ACUTE RENAL FAILURE Definition :a rapid decline in renal function .with an increase in serum creatinine level ( a relative increase of 50 % or an absolute increase of 0.5 to 1.0 mg /dl ). *ARF may be oliguric ,anuric ,or nonoliguric .Severe ARF may occur without a reduction in urine output ( nonoliguric ARF ). Wt. gain and edema are the most common clinical findings in patients with ARF.This is due to a positive water and sodium balance.
*Characterized by azotemia (elevated BUN and Cr ) A.Elevated BUN is also seen with catabolic drugs (e.g. steroids ) ,GI / soft tissue bleeding , and dietary protein intake . B.Elevated Cr is also seen with increased muscle breakdown and various drugs.The baseline Cr levelvaries propotionately with muscle mass
Cirrhosis , hepatorenal syndrome. _In patients with decreased renal perfusion ,NSAIDs ,ACE inhibitors ,and cyclosporin can precipitate prerenal failure . PATHOPHYSIOLOGY Renal blood flow decreases enough to lower the GFR which leads to decreased clearance of metabolites (BUN ,Cr ,uremic toxin ). Because the renal parenchyma is undamaged ,tubular function ( and therefore the concentrating ability )is preserved.Therefore the kidney responds apprpopriately ,conserving as much sodium and water as possible. This form of ARF is reversible on restoration of blood flow ,but if hypoperfusion persists , ischemia results and can lead to acute tubular necrosis (ATN )
LABORATORY FINDINGS *Oliguria –always found in prerenal failure ( this is to preserve volume ) . *Increased BUN to serum Cr ratio (>20 :1 is the classic ratio ) – because kidney can absorb urea. *Increased urine osmolality ( >500 mOsm/kg H2O )- because the kidney is also able to reabsorb water. *Decreased urine Na (<20 mEq /L FENa <1% ) because the Na is avidly reabsorbed . *Increased urine / plasma Cr ratio (>40 :1 ) – because much of the filtrate is reabsorbed ( but not the creatinine ) * Bland urine sediment .
INTRINSIC RENAL FAILURE A.Kidney tissue is damaged such that the glomerular filtration and tubular function are significantly impaired.The kidneys are unable to concentrate urine effectively.
CAUSES 1.Tubular disease (ATN ) –can be caused by ischemia ( most common cause ) ,nephrotoxins. 2.Glomerular disease( acute glomerulonephritis GN )- e.g. Goodpastuer s syndrome ,Wegener s granulomatosis , poststreptococcal GN, lupus . 3.Vasculardisease – e.g. renal artery occlusion ,TTP ,HUS . 4.Interstitial disease –e.g. allergic interstitial nephritis ,often due to a hypersensitivity reaction to medications
LABORATORY FINDINGS • *Decreased BUN – to serum Cr ratio (<20 :1 )in comparison with prerenal failure.Both BUN and Cr levels are still elevated , but less urea is reabsorbed than in prerenal failure. • *Increased urine Na (>40 mEq /Lwith FENa >2% to 3% ) – because Na is poorly reabsorbed • *Decreased urine osmolality ( <350 mosm /kg H2O) – because renal water reabsorption is impaired. • *Decreased urine – plasma Cr ratio ( <20 :2 ) – because filtrate can not be reabsorbed
POST RENAL FAILURE A.Least common cause of ARF. B.Obstruction of urinary tract with intact kidney ) causes increased tubular pressure ( urine produced can not be excreted ) , which leads to decreased GFR . Blood supply and renal parenchyma are intact . C.Renal function is restored if obstruction is relieved before the kidneys are damaged . D.Postrenal obstruction , if untreated ,can lead to ATN .
CAUSES *Urethral obstruction secondary to enlarged prostate (BPH ) is the most common cause . • Obstruction of the solitary kidney. *Nephrolithiasis *Obstructing neoplasm ( prostate , cervix , bladder ) *Retroperitoneal fibrosis. * Ureteral obstruction is an uncommon cause because the obstruction must be bilateral to cause renal failure .
CAUSES OF ATN *ISCHEMIC ARF -Secondary to severe decline in renal blood flow as in shock , hemorrhage , sepsis ,DIC ,heart failure. _Ischemia results in death of tubular cells. *NEPHROTOXICARF _Injury secondary to substances that directly injure renal parenchyma and result in cell death . _Causes include antibiotics ( aminoglycosides ) ,radiocontrast agents , NSAIDs( especially in the setting of CHF .), poisons myoglobinuria ( from muscle damage ,rhabdomyolysis , sternuous exercise ) , hemoglobinuria 9 from hemolysis ), chemothreapeutic drugs (cisplatin ) , and kappa and gamma chains produced in multiple myeloma .
COURSE OF ATN * Onset (insult ) *OLIGURIC PHASE -Azotemia and uremia – average length 10 to 14 days -urine output <400 -500 ml/day *DIURETIC PHASE -Begins when urine output is > 500 ml /day *High urine output due to the following : fluid overload ( excretion of retained salt , water ,other solutes that were retained during the oliguric phase ) ,osmotic diuresis due to retained solutes during the oliguric phase ; tubular cell damage ( delayed recovery of epithelial cell function relative to GFR B) *RECOVERY PHASE :recovery of tubular function .
DIAGNOSIS • 1.BLOOD TESTS • A.Elevation in BUN and Cr levels • B.Electrolytes (K ,Ca ,PO4 ), albumin levels , CBC with differential. • 2.URINALYSIS • a.A dipstick test positive for protein ( 3+ ,4+ )suggests intrinsic renal failure due to glomerular insult. • B.Microscopic examination of the urine sediment is very helpful. • *Hyaline casts are devoid of contents ( in prerenal failure ) • RBC casts indicate glomerular disease. • * WBC casts indicate renal parenchymal inflammation. • *Fatty casts indicate nephrotic syndrome
3.URINE CHEMISTRY – to distinguish between different forms of ARF . A. Urine Na , Cr , and osmolality : Urine Na depends on dietary intake. B.FENa : collect urine and plasma electrolytes simultaneously . Values below <1% suggests prerenal failure. *Values above >2% to 3% suggest ATN . * FENais most useful if oilguria is present . 4.Urine culture and sensitivity –if infection is suspected .
5.RENAL ULTRASOUND *Useful for evaluating kidney size and for excluding urinary tract obstruction ( i.e postrenal failure ) –presence of bilateral hydronephrosis or hydroureter. *Order for most patients with ARF – unless the cause of the ARF is obvious and is not postrenal. 6.CT scan ( abdomen and pelvis ) -may be helpful in some cases ; usully done if renal ultrasound shows an abnormality such as hydronephrosis. 7.Renal biopsy – useful occasionally if there is suspicion of acute GN or acute allergic interstitial nephritis. 8.Renal arteriography – to evaluate for possible renal artery occlusion ; should be performed only if specific therapy will make a difference.
COMPLICATIONS • 1.ECF volume expansion and resulting pulmonary edema – treat with diuretic (furosemide ).If there is no response within 2 hours , consider dialysis. • 2.Metabolic • A.Hyperkalemia – due to decreased excretion of K and the movement of potassium from the ICF to ECF due to tissue destruction and acidosis. • B Metabolic acidosis ( with increased anion gap )- due to decreased excretion of hydrogen ions; if severe ( below 16 mEq /L) ,correct with sodium bicarbonate. • C.Hypocalcemia –loss of ability to form active Vit. D and rapid development of PTH resistance.
d.Hyponatremia may occur if water intake is greater than body losses , or if a volume depleted patient consumes excessive hypotonic solutions. (hypernatremia may also be seen in hypovolemic states ) E.Hyperphosphatemia . F.Hyperuricemia 3.Uremia –Toxic end products of metabolism accumulate( especially from protein metabolism ) 4.Infection *Acommon and serious complication of ARF ( occurs in 50% to 60 % of cases ). The cause is probably multifactorial , but uremia itself is thought to impair immune functions . *Exampls include pneumonia , UTI ,wound infection ,and sepsis .
TREATMENT 1.General measures A.Avoid medications that decrease renal blood flow( NSAIDs) and /or that are nephrotoxic (e.g. aminoglycosides , radiocontrast agents ) B.Adjust the medication dosages for the level of the renal function . C.Correct fluid imbalance *If the patient is volume depleted . , give IV fluids .However, many patients with ARF are volume overloaded ( especially if they are oliguric or anuric ) , so diuresis may be necessary. *The goal is to strike a balance beteween correcting volume deficits and avoiding volume overload ( while maintaining adequate urine output )
*Monitor fluid balance by daily weight measurements ( most accurate estimate ) and fluid –output records. D.Correct electrolytes disturbances if present. E.Optimize cardiac output. BP should be approximately 120 to 140 /80 to 90. F.Order dialysis if symptomatic uremia ,intractable acidemia , hyperkalemia , or volume overload develop.
2.Prerenal failure A.Treat the underlying disorder. B.Give NS to maintain euvolemia and restore BP- do not give patients with edema or ascites. Stopping antihypertensive medications may be necessary. C.Eliminate any offending agents ( ACE inhibitors ,NSAIDs ). D.If the patient is unstable , Swan –Ganz monitoring is indicated for accurate assessment of intravascular volume.
3.Intrinsic A.Once ATN develops , therapy is supportive.Eliminate the cause /offending agents. B.If the patient is oliguric , a trial of furesomide may help to increase urine output.This improves fluid balance. 4.Postrenal – A bladder catheter may be inserted to decompress the urinary tract. Consider urology consultation.