Evaluation and Management of Acute Renal

Evaluation and Management of Acute Renal Failure : 

Evaluation and Management of Acute Renal Failure ????? 95/10/12

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Anuria: urine < 100ml/day Oliguria: urine <400-500 mL/d Azotemia: Increase Cr, BUN May be prerenal, renal, postrenal Does not require any clinical findings Chronic Kidney Disease: graduated loss of renal function, National kidney fundation: stage 1~5 ESRD = Loss of kidney function >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

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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

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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 < urine output +extrarenal losses Electrolytes and acid -base balance hyperkalemia hyponatremia Keep serum bicarbonate >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