Acute Kidney Injury (ARF) By: Dr. Hatim Ahmed Hassan Senior Registrar PICU.

Acute Kidney Injury (ARF)

By: Dr. Hatim Ahmed HassanSenior Registrar PICU

Objective

Introduction and background Definition Epidemiology Physiology Etiology Clinical presentation Diagnosis management

INTRODUCTION

• AKI is defined as the abrupt loss of kidney function that results in a decline in GFR, retention of urea and other nitrogenous waste products, and dysregulation of extracellular volume and electrolytes.

• The term AKI has largely replaced (ARF), as it more clearly defines renal dysfunction as a continuum rather than a discrete finding of failed kidney function.

• Pediatric AKI presents with a wide range of clinical manifestations from a minimal elevation in serum creatinine to anuric renal failure, arises from multiple causes, and occurs in a variety of clinical settings .

Background• Acute kidney injury (previously known as acute renal

failure) covers a wide spectrum of injury to the kidneys, not just kidney failure

• Up to 18% of all hospital admissions have AKI

• Inpatient AKI-related mortality is between 25 and 30%

• Between 20 and 30% of cases of AKI are preventable. Prevention could save up to 12,000 lives each year

• NHS costs related to AKI are between £434 and £620 million per year

Definition

AKI is defined as a decrease in glomerular filtration rate (GFR), which traditionally is manifested by an elevated or a rise in serum creatinine.

However, serum creatinine is often a delayed and imprecise test as it reflects GFR in individuals at steady state with stable kidney function, and does not accurately estimate the GFR in a patient whose renal function is changing. For example, a child in the early stages of severe AKI with a markedly reduced GFR may have a relatively normal or slightly elevated creatinine, as there has not been sufficient time for creatinine

accumulation..

Definition

In addition, creatinine is removed by dialysis, and it is not possible to assess renal function using serum creatinine once dialysis is initiated.

Despite these limitations, elevated or a rise in serum creatinine continues to be the most widely used laboratory finding to make the diagnosis of AKI in children

Definition

Definition

EPIDEMIOLOGY

• The precise incidence and prevalence of pediatric acute kidney injury (AKI) are not known, largely due to the lack of a consensus definition in published studies. The incidence varies based on the definition used and potentially geographic location

Epidemiology of AKI

• Community acquired AKI seen in 1% of all hospitalized patients on admission.50% of those patients have underlying CKD.

• Development of AKI in hospitalized patients is common and carries independent mortality risk.

• In patients with normal renal function, the incidence of AKI is about 5%.

• In patients with underlying CKD, the incidence is about 16%

Epidemiology of AKI

Hospital acquired AKI• 40% is due to ATN

• 15% related to medication associated AKI.

• 10% due to contrast induced nephropathy.

• AIDS associated AKI account for 5%.

PHYSIOLOGY

Types of AKI

• AKI

• AKI/CKD

• Anuric (<50ml of urine output/day)

• Oliguric (<400 ml/day)

• Non-oliguric (>400 ml/day)

ARF Pirouz Daeihagh, M.D.Internal medicine/Nephrology Wake Forest University School of Medicine. Downloaded 4.6.09

Etiology of AKI

• Prerenal Renal hypoperfusion, no structural damage to the kidneys, Cr

normalizes in 24-72 hours with correction of hypoperfused state.

• Post-renal Obstruction to the urine flow, either unilateral/bilateral, intra-ureteral

or extra-ureteral or bladder neck or intra-pelvis (renal pelvis).

• Intra-renal Damage or inflammation within the kidney, may be primary renal or

part of systemic disease.

Prerenal AKI

Decreased Extra cellular

Volume

Hemorrhage

Volume lossesEither renal, GI or other (skin)Hyperthermia etc.,

Third spacingPeritonitis, pancreatitis,

SIRS, hypoalbuminemia etc.,

Prerenal AKI

Increased ECV withArterial underfilling

Reduced CardiacOutput

Cardiogenic shock, MI, PETamponade, constrictive

Pericarditis etc.,

Peripheral VasoldilatationSepsis, anaphylaxis, anaesthesia,

Cirrhosis, other liver diseases.

Intrarenal hemodynamic changes

Intrarenal AKI

• Vascular

• Glomerular

• Interstitial

• Tubular

Vascular causes of Intrarenal AKI

• Large and Medium size vesselsRenal artery thrombosis or emboli

Renal vein thrombosis

Polyarterial nodosa

• Small vessel diseaseAtheroembolic phenomenon

Microangiopathies like TTP, HUS, HELLP and malignant HTN.

Glomerular causes of Intrarenal AKI

Nephritis• Hematuria• Proteinuria (1-2gm/d)• ARF• May present as Rapidly

progressive Glomerulonephritis

• Renal Biopsy to diagnose

Nephrosis• Minimal hematuria• Massive

proteinuria(>3gm/d)• Uncommon to present as

ARF• Renal Biopsy not needed

to diagnose.

Interstitial causes of Intrarenal AKI

Focal/diffuse edema and infiltration of the renal interstitium with inflammatory cells.

AcuteInterstitial Nephritis

Drugs Antibiotics, NSAIDs,

Phenytoin, allopurinol, diuretics etc.,

Systemic Diseases

SLE etc.,

InfectionsStaph, Strepto, CMV,

EBV, TB etc.,

Tubular causes of Intrarenal AKI, Acute Tubular Necrosis

Ischemia induced• Shock• Hemorrhage• Sepsis• Trauma• Pancreatitis

Nephrotoxin induced• Drugs like IV contrast,

Aminoglycosides, Ampho B, pentamidine, Acyclovir, Ehtylene Glycol etc.,

• Endogenous Toxins in the case of Rhabdomyolysis, Hemolysis, uric acid nephropathy

Postrenal AKI

• Intra Ureteral Stones, Clots, Pyogenic debris, Sloughed papillae in

analgesic nephropathy, sickle cell disease etc.,

• Extra Ureteral Malignancy, Retroperitoneal fibrosis, accidental ligation

etc.,

• Bladder neck/Urethral Autonomic neuropathy with urinary retention, Urethral

stricture, Blood clots/bladder stones.

CLINICAL PRESENTATION 

(Symptoms of acute renal failure depend largely on the underlying cause.)

• Fever

• Rash

• Bloody diarrhea

• Severe vomiting

• Abdominal pain

• Hemorrhage

• No urine output or high urine output

• History of recent infection

• Pale skin

CLINICAL PRESENTATION 

• History of taking certain medications• History of trauma• Swelling of the tissues• Inflammation of the eye• Detectable abdominal mass• Exposure to heavy metals or toxic solvents

Evaluation of ARF

• Careful History and tabulation of data including u.o, weights, vitals, medications etc.,.

• Physical Examination findings including signs of vol. depletion etc.,

• Urinalysis

• Urinary indices(Urine sodium, creatinine, FeNa, FeUrea etc.,)

Mortality associated with AKI

• ICU associated AKI along with respiratory failure requiring hemodialysis, the mortality is >90%.

• ICU associated AKI with out respiratory failure or hemodialysis, it is 72%

• Non-ICU renal failure associated mortality is around 32%.

Urinary Indices

Prerenal• High SpGr• No

proteinuria/hematuria• U.Na <20• U.Cr/P.Cr >40• U.Osm >500• FeNa <1%• FeUrea <35%

ATN• Sp Gr 1.010• Variable proteinuria• U.Na >40• U.Cr/P.Cr <20• U.Osm <350• FeNa >1%• FeUrea >50%

Urinalysis and Urine Sediment

• UA positive for heme and proteinuria seen in Glomerular and Interstitial renal failure.

• Urine eosinophils are seen in AIN, Atheroembolic disease etc.,

• Urine sediment positive for red cell casts seen in Glomerulonephritis.

• UA bland in Post Renal ARF.

Laboratory Data

• .Hypocomplementemia seen in SLE, MPGN, Atheroembolic disease etc.,

• Elevated ESR seen in Atheroembolic disease.

• Serologies positive in glomerular diseases, like ANA, ANCA, Anti GBM, Hepatitis, HIV

• Elevated LDH seen in RVT.

Laboratory Data (contd)

• Thrombocytopenia with microangiopathic hemolysis seen in TTP, HUS etc.,

• Low Haptoglobin, High retic count seen in microangiopathic states.

• Schistocytes (red cell fragmentation).• CPK, uric acid levels etc., to evaluate for

rhabdomyolysis, uric acid nephropathy.• Evidence of hepatic insufficiency in

diagnosing hepatorenal syndrome.

Imaging

Ultrasound• Useful in Post renal AKI. • Early obstruction may not show significant

hydronephrosis.• External obstruction encrasing the whole urinary

system may not show hydronephrosis, for e.g., retroperitoneal fibrosis.

• U/S doppler useful in diagnosing Renal vein thrombosis.

Imaging (contd)

CT scan• Useful for detecting stones, location of the

obstruction, Tumours etc.,

Isotope renography• To evaluate the function significance of

obstruction. • Done with lasix and Mag3 isotope for evaluatine

obstruction.

Imaging (contd)

Cystoscopy and Retrograde Pyelography

• To evaluate patients with high clinical suspicion of obstruction esp., in unique cases of calculi, pyogenic debris, blood clots, bladder cancer etc.,

Renal Angigraphy• In emergent cases of anuria with suspicion of

renal embolization.

Renal Biopsy

• Only in patients with no clear etiology.

• In patients with active urinary sediment (RBCs, red cell casts etc., )

• RPGN (rapidly progressive glomerulonephritis).

• Refractory ATN with out recovery despite no further renal insults.

• Acute Interstitial nephritis.

Management of AKI

• Volume repletion with isotonic fluids to improve renal perfusion pressures in prerenal states.

• CVP/ PEWS monitoring.• Supportive measures for sepsis with pressors,

antibiotics etc.,• Colloidal substances like blood products in

hemorrhagic shock.• Management of heart failure by improving

cardiac output.

Children and young people: ongoing hospital assessment

• Consider a paediatric early warning score (PEWS) to identify children and young people at risk of acute kidney injury

• Record physiological observations at admission and then according to local protocols for given PEWS

• Increase the frequency of observations if abnormal physiology is detected

• Use PEWS with multiple-parameter or aggregate weighted scoring systems that allow a graded response and include:

• heart rate • respiratory rate • systolic blood pressure • level of consciousness • oxygen saturation • temperature • capillary refill time

Management (contd)

• Drugs need to be dosed according to the renal clearance.

• Electrolyte and acid base correction.

• Renal diet, if K+ high.

• Diuretics in overt fluid overload states.

• Foley catheterization in bladder neck obstruction/prostatic obstruction.

Management (contd)

• Avoid nephrotoxic agents like Contrast dye, NSAIDs, Aminoglycosides etc.,

• Also avoid ACEI unless the underlying problem is decompensated heart failure.

• Nutritional support with parenteral or enteral feeding.

Management (contd)

Renal replacement therapyModes of dialysis:• IHD (Intermittent Hemodialysis) Quick removal of solutes over 3-4 hours,

possible hemodynamic instability. ICU, hypotensive patients are probably not the best candiadtes for this type of HD.

• CRRT (Continuous renal replacement therapy). Modality of choice in critically ill patients.

Management (contd)

• Vascular access needed for Hemodialysis.

• Peritoneal dialysis uncommonly used for managing ARF

• It may be used in locations where IHD or CRRT are not available.

Any Questions?