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ARF complicates approximately 5% of hospital admissions and up to 30% of admissions to ICU Oliguria (urine output 400 mL/d) is a frequent but not invariable clinical feature (50%) Asymptomatic, diagnosed blood urea and creatinine concentrations Most ARF reversible
ARF may complicate a wide range of diseases, which for purposes of diagnosis and management are conveniently divided into: (1) Prerenal ARF, prerenal azotemia) (55%) cause renal hypoperfusion without compromising the integrity of renal parenchyma (2) Intrinsic renal ARF, renal azotemia (40%) directly involve renal parenchyma (3) Postrenal ARF, postrenal azotemia (5%) associated with urinary tract obstruction
Penelitian
de Medonca et (2000)7, Tepel et al (2000) 9 Brivet et al (1996) 10
Definisi
al SCr 0,5 mg/dl in 24 hours
Agrawal (2000) 1
and
SCr > 2.0 mg/dl = (ARF) SCr >3.5 mg/dl and/or BUN > 100 mg/dl (Severe ARF) Swartz SCr > 0,5 mg/dl/day with UO < 400 ml/day (complete renal shutdown)
SCr between 1,5 10 mg/dl UO between 0-900 cc/day GFR >50 % with UO (hours to days)
Most common form of ARF Represents a physiologic response to mild to moderate renal hypoperfusion Prerenal ARF reversible upon restoration of renal blood flow and glomerular ultrafiltration pressure Renal parenchymal tissue is not damaged
More severe hypoperfusion ischemic injury of renal parenchyma intrinsic renal ARF Can complicate any disease that induces hypovolemia, low cardiac output, systemic vasodilatation, or selective intrarenal vasoconstriction
Hypovolemia systemic MAP activated baroreceptors trigger a coordinated series of neural and humoral responses designed to restore blood volume and arterial pressure: Activation of the sympathetic nervous system Activation of renin-angiotensinaldosterone system Release of arginine vasopressin (AVP; formerly called antidiuretic hormone)
Norepinephrine, angiotensin II, and AVP act in concert preserve cardiac and cerebral perfusion by stimulating vasoconstriction inhibiting salt loss through sweat glands stimulating thirst and salt appetite promoting renal salt and water retention
Glomerular perfusion, ultrafiltration pressure, and filtration rate are preserved during mild hypoperfusion through several compensatory mechanisms Stretch receptors in afferent arterioles trigger afferent arteriolar vasodilatation through a local myogenic reflex (autoregulation)
Biosynthesis of vasodilator prostaglandins (prostaglandin E2 and prostacyclin) dilation of afferent arterioles Angiotensin II induces constriction of efferent arterioles intraglomerular pressure is maintained the fraction of plasma flowing through glomerular capillaries that is filtered (filtration fraction) GFR is preserved
More severe hypoperfusion compensatory responses are overwhelmed GFR Prerenal ARF
NSAIDs do not compromise GFR in healthy individuals but may precipitate prerenal ARF in patients with volume depletion or in those with chronic renal insufficiency in whom GFR is maintained through prostaglandin-mediated hyperfiltration by the remaining functional nephrons
Angiotensin II preserves glomerular filtration pressure distal to stenoses by elevating systemic arterial pressure triggering selective constriction of efferent arterioles ACE inhibitors blunt these responses and precipitate ARF (usually reversible)
Causes: (1) diseases of larger renal vessels, (2) diseases of the renal microcirculation and glomeruli (3) ischemic and nephrotoxic ARF (4) tubulointerstitial inflammation
Most intrinsic renal ARF is triggered by 1. Ischemia (ischemic ARF) 2. Nephrotoxins (nephrotoxic ARF)
Patients undergoing Major cardiovascular surgery Suffering severe trauma Hemorrhage Sepsis Volume depletion
Hypoperfusion ischemic injury to renal parenchymal cells, particularly tubular epithelium bilateral renal cortical necrosis irreversible renal failure
Hours to days The initial period of renal hypoperfusion during which ischemic injury is evolving GFR declines because (1) glomerular ultrafiltration pressure as a consequence of renal blood flow (2) the flow of glomerular filtrate within tubules is obstructed by casts comprised of epithelial cells and necrotic debris derived from ischemic tubule epithelium (3) there is backleak of glomerular filtrate through injured tubular epithelium
1 2 weeks renal cell injury is established GFR stabilizes at its nadir (typically 5 to 10 mL/min) urine output is lowest uremic complications arise persistent intrarenal vasoconstriction medullary ischemia triggered by dysregulated release of vasoactive mediators from injured endothelial cells congestion of medullary blood vessels reperfusion injury
Renal parenchymal cell, particularly tubule epithelial cell, repair and regeneration and a gradual return of GFR to or towards premorbid levels
Intrarenal vasoconstriction: Radiocontrast agents (contrast nephropathy) Cyclosporine Tacrolimus (FK506) acute fall in renal blood flow and GFR a relatively benign urine sediment a low fractional excretion of sodium
Direct toxicity to tubule epithelial cells and/or intratubular obstruction are major pathophysiologic events in ARF induced by: Antibiotics + antivirus Anticancer drugs - Acyclovir - Cisplatin - Foscarnet - Carboplatin - Aminoglycosides - Ifosfamide - Amphotericin B - Pentamidine
Amphotericin B dose-related ARF intrarenal vasoconstriction and direct toxicity to proximal tubule epithelium Cisplatin and carboplatin accumulated by proximal tubule cells provoke ARF after 7 to 10 days of exposure by:
Inducing mitochondrial injury Inhibition of ATPase activity Free radicalmediated injury to cell membranes Apoptosis Necrosis
Endogenous nephrotoxins: Calcium intrarenal vasoconstriction Myoglobin Hemoglobin Urate Oxalate Myeloma light chains
Urinary tract obstruction <5% of ARF one kidney has sufficient clearance capacity to excrete the nitrogenous waste products generated daily
bladder neck Bilateral ureteric obstruction Unilateral ureteric obstruction in a patient with one functioning kidney or with preexisting chronic renal insufficiency
Less common causes of acute lower urinary tract obstruction: Blood clots Calculi Urethritis with spasm
external compression
Early stages of obstruction (hours to days) Continued glomerular filtration increased intraluminal pressure upstream to the site of obstruction gradual distention of the proximal ureter, renal pelvis, and calyces a fall in GFR