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Clin Med II > Renal Failure > Flashcards

Renal Failure Flashcards

1
Q

What is RIFLE criteria?

A

-ARF and AKI are NOT the same
-3 graded levels of injury Risk, Injury, Failure
-2 outcome measures Loss of function and End stage renal disease
-Based on either degree of serum creatinine elevation or decrease in urine output
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2
Q

What are the Functions of the Kidney?

A
  1. Regulation of water, minerals and acid-base status
  2. Removal of metabolic waste products from the blood and their excretion in the urine
  3. Removal of foreign chemicals/toxins from the blood and their excretion in the urine
  4. Secretion of hormones (Erythropoietin, renin, Vit D)
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3
Q

What conditions are at a higher risk for developing AKI?

A
  • Hypertension
  • Congestive cardiac failure
  • Diabetes
  • Multiple myeloma
  • Chronic infection
  • Myeloproliferative disorder
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4
Q

What is Prerenal AKI Etiology?

A
  • Once MAP <80mmhg steep decline in GFR
  • Hypovolemia
  • Decreased cardiac output
  • Decreased effective circulating volume
  • Impaired renal autoregulation
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5
Q

What is Pre-renal Injury?

A

-Most common cause of renal failure (50-80%)
-Results from poor renal perfusion
-Reversed with restoration of renal perfusion/glomerular pressure
-BUN/Creatinine ratio > 20:1
-Calculate fractional excretion of
sodium (FeNa)
-Urinalysis often reveals hyaline
casts

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6
Q

What are Prerenal labs?

A
  • Volume depletion
  • Decreased CO/Effective
  • Urine output
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7
Q

What is is FeNa?

A
  • FeNa = (UNa x PCr/PNa x UCr) X 100
  • FeNa < 1% is suggestive of pre-renal azotemia
  • FeNa >1% intrinsic renal failure
  • FeNa >4% post-renal failure
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8
Q

What is Prerenal Treatment?

A
  • Volume depletion
  • Decreased CO/Effective circulating volume
  • All medications cleared by renal excretion should be avoided or doses adjusted
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9
Q

What is the history of AKI?

A

Volume depletion, Cardiac failure, Radio contrast exposure, Pigment injury, Vasculitis/proliferative glomerulonephritis, Other history of hypotension, shock, exposure to nephrotoxins, new medications, vascular/cardiac surgery, anesthesia, Pertinent PMH/FH, Postrenal Sx’s

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10
Q

What is the AKI’s Physical Exam?

A

Volume depletion, Cardiac failure, Hepatorenal syndrome, Atheroembolism, Rhabdomyolysis, Interstitial nephritis, Vasculitis, Proliferative glomerulonephritis, Urine volume, Postobstructive, and Uremia

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11
Q

What is Intrinsic Renal Diseases?

A

-Acute Interstitial Nephritis (AIN)
-Acute Tubular Necrosis (ATN) 90% most
common*
-Glomerular Diseases
-Pyelonephritis
-Malignancy (MM)
-Renal artery embolism/thrombus (renal infarction)
-Vasculitis

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12
Q

What is Acute Interstitial Nephritis (AIN)?

A

-Typically allergic reaction to medication
–-Post-infectious –
-Autoimmune

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13
Q

What is the “classic presentation” of Acute Interstitial Nephritis?

A
  • After recent new drug exposure
  • Fever
  • Skin rash
  • Peripheral eosinophilia
  • Oliguria
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14
Q

What is Medications associated with acute interstitial nephritis (AIN)?

A

-Antibiotics (B-lactams, sulfonamides, vancomycin,
erythromycin, rifampin)
-Acyclovir
-NSAIDS (can cause either direct toxicity or
allergy)
-Anticonvulsants (Phenytoin, valproate, carbamazepine)

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15
Q

What is Treatment of AIN?

A
  • Discontinuation of offending agent often leads to reversal of renal injury
  • Glucocorticoid therapy may accelerate renal recovery (6 week taper prednisone or IV methylprednisolone pulse 3 days)
  • Damage may be permanent if long duration of exposure and high degree of tubular atrophy and interstitial fibrosis
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16
Q

What are Potential Nephrotoxins that cause ATN?

A 
-NSAIDs
–-Chemotherapeutic agents
–-Aminoglycosides
–-Amphotericin
–-Vancomycin
-–Radiocontrast dye
–-Poison (ethylene glycol, heavy metals)
17
Q

What is Acute Tubular Necrosis (ATN)?

A

acute tubular cell injury, usually reversible unless severe, prolonged

  1. Ischemia
  2. Sepsis
  3. Toxins
18
Q

Laboratory Data for Acute Tubular Necrosis (ATN)?

A
  • Pigmented granular casts (muddy-brown casts) on urinalysis
  • Cr/BUN elevation
  • FeNa >2%
  • Serum hyperkalemia
  • Serum hyperphosphatemia
  • Serum hyperuricemia
19
Q

What is Treatment for ATN?

A

-Aggressive volume replacement– hydrate (If nephrotoxic agent, volume depletion)
-If Oliguria present and extracellular-volume normalized consider loop-diuretic high dose (100-200mg Lasix) to improve urine output
-Protein restriction
-If it’s due to nephrotoxic agent, remove
offending agent
-Dialysis

20
Q

What is Glomerular diseases?

A
  • Infectious Disease associated Syndromes – Post-streptococcal glomerulonephritis
  • Nephrotic syndrome (Minimal change disease)
  • Diabetic nephropathy
  • Hypertensive nephropathy
21
Q

What is Post-streptococcal glomerulonephritis (PSGN)?

A

-Immune complex containing strep Ag deposited in
affected glomeruli
-Antihypertensives, salt restriction, diuretics

22
Q

What’s the Epidemiology of PSGN?

A
  • Most common cause of acute kidney injury in children globally
  • Primarily occurs in developing countries (97%)
  • In developed countries 0.3 per 100,000
  • Risk is highest in children 5-12yr & adults >60yrs
23
Q

What is the Urinalysis of PSGN?

A

+/-Red blood cell casts

24
Q

How is PSGN Diagnosed?

A
  • Hematuria, proteinuria, RBC casts
  • Positive throat, skin culture (only 25% due to timing)
  • Elevated titers of abs to strep products
25
Q

What is the treatment for IgA nephropathy?

A
  • ACE-/ARB
  • Steroids
  • Renal transplant
26
Q

What are Classic clinical presentation of Henoch Schonlein Purpura?

A
  • Rash (especially LE’s and buttocks)
  • Abdominal pain/vomiting
  • Arthralgias (knees, ankles)
  • Edema (hands, feet, scalp, ears)
  • Elevated Cr/BUN
  • Urine hematuria/proteinuria
27
Q

What is Nephrotic Syndrome?

A
  • Heavy proteinuria (>3.5g/24hr)
  • Hypoalbuminemia (<3 g/dL)
  • Peripheral edema
28
Q

What is the Etiology of Nephrotic Syndrome?

A

Membranous Nephropathy

  • Minimal Change Disease
  • Amyloidosis (secondary)
  • Systemic Lupus Erythematosus (secondary)
  • Membranoproliferative glomerulonephritis
  • Focal segmental glomerulosclerosis (FSGS)
  • IgA Nephropathy
29
Q

What is Minimal Change Disease?

A

-70-90% of nephrotic syndrome in childhood but only 10-15% of nephrotic syndrome in adults.
-Pathophysiology uncertain
-Light microscopy is normal on renal bx or only mild
mesangial cell proliferation
-Characteristic histologic finding is diffuse
effacement of the epithelial cell foot processes on electron microscopy
-Abrupt onset edema & nephrotic syndrome
-Average urine protein – 10gm/day
-Hypoalbuminemia
-HTN
-More suceptible to infection with gram+ organisms

30
Q

What are the treatments for Minimal Change Disease?

A
  • 30% of children have spontaneous remission but all children are treated with steroids
  • 90-95% of children develop complete remission after 8 weeks of steroid therapy
  • 80-85% of adults develop complete remission after 8 weeks of steroid therapy
  • Prednisone is first line therapy (up to 16 weeks of therapy)
  • ESRD is rare but may have relapses
31
Q

What is vascular AKI?

A

-Thrombus, embolus, dissection,
vasculitis
-TTP, HUS, DIC

32
Q

What is Postrenal renal failure?

A
  • Prostatic obstruction (hypertrophy, stricture or malignancy)
  • Bladder CA, stone, clots
  • Ovarian/cervical/retroperitoneal malignancy
33
Q

What is Postrenal AKI Treatment?

A
  • Bladder catheterization (Foley catheter, Suprapubic tube)

- Nephrostomy tube

34
Q

What is Polycystic Kidney Disease?

A
  • Multisystem and progressive genetic d/o with cyst formation and enlargement of the kidney (and other organs ie. Pancreas, liver, spleen)
  • 50% require transplant/dialysis by 60yo
  • Screen family members as autosomal dominant
  • Intracranial aneurysm x2 as common as general population (10%)
  • ESRD
35
Q

What are signs and symptoms of Polycystic Kidney Disease?

A 
-Pain (Abdomen, flank, back)
–-Enlargement of cysts
–-Hemorrhage into cyst or
perinephric hematoma
-Infectious (UTI, pyelonephritis, abscess, infected cyst)
–-Nephrolithiasis (20-30%)
36
Q

Diagnosis of Polycystic Kidney Disease?

A

Urinalysis (Hematuria, 1/3 microalbuminuria)

37
Q

Treatment for Polycystic Kidney Disease?

A
  • Blood pressure management (ACE-/ARB – slows progression of disease)
  • Pain control (Avoid NSAIDs, Surgical cyst decompression (can be done by IR), Nephrectomy)
  • Recurrent infections (50% develop UTI (mostly women), May develop infected cysts)
  • Hematuria (Hydrate and if substantial transfuse, Very suceptible to trauma (60% hemorrhage))

Clin Med II (9 decks)

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