NEPHROLOGY

 

Acute Renal Failure (ARF)

An abrupt decrease in renal function sufficient to result in the retention of nitrogenous waste in the body (­BUN).  Can be classified as pre-renal, renal, and post-renal.

 

1.       Pre-renal failure – 50% of ARF cases

a.       Caused by

i.                     Absolute ¯ effective blood volume (hemorrhage, skin/GI losses, diuretics, third spacing)

ii.                   Relative ¯ effective blood volume (CHF, sepsis, liver failure)

iii.                  Arterial occlusion (bilateral thromboembolism)

b.      Clinical presentation

i.                     History of fluid losses, use of NSAIDs or ACE inhibitors, thirst.

ii.                   Signs of weight loss, oliguria, orthostatic hypotension, tachycardia, dry mucous membranes.

c.       Laboratory tests

i.                     Decreased UNa (< 20 mEq/L)

ii.                   BUN/Cr > 20:1, and FENa < 1%.

iii.                  Uosm > Sosm and Uosm > 500 mOsm/kg H2O

iv.                 Urine specific gravity > 1.030

v.                   Minimal proteinuria and negative urine sediment findings

d.      Treatment

i.                     Rapid volume replacement – fluid challenge of 300-500 mL NS over 30-60 min.

ii.                   Then replace fluids to maintain urine output at 1-2 mL/min.

iii.                  Correct underlying disorder (CHF, etc.)

2.       Intrinsic renal failure

a.       Caused by

i.                     Vascular disorders (vasculitis, malignant hypertension)

ii.                   Acute glomerulonephritis (post-streptococccal)

iii.                  Acute interstitial nephriis (drug associated, e.g. methicillin)

iv.                 Acute tubular necrosis (ATN) – makes up the majority of hospital associated ARF.

(1)     Perfusional defects (shock, hypovolemia, sepsis, etc.)

(2)     Nephrotoxic agents

(a)     Exogenous toxins

(i)                   Aminoglycosides, i.e gentamicin – nonoliguric, related to duration of treatment (5-10 days), may be seen after cessation of treatment.

(ii)                 Contrast – oliguric

(iii)                Mercury, cisplatin, solvents

(b)    Endogenous toxins (hemoglobinuria, myoglobinuria, myeloma, uric acid)

b.      Laboratory tests

i.                     May or may not be oliguric

ii.                   BUN ­ by 20-40/day; Cr ­ by 2-4/day, and FENa > 1%.

iii.                  Uosm < 350 mOsm/kg, UNa elevated (> 30)

iv.                 Modest proteinuria with ATN, nephrotic range proteinuria with acute glomerulopathies.

v.                   Urine sediment – ATN = muddy brown; RPGN = RBC casts; interstitial nephritis = lymphocytes, eosinophils, and WBC casts.

c.       Treatment of ATN

i.                     Find reversible sources of ATN and treat rapidly.

ii.                   Convert oliguric ATN to nonoliguric ATN with Lasix (80-400 mg IV, repeat in 1 hr).

iii.                  Closely monitor fluid and electrolytes to avoid hyponatremia, hyperkalemia, acidosis, hyperphosphatemia, and hypocalcemia.

iv.                 Restrict fluids and electrolytes so that ins match outs.

v.                   Restrict protein intake.

vi.                 Avoid magnesium containing medications.

vii.                Dialysis – keep predialysis BUN/Cr < 100 / 8.

3.       Post-renal failure

a.       Caused by obstruction of the collecting system (bladder outlet obstruction, neoplasm, bilateral ureteral obstruction).

b.      Clinical presentation

i.                     History of dysuria, nondysmorphic hematuria, clots.

ii.                   Evidence of prostatic hypertrophy in men or pelvic pathology in women.

c.       Laboratory tests

i.                     BUN ­ by 20-40/day; Cr ­ by 2-4/day

ii.                   Enlarged kidneys with dilated calyces

iii.                  Absent proteinuria

iv.                 Urinary sediment may be negative or may have hematuria with stones.

d.      Treatment includes catheter drainage, ureteral stents, percutaneous nephrostomy.