Lecture on acute renal failure
Based on the cause of acute renal failure: shock, severe cold, hemoglobinuria, poisoning, urinary stones
Acute renal failure is a sudden loss of kidney function with creatinine/blood >0.5mg above normal (>2mg%), blood urea rising rapidly within 24 hours and urine output <20ml/hour or >20ml /hour.
60% due to surgical and traumatic causes.
40% due to internal medicine.
1-2% due to obstetrics.
Due to acute tubular necrosis: 45%.
Due to pre-renal causes 21%.
Due to 10% congestion.
Due to glomerular and vascular disease 4%.
Due to 2% interstitial nephropathy.
Due to the atherosclerotic obstruction 1%.
Due to decreased renal perfusion.
Due to volume depletion: ²Dehydration, blood loss ².
Due to circulatory failure: Shock due to acute myocardial infarction, acute cardiac tamponade, anaphylactic shock, septic shock.
Obstructive uropathy due to stone, tumor compression.
Renal failure in the kidney:
Vasculitis (vaculitis) due to malignant hypertension, TTP (thrombotic-t-purpura), scleroderma, venous thrombosis.
Drug-induced interstitial inflammation, hypercalcemia, infection of unknown etiology.
Acute tubular necrosis:
Caused by pre-renal failure.
Pigmentation: Hemoglobinuria: Due to hemolysis in malaria, G6PD deficiency, transfusion to blood type. Rhabdomyolysis: Due to rhabdomyolysis.
Increased oxygen consumption/striated muscle:
High fever, overexertion.
Decreased muscle blood volume (due to arterial insufficiency).
Alcohol (alcohol) relieves skeletal muscle.
Aminoglycoside antibiotics occur about 10-20%, are more likely to occur in:
The volume of blood reaching the kidneys is reduced.
Have pre-existing kidney disease.
Intravenous contrast media (Radiocontrast media occurs 1-2 days after the procedure, increasing serum creatinine by 25% from normal).
Renal ischemia or toxic effects on the kidneys lead to:
Renal tubular cells:
Obstruction of renal tubular cells.
Drainage of fluid from the renal tubule cells out of the interstitial tissue causes edema to compress.
Renal tubular collapse leads to increased intratubular pressure and decreased renal filtrationlower glomerular filtration rate (GFR).
Reduced surface area leads to decreased ultrafiltrationdecreased glomerular filtration rate.
Decrease renal perfusion pressure.
Increases incoming arterial force.
Decrease in arterial toneDecrease in glomerular osmolality decrease in micro glomerular filtration rate.
Clinical manifestations of acute tubular necrosis
Consists of 3 stages:
Present within 1 day of kidney damage lasting 1-2 weeks can be as short: a few hours and as long as weeks.
Urine output: 150-400ml/day little change until the diuretic phase.
Neurological manifestations: lethargy, somnolence, coma.
Gastrointestinal manifestations: loss of appetite, nausea, vomiting, intestinal paralysis, erosive ulcers in the stomach and colon, and disturbances in blood coagulation easily cause gastrointestinal bleeding, accounting for 10-20%.
Arrhythmia due to increased K+/blood.
Congestive heart failure - acute pulmonary edema.
Hypertension is uncommon in the early stages if prolonged oliguria leads to hypertension.
Pericarditis is uncommon with early dialysis.
Cardiac arrest due to increased K+/blood.
Anemia: Hct 20-30% due to:
Bone marrow reduces red blood cell production.
Bleeding caused by urea inhibits platelet activity, due to fragility of the vessel wall, in addition, can cause DIC.
Infection: 30-70% may be due to a decrease in the body's immune defenses.
Starting with an increase in urine volume, increasing day by day, although at this stage urea, creatinine and K + continue to increase, polyuria due to osmotic diuresis leads to fluid and electrolyte disturbances. At this stage, GFR decreases, kidney function has not fully recovered after 1-2 weeks, the clearance gradually increases, and the urea creatinine decreases.
The renal function continues to improve for 3-12 months after about two-thirds of patients whose GFR is still 20-40% lower than normal, but most patients return to normal. although there is a slight disturbance in renal function.
BUN increases 10-20mg%/day, when there is an infection rapidly increases 40-100mg%/day.
Creatinine increases 0.5-1mg% and rapidly increases 2-5mg%/day.
Water and electrolytes:
Increased water and salt is the most common risk that can cause complications such as acute pulmonary edema, high blood pressure.
Increase K+/blood on average 0.3-0.5mEq/l/day in the presence of tissue necrosis, infection, acidemia, K+ increase faster than 1-2mEq/l within a few hours when K+>6-6.5mEq /l has clinical symptoms and ECG.
Decrease Ca++/blood about 6.8-8.3mEq/100ml.
Increased phosphate but rarely >8mEq/100ml.
Magnesium elevation is common but rarely >4mEq/l.
Coarse granular urine sediment, many epidermal cells.
Na+/urine > 40mEq/l.
Urine osmolality < 350 m/kg.
Urine specific gravity <1.010.
Urine/plasma creatinine < 20.
Urine/plasma osmolality < 1.2.
Non-oliguria renal failure:
It accounts for about 40-50% of acute renal failure with urine output >400ml/day.
The mechanism may be due to:
Mild tubular injury.
Due to early and strong diuretic use in this form of the disease.
Urea/urine is even higher in oliguria.
Occurs suddenly, preceded by normal renal function.
Based on the cause of acute renal failure: shock, severe cold, hemoglobinuria, poisoning, urinary stones.
Urine output < 20 mL/hour or > 20 mL/hour.
Creatinine increased >2-3mg%.
Urea increases rapidly by 1.5-2g/l within 24 hours.
Urine sediment, density< 1,010.
Ure / urinaryurinary creatinine , urinary Na + , urinary K+ , urinary Na+/K+ ratio >1.
To distinguish prerenal, renal or postrenal acute renal failure based on:
History: ask carefully about the circumstances leading to acute renal failure:
Prerenal: due to volume reduction.
Post-renal: renal colic, hematuria.
In the kidney: pigmenturia, hemolysis, trauma, drug use.
Amount of urine:
Oliguria: <400ml/24 hours stable during oliguria is acute tubular necrosis.
Complete and persistent anuria is usually caused by:
Renal cortical necrosis.
Glomerulonephritis, renal vasculitis.
Prerenal: hyaline or fine-grained casts.
Post-renal: poor sediment.
In the kidney: dirty deposits, many pillars, free epidermal cells or adhesions to the pillars.
Other special tests:
Urine/plasma osmolality ratio.
Na + urine.
Urine density, Na + /K + urine, Ure.
FeNa = (Naurine x Plasma Creatinine)/(Plasma Na x
Urine Creatinine) x 100 (FeNa : Fractional excretion of Sodium).
Treatment to try: NaCl 9% 500ml + 12,5g albumin (25% 50ml) + furosemide 100mg + Dopamine 2-3 mg / kg / min. When urine output >50ml/hour: functional renal failure. Insert a urinary catheter to monitor urine every 12 hours.
Abdominal scan without preparation: Look for ureteral stones.
Renal tomography without preparation.
Ultrasound, CT Scanner looks for obstruction behind the kidney.
Pre-renal and post-renal renal failure must first be ruled out because treating the causes of these two cases will have good results.
Treatment of causes of acute renal failure and prevention
Due to volume depletion: resuscitation, blood-based on CVP, blood pressure, and urine monitoring via urinary catheter. When CVP increased, BP ³90 / 60-100 / 60mmHg we use more Furosemide + Dopamine 2 mg / kg / min.
Hemoglobinuria: fluids, blood transfusions, acidosis, and prevention of acute renal failure in the first place with furosemide.
Due to stones: remove stones.
Prevention of acute renal failure due to intravenous contrast media:
Infusion of 0.9% NaCl: 1cc/kg/h 12 hours before work and 12 hours after work.
N.acetyl cysteine (Mucomyst) 600mg x 2 before, 600mg x 2 after.
Alkaline urine with bicarbonate: 3 ampoules of 8.4% (50cc)/G 5% IV injection, dose of 3.5cc/kg 1 hour before and 1cc/kg/h for 6 hours after work.
Trial treatment with high-dose furosemide
Within the first 24-36 hours of acute renal failure with normal CVP and HA ³90 / 60-100 / 60mmHg.
Furosemide 20mg 4-10 ampoules IV/2 hours and monitor urine through urinary catheter after 15-30 minutes reach 200ml, minimum 100ml, good response >50ml/hour, minimum >30ml/hour continue using Furosemide.
If only <50ml/2 hours does not respond to furosemide, give a second dose of 20 ampoules every 2 hours if urine output is <50ml/2h, then dialysis is indicated.
Dopamine can incorporate additional dose of 2 mg / kg / min.
The following regimens can be used:
Furosemide intravenously 20mg (2-4 ampoules)/3-6h with a urine output of 100ml/h.
Furosemide IV 20mg, if no response after 30'-1h give 40mg, if no response increase dose until response and repeat dose every 8 hours.
0.1 mg/kg intravenously followed by 0.1 mg/kg/h intravenous infusion and doubled every 2 hours to achieve a dose of 0.4 mg/kg body weight.
Or give a 20mg intravenous dose, then 20mg/h infusion and increase to 40mg/h.
Maintain Furosemide in response to fluid resuscitation and depending on urine output (1 liter Glucose 5% + 4-6g NaCl + 1.5-2g KCl) keep urine output 2-2.5 liters/24 hours .
Upon failure of a trial with furosemide, the patient developed acute tubular necrosis
Conservative treatment when:
There is still urine.
Using Furosemide has a urine response >50ml/hour and BUN, K+ do not increase rapidly.
Without conservative treatment:
BUN and K+ increase rapidly.
Furosemide did not respond.
Regulate water, electrolytes, acid-base
Water intake = depending on the amount of urine/day + 500ml (if edema, hypertension only compensates ½.).
Na+ compensates by the amount of Na+ lost each day in the urine, only compensates for Na+ when: no edema, urinating (Na+ blood decreases).
K+ 5.5-6mEq/l stops the sources of potassium entering the body.
K+ >6mEq temporarily lowers K+ blood by:
Calcium gluconate 10% 10ml IV/2 minutes, after 5 minutes of no effect, repeat the second time, lasting for 1 hour.
Sodium bicarbonate 45mEq IV/5 minutes, repeat after 15-30 minutes, lasting 1-2 hours.
Glucose 20% 250cc + 20 UI Intravenous insulin 30-60 minutes, lasting 3-6 hours.
Or Glucose 50% 25g IV + Insulin 10UI IV.
Or Glucose 10% 1000cc + 2 tubes of SB 8.4% TTM, Insulin 25UI TDD, 300cc within 30 minutes, then remaining for 3 hours.
Ion exchange: Resonium A, Kayexalate 20g x 4 times/day + Sorbitol 20% 50-100cc 1 time within 1-2 days.
When K+ > 6.5mEq/l: dialysis.
Antiacid: Sodium carbonate 1.4% 250-500ml/day or 8.4% 50mEq for pH > 7.2 and HCO3- >16-18mEq/l.
Diet GG energy 2,000 calories/day.
Glucose 100-200g/day, vegetable oil, 2 eggs (yolk.).
0,5-1g protein / kg / day using proteins with high nutritional value (eggs, milk, meat).
NaCl 2-4g a day mainly compensates for loss through urine, no edema, no hypertension.
Do not use potassium-rich foods such as old bananas, coconuts, oranges.
Treatment of complications
Gastrointestinal bleeding: DDAVP 0.3 mg / kg IV or Desmopressin 0.3 mg / kg / 50ml NaCl 9% PIV 30 minutes x 4-6 / 24 hours or prophylactic H2 inhibitors or proton pump inhibitors , keep Hb >10g/l.
Treat the cause
Hyperhydration or acute pulmonary edema due to excess water.
Severe hyperK+/blood >6.5mEq/l.
Severe metabolic acidosis not treatable by medical therapy with pH <7-7.2 (HCO-3 10-15mEq/l).
Decreased Na+/blood <120mEq/l.
Anuria (<10ml/h) with BUN >50mg% and K+ >6mEq/l lasting >12 hours.
Increased regressive with 30 to 40mg% increase in BUN, or 1-2mg increase in creatinine within 24 hours, 1mEq/24 hour increase in K+/blood.
BUN >80mg% or Creatinine >8mg% and K+ >6mEq/l.
Gastrointestinal bleeding, acute pericarditis, neuropsychiatric disorders due to high blood urea syndrome.
Prerenal renal failure after adequate fluid resuscitation and failed Furosemide test.
Kidney failure after kidney obstruction.
Urine output per hour for 24 hours.
Urea, blood creatinine, blood ion, HCO3-.
Urea, urinary creatinine, urine ion.
Blood pressure, edema.
Overall mortality 30-60% of complications:
Internal medicine 30-50%.
Postoperative trauma 50-70%.
Due to production 10-20%.