AcRenFail.

doc
Андрій Миколайович Лобода

2014
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Acute renal failure (ARF) denotes an acute impairment of renal function, which results in several clinical
and biochemical derangements. Anuria or severe oliguria (urine flow less than 300 ml/m 2/day or 10-12
ml/kg/day - necessary quantity of urine for excretion of 600 mosmol of osmotic active substances,
created during 24 hours in normal diet and metabolism) is the most important feature, although rarely
urine output may not be decreased. K.N. Drammond considers that in infants oliguria - it is urine flow less
than 180 ml/m 2/d, anuria - 60 ml/m 2/d (2-3 ml/kg/d), except newborns of first two days when anuria - it is
urine flow less than 1 ml/kg/d.
Etiology. Pre-renal, renal and post-renal (obstructive) ARF are marked out.
Pre-renal ARF (renal hypoperfusion): hypovolemia and/or hypotension caused by dehydration
(vomiting, diarrhea, severe and prolonged fever, decrease of colloid-oncotic blood pressure (protein loss
in exudative enteropathy, nephrotic syndrome), peritonitis, ascites, burns, septic chock, hemorrhage,
congenital heart failure.
Renal:

Acute tubular necrosis: fluid loss, hemorrhage, shock, intravascular hemolysis, sepsis, nephrotoxic
drugs, chemical, radiocontrast media, major surgical procedures, road accidents, extensive burns,
hepatic failure, congenital cardiac failure;
Glomerular disease: acute glomerulonephritis, hemolytic uremic syndrome;

- Interstitial nephritis: acute bacterial pyelonephritis, meticillin, sulfonamides;

- Miscellaneous: snakebite, renal vein thrombosis;
Post-renal (obstructive).
Calculi, blood dots, crystals of uric acid, sulfonamides.

Pathogenesis. It has been extensively studied in experimental models. Leakage of glomerular filtrate
back into the circulation across the damaged tubular epithelium and tubular obstruction from impaction
of proteinaceous casts and cellular debris has been long considered to be responsible for oliguria. The
latter may be important in intravascular hemolysis and methemoglobinuria with renal failure. Glomerular
filtration rate (GFR) and renal blood flow are markedly reduced, the latter by 50 to 75 percents. The
importance of tubular obstruction, back leak of filtrate and persistent renal vasoconstriction will vary,
depending on the cause and duration of renal failure. Intense renal vasoconstriction may be caused by
increased renin-angiotensin activity which could follow increased delivery of sodium to the macula densa
due to proximal tubular dysfunction. Intravascular coagulation may play an important role in cases with
sepsis and hemolitic uremic syndrome. Patients with glomerulonephritis and renal failure show severe
glomerular lesions, often characterized by extensive crescents.
Ischemic changes consist of focal or patchy necrosis in any part of tubule, but most frequently in distal
tubules especially at the corticomedullary junction. Proximal tubules are often dilated, but necrosis is
uncommon. Nephrotoxic agents cause strong and uniform epithelial damage especially in the proximal
tubules, without disruption of tubular basement membrane. In post-is-chemic injury there is poor
correlation between histologic changes and renal functional impairment. Subtle changes in intracellular
organelles may be observed by electronmicroscopy in the cells which are not clearly necrotic.
Clinical features. A history of anuria or severe oliguria is present. In a small proportion of cases urine
output may not be diminished ("nonoliguric" ARF). Depending upon the underlying cause and the
duration of renal failure, the child may look remarkably well or extremely sick.
There are 4 phases in ARF:

1. Initial (pre-anuric);
2. oligo-anuric;
3. diuretic;
4. convalescence.

In initial phase clinical features of main disease may be seen (1-3 days).
Oligo-anuric phase (2-2,5 weeks): decrease of urine output, deterioration of general condition, pallor
with jaundice (sometimes hemorrhages on skin, itch), adynamia, headache, weakness, nausea, vomiting,
diarrhea, tachycardia, decrease of BP, especially diastolic, and after it - hypertension, irregularities of
cardiac rhythm and conduction, acidotic breathing, convulsions, abdomen pains, pulmonary edema are
seen. Signs of hyperkalemia may be present (muscular weakness, arrhythmia, cardiac arrest), as well as
signs of fluid overload (edema of optic papilla, hypertension, cardiac enlargement, gallop rhythm,
increase of body weight, pulmonary edema). It is life threatening situation where proper assessment and
adequate treatment is highly rewarding.
Diuretic phase (1-6 weeks): urine output starts to increase steadily, general condition improves, but
hypoisostenuria, hyponatremia, hypokalemia, hypomagnemia, hypocalcemia, polyuria appear. The
patient may get dehydrated if these losses are not adequately replaced. Anemia is progresses.
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Infections are deposited because of depression of humoral and cellular immunity. Infectious
complications are the main cause of death in patients with ARF.
Diagnosis. It is important to detect functional oliguria ("pre-renal type of ARF") which will rapidly
respond to fluid replacement. The bladder should be catheterized for accurate measurement of the urine
output. Increase in urine flow (6 to 10 ml/kg in 1 to 3 hours) is indicative of intact renal function.
Determination of ratios of urine and plasma urea and osmolality, and fractional excretion of sodium also
help in differentiating functional oliguria from established renal failure. These are based on the
impairment of tubular functions in the latter situation, resulting in increased sodium excretion in the urine
and failure to concentrate the urine. Anemia, elevated ESR, azotemia with concentration of RN more
than 72 mmol/l, urea more than 16,7 mmol/l, creatinine more than 0,18 mmol/l, hyperkalemia more than
6 mmol/l, hypocalcemia more than 2 mmol/l, hyperphosphatemia more than 1,8 mmol/l,
decompensated metabolic acidosis (BE more than 10mmol/l) are typical for ARF.
Treatment. Diet, fluid and electrolytes. It is important to provide sufficient calories to meet nutritional
needs. It will also reduce endogenous protein breakdown and thus the metabolic load. Sugar and fat may
be freely given. Proteins, sodium and potassium should not be allowed initially. Insensible losses
(300ml/m 2/day) should be replaced in the form of water with sugar. This amount should be increased to
quantitatively replace the previous 24 hours urine output and any other losses. Administration of calories
becomes difficult in presence of vomiting and infusion of intravenous glucose may have to be resorted
to. The daily vitamin requirement should be given. The child should be accurately weighed daily. With
proper management the child should loss about 0,5% of his body weight per day, because of tissue
breakdown.
Hyperkalemia. Raised serum potassium level can be temporarily brought down by intravenous
administration of glucose 0,5 g/kg along with soluble insulin 0,1U/kg over a period of 90 min. Calcium
antagonizes the cardiotoxicity of hyperkalemia, and intravenous administration of calcium gluconate may
be employed for its immediate effect during an emergency (serum potassium >8 mEq/l). It should be
injected very slowly, the dose being 2,0 ml/kg of a 10% solution over a period of 5 minutes. Persistent
hyperkalemia, especially when anuria, infection, hemolysis and trauma are present, requires prompt
institution of dialysis. Administration of sodium bicarbonate promptly lowers serum level of potassium by
favoring its uptake by the cell; 3 ml/kg of a 7,5% solution of NaHCO3 should be injected.
Metabolic acidosis. Severe acidosis manifested by deep rapid breathing should be treated by
administration of sodium bicarbonate, 1 to 2 mEq/kg, the aim being to raise the serum bicarbonate level
to above 15 mEq/l. Since sodium cannot be excreted, it will increase fluid retention and may aggravate
hypertension. Persistent acidosis requires dialysis treatment.
Hypertension. Severe hypertension may occur with acute glomerulonephritis and hemolitic uremic
syndrome leading to encephalopathy and heart failure. Furosemide 1-2 mg/kg i.v., nifedipine 0,15 mg/kg
sublingually may be used. Diazoxid also has a prompt effect and is given as i.v. bolus in a dose of 2 to 5
mg/kg/dose. Hydralasine (0,2 mg/kg) may be given i.v. or i.m. and repeated after 3 hours; a precipitous
fall of BP may occasionally occur and cause cerebral or ocular complications. Controlled infusion of
sodium nitroprussid with close monitoring of BP is safer in managing hypertensive encephalopathy. After
the blood pressure has been brought down, methyldopa or hydralasine may be continued to keep it
under control.
General supportive care. The child with acute renal failure should be isolated and managed under
intensive care conditions. Accurate records of intake and output and daily weight should be maintained.
Urine should be collected by condom drainage; bladder should not be catheterized. The risk of infection is
very high and appropriate preventive measures should be undertaken. Venipuncture and venisection
should be done with strict aseptic precautions. Prophylactic antibiotics are not recommended but
infections should be detected early and vigorously treated. Their clinical manifestations are often mild
and subtle. Sepsis may be indicated by low grade fever, tachycardia and hypotension. Attempts should
be made to identify the pathogens, since unusual and opportunistic organisms may be involved. The
dosage of antibiotics should be appropriately modified since their excretion is impaired. The total dose or
dosing interval or both of these may be varied. The longer the child remains in renal failure, the higher is
the incidence of infection.
Dialysis. Increasing deterioration of clinical and biochemical status necessitates institution of dialysis.
In most cases peritoneal dialysis is the procedure of choice in view of its simplicity and easy availability.
The need for dialysis should be anticipated. The procedure must be not delayed till the child becomes
critically ill. Early dialysis is particularly indicated in the patients with hemolytic uremic syndrome,
infections and extensive trauma.
The usual guidelines indicating the need for dialysis include: 1) blood urea level of over 250 mg/dL or
rapidly rising values; 2) serum potassium higher then 7 mEq/L; 3) serum bicarbonate below 10 mEq/L; 4)
overhydration with cardiac embarrassment; 5) sensorial changes or rapid deterioration of neurological
status. The decision to dialyze is seldom based on any one criterion, but on careful evaluation of all
clinical and biochemical data.
Outcome. Acute renal failure still carries a very high mortality, particularly in infants. It is chiefly related
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to the underlying etiologic condition and the duration of renal failure, which increases chances of
infection. Septicemia, hemolytic uremic syndrome and glomerulonephritis with prolonged anuria are
usually associated with a poor prognosis. The outlook is satisfactory in cases of acute tubular necrosis
without complicating factors.
Continuous arteriovenous hemofiltration (CAVH). It is an extracorporeal method for the management
of hypervolemia and electrolyte disorders in patients with oliguria. CAVH has been reported to be
especially useful for critically ill patients having undergone major surgery and multiorganic failure, who
are he-modynamically unstable and where peritoneal dialysis cannot be performed.