Tubular diseases: Presentations, Etiologies and Complications Flashcards

1
Q

What are the causes of postrenal azotemia?

A
  • Prostate hypertrophy or cancer
  • Stone in the ureter
  • Cervical cancer
  • Urethral stricture
  • Neurogenic (atonic) bladder
  • Retroperitoneal fibrosis (from bleomycin, methylsergide or radiation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the causes of intrinsic renal disease?

A
  • ATN from toxins (contrast agents, aminoglycosides, cisplatin, amphotericin, cyclosporine, and NSAIDs)or prolonged ischemia
  • Acute (allergic) interstitial nephritis (commonly from meds e.g. penicillin)
  • Rhabdomyolysis and hemoglobinuria
  • Crystals from hyperuricemia, hypercalcemia, or hyperoxaluria
  • Proteins e.g. Bence-Jones proteins in multiple myeloma
  • Poststreptococcal infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the presentation of acute kidney injury (AKI)?

A

May be only an asymptomatic rise in BUN and Cr.

When symptomatic, the pt presents with:

  • Nausea and vomiting
  • Fatigue/malaise
  • Weakness
  • SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the features of severe AKI?

A
  • Confusion
  • Arrhythmia from hyperkalemia and acidosis
  • Sharp, pleuritic chest pain from pericarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the typical presentation of postrenal azotemia?

A

Enlargement/distention of the bladder and massive diuresis after placement of a Foley catheter. Hydronephrosis may be seen unilaterally or bilaterally on sonogram.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the onset of AKI with the following toxins:

  • Contrast media
  • Vancomycin, gentamicin, amphotericin, cisplatin
  • Tumor lysis syndrome
A
  • Contrast media: very rapid onset injury, with Cr rising the next day
  • Vancomycin, gentamicin, amphotericin, cisplatin, acyclovir: slower onset injury of 5-10 days
  • Tumor lysis syndrome (hyperuricemia): onset of 2 days following start of chemotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the causes of rhabdomyolysis?

A
  • Trauma
  • Snake bite
  • Prolonged immobility
  • Seizures
  • Crush injuries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In ATN, what increases the risk of aminoglycoside or cisplatin toxicity?

A

Low magnesium level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does AKI from ethylene glycol present?

A

Pt who ingested an unknown substance presents with renal failure 3 days later along with a low calcium level and abnormal UA.

The calcium is low because it was used to form the envelope-shaped oxalate crystals that caused the AKI.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does the risk of ATN relate to the age of the pt?

A

The risk of ATN is directly proportional to age. This is because we lose 1% of our renal function for every year past age 40.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is hepatorenal syndrome? How does it present? With which type of AKI does it share lab values?

A

HR syndrome is renal failure that results secondary to liver disease. The kidneys are intrinsically normal. Look for:

  • Severe liver disease (cirrhosis)
  • New-onset renal failure with no other explanation
  • Very low urine sodium 20:1

HR syndrome shares lab values with prerenal azotemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do atheroemboli cause AKI? What is the presentation?

A

Cholesterol plaques may be broken off the aorta or coronary arteries during catheter procedures and the emboli can get lodged in the kidneys, leading to AKI.

Along with signs and Sx of AKI, the pt will present with:

  • Blue/purplish skin lesions in fingers and toes
  • Livedo reticularis
  • Ocular lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is acute (allergic) interstitial nephritis? What are the causes of it?

A

AIN is a form of AKI in which antibodies and eosinophils attack the cells lining the tubules as a reaction to drugs (70%), infection, and autoimmune disorders (SLE, Sjögren syndrome, sarcoidosis).

The most common medications that cause AIN are:

  • Penicillins and cephalosporins
  • Sulfa drugs
  • Phenytoin
  • Rifampin
  • Quinolones
  • Allopurinol
  • PPIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The drugs that cause AIN are penicillins, cephalosporins, sulfa drugs, phenytoin, rifampin, quinolones, allopurinol, and PPIs. What else do all of these drugs have in common?

A

The drugs that cause AIN also cause:

  • Drug allergy and rash
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis (TEN)
  • Hemolysis

*They all can damage the skin, kidneys, and RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the presentation of AIN?

A

Look for AKI (elevated BUN and Cr) with:

  • Fever (80%)
  • Rash (50%)
  • Arthralgias
  • Eosinophilia and eosinophiluria (80%)

*AIN from NSAIDs does NOT present with eosinophiluria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the presentation of analgesic nephropathy?

A
  • ATN from direct toxicity to the tubules
  • AIN
  • Membranous glomerulonephritis
  • Vascular insufficiency of the kidney from inhibiting prostaglandins
  • Papillary necrosis
17
Q

What is papillary necrosis? What are the causes?

A

Papillary necrosis is sloughing off of the renal papillae. It is caused by:

  • Toxins e.g. NSAIDs
  • Sudden vascular insufficiency

PN does not happen to healthy pts. Look for extra NSAID use with a history of:

  • Sickle cell disease
  • Diabetes
  • Urinary obstruction
  • Chronic pyelonephritis
18
Q

What is the pres. of papillary necrosis?

A

Sudden onset of flank pain, fever, and hematuria in a pt with one of the diseases previously listed.

*It may be very hard to distinguish PN from pyelonephritis

19
Q

Summary of tubular disease

A
  • Generally, they are acute
  • Tubular diseases are caused by toxins, infections and autoimmune diseases
  • NONE of them EVER cause nephrotic syndrome or give massive proteinuria
  • Biopsy is NOT needed to establish diagnosis
  • They are NOT treated with steroids
  • They are NOT treated with immunosuppressive drugs
  • The underlying cause is treated (correcting hypoperfusion and removing the toxins)
20
Q

What are the causes of prerenal azotemia?

A
  • Hypotension: sepsis, anaphylaxis, bleeding or dehydration
  • Hypovolemia: diuretics, burns, pancreatitis
  • Renal artery stenosis
  • Relative hypovolemia: CHF, constrictive pericarditis, tamponade
  • Hypoalbuminemia
  • Cirrhosis
  • NSAIDs (constrict the afferent arteriole)
  • ACEIs (dilate the efferent arteriole)