Online Test Banks
Score higher
See Online Test Banks
eLearning
Learning anything is easy
Browse Online Courses
Mobile Apps
Learning on the go
Explore Mobile Apps
Dummies Store
Shop for books and more
Start Shopping

Physician Assistant Exam: Kidney Failure

The Physician Assistant Exam will expect you to be aware of some common causes of renal failure. Acute renal failure (ARF) (or acute kidney injury — AKI) is defined as an abrupt rise in the creatinine (Cr) level or an abrupt decrease in the glomerular filtration rate (GFR) from baseline.

Prerenal azotemia

The easiest kidney-failure-related condition to diagnose is prerenal azotemia. With prerenal azotemia, the blood urea nitrogen (BUN) can be elevated (BUN/Cr ratio > 1), and the urinalysis is negative for blood or protein. You may see hyaline casts on the urinary sediment. Clinically, acute renal failure from prerenal azotemia improves with volume repletion.

In evaluating causes of acute renal failure, an important diagnostic tool (in addition to the urinalysis) is the fractional excretion of sodium (FENa). The kidney can detect subtle changes in perfusion, for example, secondary to volume loss or gastrointestinal bleeding.

In those situations, the job of the kidney is to hold on to all the sodium it can in order to maintain kidney perfusion. That’s why in prerenal azotemia or volume depletion, you see a low FENa. Other states where you can see a low FENa include glomerulonephritis and certain forms of acute tubular necrosis.

Acute tubular necrosis (ATN)

Acute tubular necrosis (ATN) is the most common condition of acute of acute kidney failure in the hospital setting. This type of acute renal failure is often diagnosed by looking at the clinical setting. You should recognize both the causes of acute tubular necrosis and what you can do to prevent the acute renal failure in the first place.

Common causes of acute tubular necrosis are shock, low blood pressure, dye nephropathy related to contrast studies, and medications, including chemotherapy agents like cisplatin (Platinol), the antifungal agent amphotericin B, and aminoglycoside antibiotics. Medications like these cause a nephrotoxic acute tubular necrosis. Acute tubular necrosis related to low blood pressure or low perfusion states is called ischemic acute tubular necrosis.

Important lab findings that can help in diagnosing acute tubular necrosis are the urinalysis and the fractional excretion of sodium (FENa). On urinalysis, the most common reported finding is muddy brown granular casts. In many cases, the urinalysis is completely normal. Most causes of acute tubular necrosis cause an FENa of > 3. The exceptions are contrast nephropathy and rhabdomyolysis, where it’s < 1.

Contrast-induced nephropathy (CIN) is defined as a rise in the serum creatinine by 25 percent, or 0.5 mg/dL, which usually occurs 24 to 48 hours after an interventional study such as a cardiac catheterization or an angiogram. This is a common etiology of acute tubular necrosis in the hospital setting. Risk factors for contrast nephropathy include diabetes, volume depletion, underlying kidney disease, and multiple myeloma.

The only proven therapy for the prevention of contrast-induced nephropathy is administering isotonic saline at least 12 hours prior to the intended procedure. N-acetylcystein is an antioxidant that’s also used in preventing contrast-induced nephropathy.

An important clinical distinction is the difference between atheroembolic renal disease (AERD) and contrast nephropathy. Although both can occur after an interventional study, there are subtle differences:

  • Atheroembolic renal disease usually occurs several weeks after an interventional study, whereas contrast-induced neuropathy occurs 24 to 48 hours after an interventional study.

  • With atheroembolic renal disease, you see digital infarcts and livedo reticularis on physical exam.

In a common test question scenario, a patient had an interventional study and now presents with acute renal failure. The time course is the clincher: If the acute renal failure occurred 24 to 48 hours after the study, the answer is contrast-induced neuropathy. If the kidney function worsened 2 to 3 weeks after the study, the answer is atheroembolic renal disease.

Obstructive uropathies: Urinary blockages

Obstructive uropathies are very common causes of acute kidney disease, especially in the older male population. Understanding the basic approach to evaluating and treating an obstructive process is important. Here are a few general points concerning the causes and evaluation of an obstructive process:

  • The most common cause of obstruction in men is benign prostate hyperplasia (BPH).

  • The most common cause of obstruction in a young woman is cervical cancer. In an older woman, think about ovarian cancer as the cause.

  • You can diagnose an obstruction by kidney ultrasound, CT scan, or MRI.

  • If you see a bilateral hydronephrosis on ultrasound, your next step is to have a Foley catheter placed.

As an imaging modality, the kidney ultrasound is important in a number of ways other than determining whether an obstruction is present.

  • If both kidneys are small, are echogenic, or show cortical thinning, think of chronic kidney disease.

  • If one kidney is small compared to the other, the difference can be congenital, unilateral renal artery stenosis, or unilateral reflux nephropathy.

  • If both kidneys are large by ultrasound criteria, think about HIV, diabetes, polycystic kidney disease, multiple myeloma, and/or amyloidosis.

Polycystic kidney disease (PKD)

Polycystic kidney disease (PKD) is the most common hereditary cause of kidney disease in the United States. It’s characterized by cysts that can grow so large they can overwhelm the kidney and other organs, including the liver and pancreas. Here are some key points about this condition:

  • Polycystic kidney disease is inherited in an autosomal dominant fashion. This means that if one parent has the condition, a son or daughter has a 50 percent chance of inheriting the condition. There’s also an autosomal recessive form that affects very young children and can affect the liver big time.

  • The diagnosis of polycystic kidney disease is confirmed by kidney ultrasound.

  • If the blood pressure is elevated, the treatment is to use an ACE inhibitor or ARB.

  • Polycystic kidney disease can affect the brain. Screening for berry aneurysms is important, especially if the patient has a family history of these aneurysms. Magnetic resonance angiography (MRA) with contrast is the diagnostic procedure of choice to diagnose the aneurysms.

  • Add a Comment
  • Print
  • Share
blog comments powered by Disqus
Advertisement

Inside Dummies.com

Dummies.com Sweepstakes

Win $500. Easy.