NCP Renal Failure : Acute

Acute renal failure (ARF) has four well-defined stages: onset, oliguric or anuric, diuretic, and convalescent. Treatment depends on stage and severity of renal compromise. ARF can be divided into three major classifications, depending on site:

Prerenal: Prerenal failure is caused by interference with renal perfusion (e.g., blood volume depletion, volume shifts [“third-space” sequestration of fluid], or excessive/too-rapid volume expansion), manifested by decreased glomerular filtration rate (GFR). Disorders that lead to prerenal failure include cardiogenic shock, heart failure (HF), myocardial infarction (MI), burns, trauma, hemorrhage, septic or anaphylactic shock, and renal artery obstruction.

Renal (or intrarenal): Intrarenal causes for renal failure are associated with parenchymal changes caused by ischemia or nephrotoxic substances. Acute tubular necrosis (ATN) accounts for 90% of cases of acute oliguria. Destruction of tubular epithelial cells results from (1) ischemia/hypoperfusion (similar to prerenal hypoperfusion except that correction of the causative factor may be followed by continued oliguria for up to 30 days) and/or (2) direct damage from nephrotoxins.

Postrenal: Postrenal failure occurs as the result of an obstruction in the urinary tract anywhere from the tubules to the urethral meatus. Obstruction most commonly occurs with stones in the ureters, bladder, or urethra; however, trauma, edema associated with infection, prostate enlargement, and strictures also cause postrenal failure.

Note: Iatrogenically induced ARF should be considered when failure develops during or shortly after hospitalization.

The most common causative factor is administration of potentially nephrotoxic agents.


Inpatient acute medical or surgical unit


Metabolic acidosis (primary base bicarbonate deficiency)

Fluid and electrolyte imbalances

Psychosocial aspects of care

Renal dialysis

Renal failure: chronic


Total nutritional support: parenteral/enteral feeding

Upper gastrointestinal/esophageal bleeding

Patient Assessment Database


May report: Fatigue, weakness, malaise

May exhibit: Muscle weakness, loss of tone


May exhibit: Hypotension or hypertension (including malignant hypertension, eclampsia/pregnancyinduced hypertension)

Cardiac dysrhythmias

Weak/thready pulses, orthostatic hypotension (hypovolemia)

Jugular venous distension (JVD), full/bounding pulses (hypervolemia); flat neck veins (diuretic phase)

Generalized tissue edema (including periorbital area, ankles, sacrum)

Pallor (anemia); bleeding tendencies


May report: Change in usual urination pattern: Increased frequency, polyuria (early failure and early recovery), or decreased frequency/oliguria (later phase)

Dysuria, hesitancy, urgency, and retention (inflammation/obstruction/infection)

Abdominal bloating, diarrhea, or constipation

History of benign prostatic hyperplasia (BPH), or kidney/bladder stones/calculi

May exhibit: Change in urinary color, e.g., absence of color, deep yellow, red, brown, cloudy

Oliguria (may last 12–21 days and occurs in 70% of patients); polyuria (2–6 L/day of urine, lacking concentration and regulation of waste products)


May report: Weight gain (edema), weight loss (dehydration)

Nausea, anorexia, heartburn, vomiting

Metallic taste

Use of diuretics

May exhibit: Changes in skin turgor/moisture

Edema (generalized, dependent)


May report: Headache, blurred vision

Muscle cramps/twitching; “restless leg” syndrome; numbness, tingling

May exhibit: Altered mental state, e.g., decreased attention span, inability to concentrate, loss of

memory, confusion, decreasing level of consciousness (LOC) (azotemia, electrolyte and acid-base imbalance)

Twitching, muscle fasciculations, seizure activity


May report: Flank pain, headache

May exhibit: Guarding/distraction behaviors, restlessness


May report: Shortness of breath

May exhibit: Tachypnea, dyspnea, increased rate/depth (Kussmaul’s respiration); ammonia breath

Cough productive of pink-tinged sputum (pulmonary edema)


May report: Recent transfusion reaction

May exhibit: Fever (sepsis, dehydration)

Petechiae, ecchymotic areas on skin

Pruritus, dry skin


May report: Family history of polycystic disease, hereditary nephritis, urinary calculus, malignancy

History of exposure to toxins, e.g., drugs, environmental poisons; substance abuse

Current/recent use of nephrotoxic drugs, e.g., aminoglycoside antibiotics, amphotericin B;

anesthetics; vasodilators; nonsteroidal anti-inflammatory drugs (NSAIDs)

Recent diagnostic testing with radiographic contrast media

Concurrent conditions: Tumors in the urinary tract, Gram-negative sepsis; trauma/crush injuries, hemorrhage, disseminated intravascular coagulation (DIC), burns, electrocution injury; autoimmune disorders (e.g., scleroderma, vasculitis), vascular occlusion/surgery, diabetes mellitus (DM), cardiac/liver failure

Discharge plan

DRG projected mean length of inpatient stay: 5.9 days

May require alteration/assistance with medications, treatments, supplies; transportation, homemaker/maintenance tasks

Refer to section at end of plan for postdischarge considerations.



Volume: Usually less than 100 mL/24 hr (anuric phase) or 400 mL/24 hr (oliguric phase), which occurs within 24–48 hr after renal insult. Nonoliguric (more than 400 mL/24 hr) renal failure also occurs when renal damage is associated with nephrotoxic agents (e.g., contrast media or antibiotics).

Color: Dirty, brown sediment indicates presence of RBCs, hemoglobin, myoglobin, porphyrins.

Specific gravity: Less than 1.020 reflects kidney disease, e.g., glomerulonephritis, pyelonephritis with loss of ability to concentrate; fixed at 1.010 reflects severe renal damage.

pH: Greater than 7 found in urinary tract infections (UTIs), renal tubular necrosis, and chronic renal failure (CRF).

Osmolality: Less than 350 mOsm/kg is indicative of tubular damage, and urine/serum ratio is often 1:1.

Creatinine (Cr) clearance: Renal function may be significantly decreased before blood urea nitrogen (BUN) and serum Cr show significant elevation.

Sodium: Usually increased if ATN is cause for ARF, more than 40 mEq/L if kidney is not able to resorb sodium, although it may be decreased in other causes of prerenal failure.

Fractional sodium (FeNa): Ratio of sodium excreted to total sodium filtered by the kidneys reveals inability of tubules to reabsorb sodium. Readings of less than 1% indicate prerenal problems, higher than 1% reflects intrarenal disorders.

Bicarbonate: Elevated if metabolic acidosis is present.

Red blood cells (RBCs): May be present because of infection, stones, trauma, tumor, or altered glomerular filtration (GF).

Protein: High-grade proteinuria (3–4+) strongly indicates glomerular damage when RBCs and casts are also present. Low-grade proteinuria (1–2+) and white blood cells (WBCs) may be indicative of infection or interstitial nephritis. In ATN, proteinuria is usually minimal.

Casts: Usually signal renal disease or infection. Cellular casts with brownish pigments and numerous renal tubular epithelial cells are diagnostic of ATN. Red casts suggest acute glomerular nephritis.


BUN/Cr: Elevated and usually rise in proportion with ratio of 10:1 or higher.

Complete blood count (CBC): Hemoglobin (Hb) decreased in presence of anemia. RBCs often decreased because of increased fragility/decreased survival.

Arterial blood gases (ABGs): Metabolic acidosis (pH less than 7.2) may develop because of decreased renal ability to excrete hydrogen and end products of metabolism. Bicarbonate decreased.

Sodium: Usually increased, but may vary.

Potassium: Elevated related to retention and cellular shifts (acidosis) or tissue release (red cell hemolysis).

Chloride, phosphorus, and magnesium: Usually elevated.

Calcium: Decreased.

Serum osmolality: More than 285 mOsm/kg; often equal to urine.

Protein: Decreased serum level may reflect protein loss via urine, fluid shifts, decreased intake, or decreased synthesis because of lack of essential amino acids.

Radionuclide imaging: May reveal calicectasis, hydronephrosis, narrowing, and delayed filling or emptying as a cause of ARF.

Kidney, ureter, bladder (KUB) x-ray: Demonstrates size of kidneys/ureters/bladder, presence of cysts, tumors, ad kidney displacement or obstruction (stones).

Retrograde pyelogram: Outlines abnormalities of renal pelvis and ureters.

Renal arteriogram: Assesses renal circulation and identifies extravascularities, masses.

Voiding cystoureterogram: Shows bladder size, reflux into ureters, retention.

Renal ultrasound: Determines kidney size and presence of masses, cysts, obstruction in upper urinary tract.

Nonnuclear computed tomography (CT) scan: Cross-sectional view of kidney and urinary tract detects presence/extent of disease.

Magnetic resonance imaging (MRI): Provides information about soft tissue damage.

Excretory urography (intravenous urogram or pyelogram): Radiopaque contrast concentrates in urine and facilitates visualization of KUB.

Endourology: Direct visualization may be done of urethra, bladder, ureters, and kidney to diagnose problems, biopsy, and remove small lesions and/or calculi.

Electrocardiogram (ECG): May be abnormal, reflecting electrolyte and acid-base imbalances.


1. Reestablish/maintain fluid and electrolyte balance.
2. Prevent complications.
3. Provide emotional support for patient/significant other (SO).
4. Provide information about disease process/prognosis and treatment needs.


1. Homeostasis achieved.
2. Complications prevented/minimized.
3. Dealing realistically with current situation.
4. Disease process/prognosis and therapeutic regimen understood.
5. Plan in place to meet needs after discharge.