Acute renal injury Flashcards
ARF Definition
ACUTE RENAL FAILURE:
DEFINITION: rapid reduction in renal function, reduction of GFR, resulting in the retention of nitrogen waste products such as urea, creatinine and other uremic toxins.
RENAL NORMOFUNZIONE
Sudden increase in creatinine values above 2 mg/dl
REDUCED RENAL FUNCTION
Sudden increase in creatinine by at least 50% of the existing value
ACUTE RENAL insufficiency: CLASSIFICATION
ACUTE RENAL insufficiency: CLASSIFICATION
PRE-RENAL ARI (FUNCTIONAL)
RENAL ARI (ORGANIC)
POSTRENAL ARI (OBSTRUCTIVE)
CAUSES OF PRERENAL KIDNEY FAILURE
ACUTE (IRA) OR FUNCTIONAL
CAUSES OF KIDNEY FAILURE
PRERENAL ACUTE (IRA) OR FUNCTIONAL
1. Hypovolemia
2. Reduced cardiac output
3. systemic hemodynamic Causes
4. renal hemodynamic Causes
FUNCTIONAL ARI
description
FUNCTIONAL ARI - prerenal ARI is due to a reduction in renal perfusion, either in terms of renal arthery blood flow and/or renal perfusion pressure or due to intrarenal ischemia.
• Falls within the physiological response to the reduction of Renal perfusion, whose purpose is the defense of blood volume to prevent a severe systemic hypoperfusion.
- The first effect of this answer is the increase aproximal and distal tubular reabsorption for direct and indirect mechanisms (neuroumorali systems: AII, SNS, ET-1, etc.)
- The decreased F.G. (ARI) appears when the reduction renal blood flow. It is serious and is determined by a further activation of neurohumoral vasoconstrictive systems and/or inadequate response vasodilatanti systems
Organic acute renal insufficiency classification and incidence
tubular (85%) (ischemic - 50%, toxic - 35%)
interstitial(10%)
glomerular(5%)
Organic acute renal insufficiency causes
CAUSE DELL’IRA ORGANICA (O RENALE)
Acute tubular necrosis
acute interstitial nefritis
glomerular cuases
vascular causes
TUBULOGLOMERULARE FEEDBACK (TGF)
TUBULOGLOMERULARE FEEDBACK (TGF)
- defense mechanism against volume depletion
- always active (stimulus: [NaCl] at the Macula Densa)
- the sensitivity depends [AII] intrarenale
- effect: afferent arteriole tone adjustment (GFR)
ARI FROM AMINOGLYCOSIDES
incidence, pathogenesis
ARI FROM AMINOGLYCOSIDES
INCIDENCE: 4-10% of IRA forms
PATHOGENESIS:
Accumulation in proximal tubular cells with interference of Lysosomal activity; insensitivity of the collector to ADH
ARI from aminoglycosides
CLINIC, LABORATORY
ARI from aminoglycosides
CLINIC:
Delayed onset (1 week) and prolonged even
after discontinuation of the drug
Non-oliguric ARI
LABORATORY:
Alterations not features, lower incidence of
Hydro electrolytic abnormalities (diuresis preserved)
ARI from aminoglycosides. risk factors.
- *IDENTIFICATION AND CORRECTION OF RISK FACTORS**
- *drug-related:**
- dose
- previous therapy of aminoglycosides
- type of drug
- therapies associated: diuretics, nsaids, cyclosporine, etc.
patient-related:
• Advanced age
• Renal and / or
pre-existing liver
• Dehydration
Interstitial nephritis
indications, patogenesis
interstitial nephritis
IMPLICATIONS: 10% of the forms of IRA
pathogenesis:
• Hypersensitivity to drugs, infection, inflammation
immunomediated
Interstitial nephritis. clinic, laboratory
CLINIC:
• Rapid onset
• Low back pain (sometimes)
• Hypertension, fever, skin rash
LABORATORY:
• Increased IgE, eosinophilia (sometimes)
• modest Proteinuria, hematuria, leucocyturia,
eosinofiluria (sometimes)
CAUSES OF THE OBSTRUCTIVE (POST-RENAL) ARI
1. Intrarenal obstruction (Tubular)
crystals, from proteins
2. Obstruction extrarenal
ureteral, bladder, urethral
Clinical symptoms of ARI
Clinical symptoms of ARI
- Alterations of spare hydrosaline
- Hyperkalaemia (acidosis, hypercatabolism)
- Hyponatremia (iatrogenic) - Changes in the calcium-phosphorus balance
- Hypocalcemia and hyperphosphatemia (same mechanisms
IRC, but less severe for the shorter duration) - Metabolic acidosis
- hypercatabolism
- anemia normochromic normocytic
- Hyperuricemia
- Alterations coagulation
Acute or chronic renal injury?
DIAGNOSTIC APPROACH TO ‘IRA
Renal ultrasonography
Previous value of creatinine: acute normal, chronic high
haemoglobin: acute normal, chronic reduced.
DIagnostic approach to acute renal injury
IRA PRE-RENAL no edema, decreased arterial pressure and duresis
IRA ORGANIC yes/no oedema, variable a.pressure and duresis
IRA OBSTRUCTIVE yes edema, increased a.pressure, decreased diuresis
Diagnosis of ARI history
Volume Intravascular
hypovolemia (bleeding, loss GI, renal losses, skin losses)
redistribution of the volume: (peritonitis, ascties, pancreatites)
• Heart deficit
- Heart attack, heart failure, valvular heart disease, pericarditis, arrhythmias
- Vasodilatation (sepsis, drugs, anaphylaxis)
DIAGNOSIS OF prerenal ARI
PHYSICAL EXAMINATION
•body weight
•diuresis
• dry skin, inelastic
• Hypotension
(Normotension or in the absence of drugs if the
patient was previously hypertensive)
• Tachycardia
DIAGNOSIS OF OBSTRUCTIVE ARI.
HISTORY
• Anuria total
• Fluctuations in the urine volume
• Previous chronic urinary pathologies
• Nocturia
• urination difficult
• Inflammation urinary
• Conditions predisposing the papillary necrosis:
- Diabetes, sickle cell anemia, abuse
analgesics
Diagnosis of obstructive ARI. physical examination.
Diagnosis of obstructive ARI.
physical examination.
• Globe bladder
• Back Pain
• Mass palpable, painful abdominal
• General not compromise
Resolving organic ARI
RESOLUTION OF THE ORGANIC ARI (NTA)
Correction
hypovolemia
Dissolution of
necrotic debris
Regeneration
tubular epithelium
Restoring
Tubular flow
Resuming
diuresis
organic ARI prognosis.
PATIENTS WITH IRA
MORTALITY - 60%
Survival - 40%
Remission
Full
65%
Remission
Partial
30%
None
Remission
5%
COMPLICATIONS OF ARI
Responsible for the high mortality in the course of ARI:
- Infectious (50%)
- Cardiovascular
• acute pulmonary edema,
• congestive(stazinis) heart failure
• aritmie
- Gastrointestinal
• anorexia nausea, vomiting,
• bleeding
Therapy of acute renal failure. prerenal.
symptoms -> treatment
IRA PRE-RENAL
• Vomiting
• Diarrhea
• Sweating
• Drains GI
then inject physiological solution
• Hemorrhage
INFUSIONS OF
BLOOD
- Burns
- Cirrhosis
- Cachexia
then human albumin
• Diarrhea
• Acidosis
then NaHCO3
catabolism then
Glucose
AMINO
LIPIDS
(+ NaCl)
