ACUTE RENAL FAILURE (ARF)
Clinical conditions associated with rapid (days or weeks), steadily
decreasing renal function (azotemia), with or without oliguria.
CLASSIFICATION AND ETIOLOGY
Pre-renal
Renal
Post-renal
causes
Potentially reversible if diagnosed and treated early.
 some renal causes resulting in acute glomerular vascular or interstitial
nephropathy also are treatable
(malignant hypertension, glomerulonephritis, vasculitis, bacterial
infections, drug reactions, metabolic disorders such as hypercalcemia,
hyperuricemia)
- Pre renal azotemia: 50-80% of ARF, inadequate renal perfusion results
from extracellular fluid volume depletion or from cardiovascular
disease.
- Post renal azotemia: 5-10% of ARF; various types of obstruction in the
voiding and collecting parts of the urinary system.
- Intrinsic renal causes: associated with prolonged renal ischemia
(hemorrhage, surgery), or a nephrotoxin. Acute tubulointerstitial
nephritis or acute glomerulonephritis can also present as ARF.
 IN many patients no single cause of ARF identified.
Factors that initiate and those that maintain ARF may differ.
PATHOPHYSIOLOGY
PRE-RENAL: Oliguria (urine <500 ml/day) from reduced GFR and
enhanced Na+ and H2O reabsorbtion, a normal response to ineffective
circulating blood volume.
POST-RENAL: Bladder outlet obstruction most common cause (prostatic
hyperplasia, cancer of prostate or cervix, retroperitoneal disorders).
Occlusion of both urinary outflow tracts.
Less frequent intraluminal causes: bilateral renal calculi, papillary
necrosis, coagulated blood, bladder carcinoma.
Extraluminal causes: retroperitoneal fibrosis, colorectal tumor, neoplasia.
In children: congenital obstructive defects.
RENAL: Hypofiltration includes decrease in renal blood flow, reduced
glomerular permeability, tubular obstruction, injured tubular epithelium.
(Variability in factors, inadequacy of former term “acute tubular necrosis”)
Renal vasculature very sensitive to endothelin  antiendothelin antibodies
or endothelin-receptor antagonists may protect against ischemic ARF
Structura changes in the tubules depend on the insult, edema and
inflammation always present.
ARF accompanied by hypocalcemia, hyperphosphatemia and secondary
hyperparathyroidism.  Temporary loss of calcitriol production by the
injured kidney and phosphate retention
SYMPTOMS AND SIGNS
- In community acquired ARF often only finding is passage of colacolored urine followed by oliguria or anuria.
- In hospitalized patients: recent traumatic, surgical or medical event
- A relatively preserved urine output (1-2.4 l/day) common. Oliguria
may occur. Anuria suggests bilateral renal artery occlusion, obstructive
uropathy, acute cortical necrosis, rapidly progressive glomerulonephritis
- Intrinsic renal disease: 3 phases.
 prodromal phase (depends on cause)
 Oliguric phase 10-14 days, Urine output 50-400 mL/day (non
oliguric patients better prognosis). Serum creatinine typically increases by
1-2 mg/dL/day and urea nitrogen by 10-20 mg/dL Urea nitrogen may be
misleading as an early index of renal function (elevated by increased
proteine catabolism).
 Postoliguric phase: urine output gradually back to normal, but serum
creatinine and urea levels may not fall for several days. Tubular
dysfunction may persists (Na wasting, polyuria, hyperchloremic metabolic
acidosis)
- Glomerulonephritis suggested by edema, nephrotic syndrome, signs of
arteritis in the skin and retina
- Hemoptysis suggests Wegener’s granulomatosis or Goodpasture’s
syndrome
- Skin rash suggests polyarteritis or SLE.
DIAGNOSIS
- Progressive daily rise in serum creatinine diagostic of ARF.
- Improvement by correction of hemodynamic abnormality (Pre-renal)
- Urinary and serum chemical analysis  renal failure index
renal failure index: Urine NA / U/P creatinine ratio
- Recommended blood tests: creatinine, CO2, K+, serum Na++, Ca++,
Phosphate, BUN, uric acid, CK, Antistreptolysin-O and complement
titres, antinuclear antibodies, antinuclear cytoplasmic antibodies, Urine
Na and creatinine, blood and urine cultures.
- Typical laboratory findings: progressive azotemia, acidosis (moderate,
plasma CO2 12-20 mmol/L) , hyperkalemia, hyponatremia (surplus of
water), normochromic, normocytic anemia.
- Urinary sediment: WBCs, RBDs, casts (granular and tubular cells). In
primary renal injury tubular cells, tubular cells casts, brown granular
casts
- X-ray abdomen: 90% urinary calculi (radiopaque)
- Ultrasonography (sensitivity 80-85%)
- If obstruction suspected, antegrade or retrograde contrast studies
- Post-voiding urethral catheterization
- Ultrasonography or CT: a normal or enlarged kidney favours
reversibility, whereas small sizes suggest chronic renal insufficiency
- Renal arteriography or venography
- MRI if radiocontrast dangerous
- Radionuclide studies only to exclude renal artery occlusion
- Renal biopsy if cause elusive.
PROGNOSIS
ARF and complications (hypervolemia, metabolic acidosis, hyperkalemia,
uremia, bleeding diathesis) treatable, but survival 60%
PROPHYLAXIS AND TREATMENT
Prevention by:
- maintenance of normal fluid balance, blood volume, and BP during and
after major surgery
- isotonic NaCl infusions in patients with severe burns,
- prompt transfusions in hemorrhagic hypotension
Vasopressor drug: dopamine 1-3 mcg/Kg/min I.V. may augment renal
blood flow and urine output
Incipient ARF: furosemide with mannitol or dopamine may reestablish
normal urine output
Dehydration and ECF depletion should be avoided in patients with
cholecystography or in renal insuff patients requiring urography (mainly if
with multiple myeloma). Urography and angiography should be avoided
in patients with renal insufficiency because of high incidence of renal
deterioration.
Before cytolitic therapy in patients with lymphoma or leukemia treatment
with allopurinol along with alkalizing urine (Na bicarbonate or
acetazolamide) and increasing urine flow with increased oral or IV fluids
to reduce urate crystalluria.
DIALYSIS
Improves fluid and electrolyte imbalance. Allows adequate nutrition.
ARF should be managed without dialysis only when dialysis unavailable
or ARF uncomplicated and existed < 5 days.
Water intake restricted to a volume equal to urine output + measured
extrarenal losses + 500 ml/day for insensible loss.
Body weight is an indicator of fluid intake.
To reduce nitrogen loss oral of IV essential amino acids with glucose
To keep serum K+ < 6 mmol/L in the absence of dialysis , cationexchange resin (sodium polystyrene sulfonate) 15 g PO or rectally 1-4
times /day.
When obstruction is relieved polyuria with escretion of large amounts of
Na, K, Mg. Possible contraction of ECF volume with vascular collapse
may occur
IN the post oliguric phase close attention to fluid and electrolyte balance is
mandatory.