Step-Up To Medicine: Renal/gu

Front 1

Define acute renal failure (ARF).

Back 1

(1) A rapid decline in renal function, with an increase in serum creatinine level (a relative increase of 50% or an absolute increase of 0.5 to 1.0 mg/dL).
(2) Can be oliguric, anuric, or nonoliguric
(3) Most common findings are weight gain and edema, due to positive water and sodium balance
(4) Characterized by azotemia (elevated BUN and Cr)

Front 2

What is the general prognosis in the setting of ARF?

Back 2

(1) More than 80% of patients recover completely
(2) The prognosis varies widely, however, depending on the severity of renal failure and the presence of comorbid conditions.
(3) The older the patient and the more severe the insult, the lower is the likelihood of complete recovery.
(4) The most common cause of death in ARF is infection (75% of cases), followed by cardiopulmonary complications

Front 3

What are the three categories of ARF?

Back 3

(1) Prerenal azotemia—decreased in renal blood flow (60%-70% of cases); most common case of ARF; potentially reversible
(2) Intrinsic renal failure—damage to renal parenchyma (25%-40% of cases); kidney tissue is damaged such that glomerular filtration and tubular function are significantly impaired
(3) Postrenal failure—Least common cause of ARF (5-10% of cases); associated with obstruction of urinary tract which causes increased tubular pressure, leading to decreased GFR. Blood supply and renal parenchyma are intact.

Front 4

What are the main causes of prerenal failure?

Back 4

(1) Generally, decrease in systemic arterial blood volume or renal perfusion)—can complicate any disease that causes hypovolemia, low CO, or systemic vasodilation
(2) Hypovolemia—dehyrdation, excessive diuretics, poor fluid intake, vomiting, diarrhea, burns, hemorrhage
(3) CHF
(4) Peripheral vasodilation—sepsis, excessive antihypertensive medications
(5) Renal arterial obstruction
(6) Cirrhosis, hepatorenal syndrome
(7) In patients with decreased renal perfusion (e.g. renal artery stenosis), NSAIDs, ACE inhibitors, and cyclosporine can precipitate prerenal failure

Front 5

Describe the basic pathophysiology of prerenal azotemia.

Back 5

(1) RBF decreases enough to lower the GFR, leading to decreased clearance of metabolites (BUN, Cr, uremic toxins)
(2) Because the renal parenchyma is undamaged, tubular function (and therefore the concentrating ability) is preserved; kidney responds appropriately
(3) Reversible on restoration of blood flow; if hypoperfusion persists, ischemia results and can lead to ATN

Front 6

What are the main clinical features of prerenal azotemia?

Back 6

(1) Signs of volume depletion
(2) Dry mucous membranes
(3) Hypotension
(4) Tachycardia
(5) Decreased tissue turgor
(6) Oliguria/anuria

Front 7

Describe the laboratory findings in prerenal azotemia.

Back 7

(1) Oliguria – always found in prerenal failure (to preserve volume)
(2) Increased BUN to serum Cr ratio (>20:1 is the classic ratio)—because kidney can reabsorb urea
(3) Increased urine osmolality (>500 mOsm/kg H2O)—because kidney is able to reabsorb water
(4) Decreased urine Na+ (<20 mEq/L); FEna <1%; because sodium is avidly reabsorbed
(5) Increased urine/plasma Cr ratio (>40:1)—because much of the filtrate is reabsorbed (but not the creatinine)
(6) Bland urine sediment

Front 8

What is the diagnostic approach in ARF?

Back 8

(1) History and physical examination
(2) Determine the duration of renal failure by obtaining a baseline Cr level
(3) Determine whether ARF is due to prerenal, intrarenal, or postrenal causes; done by a combination of H&P and labs.
(4) Medication review
(5) Urinalysis
(6) Urine chemistry (FENa, osmolality, urine Na+, urine Cr
(7) Renal ultrasound (to rule out obstruction)

Front 9

List the main causes of intrinsic renal failure.

Back 9

(1) Tubular disease—ischemia, nephrotoxins
(2) Glomerular disease—acute GN (e.g. Goodpasture’s, Wegener’s, post-streptococcal GN, lupus
(3) Vascular disease—e.g. renal artery occlusion, TTP, HUS
(4) Interstitial disease—e.g. allergic interstitial nephritis, often due to a hypersensitivity reaction to medication

Front 10

What are the typical lab findings in the setting of intrinsic renal failure?

Back 10

(1) Decreased BUN:Cr (<20:1); both BUN and Cr are still elevated, but less urea is reabsorbed than in prerenal failure
(2) Increased urine Na+ (>40 mEq/L w/ FENa >2%-3%)—because Na+ is poorly absorbed
(3) Decreased urine osmolality (<350 mOsm/kg H2O)—because renal water reabsorption is impaired
(4) Decreased urine-plasma Cr ratio (<20:1)—because filtrate cannot be reabsorbed

Front 11

List the most common causes of postrenal failure.

Back 11

(1) Urethral obstruction secondary to enlarged prostate (MCC)
(2) Obstruction of solitary kidney
(3) Nephrolithiasis
(4) Obstructing neoplasm
(5) Retroperitoneal fibrosis
(6) Ureteral obstruction is an uncommon cause because obstructions have to be bilateral to cause renal failure