Acute Renal FailureBy: Dr. Muhammad Asim FazalMeeqat General Hospital (ICU)

Al-Madinah Al-Munawwara

Objective

• Definition

• Classification

• Epidemiology

• Etiology

• Management– Diagnosis

– Treatment

Definition

• There are more than 35 definitions of AKI (formerly acute renal failure) in literature! - shows the complexity of the problem.

• Deterioration of renal function over a period of hours to days, resulting in • The failure of the kidney to excrete nitrogenous

waste products and

• The failure to maintain fluid and electrolyte homeostasis

Classification

• Can be Classified into 3 ways• 1* Oliguric / Non-Oliguric• 2* Pre-Renal / Renal / Post-Renal• 3* RIFLE Criteria

Oliguric / Non-Oliguric

• Oliguric : AKI associated with decrease urine output (<400ml/24 hours)

• Non-Oligguric: AKI associated with normal urine output (>400ml/24 hours)

• Very simple classification but not much helpful except that non-oliguric AKI has better prognosis.

Acute Kidney Injury

PRERENAL

AKI

INTRINSIC POSTRENAL

Acute Kidney Injury

• PRERENAL: 40-80%– Volume loss/Sequestration

– Impaired Cardiac Output

– Hypotension (and potentially hypo-oncotic states)

• Net result: glomerular hypoperfusion

Acute Kidney Injury

• Prerenal Azotemia: fall in GFR secondary to renal hypoperfusion that potentially has rapid reversible component

• Restoration of effective intravascular volume, perfusion pressure

• By current detectable methods, AKI reverses with minimal evidence of tubular ischemia

Acute Kidney Injury

• RENAL/INTRINSIC: 10-30%– Vascular disorders:

– small vessel– large vessel

– Glomerulonephritis– Interstitial disorders:

– Inflammation

– Tubular necrosis:– Ischemia– Toxin– Pigmenturia

Acute Kidney Injury• Prerenal and ATN encountered most often in

the hospital setting: 70-75% in many studies• Most common diagnostic consideration is

therefore between these two conditions• Prerenal:

1. Intravascular volume depletion2. Hypotension3. Edematous states4. Localized renal ischemia

• ATN:1. All causes for prerenal, leading to post-ischemic ATN2. Toxins

• Stones• Blood clots• Papillary necrotic tissue• Urethral disease

anatomic: posterior valvefunctional: anticholinergics, L-DOPA

• Prostate disease• Bladder disease

anatomic: cancer, schistosomiasisfunctional: neurogenic bladder

Postrenal azotemia

RIFLE Criteria

– Risk• 1.5X increase in creatinine or UO < 0.5 ml/kg for 6 hours

– Injury• 2X increase in creatinine or UO < 0.5 ml/kg for 12 hours

– Failure• 3X increase in creatinine or UO < 0.3 ml/kg for 24 hours or anuria

for 12 hours

– Loss• Complete loss of function for more than 4 weeks

– ESRD• Complete loss of function for more than 3 months

Epidemiology

• AKI occurs in ≈ 7% of hospitalized patients. 36 – 67% of critically ill patients (depending

on the definition). 5-6% of ICU patients with AKI require Renal

Replacement Therapy.

Mortality

• Dialysis requiring 40-90%

• Increased mortality even in patients not requiring dialysis

• 25% increase in creatinine associated with a mortality rate of 31% compared with 8% for matched patients without renal failure.

Etiology

• Categorize the different causes of acute renal insufficiency.– Prerenal: volume depletion and relative hypotension– Vascular: Consider vasculitis, TTP, nephrosclerosis, renal

artery stenosis– Glomerular: Consider the nephritic and nephrotic

syndromes– Tubular/interstitial: Consider ATN, drugs, PCKD, myeloma,

autoimmune disorders– Obstructive: Consider prostate disease, stones,

metastatic cancer

Management

• Consists of 2 Parts:• 1* Diagnosis• 2* Treatment History and Physical exam Detailed review of the chart, drugs

administered, procedures done, hemodynamics during the procedures.

Diagnosis

• The following tests can aid in the diagnosis and assessment of AKI:

• Kidney function studies: Increased levels of blood urea nitrogen (BUN) and creatinine are the hallmarks of renal failure; the ratio of BUN to creatinine can exceed 20:1 in conditions that favor the enhanced reabsorption of urea, such as volume contraction (this suggests prerenal AKI)

• Complete blood count• Peripheral smear• Serologic tests: These may show evidence of

conditions associated with AKI, such as schistocytes in disorders such as hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura

• Fractional excretion of sodium and urea

AKI: Diagnostic studies-urine

• Urinalysis for sediment, casts• Response to volume repletion with return to

baseline SCr 24-72 hr in prerenal event• Urine Na; FENa FENa (%) = UNa x SCr x 100 SNa x UCr

– FENa < 1%: Prerenal– FENa 1-2%: Mixed– FENa > 2%: ATN

• Hansel’s stain

Acute Kidney Injury

OTHER LABORATORY DATA• HCO3ˉ: anion gap, lactic acid, ketones• Serum Electrolytes especially serum K level• CPK/LDH/Uric acid/liver panel• Serologies:

– Complement– ESR, RF, ANA, ANCA, AntiGBM– Electrophoresis

• Toxicology studies

Acute Kidney Injury

IMAGING STUDIES• Ultrasound: evaluates renal size, able to

detect masses, obstruction, stones. • Renal biopsy: Can be useful in identifying

intrarenal causes of AKI

AKI: Acute Tubular Necrosis• Non-oliguric vs. Oliguric

• Prognosis worse with oliguric ATN in most series

• Ischemic insult: medulla most susceptible to hypoxic event, cellular ATP depletion, oxidative injury

• AKI/ARF phase of ATN: 7-21 days on average• Recovery phase of ATN: also known as diuretic

phase• High urine output (>3-4 L)• K, Mg, PO4 wasting

• Associated with high FENa

Treatment of AKI

• It cannot be overstated that the current treatment for AKI is mainly supportive in nature; no therapeutic modalities to date have shown efficacy in treating the condition.

• Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary goals of AKI treatment and may include the following measures:

• Correction of fluid overload with furosemide• Correction of severe acidosis with bicarbonate

administration, which can be important as a bridge to dialysis

• Correction of hyperkalemia• Correction of hematologic abnormalities (eg,

anemia, uremic platelet dysfunction) with measures such as transfusions and administration of desmopressin as needed.

Dietary Modification

• Dietary changes are an important facet of AKI treatment. Restriction of salt and fluid becomes crucial in the management of oliguric renal failure, wherein the kidneys do not adequately excrete either toxins or fluids.

• In the polyuric phase of AKI, potassium and phosphorus may be depleted, so that patients may require dietary supplementation and IV replacement.

Avoid Nephrotoxic agents

• In AKI, the kidneys are especially vulnerable to the toxic effects of various chemicals. All nephrotoxic agents (eg, radiocontrast agents, antibiotics with nephrotoxic potential, heavy metal preparations, cancer chemotherapeutic agents, nonsteroidal anti-inflammatory drugs [NSAIDs]) should be avoided or used with extreme caution.

• Similarly, all medications cleared by renal excretion should be avoided, or their doses should be adjusted appropriately.

Acute Kidney InjuryINDICATIONS FOR RENAL REPLACEMENT THERAPY• Consensus generally includes:

1. Refractory volume overload2. Severe metabolic acidosis; HCO3 may be variable,

but declining level of factor; also falling pH to 7.1-7.2

3. Hyperkalemia, with levels > 6.5, or documented rapid rise refractory to medical therapy

4. Major uremic target organ manifestations i.e. pericarditis, progressive neuropathy, seizure

5. Platelet dysfunction, bleeding diasthesis6. AKI in setting of dialyzable drug/toxin

CRRT

• CRRT may have a role in patients who are hemodynamically unstable and who have had prolonged renal failure after a stroke or liver failure.

• Such patients may not tolerate the rapid shift of fluid and electrolytes caused during conventional hemodialysis.

Acute : Conclusions• Major advances in understanding AKI, but no clear

definition that guides research on prophylaxis, prognosis• AKI still carries high M/M risk, especially in ICU setting• Improving volume status, hemodynamics rapidly aids in

minimizing ischemic AKI risk; volume resuscitation, relief of urinary obstruction can be done concurrently

• Patient history, hosp chart review, PEx coupled with routine labs, UA may establish cause in 40-60% of AKI

• Serologies and consideration of Bx are also adjuncts

THANKYOU