Acute renal failure is defined by a rapid decrease (hours to 1-2 weeks) of renal function, constituting an electrolyte imbalance and acid-base brutal.
classically There are 3 major groups of acute renal failure (ARF), as the mechanism involved in the infringement:
– Functional or Prerenal IRA;
– Renal IRA (or organic);
– Obstructive or post-renal ARF.
Symptoms specific to renal insufficiency are nonspecific (nausea, asthenia, etc.), And it is often the underlying disease which perform laboratory tests.
The diagnosis of ARF is focused on the standard biology before an elevated creatinine.
The degree of renal impairment is then evaluated according to sex, age and weight (Cockroft formula: CI = (140 – age) x weight (kg) × K / creatinine (mmol / L) with K = 1.04 in women and 1.23 in men). Sometimes the acute nature is difficult to assert before an asymptomatic patient and without previous data creatinine. The presence of normal kidney size (in the absence of diabetes, amyloidosis and multiple myeloma) on an iconographic data (ASP / ultrasound) is necessary (ASP: abdomen without preparation).
The ARI management requires first search prerenal etiology (functional IRA) or post-renal (obstruction) before rolling the etiologies “organic”, and undertake at the same time the rapid correction of disorders hydroelectrolytic threatening.
Most often achieve is reversible if one tries to treat the cause.
This is the most common cause of acute impairment of kidney function in an ambulatory patient.
From a pathophysiological point of view, this is a decrease in the glomerular filtration by significant systemic hypotension and / or vasoconstriction of the afferent glomerular arterioles (decreased renal blood flow).
It is reversible upon restoration of hemodynamics.
Clinically, there is a trace anuria (urine output <20 ml / hr or <500 mL / d).
The context may be evocative: hypotension (hypovolemia, heart failure, severe sepsis), digestive salt and water losses, hepatorenal syndrome (decompensated liver cirrhosis), iatrogenic (NSAIDs [nonsteroidal anti-inflammatory] or IEC [inhibitor of the enzyme conversion] in a dehydrated or sick with bilateral renal artery stenosis).
Biology is often evocative.
The treatment is the cause of the effective hypovolemia (fluid resuscitation, treatment of a possible shock, cardiac specific treatments), associated with metabolic necessary corrections.
The evolution of renal disease has a good prognosis if the treatment was early and treatable aetiology (there are few effective treatment for hepatorenal syndrome, which remains poor prognosis).
IRA OR OBSTRUCTIVE postrenal:
From a pathophysiological point of view, this is obstruction of the urinary tract on an intrinsic or extrinsic obstacle. It can be a bilateral obstruction of both ureters (retroperitoneal fibrosis or pelvic tumor), unilateral (one functioning kidney: stones +++) or urinary retention. The lifting of the obstacle can recover kidney function.
Whatever the IRA mechanism, the immediate risk is related to the biological consequences associated with the loss of homeostasis: hyperkalemia (acidosis and hypercatabolism), hyponatremia (dilution), hypocalcemia (usually delayed), metabolic acidosis ( removing defect H + and reabsorption HCO3-), nitrogen retention (urea, creatinine, uric acid).
Clinically, we retain a total anuria (<5 mL / h), a brutal start in a painful context (neoplasia, renal colic, acute urinary retention, etc.).
Diagnosis is based on the systematic imaging to an IRA: ASP (calculations images rarely seen) and especially ultrasound (dilated pyélocalicielles cavities, gallstones, fibrosis, tumor).
Urgent treatment is based on the drainage of urine (percutaneous nephrostomy, double J stent or urinary catheter), with compensation resulting polyuria. The use of renal replacement therapy is rare except in cases of uncontrollable biological threat.
IRA RENAL OR ORGANIC:
The lesion interested reached the kidney itself.
The biology of the organic IRA is described in Table I.
Acute Tubular Necrosis:
It is the leading cause of organic IRA.
From a pathophysiological point of view, it is an acute or renal toxicity secondary to prolonged functional IRA, with persistent vasoconstriction of the efferent glomerular arterioles resulting in necrosis of tubular cells.
The extrarenal context is often high: shock, rhabdomyolysis (muscle injury, sustained arterial ischemia, viral disease, intense exercise), acute hemolysis [jaundice, hyperbilirubinemia, anemia, hemoglobinuria (pernicious malaria +++)] intoxication [paraquat (weedkiller), trichlorethylene, methanol, ethylene glycol, arsenic, mercury] or iatrogenic (aminoglycosides, NSAIDs, ACE inhibitors, chemotherapy, iodinated contrast agents).
Treatment is based on the rapid correction of shock and offsetting hydrosodées losses associated if persistent oligoanuria the high-dose furosemide (> 500 mg / d). The addition of low-dose dopamine (3 ìg / kg / min) can be discussed.
The renal replacement therapy is indicated in cases of hyperkalemia> 6.5 mmol / L (or ECG signs), major acidosis (pH <7.20), uremia> 50 mmol / L and / or serum creatinine> 700 ol / L.
The evolution is towards the progressive worsening often with important metabolic disorders (hyperkalemia sometimes critical, aggravated by acidosis and hyponatremia that exposes a convulsive risk).
The decline comes after control of the case, with resumption of diuresis after 4 weeks.
The outcome is often fatal (about 60% of cases), mainly related to the underlying cause. There is a definite risk renal failure when associated cortical necrosis (in the absence of recovery of diuresis after 6 weeks, kidney biopsy confirms the diagnosis).
The forms with preserved diuresis are seen more readily in iatrogenic IRA or when shocks quickly corrected: biological signs are often minimized and easier to correct, the rarely needed dialysis.
From a pathophysiological point of view, it will decrease the flow and glomerular filtration area and a disorder of glomerular permeability (proteinuria, hematuria).
Symptoms often preexist depending on the aetiology. Proteinuria is constant, the often high blood pressure.
The classification of these rapidly progressive glomerulonephritis is based on renal histology, the nature of circulating autoantibodies and systemic manifestations associated (extracapillary glomerulonephritis and anti-basement membrane antibodies glomerular of Goodpasture, and antineutrophil cytoplasmic antibody of Wegener, etc. ).
The classic endocapillary post-streptococcal acute glomerulonephritis usually carries an acute nephritic syndrome (edema, hypertension, proteinuria, hematuria, etc.).
Treatment is based on the etiology and data in renal biopsy.
The evolution is variable.
From a pathophysiological point of view, is the infiltration of the interstitial tissue, polynuclear, tumor cells or inflammatory mediators in case of allergy.
The interstitial infiltration may be related to an infectious disease (acute pyelonephritis, legionellosis, septicemia BGN [Gram-negative bacillus] or Staphylococcus aureus, leptospirosis, etc.), Immuno-allergic mechanism (beta-lactams, sulfonamides, NSAIDs, allopurinol etc.) or metabolic (hypercalcemia, hyperuricemia) or occur as part of a broader disease (sarcoidosis, Gougerotcsjrogren, lymphoma or hematologic malignancy).
Clinically, urine output is often preserved.
The treatment is the cause.
Evolution is usually healing. ESRD is rare.
It is rare.
From a pathophysiological point of view, it meets a sudden occlusion of the renal arteries or their branches, which occurs on vascular and atherosclerotic field or during endovascular maneuvers (illness cholesterol emboli).
Clinically, the onset is sudden, with abdominal or back pain. Often found hematuria and acute hypertension.
The diagnosis of renal artery occlusion is achieved using a CT angiography or arteriography. The disease of cholesterol embolism is suspected in a livedo lower back and lower limbs, purple toes and / or necrosis of the pulp.The fundus (OF) can find cholesterol emboli.
In children, thrombotic microangiopathy (hemolytic uremic syndrome [HUS] and thrombotic thrombocytopenic purpura [PTT]) are more frequent. It combines a trace anuric IRA quick installation, hemolytic anemia with schizocytosis, thrombocytopenia and often hypertension. The neurological signs and fever are common in the PTT.
The etiology of HUS often gastroenteritis E. coli serotype 0157: H7 secreting a verotoxin (VTEC), thrombotic microangiopathy but can occur in malignant néphroangiosclérose, preeclampsia, shigellosis (Shiga toxin) or HIV infection, hormonal therapy, immunosuppressants (tacrolimus, cyclosporine ), ticlopidine or some chemotherapy (mitomycin), as well as in the antiphospholipid syndrome.
Treatment consists of plasma exchange with fresh plasma transfusion.