Acute renal failure (ARF)
Definition
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is a clinical syndrome in which a sudden deterioration in renal function results
in the inability of the kidneys to maintain fluid and electrolyte homeostasis.
Etiological classification
Prerenal ARF,, is characterized by diminished effective circulating arterial
volume,Common causes of prerenal ARF include
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dehydration,
sepsis,
hemorrhage,
severe hypoalbuminemia, and
cardiac failure.
Intrinsic renal ARF includes a variety of disorders characterized by renal
parenchymal damage, Causes includes:
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sustained hypoperfusion and ischemia.
glomerulonephritis,
Hemolytic-uremic syndrome (HUS)
Acute tubular necrosis (ATN) nephrotoxic and/or perfusion insults.
Tumor lysis syndrome spontaneous or chemotherapy-induced cell lysis in
patients with lymphoproliferative malignancies. This disorder is primarily
caused by obstruction of the tubules by uric acid crystals
Acute interstitial nephritis hypersensitivity reaction to a therapeutic agent or
various infectious agents
Postrenal ARF
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includes a variety of disorders characterized by obstruction of the urinary tract.
Relief of the obstruction usually results in recovery of renal function except in
patients with associated renal dysplasia or prolonged urinary tract obstruction.
Clinical evaluation
History
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Age
History of vomiting and diarrhea ,haemorrage ,CHF, protracted hypotension
,sepsis (prerenal ARF).
a recent pharyngitis , periorbital edema, hypertension, and gross hematuria
(GN).
nephrotoxic medications most likely has ATN.
lymphoproliferative malignancies,chemotherapy (TLS).
bloody diarrhea ,haematuria (HUS).
A neonate with a history of hydronephrosis on prenatal ultrasound (post renal).
Examination
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Volume status. ( Peripheral edema, rales, and a cardiac gallop suggest volume
overload and the).
Poor peripheral perfusion suggest inadequate circulating volume and the
possibility of prerenal ARF
The presence of a rash and arthritis might suggest systemic lupus
erythematosus (SLE) or Henoch-Schonlein purpura nephritis.
Palpable flank masses might suggest renal vein thrombosis, tumors, cystic
disease, or urinary tract obstruction.
Investigations
Blood
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Anemia (the anemia is usually dilutional or hemolytic, as in SLE, renal vein
thrombosis, HUS);
Leukopenia (SLE, sepsis);
Thrombocytopenia (SLE, renal vein thrombosis, sepsis, HUS);
Urea , creatnine
Serum electrolytes
ABG
BUN/cr(more than 20 suggest prerenal dis)
Urine
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hematuria, proteinuria, and red blood cell or granular urinary casts (glomerular
disease)
The presence of white blood cells and white blood cell casts, with low-grade
hematuria and proteinuria, Urinary eosinophils (tubulointerstitial disease).
Fractional excretion of sodium (FENa) <1% , most likely have prerenal ARF.
Image
Abdominal USS (role out renal anomalies, obstruction)
Biopsy
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Clinical evidence of glomerular injury (nephritic ,nephrotic)
Susception of inherited cause
Not detected cause by other investigations
Suggested algorism for ARF diagnosis
Suspect
ARF if
Clinical evidence predispose for ARF(review the aetiology)
Oliguria,anuria ,volume over load
Confirm with elevated
BUN , CR
Review history
,examination and
ivestigations
Role out post renal
failure by image
Urological referal
Unclear etiology
detected
Clear etiological
diagnosis for prrenal
insult or intrinsic renal
failure
Follow up to
detect the
aetiology as
possible
Management of ARF
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Spefic ttt
Fluid resus
Immunosuppssive ,etc
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Fluid mamagemnt
Ttt of hyperkalemia and other electrolytes
disturbance
Ttt of acid bace disturbance
Hypertension
Anemia, neurological manifestations
Dialysis
(see later)
Fluid management
Determine volume status and exclude volume
overload or cardiac failure (best determined by
CVP , or examination of neck veins)
Fluid resuscitation 20ml/kg up to 60ml/kg ,
isotonic saline , over 30 min
Adequate prepherial perfusion
Adequate prepherial perfusion
In adequate perfusion
Adequate urine out put
no urine out put (after 6oml/kg)
No urine out put
Diuretic challenge +
dopamine infusion
No urine out put
After exclusion of
causes of obstructive
shock
Diuretic challenge
Frusimide (1mg/kg/dose) ,
can be repeated twice at 30
min intervals ,then the dose
can be increased up to
4mg/kg/dose and if in
effective continous infusion
in
conjunction
with
dopamine (0.05mg/kg/h)
Consider aggressive
fluid resuscitation and
inotropes +
norepinephreine
Consider intrinsic or
obstructive renal failure
Restrict fluid (30 ml/kg/d)
Montoir (dialy)
Or
Fluid balance
400ml/m2/d
Body weight
+
Serum chemistries
Uop & GIT loss (omitted if
sever hypervolemiea)
Hyperkalemia
(serum potassium level >6 mEq/L)
Risk
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cardiac arrhythmia,
cardiac arrest, and death.
ECG changes
The earliest electrocardiographic change seen in patients with developing
hyperkalemia is the appearance of peaked T waves. This may be followed by
widening of the QRS intervals, ST segment depression, ventricular arrhythmias, and
cardiac arrest
Measurements
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Exogenous sources of potassium (dietary, intravenous fluids, total parenteral
nutrition) should be eliminated.
More-severe elevations in serum potassium (>7 mEq/L), especially if
accompanied by electrocardiographic changes, require emergency measures .
Calcium gluconate 10% solution, 1.0 mL/kg IV, over 3-5 min
Sodium bicarbonate, 1-2 mEq/kg IV, over 5-10 min
Regular insulin, 0.1 U/kg, with glucose 50% solution, 1 mL/kg, over 1 hr
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If above measures failed dialysis is indicated
Metabolic acidosis
Indications for correction
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arterial pH < 7.15;
serum bicarbonate < 8 mEq/L
contributes to hyperkalemia.
Correction
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corrected partially by the intravenous route, generally giving enough bicarbonate to
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raise the arterial pH to 7.20 (which approximates a serum bicarbonate level of 12
mEq/L).
Correction of metabolic acidosis with intravenous bicarbonate can precipitate tetany
in patients with renal failure as rapid correction of acidosis reduces the ionized
calcium concentration.
Hypocalcemia
Risk
Tetany
Correction
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Primarily treated by lowering the serum phosphorus level..
Patients should be instructed to follow a low-phosphorus diet, and phosphate
binders should be orally administered to bind any ingested phosphate and
increase GI phosphate excretion.
Common agents include sevelamer (Renagel), calcium carbonate (calcimate),
and calcium acetate (PhosLo). Aluminum-based binders, commonly employed
in the past, should be avoided because of the established risk of aluminum
toxicity.
Caution
Calcium should not be given intravenously, except in cases of tetany, to avoid
deposition of calcium salts into tissues
Hyponatremia
Risk
Neurological manifestations
Correction
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Corrected by fluid restriction rather than sodium chloride administration.
Administration of hypertonic (3%) saline should be limited to patients with
symptomatic hyponatremia (seizures, lethargy) or those with a serum sodium
level <120 mEq/L.
Acute correction of the serum sodium to 125 mEq/L (mmol/L) should
beaccomplished using the following formula:
Hypertension
See chapter of hypertension
Neurologic symptoms
Include
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headache,
seizures,
Lethargy and confusion (encephalopathy).
Etiology
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hyponatremia,
hypocalcemia,
hypertension,
cerebral hemorrhage,
cerebral vasculitis, and the
uremic state.
Measures
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Diazepam is the most effective agent in controlling seizures,
therapy should be directed toward the precipitating cause.
Anemia
Etiology
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Diultional
Active bleeding (HUS)
Indications for transfusion
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hemoglobin level falls below 7 g/dL.
Transfusion rules
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Itransfusion with packed red blood cells (10 mL/kg) diminishes the risk of
hypervolemia.
The use of fresh washed red blood cells minimizes the risk of hyperkalemia.
In the presence of severe hypervolemia or hyperkalemia, blood transfusions are most
safely administered during dialysis or ultrafiltration.
Dialysis
Indications for dialysis in ARF include the following:
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Volume overload with evidence of hypertension and/or pulmonary edema
refractory to diuretic therapy
Persistent hyperkalemia (7meq/l or above)
Severe metabolic acidosis unresponsive to medical management
Neurologic symptoms (altered mental status, seizures)
Blood urea nitrogen >100-150 mg/dL (or lower if rapidly rising)
Calcium:phosphorus imbalance, with hypocalcemic tetany
Follow up
Clinical follow up (for dialysis indications or improvement)
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Conscious level ( q/6hrs)
Convulsion (all time)
Chest auscultation
Liver palpation
Blood pressure ( q/4hrs)
Capillary refill ( q/6hrs)
Hydration state (dialy)
Urine out put(dialy)
Fluid input(dialy)
Bleeding (all time)
Lab. Follow up (for dialysis indications or improvement)
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ABG (dialy)
Urea , creat (dialy)
Serum electrolytes (dialy)
Hb (q72hrs)