Renal Syndrome

(Wegner’s, Goodpasture’s)– Trauma/crush injury – rhabdomyolysis– Exposure to nephrotoxins – aminoglycosides,

amphotericin-B, chemotherapy Rx• PxEx:

– Tachycardia, dry MM, sunken eyes/fontanel, orthostatic BP, decreased skin turgor

– Edema – nephrotic syndrome, heart failure, liver failure– Skin findings – purpura, petechiae, malar rash,

maculopapular – HSP/SLE, AIN

Reabsorption of water and sodium:

- intact in pre-renal failure

- impaired in tubulo-interstitial disease and ATN

Since urinary indices depend on urine sodium concentration, they should be interpreted

cautiously if the patient has received diuretic therapy

renal indices

Fractional Excretion of Na (FENa)

FENa: [ urine Na/serum Na] x 100 %

[urine creatinine/serum creatinine]

renal indices

prerenal azotemia:

– Urine sediment: hyaline and fine granular casts

– Urinary to plasma creatinine ratio: high

– Urinary Na: low

– FENa: low

Increased urine output in response to hydration

• renal azotemia:

– Urine sediment: brown granular casts and tubular epithelial cells

– Urinary to plasma creatinine ratio: low

– Urinary Na: high

– FENa: high

Urine Sediment

Monomorphic RBCs Dysmorphic RBCs

Hyaline castRBC cast

Urine Sediment

RTE cast

Fatty cast ATN

WBC cast

urine and serum laboratory values

Prenal Renal

BUN/ Cr >20 <20

FeNa <1% >1%

RFI <1% >1%

UNa (mEq/ L) <20 > 40

Specific gravity high low

hemoglobinuria + myoglobinuria

hemoglobinuria:transfusion reactions, HUS

myoglobinuria:crush injuries, rhabdomyolisisurine (+) blood but (-) red blood cells CPK K+

treatment aggressive hydration + urine alkalinizationmannitol / furosemide

acute renal failure: management

• treat the underlying disease• strictly monitor intake and output (weight, urine

output, insensible losses, IVF)• monitor serum electrolytes• adjust medication dosages according to GFR• avoid highly nephrotoxic drugs• attempt to convert oliguric to non-oliguric renal

failure (furosemide )

acute renal failure: fluid therapy

If patient is fluid overloaded• fluid restriction (insensible losses)• attempt furosemide 1-2 mg/kg• Renal replacement therapy

If patient is dehydrated: • restore intravascular volume first• then treat as euvolemic (below)

If patient is euvolemic:• restrict to insensible losses (30-35

ml/100kcal/24 hours) + other losses (urine, chest tubes, etc)

sodium

• most patients have dilutional hyponatremia which should be treated with fluid restriction

• Na< 120mEq/L or symptomatic: hypertonic saline

potassiumOliguric renal failure is often complicated by hyperkalemia, increasing the risk in cardiac arrhythmiasK>6 resinK>7 emergency treatmentTreatment of hyperkalemia:

.calcium gluconate ( 1cc/kg IV ) over 3-5 min •sodium bicarbonate (1-2 mEq/kg) over 5-10 min

• insulin + hypertonic dextrose: 0.1 U/kg with 1 cc/kg 50% glucose over 1 hour

• sodium polystyrene (Kayexalate): 1 gm/kg . Can be repeated qh. (Hypernatremia and hypertension are potential complications)

• dialysis

nutrition

• provide adequate caloric intake• limit protein intake to control increases in BUN• minimize potassium and phosphorus intake• limit fluid intake

If adequate caloric intake can not be achieved due to fluid limitations, some form of dialysis should be considered

Management

• Anemia Hb<7

• Acidosis PH<7.15 HCO3<8

• Neurologic

• Hypertension

Indication for dialysis

• Volume overload

• Refractory electrolyte imbalance & acidosis

• BUN> 100-150 or lower if rapidly rising

• Pericarditis

• Uremic encephalopathy