Renal failure

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  1. Term applied to the impairment of glomerular filtration rate (GFR); GFR is estimated from the plasma creatinine concentration or the creatinine clearance and reflects the number of functioning nephrons
    1. normal GFR is 100 cc/min
    2. oliguria- urine output less than 0.5 mj/kg/h
    3. chronic renal failure patients may survive without symptoms with a GFR of 20 cc/min
  2. acute renal failure
    1. recent (<1 month) increase in plasma creatinine concentration of at least .5 mg/dL if the baseline plasma creatinine concentration is less than 3.0 or an increase of at least 1.0 mg/dL if the baseline plasma creatinine concentration is higher
    2. causes of acute renal failure: prerenal causes, glomerular disease (see red cells and proteinuria which is pathognomonic), vascular disease, tubulointerstitial disease (white cells and some red cells are highly suggestive of acute interstitial nephritis, granular casts with epithelial cells are very suggestive of acute tubular necrosis), urinary tract obstruction (usually normal uninalysis)
      1. distinction between ATN and prerenal disease – determining factor is the response to a fluid load – an improvement in renal function back to the baseline plasma creatinine concentration is considered diagnostic of prerenal disease while a continued elevation of plasma creatinine points toward ATN
      2. BUN:Creatinine ratio is also helpful in distinguishing prerenal syndrome as those patients will have a 20:1 ratio as opposed to the normal 10-15:1
      3. Retention of Na is enhanced in prerenal syndrome and decreased in ATN (prerenal urine concentration of Na <20 mEq/L and above 40 mEq/L in ATN; the fractional excretion of sodium (FENa)=Urine [Na]/Plasma [Na]: Urine[Cr]/Plasma{Cr]; FENa < 1%- prerenal condition; FENa >2%- renal injury
      4. ATN has two major types: (both are associated with denuding of epithelial cells and occlusion of the tubular lumens by cellular debris and casts
        1. Postischemic – volume depletion can lead to ATN, greatest risk in sepsis or hypotension
        2. Toxic – e.g aminoglycosides (number of amino groups on the aminoglycoside determines its nephrotooxicity)
    3. renal tubular acidosis (RTA) – impaired ability to secrete hydrogen ions in the distal nephron or to resorb bicarbonate ions proximally, leading to chronic metabolic non anion gap acidosis and hypokalemia; in the distal form, may be accompanied by rickets or osteomalacia
      1. RTA type I – (classic) – a distal tubule problem where the ability to develop a high concentration of H+ ions in the distal tubule and collecting duct is impaired so that urine pH does not fall below 6; hypokalemia and hypercalciuria are seen
        1. Thiazide diuretics may cause hypokalemia from renal potassium loss, hyperuricemia from uric acid retention, carbohydrate intolerance, and hyperlipidemia
      2. RTA type II – capacity off the proximal tubule to resorb HCO3 is diminished so that increased amounts of HCO3 reach the distal tubue and are excreted in the urine
      3. Treatment: bicarb
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