PANCE Blueprint Genitourinary (6%)

Acute renal failure (ReelDx + Lecture)


Acute Renal Failure

8-year-old with decreased urine output, edema, rapid and unexplained weight gain, fatigue, and leg pain (watch video)

Patient will present as → a 52-year-old male with a past medical history of diabetes mellitus presents with fever and acute onset left lower quadrant abdominal pain. CT scan with contrast shows acute diverticulitis. He is started on broad-spectrum antibiotics. The next day, labs reveal a rise in creatinine from 0.7 mg/dL to 2.0 mg/dL. Urinalysis is obtained and a significant amount of muddy brown casts is found.

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Acute renal failure is a rapid but usually reversible, reduction in renal excretory function sufficient to cause azotemia, urine output may or may not be reduced

  • Azotemia: retention of nitrogenous wastes
  • Uremia: symptomatic azotemia, with nausea, vomiting, and lethargy
  • Acute: sudden, hours or days and is reversible
  • Chronic: progressive, irreversible
  • Oliguria: urine output less than 400 ml/day

- 30% of ICU admissions have acute renal failure and 5% of total admissions, 25% of hospitalized patients will develop it

Serum creatinine is the most convenient marker, in the absence of functioning kidneys creatinine rises 1-1.5 mg/dl per day (or faster)

There are three mechanisms of acute renal failure:

  1. prerenal - perfusional (50%)
  2. renal - glomerular, tubular, interstitial (45%)
  3. postrenal - obstructive (5%)
Index Prerenal Renal
Urine specific gravity > 1.030 < 1.010
BUN/CR > 20 < 10
Urine osmolality > 500 < 300
FENA (fractional excretion of sodium) < 1 (kidney has decreased perfusion which results in ↑ aldosterone and NA+ retention in an attempt to increase pressure) > 1

Prerenal - Kidney is working fine it's the things that make the kidney perfuse that aren't working properly

  • Volume loss (blood or water), heart failure (the pump stops working = no kidney perfusion), or a loss of peripheral vascular resistance (think sepsis or anesthesia)
  • Pt will be weak, decreased urine output, dizziness, sunken eyes, tachycardia, orthostatic blood pressure changes
  • Fractional excretion of sodium will be normal < 1: Can your kidneys concentrate your urine properly? In prerenal failure, the answer is yes, this distinguishes this from ATN.
  • In prerenal disease, the secretion will be normal
  • BUN/CR  > 20:1
  • You treat with fluids, cardiac support and/or treat shock.

Postrenal - obstruction (most likely prostate)

  • Will typically have low or no urine output and possibly suprapubic pain
  • Place foley catheter to find the source of the obstruction
  • If you get a large urine volume after the foley = bladder, urethra, BPH if little urine = ureter obstruction or pathology
  • Renal US look for tumors or hydronephrosis

Renal - glomerular, tubular, interstitial

  • RBC casts = glomerulonephritis
  • WBC casts = pyelonephritis
  • Muddy casts = Acute tubular necrosis
  • Hyaline casts = normal
  • Waxy casts = chronic renal disease
  • ↑ Osmolality FENa > 2% = Acute tubular necrosis

Acute renal failure causes

  • Acute Tubular Necrosis (ATN) (85%)
  • Interstitial nephritis (10-15%)
  • Glomerulonephritis (5%)

1. Acute tubular necrosis (Muddy Casts)

  • Etiology: Kidney ischemia or toxins
  • Urinalysis: Muddy brown casts

  • Damage to the tubules means you are unable to concentrate urine which means a high FENa
  • Prerenal failure is the most common cause
  • Major causes are:
    • Drugs and toxins: amphotericin B ("amphoterrible"), cisplatin, aminoglycosides, radiocontrast media, NSAIDs, ACE
    • Ischemic (dehydration, shock, sepsis)
  • FENa (Fractional Excretion of Sodium is going to be GREATER than 2%) + Muddy Casts + High Urine Osmolality
  • Just like pre-renal: think post-dye using procedure, use of aminoglycosides or muscle breakdown (marathon runner or cocaine use)

2. Interstitial nephritis (Eosinophils) 

  • Etiology: Immune-mediated response
    • Drugs: PCN, sulfa, NSAIDs, phenytoin etc.
    • Immunologic and infectious disease: strep, SLE, CMV, Sjogren’s, Sarcoidosis
  • Urinalysis: WBC casts and eosinophils

  • Eosinophils, WBC casts, and hematuria
  • Acute azotemia (accumulation of nitrogen waste)
  • Major causes - immune-mediated response
    • Drugs: PCN, sulfa, NSAIDs, phenytoin etc.
    • Immunologic and infectious disease: strep, SLE, CMV, Sjogren's, Sarcoidosis
  • Diagnose with renal biopsy - will see interstitial inflammatory cell infiltrates Treat by discontinuing the offending drug, corticosteroids, Dialysis if needed, usually self-limiting if caught early

3. Glomerulonephritis (will be covered in Glomerulonephritis NCCPA Blueprint section)

  • Etiology: IGA Nephropathy (Berger disease), postinfectious, membranoproliferative
  • Urinalysis: Oliguria, hematuria and RBC casts

  • Hematuria and red cell casts
  • Acute azotemia with mild proteinuria
  • Causes - Group A strep, IGA, anti-GBM, ANCA

Types of acute renal failure secondary to glomerulonephritis (Glomerulonephritis NCCPA Blueprint section)

  1. Postreptococcal Glomerulonephritis
  2. Post Infectious (i.e viral)
  3. Glomerular diseases - AMCA. Wegener's, Churg-Strauss, anti-GBM, Goodpasture's syndrome, IgA nephropathy (Berger's)

Acute renal failure is suspected when urine output falls or serum BUN and creatinine rise

Evaluation should determine the presence and type of acute renal failure and seek a cause. Blood tests generally include CBC, BUN, creatinine, and electrolytes (including Ca and phosphate). Urine tests include Na and creatinine concentration and microscopic analysis of sediment. Early detection and treatment increase the chances of reversing renal failure and in some cases preventing it.

  • Blood tests generally include CBC, BUN, creatinine, and electrolytes (including Ca and phosphate)
  • Urine tests generally include Urinary sediment (casts), FENa
  • Postvoid residual bladder volume if postrenal cause suspected


  • ATN:  FENa (Fractional Excretion of Sodium is going to be GREATER than 2%) + MUDDY, PIGMENTED, GRANULAR CASTS, Renal tubular epithelial cells, + High Urine Osmolality
  • Interstitial nephritis: Eosinophils, WBC casts, and hematuria
  • Glomerulonephritis: Hematuria and red cell casts

Treatment depends on the cause of the acute renal failure

Congratulations - you have completed Acute Renal Failure. You scored %%SCORE%% out of %%TOTAL%%. Your performance has been rated as %%RATING%% %%FORM%%
Your answers are highlighted below.
Question 1
A 15 year old boy comes to your clinic after having a sore throat, he wasn't treated.  He now has hematuria, pretibial edema and hypertension. What antibody do expect on lab findings?
ANCA is positive in Churg Strauss or Wegner's
ANA is positive in lupus
Anti GBM
Anti GBM is positive in Goodpasture's
Question 1 Explanation: 
This patient has classic symptoms of hematuria, pretibial edema and hypertension indicative of nephritic syndrome. The history of an untreated sore throat is key to the diagnosis of post streptococcal glomerulonephritis. He would have a positive ASO titer.
Question 2
Lab results for a post-operative oliguric patient reveals an increased BUN to creatinine ratio. The patient has a low fractional excretion of sodium (less than 1%). Which of the following is the most likely diagnosis?
prerenal azotemia
acute tubular necrosis
Acute tubular necrosis may occur in the post-operative setting but these kidneys are damaged and unable to save sodium.
acute glomerulonephritis
Acute glomerulonephritis is a complication of a streptococcal infection wherein the immune complexes damage the glomeruli and lead to hematuria, red blood cell casts, and proteinuria.
obstructive uropathy
Question 2 Explanation: 
Patients who have prerenal azotemia with otherwise normal kidneys will have severe sodium retention in order to help to save fluid. The amount of sodium in the urine is therefore very low.
Question 3
A urinalysis performed during a routine physical examination on a 43 year-old male reveals 1-2 hyaline casts/HPF. The remainder of the UA is normal. Based upon these results, the physician assistant should
collect a urine for culture and sensitivity
See B for explanation.
do nothing, since these casts are considered normal
refer the patient to a nephrologist
See B for explanation.
schedule the patient for a CT scan
See B for explanation.
Question 3 Explanation: 
Hyaline casts are not indicative of renal disease. They can be found following strenuous exercise and with concentrated urine or during a febrile illness.
Question 4
A 27 year-old patient presents with crush injuries to both lower extremities after being involved in an automobile accident. Within six hours of the accident, urine output has decreased to less than 10 cc per hour. Within 24 hours the serum creatinine increased from 0.9 mg/dl to 2.9 mg/dl and serum CPK is now 12,000 U/L. In addition to a fluid challenge with normal saline, which of the following is the most appropriate treatment as this time?
IV calcium chloride
While hypocalcemia is common in rhabdomyolysis and acute renal failure, treatment is not needed unless clinical signs such as tetany are noted.
Oral captopril (Capoten)
The use of ACE inhibitors, such as captopril, may worsen renal function and are not indicated in this case.
IV sodium bicarbonate
Oral sevelamer (Renagel)
Sevelamer is a phosphate binder used to treat elevated phosphate levels in patients with end stage renal disease.
Question 4 Explanation: 
Treatment of acute renal failure due to rhabdomyolysis is best accomplished with IV fluids and forced alkaline diuresis.
Question 5
Which of the following medications is most likely to cause acute tubular necrosis?
Trimethoprim-sulfamethoxazole (Bactrim)
See D for explanation.
Acute renal failure can develop as a result of acetaminophen overdose however this is rare.
Cephalothin (Kefzol)
Some first generation cephalosporins may cause renal insufficiency this too is rare. Aminoglycosides are still more nephrotoxic.
Question 5 Explanation: 
In hospitalized patients up to 25% of patients receiving aminoglycosides sustain some degree of acute tubular necrosis. Gentamicin is one of the most toxic aminoglycosides, streptomycin is the least nephrotoxic of the aminoglycosides.
Question 6
An elderly appearing adult male patient is transported to the emergency room with unconsciousness for an underdetermined amount of time. There is no family and the only history is provided by the paramedics. The patient arouses to verbal and painful stimuli. VS: T-97.0 degrees F rectally, P-52 bpm, R-10, BP-95/60 mmHg. Physical examination is unremarkable except for ecchymosis across his extremities. A Foley catheter is inserted draining a small amount of dark brown urine. Urine dipstick reveals 4+ positive hemoglobin and protein. Microscopic urinalysis reveals no RBCs but many renal tubular epithelial cells and renal tubular casts. Drug screen is negative, blood alcohol is 2.5 mg/dL, and creatinine is 4.9 mg/dL. What is the most likely diagnosis?
Rhabdomyolysis causing acute renal failure
Obstructive uropathy causing acute renal failure
See A for explanation.
Ethanol ingestion causing acute renal failure
See A for explanation.
Methanol ingestion causing acute renal failure
See A for explanation.
Question 6 Explanation: 
Since the patient was found unconscious for an undetermined amount of time and the blood alcohol is elevated the patient has been in a state of prolonged immobilization resulting in muscle ischemia resulting in myoglobinuria. This is responsible for turning the dipstick positive without the RBCs seen on the urinary microscopy. The myoglobin causes an acute tubular necrosis resulting in the sloughing of the renal tubular epithelium. Obstructive uropathy does not cause acute tubular necrosis and occurs over time. Methanol ingestion causes visual symptoms, ethylene glycol causes renal failure.
Question 7
Which of the following is a cause of acute kidney failure due to prerenal azotemia?
Excessive diuresis
Urinary tract obstruction
Postrenal azotemia is due to obstruction of urinary flow from both of the kidneys.
Radiologic contrast media
Radiologic contrast media can be directly nephrotoxic causing acute tubular necrosis, which is an intrinsic renal disease.
Exogenous nephrotoxins, such as aminoglycosides, cause acute tubular necrosis, which is an intrinsic renal disease.
Question 7 Explanation: 
Prerenal azotemia is due to renal hypoperfusion which can occur with intravascular volume depletion such as excessive diuresis, hemorrhage, and gastrointestinal losses.
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