I-Pathophysiology:
*Prerenal ARF:
Causes: "effective" hypovolemia
Normal compensatory mechanisms at kidney:
-the reduction in perfusion pressure → stretch receptors in afferent arterioles trigger afferent arteriolar vasodilatation through a local myogenic reflex: autoregulation
-Angiotensin II: increase biosynthesis of vasodilator prostaglandins →afferent arteriolar vasodilation, induce constriction of efferent arterioles.
=> Risk: 1.the elderly and patients with diseases that affect the integrity of afferent arterioles (e.g., hypertensive nephrosclerosis, diabetic vasculopathy and other forms of occlusive (including atherosclerotic) renovascular disease)
2. Drugs: NSAIDs, ACE inhibitors, ARBs
*Intrinsic ARF:
Causes: ischemic or nephrotoxic tubular injury, tubulointerstitial diseases, diseases of the renal microcirculation and glomeruli, and diseases of larger renal vessels.
Ischemic ATN (acute tubular necrosis):four phases: is typically characterized initiation, extension, maintenance, and recovery.
Nephrotoxic ATN:
-Radiocontrast agents, cyclosporine →intrarenal vasoconstriction
-Antibiotics (aminoglycoside antibiotics) and anticancer drugs →direct toxicity to the tubular epithelial cells and/or intratubular obstruction
-Endogenous nephrotoxins (calcium, myoglobin, hemoglobin, urate, oxalate, and myeloma light chains): calcium →intrarenal vasoconstriction
myoglobin, hemoglobin →intrarenal vasoconstriction,
injury to tubular epithelial cells
myeloma light chains →directly toxic to tubule epithelial cells
hyperuricosuria or hyperoxaluria → Intratubular obstruction
Allergic interstitial nephritis: antibiotics (e.g., penicillins, cephalosporins, quinolones, sulfonamides, rifampin) and NSAIDs
*Postrenal ARF:
Causes: Urinary tract obstruction
II- Clinical features and differential diagnosis:
1.The first step in evaluating a patient with renal failure is to determine if the disease is acute or chronic.
-review of laboratory records: demonstrates that the rise in blood urea nitrogen and creatinine is recent →suggests ARF
-if not, findings that suggest chronic kidney disease (anemia, evidence of renal osteodystrophy (radiologic or laboratory), and small scarred kidneys)
2.A diagnosis of ARF →determine the etiology of ARF
3.The prevention and management of complications should be instituted
*Urinalysis:
-In prerenal ARF: the sediment is characteristically acellular and contains transparent hyaline casts
-Postrenal ARF: an inactive sediment, hematuria, pyuria
-Intrinsic ARF:
Pigmented "muddy brown" granular casts and casts containing tubule epithelial cells in association with mild "tubular" proteinuria (<1 g/d): suggest ATN.
Red blood cell casts: indicate glomerular injury
White cell casts and nonpigmented granular casts: suggest interstitial nephritis
Abundant uric acid crystals :suggest acute urate nephropathy
*The fractional excretion of sodium (FENa)
-Prerenal ARF: FENa <1.0%
-The FENa in ischemic or nephrotoxic intrinsic renal ARF: higher
III-Treatment:
-Prevention: paramount importance
-Special therapies:
Prerenal ARF: correction of the primary hemodynamic abnormality
Postrenal ARF: relief of obstruction
ATN: no specific therapies
-Prevention and treatment of complcations