Evaluation and Management of Acute Renal Failure :Evaluation and Management of Acute Renal Failure ????? 95/10/12
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Slide 3:Anuria: urine 3 months
Blood Urea Nitrogen (BUN) :Blood Urea Nitrogen (BUN) Catabolism of aminoacids generates NH3
NH2
2 NH3 + CO2 = C = 0 + H2O
NH2
Urea Mol wt : 60; BUN Mol wt. : 28
Normal BUN 10-20 mg/dl
After filtration › 50% is reabsorbed by the tubule
BUN level is related to: Renal function, protein intake, liver function, GI bleeding, steroid, hyper catabolic states
Creatinine :Creatinine Formed at a constant rate by dehydration of muscle creatine
Normally 1–2% of muscle creatine is broken into creatinine
Mol. Wt. 113
Creatinine is freely filtered by the glomerulii and is not reabsorbed 10–15% is secreted into proximal tubule
GFR Estimation by Plasma Creatinine :GFR Estimation by Plasma Creatinine Cockcroft and Gault Formula*
Calculated creatinine clearance
= (140–age) x wt (kg)
72 X serum creatinine(mg/dl)
For females, subtract 15% (or multiply by 0.85); for paraplegics multiply by 0.8, for quadriplegics, multiply by 0.6
*Applicable only when patient is in a steady state, not edematous and not obese
Factors that affect serum creatinine concentration :Factors that affect serum creatinine concentration
Acute Renal Failure :Acute Renal Failure Definition:
Rapid (hours to weeks) decline in glomerular filtration rate and retention of waste products
It is a clinical syndrome cause by many renal or extrarenal diseases
Lack a uniform definition
Cr > 1.5x, urine output <0.5ml/kg/hr
Cr increase = 1.0 mg/dl/2d
Slide 9:The Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group
The facts you need to know about ARF :The facts you need to know about ARF Acute renal failure may reversible and should look for the causes to management
Incidence:
- 2-5% of hospitalized patients(55% iatrogenic)
- 7-23% of ICU patients
- 20-60% require dialysis; of those who survive initial dialysis, <25% require long-term dialysis
The facts you need to know about ARF :The facts you need to know about ARF Motality:
Liano(1996) reported mortality rate of 60% for patient with ATN, 35% for acute on chronic renal failure, 27% for obstructive ARF and 26% for renal disorder other than ATN.
Knaus(1986)50% for combination of acute renal and respiratory failure towards 100% with 5 system failure
In community-acquired ARF with mostly prerenal and postrenal causes and the prognosis is better.
Rates not significantly decreased over past 50 years despite advances in dialysis and critical care (increased patient age and co morbid illnesses)
Symptoms and Signs of Renal Failure :Symptoms and Signs of Renal Failure Retention of nitrogenous waste products
Nausea, vomiting, diarrhea, hiccup, foul taste, dry crusted mouth, itching,
Drowsiness, clouding of consciousness, neuropathy, pericarditis, GI bleeding,
Coma
Retention of salt and water
Pulmonary edema, peripheral edema, ascites, pleural effusion
Symptoms and Signs of Renal Failure :Symptoms and Signs of Renal Failure Retention of potassium
Weakness, lassitude, paralysis, EKG changes with tenting T waves, widening of QRS complex, increased PR interval, sine wave pattern, cardiac arrest, VT
Retention of acid
Kussmaul respiration, hyperreflexia, hypotension
Slide 14:A: Cr, BUN
B: H, P, K
C: NaCl
Classification of ARF :Classification of ARF Acute Renal Failure Pre-renal Intrinsic Post-renal Glomerular Interstitial Vascular Tubular
Pre-renal ARF :Pre-renal ARF Accounts for 60-70% of cases of ARF
Represents physiologic response to mild-moderate renal hypoperfusion
Renal parenchymal tissue is not damaged therefore rapidly reversible upon restoration of RBF and glomerular filtration pressure
Elderly and those with pre-existing renal disease at increased risk
Pre-renal ARF :Pre-renal ARF I. Hypovolemia
A. Hemorrhage, burns, dehydration
B. GI fluid loss: vomiting, surgical drainage, diarrhea
C. Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes mellitus), hypoadrenalism
D. Sequestration in extravascular space: pancreatitis, peritonitis, trauma, burns, severe hypoalbuminemia
II. Low cardiac output
A. Diseases of myocardium, valves, and pericardium; arrhythmias; tamponade
B. Other: pulmonary hypertension, massive pulmonary embolus, positive pressure mechanical ventilation
Pre-renal ARF :Pre-renal ARF III. Altered renal systemic vascular resistance ratio
A. Systemic vasodilatation: sepsis, antihypertensives, afterload reducers, anesthesia, anaphylaxis
B. Renal vasoconstriction: hypercalcemia, norepinephrine, epinephrine, cyclosporine, tacrolimus, amphotericin B
C. Cirrhosis with ascites (hepatorenal syndrome)
IV. Renal hypoperfusion with impairment of renal autoregulatory responses
Cyclooxygenase inhibitors, ACEI
V. Hyperviscosity syndrome (rare)
Multiple myeloma, macroglobulinemia, polycythemia
Intrinsic Renal Causes :Intrinsic Renal Causes Accounts for 25-40% of cases of ARF
Types:
Acute glomerulonephritis <5%
Interstitial nephritis 10%
Intrarenal vascular disease <5%
ATN 85%
Intrinsic Renal Causes :I. Renovascular obstruction (bilateral or unilateral in the setting of one functioning kidney)
A. Renal artery obstruction: atherosclerotic plaque, thrombosis, embolism, dissecting aneurysm, vasculitis
B. Renal vein obstruction: thrombosis, compression
II. Disease of glomeruli or renal microvasculature
A. Glomerulonephritis and vasculitis
B. Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, toxemia of pregnancy, accelerated hypertension, radiation nephritis, systemic lupus erythematosus, scleroderma Intrinsic Renal Causes
Intrinsic Renal Causes :Intrinsic Renal Causes III. Acute tubular necrosis
A. Ischemia(60%): as for prerenal ARF (hypovolemia, low cardiac output, renal vasoconstriction, systemic vasodilatation), obstetric complications (abruptio placentae, postpartum hemorrhage)
B. Toxins(40%)
1. Exogenous: radiocontrast, cyclosporine, antibiotics (e.g., aminoglycosides), chemotherapy (e.g., cisplatin), organic solvents (e.g., ethylene glycol), acetaminophen, illegal abortifacients
2. Endogenous: rhabdomyolysis, hemolysis, uric acid, oxalate, plasma cell dyscrasia (e.g., myeloma)
Intrinsic Renal Causes :Intrinsic Renal Causes IV. Interstitial nephritis
A. Allergic: antibiotics (e.g., -lactams, sulfonamides, trimethoprim, rifampicin), nonsteroidal anti-inflammatory agents, diuretics, captopril
B. Infection: bacterial (e.g., acute pyelonephritis, leptospirosis), viral (e.g., cytomegalovirus), fungal (e.g., candidiasis)
C. Infiltration: lymphoma, leukemia, sarcoidosis
D. Idiopathic
V. Intratubular deposition and obstruction
Myeloma proteins, uric acid, oxalate, acyclovir, methotrexate, sulphonamides
VI. Renal allograft rejection
Post-renal Causes of ARF :Post-renal Causes of ARF Account for 5% of cases of ARF
ARF occurs when both urinary outflow tracts are obstructed or when one tract is obstructed in a patient with a single functional kidney
Post-renal Causes of ARF :Post-renal Causes of ARF I. Ureteric
Calculi, blood clot, sloughed papillae, cancer, external compression (e.g., retroperitoneal fibrosis)
II. Bladder neck
Neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clot
III. Urethra
Stricture, congenital valve, phimosis
Investigations :Investigations ARF: Focused History
Nausea? Vomiting? Diarrhea?
Hx of heart disease, liver disease, previous renal disease, kidney stones, BPH?
Any recent illnesses?
Any edema, change in
urination?
Any new medications?
Any recent radiology studies?
Rashes?
Investigations :Investigations Physical Examination:
Infection sign ? Blood pressure, vital sign
Volume Status
Mucus membranes, orthostatics, skin turgor, Edema
Cardiovascular
JVD, rubs
Pulmonary
Decreased breath sounds
Rales
Abd and back: bladder distension, masses, ascites, CVA tenderness, large prostate
Rash (Allergic interstitial nephritis)
Investigations :Investigations Blood
CBC-DC
Electrolyte, Ca, Mg, P
Urea, Creatinine
Others: LDH, Alb, CRP…
Urine
Urine sodium, Cr
Urine osmolality
Urinalysis
Renal echo
FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr) :FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr) FeNa <1%
1. PRERENAL
Urine Na < 20. Functioning tubules reabsorb lots of filtered Na
2. ATN (unusual)
Postischemic dz: most of UOP comes from few normal nephrons, which handle Na appropriately
ATN + chronic prerenal dz (cirrhosis, CHF)
3. Glomerular or vascular injury
Despite glomerular or vascular injury, pt may still have well-preserved tubular function and be able to concentrate Na
More FeNa :More FeNa FeNa 1%-2%
Prerenal-sometimes
ATN-sometimes
AIN-higher FeNa due to tubular damage
FeNa >2%
ATN Damaged tubules can't reabsorb Na
Calculating FeNa after pt has gotten Lasix.
1. Fractional Excretion of Lithium (endogenous) (<7% in prerenal )
2. Fractional Excretion of Uric Acid (<7% in prerenal )
Is the renal failure really acute? :Is the renal failure really acute? Factors suggesting chronicity
Duration of symptoms for months
Absence of acute illness in the face of very high urea and creatinine
Anaemia of chronic disorders
Bone disease (renal osteodystrophy)
Sexual dysfunction
Skin disorders, pruritus
Neurological complications
Small kidneys on renal imaging
Management :Management Prevention
  Etiology treatment
  Prevention additional injury
  Treatment of complication
  Conservative measurement
  Renal replacement therapy
Prevention :Prevention Identification of high-risk patients for pharmacologic agents-induced nephrotoxicity
iodinated radiocontrast medium, NSAIDs
Aggressive surveillance for nephrotoxin-induced renal dysfunction
cisplatin, amphotericin B, aminoglycoside
Use of volume expansion in selected clinical settings
Hyperpigmenturia: hemoglobinuria, myoglobinuria
Crystaluria: uric acid, acyclovir, methotrexate, sulfonamides
Minimalization of catheters use to avoid nosocomial sepsis
Etiology Treatment :Etiology Treatment Correct postrenal factor
Correct prerenal factor
Treat underlying sepsis
Stop nephrotoxic drugs
Conservative Measurement :Conservative Measurement Fluid balance
Careful monitoring of I/O and body weight
Fluid restriction
(usually less than 1 L/day in oliguric ARF)
Total intake 15
hyperphosphatemia
Treat hypocalcemia only if symptomatic
Guide of Volume Expansion :Guide of Volume Expansion CVP 8-14 cm H2O (5-2 rule)
PAWP 12-16 mmHg (7-3 rule)
Urine output 0.5-1.0ml/kg/hour
Weighing the patient daily
Insensible water loss from the skin and respiratory tract (500 ml/day)
Dietary modification :Dietary modification total caloric intake– 35~ 50 kcal/kg/day
to avoid catabolism
Salt restriction– 2~4 g/day
Potassium intake– 40 meq/day
Phosphorus intake– 800 mg/day
Conservative Measurement :Uremia-nutrition
Restriction protein is not necessary in ARF, maintain caloric intake
Carbohydrate = 100gm/day to minimize ketosis and protein catabolism
Drug
Review all medication, Stop magnesium-containing medication
Adjusted dosage for renal failure, Readjust with improvement of GFR Conservative Measurement
Indication of Dialysis : Absolute indication
CCr ? 5 ml/min or serum Cr ? 10.0 mg/dl
Relative indication
CCr ? 10 ml/min or serum Cr ? 8.0 mg/dl
With accompanied symptoms or signs
= CHF/Pulmonary edema = Uremic pericarditis= Bleeding tendency = Neurologic symptoms= Drug-resistant hyper-K = Drug-resistant metabolic acidosis = Drug-resistant nausea/vomiting= Others Indication of Dialysis
Take Home Points :Take Home Points Features of the history and physical examination in addition to relevant lab and radiologic investigations help to determine the most likely cause(s) of ARF in a given patient
Take Home Points :Take Home Points Management of a patient with ARF involves:
Treating potentially life-threatening complications
Reversing pre-renal and post-renal causes
Minimizing further hemodynamic and toxic insults to the kidney
Admission and appropriate consultation
Lack of evidence for converting oliguric to non-oliguric ARF