STEPUP Renal and Genitourinary System: Renal Failure

Question 1

What is the definition of acute kidney injury? Can creatinine be normal in acute kidney injury?

Answer 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) The creatinine may be normal despite markedly reduced glomerular filtration rate (GFR) in the early stages of acute kidney injury (AKI) due to the time it takes for creatinine to accumulate in the body

Question 2

What are the RIFLE criteria of AKI?

Answer 2

1) RISK: 1.5-fold increase in the serum creatinine or GFR decrease by 25% or urine output <0.5mL/kg/hr for 6 hours
2) INJURY: Twofold increase in the serum creatinine or GFR decrease by 50% or urine output <0.5mL/kg/hr for 12 hours
3) FAILURE: Threefold increase in the serum creatinine or GFR decrease by 75% or urine output of <0.5 mL/kg/hr for 24 hours, or anuria for 12 hours
4) LOSS: Complete loss of kidney function (i.e., requiring dialysis) for more than 4 weeks
5) ESRD: Complete loss of kidney function (i.e., requiring dialysis for more than 3 months

Question 3

What are different levels of urine output in AKI? Can you have severe AKI without reduction in urine output?

Answer 3

1) Nonoliguric, oliguric, or anuric

2) Yes, severe AKI may occur without a reduction in urine output (nonoliguric AKI)

Question 4

What are the most common findings in patients with AKI? What are these findings due to?

Answer 4

1) Weight gain and edema

2) This is due to a positive water and sodium (Na+) balance

Question 5

What is AKI characterized by? What is an elevated BUN also seen with aside from AKI? What is an elevated Cr also seen with aside from AKI?

Answer 5

1) Azotemia (elevated BUN and Cr)
2) Elevated BUN is also seen with catabolic drugs (e.g., steroids), GI/soft tissue bleeding, and dietary protein intake
3) Elevated Cr is also seen with increased muscle breakdown and various drugs. The baseline Cr level varies proportionately with muscle mass

Question 6

What is the prognosis of AKI in most patients? What does the prognosis depend on? How does the prognosis change in an older patient with a more severe insult?

Answer 6

1) More than 80% of patients in whom AKI develops recover completely
2) Prognosis varies widely depending on the severity of renal failure and other comorbidities
3) The older the patient and the more severe the insult, the lower is the likelihood of complete recovery

Question 7

What is the most common cause of death in AKI patients?

Answer 7

Infection (75% of all deaths) followed by cardiorespiratory complications

Question 8

What are the three categories/types of AKI?

Answer 8

1) Prerenal AKI - decrease in renal blood flow (60% to 70% of cases)
2) Intrinsic AKI - damage to renal parenchyma (25% to 40% of cases)
3) Postrenal AKI - urinary tract obstruction (5% to 10% of cases)

Question 9

What type of AKI is the most common? Is it reversible?

Answer 9

1) Prerenal AKI

2) Potentially reversible

Question 10

What is the cause of prerenal AKI?

Answer 10

1) Decrease in systemic arterial blood volume or renal perfusion
2) Can complicate any disease that causes hypovolemia, low cardiac output, or systemic vasodilation

Question 11

What are the etiologies of prerenal AKI?

Answer 11

1) Hypovolemia - dehydration, excessive diuretic use, poor fluid intake, vomiting, diarrhea, burns, hemorrhage
2) CHF
3) Hypotension (systolic BP below 90 mm Hg), from sepsis, excessive antihypertensive medications, bleeding, dehydration
4) Renal arterial obstruction (kidney is hypoperfused despite elevated blood pressure)
5) Cirrhosis, hepatorenal syndrome
6) In patients with decreased renal perfusion, NSAIDs (constrict afferent arteriole), ACE inhibitors (cause efferent arteriole vasodilation), and cyclosporin can precipitate prerenal failure

Question 12

What should you monitor and watch out for in a patient with AKI?

Answer 12

1) Daily weights, intake, and output
2) BP
3) Serum electrolytes
4) Watch Hb and Hct for anemia
5) Watch for infection

Question 13

What happens to renal blood flow in prerenal failure and how does this affect GFR? What happens to the renal parenchyma and tubular function? Is prerenal renal failure reversible? What can it lead to?

Answer 13

1) Renal blood flow decreases enough to lower the GFR, which leads 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. Therefore, the kidney responds appropriately, conserving as much sodium and water as possible
3) This form of AKI is reversible on restoration of blood flow; but if hypoperfusion persists, ischemia results and can lead to acute tubular necrosis (ATN)

Question 14

What are clinical features of prerenal kidney failure?

Answer 14

Signs of volume depetion (dry mucous membranes, hypotension, tachycardia, decreased tissue turgor, oliguria/anuria)

Question 15

What happens to urine output in prerenal failure? BUN-to-serum Cr ratio? Urine osmolality? Urine Na+? Urine-plasma Cr ratio? What type of urine sediment is found?

Answer 15

1) Oliguria - always found in prerenal failure (this is 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 the kidney is able to reabsorb water
4) Decreased urine Na+ (<20 mEq/L with fractional excretion of sodium [FENa] <1%) because Na+ 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

Question 16

What is the definition of intrinsic renal failure? Are the kidneys able to concentrate urine?

Answer 16

1) Kidney tissue is damaged such that glomerular filtration and tubular function are significantly impaired
2) The kidneys are unable to concentrate urine effectively

Question 17

What are causes of intrinsic renal failure?

Answer 17

1) Tubular disease (ATN)
2) Glomerular disease (acute glomerulonephritis [GN])
3) Vascular disease
4) Interstitial disease

Question 18

What is the cause of acute tubular necrosis?

Answer 18

Can be caused by ischemia (most common cause) and nephrotoxins

Question 19

What are examples of glomerular disease in intrinsic renal failure?

Answer 19

Goodpasture syndrome, Wegener granulomatosis, poststreptococcal GN, and lupus

Question 20

What are examples of vascular disease in intrinsic renal failure?

Answer 20

Renal artery occlusion, TTP, and HUS

Question 21

What is the first thing to do in diagnosis of AKI? What first test should you check? What should you determine next? What are some signs to look for that suggest prerenal etiology? What does an allergic reaction (rash) suggest etiology of? What suggests a postrenal etiology? What other things should be reviewed and what other tests should be done for AKI?

Answer 21

1) History and physical examination
2) The first thing to do is to determine the duration of renal failure. A baseline Cr level provides this information.
3) The second task is to determine whether AKI is due to prerenal, intrarenal, or postrenal causes. This is done via a combination of H&P and laboratory findings
4) Signs of volume depletion and CHF suggest a prerenal etiology
5) Signs of an allergic reaction (rash) suggest acute interstitial nephritis (an intrinsic renal etiology)
6) A suprapubic mass, BPH, or bladder dysfunction
7) Medication review, urinalysis, urine chemistry (FENa, osmolality, urine Na+, urine Cr), renal ultrasound (to rule out obstruction)

Question 22

How does urinalysis differ in prerenal and intrinsic renal AKI? BUN/Cr ratio? FENa? Urine Osmolality? Urine Sodium?

Answer 22

1) Prerenal:
a) Urinalysis: Hyaline casts
b) BUN/Cr Ratio: >20:1
c) FENa: <1%
d) Urine Osmolality: >500 mOsm
e) Urine Sodium: <20
2) Intrinsic Renal:
a) Urinalysis: Abnormal
b) BUN/Cr Ratio: <20:1
c) FENa: >2%-3%
d) Urine Osmolality: 250-300mOsm
e) Urine Sodium: >40

Question 23

How do urine osmolarity, urine Na+, FENa, and urine sediment differ in prerenal failure and ATN?

Answer 23

1) Prerenal failiure:
a) Urine osmolarity: >500
b) Urine Na+: <20
c) FENa: <1%
d) Urine sediment: Scant
2) ATN:
a) Urine osmolarity: >350
b) Urine Na+: >40
c) FENa: >1%
d) Urine sediment: Full brownish pigment, granular casts with epithelial casts

Question 24

What is important to note about prerenal azotemia and ischemic AKI in terms of renal hypoperfusion?

Answer 24

1) Note that prerenal azotemia and ischemia AKI are part of a spectrum of manifestations of renal hypoperfusion
2) The latter differs in that injury to renal tubular cells occurs

Question 25

What is rhabdomyolysis caused by? What happens in rhabdomyolysis? What laboratory studies are elevated in rhabdo? What is the treatment?

Answer 25

1) Skeletal muscle breakdown caused by trauma, crush injuries, prolonged immobility, seizures, snake bites 2) Release of muscle fiber contents (myoglobin) into bloodstream. Myoglobin is toxic to kidneys, which can lead to AKI 3) Presents with markedly elevated creatine phosphokinase (CPK), hyperkalemia, hypocalcemia, hyperuricemia 4) Treat with IV fluids, mannitol (osmotic diuretic) and bicarbonate (drives K back into cells)

Question 26

What are two causes of acute tubular necrosis (ATN)?

Answer 26

1) Ischemic AKI | 2) Nephrotoxic AKI

Question 27

What is ischemic AKI caused by? What does it lead to in ATN?

Answer 27

1) Secondary to severe decline in renal blood flow, as in shock, hemorrhage, sepsis, disseminated intravascular coagulation, heart failure 2) Ischemia results in the death of tubular cells

Question 28

What is nephrotoxic AKI caused by that results in ATN?

Answer 28

1) Injury secondary to substances that directly injure renal parenchyma and result in cell death 2) Causes include antibiotics (aminoglycosides, vancomycin), radiocontrast agents, NSAIDs (especially in the setting of CHF), poisons, myoglobinuria (from muscle damage, rhabdomyolysis, strenuous exercise), hemoglobinuria (from hemolysis), chemotherapeutic drugs (cisplatin), and kappa and gamma light chains produced in multiple myeloma

Question 29

What do the clinical features of intrinsic renal failure depend on? What symptom is usually present? Is recovery possible?

Answer 29

1) Clinical features depend on the cause 2) Edema is usually present 3) Recovery may be possible but takes longer than in prerenal failure

Question 30

What are laboratory findings in intrinsic renal failure for BUN-to-serum Cr ratio? Urine Na+? Urine osmolality? Urine-plasma Cr ratio?

Answer 30

1) Decreased BUN-to-serum Cr ratio (<20:1, typically closer to 10:1 ratio) in comparison with prerenal failure. Both BUN and Cr levels are still elevated, but less urea is reabsorbed than in prerenal failure 2) Increased urine Na+ (>40 mEq/L with FENa > 2% to 3%) - because Na+ is poorly reabsorbed 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

Question 31

How common of a cause of AKI is postrenal failure? What is the etiology of postrenal failure and what must happen for creatinine to rise? What happens to renal function if postrenal failure is treated? If postrenal failure is untreated, what happens? What are causes of postrenal failure?

Answer 31

1) Least common cause of AKI 2) Obstruction of any segment of the urinary tract (with kidney) causes increased tubular pressure (urine produced cannot be excreted), which leads to decreased GFR. Blood supply and renal parenchyma are intact. Note that both kidneys must be obstructed for creatinine to rise 3) Renal function is restored if obstruction is relieved before the kidneys are damaged 4) Postrenal obstruction, if untreated, can lead to ATN 5) Causes: a) Urethral obstruction secondary to enlarged prostate (BPH) is the most common cause b) Obstruction of solitary kidney c) Nephrolithiasis d) Obstructing neoplasm (bladder, cervix, prostate, and so on) e) Retroperitoneal fibrosis f) Ureteral obstruction is an uncommon cause because obstruction must be bilateral to cause renal failure

Question 32

Describe the course of ATN in phases

Answer 32

1) Onset (insult) 2) Oliguric phase 3) Diuretic phase 4) Recovery phase

Question 33

Describe the oliguric phase of ATN

Answer 33

1) Azotemia and uremia - average length 10 to 14 days | 2) Decreased urine output

Question 34

Describe the diuretic phase of ATN

Answer 34

1) Begins when urine output is >500mL/day 2) High urine output due to the following: fluid overload (excretion of retained salt, water, other solutes that were retained during oliguric phase); osmotic diuresis due to retained solutes during oliguric phase; tubular cell damage (delayed recovery of epithelial cell function relative to GFR)

Question 35

What is urine osmolality? How does dehydration affect urine osmolality? What happens to urine osmolality in ATN and why?

Answer 35

1) Urine osmolality is a measure of urine concentration. The higher the osmolality, the more concentrated the urine 2) Dehydration in a healthy person leads to increase in urine concentration (osmolality) as follows: Dehydration causes low intravascular volume, which triggers ADH release, which stimulates reabsorption of water from kidney to fill the vasculature. Increased water reabsorption leads to more concentrated urine 3) In ATN, the tubule cells are damaged and cannot reabsorb water (or sodium); so the urine cannot be concentrated, which leads to low urine osmolality

Question 36

What tests can you do to diagnose AKI?

Answer 36

1) Blood tests 2) Urinalysis 3) Urine chemistry 4) Urine culture and sensitivities 5) Renal ultrasound 6) CT scan 7) Renal biopsy 8) Renal arteriography

Question 37

What blood tests can be used to diagnose AKI?

Answer 37

1) Elevation in BUN and Cr levels | 2) Electrolytes (K+, Ca2+, PO43-), albumin levels, CBC with differential

Question 38

What are two ways in which a urinalysis can be used to diagnose AKI? What do findings on microscopic examination of the urine sediment indicate?

Answer 38

1) A dipstick test positive for protein (3+,4+) suggests intrinsic renal failure due to glomerular insult 2) Microscopic examination of the urine sediment: a) Hyaline casts are devoid of contents (seen in prerenal failure) b) RBC casts indicate glomerular disease c) WBC casts indicate glomerular disease d) Fatty casts indicate nephrotic syndrome

Question 39

What are three basic tests for postrenal failure?

Answer 39

1) Physical examination - palpate the bladder 2) Ultrasound - look for obstruction, hydronephrosis 3) Catheter - look for large volume of urine

Question 40

How is the diagnosis of AKI usually made? Is the patient symptomatic?

Answer 40

1) Diagnosis of AKI is usually made by finding elevated BUN and Cr levels 2) The patient is usually asymptomatic

Question 41

What tests should you obtain in any patient with AKI?

Answer 41

1) Urinalysis 2) Urine chemistry 3) Serum electrolytes (Na+, K+, BUN, Cr), CBC 4) Bladder catheterization to rule out obstruction (diagnostic and therapeutic) 5) Renal ultrasound to look for obstruction

Question 42

What urine chemistry tests can be used to distinguish between different forms of AKI? How do you measure/calculate each of these tests? What do values of these tests indicate?

Answer 42

1) Urine Na+, Cr, and osmolality: Urine Na+ depends on dietary intake 2) FENa: collect urine and plasma electrolytes simultaneously = [(UNa)/(PNa)/(UCr)/PCr) x 100], where U = urine and P = plasma a) Values below 1% suggest prerenal failure b) Values above 2% to 3% suggest ATN c) FENa is most useful if oliguria is present 3) Renal failure index 5 (UNa/[UCr/PCr]) x 100) a) Values below 1% suggest prerenal failure b) Values above 1% suggest ATN

Question 43

When do you run urine culture and sensitivities for AKI?

Answer 43

If infection is suspected

Question 44

Why is a renal ultrasound in AKI useful? Is it frequently ordered in AKI?

Answer 44

1) Useful for evaluating kidney size and for excluding urinary tract obstruction (i.e., postrenal failure) - presence of bilateral hydronephrosis or hydroureter 2) Order for most patients with AKI - unless the cause of the AKI is obvious and is not postrenal

Question 45

When is a CT scan of the abdomen and pelvis usually done?

Answer 45

It may be helpful in some cases; usually done if renal ultrasound shows an abnormality such as hydronephrosis

Question 46

When is a renal biopsy done in the setting of AKI?

Answer 46

Useful occasionally if there is suspicion of acute GN or acute allergic interstitial nephritis

Question 47

When is renal arteriography done for AKI?

Answer 47

To evaluate for possible renal artery occlusion; should be performed only if specific therapy will make a difference

Question 48

What should first be excluded when evaluating a patient with AKI?

Answer 48

First exclude prerenal and postrenal causes, and then, if necessary, investigate intrinsic renal causes

Question 49

What are the most common mortal complications in the early phase of AKI?

Answer 49

1) Hyperkalemic cardiac arrest | 2) Pulmonary edema

Question 50

What are 4 categories of complications in AKI?

Answer 50

1) ECF volume expansion and resulting pulmonary edema 2) Metabolic 3) Uremia 4) Infection

Question 51

How do you treat ECF volume expansion and resulting pulmonary edema in AKI?

Answer 51

Diuretic (furosemide)

Question 52

What metabolic abnormalities can happen in AKI?

Answer 52

1) Hyperkalemia 2) Metabolic acidosis (with increased anion gap) 2) Hypocalcemia 4) Hyponatremia 5) Hyperphosphatemia 6) Hyperuricemia

Question 53

How does hyperkalemia occur in AKI?

Answer 53

It is due to decreased excretion of K+ and the movement of potassium from ICF to ECF due to tissue destruction and acidosis

Question 54

How does metabolic acidosis occur in AKI? When and how is it treated?

Answer 54

1) It is due to decreased excretion of hydrogen ions | 2) If severe (below 16 mEq/L), correct with sodium bicarbonate

Question 55

How does hypocalcemia occur in AKI?

Answer 55

Loss of ability to form active vitamin D and rapid development of PTH resistance

Question 56

How does hyponatremia occur in AKI?

Answer 56

1) Hyponatremia may occur if water intake is greater than body losses 2) If a volume depleted patient consumes excessive hypotonic solutions (Hypernatremia may also be seen in hypovolemia states)

Question 57

How does uremia occur in AKI?

Answer 57

Toxic end products of metabolism accumulate (especially from protein metabolism)

Question 58

Is infection in AKI common? What is the cause? What are examples?

Answer 58

1) Infection is a common and serious complication of AKI (occurs in 50% to 60% of cases) 2) The cause is probably multifactorial, but uremia itself is thought to impair immune function 3) Examples include pneumonia, UTI, wound infection, and sepsis

Question 59

What are general treatment measures for AKI?

Answer 59

1) Avoid medications that decrease renal blood flow (NSAIDs) and/or that are nephrotoxic (e.g., aminoglycosides, radiocontrast agents) 2) Adjust medication dosages for level of renal function 3) Correct fluid imbalance 4) Correct electrolyte disturbances if present 5) Optimize cardiac output. BP should be approximately 120 to 140/80 to 90 6) Order dialysis if symptomatic uremia, intractable acidemia, hyperkalemia, or volume overload develop

Question 60

How do you correct fluid imbalance in AKI if volume depleted? If volume overloaded? What is the goal of correcting fluid imbalance? What should you monitor? What should also take into account?

Answer 60

1) If volume depleted, give IV fluids 2) Many patients with AKI are volume overloaded (especially if they are oliguric or anuric), so diuresis may be necessary 3) The goal is to strike a balance between correcting volume deficits and avoiding volume overload (while maintaining adequate urine output) 4) Monitor fluid balance by daily weight measurements (most accurate estimate) and intake-output records 5) Be sure to take into account the patient's cardiac history when considering treatment options for fluid imbalances (i.e., do not give excessive fluid to a patient with CHF)

Question 61

What should you focus on in treating prerenal AKI? What fluids should you give and why? Which patients should you not give fluids to? What medications may it be necessary to stop? What should you eliminate? What should you do if a patient is unstable?

Answer 61

1) Treat the underlying disorder 2) Give NS to maintain euvolemia and restore blood pressure 3) Do not give fluids to patients with edema or ascites 4) May be necessary to stop antihypertensive medications 5) Eliminate any offending agents (ACE inhibitors, NSAIDs) 6) If patient is unstable, Swan-Ganz monitoring for accurate assessment of intravascular volume

Question 62

How can radiographic contrast media be nephrotoxic? How can this be prevented?

Answer 62

1) Can cause ATN (typically very rapidly) by causing spasm of the afferent arteriole 2) Can be prevented with saline hydration

Question 63

What type of urine sediment is found on urinalysis in prerenal AKI? Intrarenal ATN? Intrarenal acute glomerulonephritis? Intrarenal AIN? Postrenal AKI?

Answer 63

1) Benign sediment - few hyaline casts 2) "Muddy brown" casts, renal tubular cells/casts, granular casts 3) Dysmorphic RBCs, RBCs with casts, WBCs with casts, fatty casts 4) RBCs, WBCs, WBCs with casts, eosinophils 5) Benign; may or may not see RBCs, WBCs

Question 64

Is there protein found in urinalysis in prerenal AKI? Intrarenal ATN? Intrarenal acute glomerulonephritis? Intrarenal AIN? Postrenal AKI?

Answer 64

1) Negative 2) Trace 3) 4+ 4) 1+ 5) Negative

Question 65

Is there blood found in urinalysis in prerenal AKI? Intrarenal ATN? Intrarenal acute glomerulonephritis? Intrarenal AIN? Postrenal AKI?

Answer 65

1) Negative 2) Negative 3) 3+ 4) 2+ 5) Negative

Question 66

What are prognostic factors that determine the severity of renal failure in AKI?

Answer 66

1) Magnitude of increase in Cr 2) Presence of oliguria 3) Fractional excretion of sodium 4) Requirement for dialysis 5) Duration of severe renal failure 6) Marked abnormalities on urinalysis

Question 67

What are prognostic factors that determine the underlying health of the patient in AKI?

Answer 67

1) Age | 2) Presence, severity, and reversibility of underlying disease

Question 68

What are prognostic factors that determine the clinical circumstances of the patient in AKI?

Answer 68

1) Cause of renal failure 2) Severity and reversibility of acute process(es) 3) Number and type of other failed organ systems 4) Development of sepsis and other complications

Question 69

What factors favor CKD over AKI?

Answer 69

1) History of kidney disease, HTN, abnormal urinalysis, edema 2) Small kidney size on renal ultrasound 3) Hyperkalemia, acidemia, hyperphosphatemia, anemia 4) Urinalysis with broad casts (i.e., more than two to three WBCs in diameter)

Question 70

What factors favor AKI over CKD?

Answer 70

1) Return of renal function to normal with time 2) Hyperkalemia, acidemia, hyperphosphatemia, anemia 3) Urine output <500mL/day without uremic symptoms

Question 71

What is the first thing to do whenever a patient has elevated Cr levels? Why is this helpful?

Answer 71

1) Determine the patients baseline Cr level, if possible 2) This helps determine whether the patient has AKI, CKD, or chronic renal insufficiency/failure with superimposed AKI (This condition is known as "acute on chronic" renal failure)

Question 72

What is azotemia? What is uremia?

Answer 72

1) Azotemia refers to the elevation of BUN 2) Uremia refers to signs and symptoms associated with accumulation of nitrogenous wastes due to impaired renal function. It is didficult to predict when uremic symptoms will appear, but it rarely occurs unless the BUN is > 60mg/dL

Question 73

What are the most common causes of ESRD?

Answer 73

1) Diabetes | 2) Hypertension

Question 74

What is ESRD defined by?

Answer 74

1) Not defined by BUN or creatinine levels | 2) Defined by loss of kidney function that leads to laboratory and clinical findings of uremia

Question 75

What is the treatment for intrinsic renal AKI? What if the patient is oliguric?

Answer 75

1) Once ATN develops, therapy is supportive. Eliminate the cause/offending agent 2) If oliguric, a trial of furosemide may help to increase urine flow. This improves fluid balance

Question 76

What is the treatment for postrenal AKI?

Answer 76

A bladder catheter may be inserted to decompress the urinary tract. Consider urology consultation

Question 77

What two things can chronic kidney disease (CKD) be defined as?

Answer 77

1) Decreased kidney function (GFR < 60mL/min) | 2) Kidney damage (structural or functional abnormalities) for at least 3 months, regardless of cause

Question 78

What are causes of CKD?

Answer 78

1) Diabetes is the most common cause (30% of cases) 2) HTN is responsible for 25% of cases 3) Chronic GN accounts for 15% of cases 4) Interstitial nephritis, polycystic kidney disease, obstructive uropathy 5) Any of the causes of AKI may lead to CKD if prolonged and/or if treatment is delayed

Question 79

What is the relationship between Cr and GFR in CKD? What is the most common clinical measure of GFR? What does an increase in plasma Cr indicate? Decrease in plasma Cr? What do most laboratories now also report?

Answer 79

1) Plasma Cr varies inversely with GFR 2) Cr clearance is the most common clinical measure of GFR 3) An increase in plasma Cr indicates disease progression, whereas a decrease suggests recovery of renal function (assuming muscle mass has not changed) 4) Most laboratories now also report an estimated GFR (eGFR) each time the creatinine is ordered

Question 80

In which race is CKD more common?

Answer 80

More common in African-American than in Caucasian patients

Question 81

What organ systems have clinical features of CKD that may be present?

Answer 81

1) Cardiovascular 2) GI 3) Neurologic 4) Hematologic 5) Endocrine/metabolic 6) Fluid and electrolyte problems 7) Immunologic

Question 82

What are clinical features of the cardiovascular system that may be present in CKD and why?

Answer 82

1) HTN a) Secondary to salt and water retention - decreased GFR stimulates renin-angiotensin system and aldosterone secretion to increase, which leads to an increase in BP b) Renal failure is the most common cause of secondary HTN 2) CHF - due to volume overload, HTN, and anemia 3) Pericarditis (uremic)

Question 83

What are clinical features of the GI system that may be present in CKD and why?

Answer 83

1) Nausea, vomiting (usually due to uremia) | 2) Loss of appetite (anorexia)

Question 84

What are symptoms of the neurologic system that may be present in CKD? Physical exam findings? What features of hypocalcemia can mimic symptoms of the neurologic system?

Answer 84

1) Symptoms include lethargy, somnolence, confusion, peripheral neuropathy, and uremic seizures 2) Physical findings include weakness, asterixis, and hyperreflexia. Patients may show "restless legs" - neuropathic pain in the legs that is only relieved with movement 3) Hypocalcemia can cause lethargy, confusion, and tetany

Question 85

What are symptoms of the hematologic system that may be present in CKD and why?

Answer 85

1) Normocytic normochromic anemia (secondary to deficiency of erythropoietin) - may be severe 2) Bleeding secondary to platelet dysfunction (due to uremia). Platelets do not degranulate in uremic environment

Question 86

Why do hyperphosphatemia and hypocalcemia occur in CKD? Can hypercalcemia be present? What can secondary hyperparathyroidism result in? What is calciphylaxis?

Answer 86

1) Decreased renal clearance of phosphate leads to hyperphosphatemia, which results in decreased renal production of 1,25-dihydroxy vitamin D. This leads to hypocalcemia, which causes secondary hyperparathyroidism 2) So, hypocalcemia and hyperphosphatemia are usually seen, but long-standing secondary hyperparathyroidism and calcium-based phosphate binders may sometimes cause hypercalcemia 3) Secondary hyperparathyroidism causes renal osteodystrophy, which causes weakening of bones and possibly fractures 4) Hyperphosphatemia may cause calcium and phosphate to precipitate, which causes vascular calcifications that may result in necrotic skin lesions. This is called calciphylaxis

Question 87

What are sexual/reproductive symptoms that may arise in CKD?

Answer 87

Sexual/reproductive symptoms due to hypothalamic-pituitary disturbances and gonadal response to sex hormones: in men, decreased testosterone; in women, amenorrhea, infertility, and hyperproactinemia

Question 88

Is pruiritus (multifactorial etiology) common in CKD? What is the treatment?

Answer 88

1) Common and difficult to treat | 2) Dialysis and UV light

Question 89

What are fluid and electrolyte problems in CKD?

Answer 89

1) Volume overload - watch for pulmonary edema 2) Hyperkalemia - due to decreased urinary secretion 3) Hypermagnesemia - occurs secondary to reduced urinary loss 4) Hyperphosphatemia 5) Metabolic acidosis - due to loss of renal mass (and thus decreased ammonia production) and the kidney's inability to excrete H+

Question 90

What is the immunologic effect of CKD?

Answer 90

Uremia inhibits cellular and humoral immunity

Question 91

When is the term chronic renal insufficiency used? To whom is it generally applied to?

Answer 91

1) When a patient's renal function is irreversibly compromised but not failed 2) To those with a chronic elevation of serum creatinine of 1.5 to 3.0 mg/dL

Question 92

What is a major cause of mortality in patients with CKD?

Answer 92

Increased susceptibility to infections

Question 93

Why do patients with CKD get weak bones and become susceptible to fracture?

Answer 93

Hypocalcemia leads to secondary hyperparathyroidism, which removes calcium from bones, making them weak and susceptible to fracture

Question 94

What are the most common complications that require urgent intervention in a patient with CKD?

Answer 94

1) Symptomatic volume overload | 2) Severe hyperkalemia

Question 95

What tests should be run to diagnose CKD and what should you look for in each of these tests? What do small kidneys suggest? What do normal-sized or large kidneys suggest? When should a renal biopsy be done?

Answer 95

1) Urinalysis - examine sediment 2) Measure Cr clearance to estimate GFR 3) CBC (anemia, thrombocytopenia) 4) Serum electrolytes (e.g., K+, Ca2+, PO43-, serum protein) 5) Renal ultrasound - evaluate size of kidneys/rule out obstruction a) Small kidneys are suggestive of chronic renal insufficiency with little chance of recovery b) Presence of normal-sized or large kidneys does not exclude CKD c) Renal biopsy - in select cases to determine specific etiology

Question 96

What are the components of treatment for CKD?

Answer 96

1) Diet 2) ACE inhibitors 3) BP control 4) Glycemic control 5) Smoking cessation 6) Correction of electrolyte abnormalities 7) Anemia 8) Pulmonary edema 9) Pruritis 10) - Dialysis 11) Transplantation

Question 97

What is the protein intake in a diet for CKD? Salt intake? Potassium, phosphate, and magnesium intake?

Answer 97

1) Low protein - 0.7 to 0.8 g/kg body weight per day 2) Use a low-salt diet if HTN, CHF, or oliguria are present 3) Restrict potassium, phosphate, and magnesium intake

Question 98

How do ACE inhibitors help in CKD? If used early on? Why should you use caution?

Answer 98

1) Dilate efferent arteriole of glomerulus 2) If used early on, they reduce the risk of progression to ESRD because they slow the progression of proteinuria 3) Use with great caution because they can cause hyperkalemia

Question 99

Why is strict BP control helpful in CKD? What is the preferred agent to use in controlling BP in CKD?

Answer 99

1) Strict control decreases the rate of disease progression | 2) ACE inhibitors are the preferred agents. Multiple drugs, including diuretics, may be required

Question 100

What is the benefit of glycemic control in CKD if the patient is diabetic?

Answer 100

Prevents worsening of proteinuria

Question 101

What electrolyte abnormalities should you treat in CKD and how?

Answer 101

1) Correct hyperphosphatemia with calcium citrate (a phosphate binder) 2) Patients with chronic renal disease are generally treated with long-term oral calcium and vitamin D in an effort to prevent secondary hyperparathyroidism and uremia osteodystrophy 3) Acidosis - treat the underlying cause (renal failure). Patients may require oral bicarbonate replacement

Question 102

How do you treat anemia in CKD?

Answer 102

Erythropoietin

Question 103

How do you treat pulmonary edema in CKD?

Answer 103

1) Diuretics | 2) If unresponsive, arrange for dialysis

Question 104

How do you treat pruritis in CKD?

Answer 104

1) Capsaicin cream 2) Cholestyramine 3) UV light

Question 105

What is the only cure of CKD?

Answer 105

Kidney transplantation

Question 106

What are life-threaning complications in CKD and how should you check for each?

Answer 106

1) Hyperkalemia - obtain an ECG (be aware that potassium levels can be high without ECG changes) 2) Pulmonary edema secondary to volume overload - look for recent weight gain 3) Infection (e.g., pneumonia, UTI, sepsis)

Question 107

What are absolute indications for dialysis?

Answer 107

1) Acidosis - significant, intractable metabolic acidosis 2) Electrolytes - severe, persistent hyperkalemia 3) Intoxications - methanol, ethylene glycol, lithium, aspirin 4) Overload - hypervolemia not managed by other means 5) Uremia (severe) - based on clinical presentation, not laboratory values (e.g., uremic pericarditis is an absolute indication for dialysis)

Question 108

Is creatinine level an absolute indication for dialysis?

Answer 108

No

Question 109

What is dialysis? In all forms of dialysis, what does the blood interface with and what happens?

Answer 109

1) Dialysis is the artificial mechanism by which fluid and toxic solutes are removed from the circulation when the kidneys cannot do so sufficiently 2) In all forms of dialysis, the blood interfaces with an artificial solution resembling human plasma (called the dialysate), and diffusion of fluid and solutes occurs across a semipermeable membrane

Question 110

What are the two major methods of dialyzing a patient?

Answer 110

1) Hemodialysis | 2) Peritoneal dialysis

Question 111

Where do the majority of dialysis patient in the US receive hemodialysis?

Answer 111

At hospitals or dialysis centers, but more and more patients are opting for chronic ambulatory peritoneal dialysis (CAPD)

Question 112

What can be used for constant renal support for patients with life-threatening complications of AKI?

Answer 112

Continuous renal placement therapy (CRRT)

Question 113

What are settings with CKD, AKI, and overdose in which dialysis is considered?

Answer 113

1) CKD - dialysis serves as a bridge to renal transplantation or as a permanent treatment when the patient is not a transplantation candidate 2) AKI - dialysis is often required as a temporary measure until the patient's renal function improves 3) Overdose of medications or ingestions of substances cleared by the kidneys - some, but not all medications and toxins can be dialyzed

Question 114

What are specific nonemergent indications for dialysis?

Answer 114

1) Cr and BUN levels are not absolute indications for dialysis 2) Symptoms of uremia a) Nausea and vomiting b) Lethargy/deterioration in mental status, encephalopathy, seizures c) Pericarditis

Question 115

What are specific emergent indications (usually in the setting of renal failure) for dialysis?

Answer 115

1) Life-threatening manifestations of volume overload a) Pulmonary edema b) Hypertensive emergency refractory to antihypertensive agents 2) Severe, refractory electrolyte disturbances, for example, hyperkalemia, hypermagnesemia 3) Severe metabolic acidosis 4) Drug toxicity/ingestions (particularly in patients with renal failure): methanol, ethylene glycol, lithium, aspirin

Question 116

Describe the process of hemodialysis

Answer 116

1) The patient's blood is pumped by an artificial pump outside of the body through the dialyzer, which typically consists of fine capillary networks of semipermeable membranes. The dialysate flows on the outside of these networks, and fluids and solutes diffuse across the membrane 2) The patient's blood must be heparinized to prevent clotting in the dialyzer

Question 117

How frequent is dialysis done?

Answer 117

Most hemodialysis patients require 3 to 5 hours of dialysis 3 days per week

Question 118

What are different types of access to use for hemodialysis? Describe each.

Answer 118

1) Use the central catheter placed using the Seldinger technique most often in the subclavian or jugular vein for temporary access 2) Tunneled catheters are placed under the skin which leads to a lower rate of infection. These catheters are often suitable for use up to 6 months 3) Arteriovenous fistula a) Best form of permanent dialysis access b) It requires vascular surgery to connect the radial or brachial artery to veins in the forearm c) An audible bruit over the fistula indicates that it is patent 4) An alternative to an arteriorvenous fistula is an implantable graft - typically made of polytetrafluoroethylene (PTFE)

Question 119

What are alternatives to traditional hemodialysis that are usually used in unstable patients? What allows these types of dialysis to occur while minimizing rapid shifts in volume and osmolality? What do they require to be effective?

Answer 119

1) Continuous arteriovenous hemodialysis (CAVHD) and continuous venovenous hemodialysis (CVVHD) are often used in hemodynamically unstable patients, such as ICU patients with AKI 2) Lower flow rates of blood and dialysate enable dialysis to occur while minimizing rapid shifts in volume and osmolality 3) They require highly efficient dialyzers to be effective

Question 120

What are advantages of hemodialysis?

Answer 120

1) It is more efficient than peritoneal dialysis. High flow rates and efficient dialyzers shorten the period of time required for dialysis 2) It can be initiated more quickly than peritoneal dialysis, using temporary vascular access in the emergent setting

Question 121

What are disadvantages of hemodialysis?

Answer 121

1) It is less similar to the physiology of natural kidney function than is peritoneal dialysis, predisposing the patient to the following: a) Hypotension due to rapid removal of intravascular volume leading to rapid fluid shifts from the extravascular space into cells b) Hypo-osmolality due to solute removal 2) Requires vascular access

Question 122

What are 4 dialyzable substances?

Answer 122

1) Salicylic acid 2) Lithium 3) Ethylene glycol 4) Magnesium-containing laxatives

Question 123

Describe the process of peritoneal dialysis

Answer 123

1) The peritoneum serves as the dialysis membrane. Dialysate fluid is infused into the peritoneal cavity, the fluids and solutes from the peritoneal capillaries diffuse into the dialysate fluid, which is drained from the abdomen 2) A hyperosmolar (high-glucose) solution is used, and water is removed from the blood via osmosis

Question 124

How frequent is peritoneal dialysis done?

Answer 124

Dialysate fluid is drained and replaced every hour in acute peritoneal dialysis, but only once every 4 to 8 hours in CAPD

Question 125

How do you get access in peritoneal dialysis?

Answer 125

1) With CAPD, dialysate is infused into the peritoneal fluid via an implanted catheter 2) A temporary catheter is used for acute peritoneal dialysis

Question 126

What are two advantages of peritoneal dialysis?

Answer 126

1) The patient can learn to perform dialysis on his or her own 2) It mimics the physiology of normal kidney function more closely than hemodialysis in that it is more continuous

Question 127

What are four disadvantages of peritoneal dialysis?

Answer 127

1) High glucose load may lead to hyperglycemia and hypertriglyceridemia 2) Peritonitis is a significant potential complication 3) The patients must be highly motivated to self-administer it 4) Cosmetic - there is increased abdominal girth due to dialysate fluid

Question 128

What are general limitations of dialysis?

Answer 128

1) Dialysis does not replicate the kidney's synthetic functions 2) Therefore, dialysis patients are still prone to erythropoietin and vitamin D deficiency, with their associated complications

Question 129

What are six complications associated with hemodialysis?

Answer 129

1) Hypotension - may result in myocardial ischemia, fatigue, and so on 2) The relative hypo-osmolality of the ECF compared with the brain may result in nausea, vomiting, headache, and rarely, seizures or coma 3) "First-use syndrome" - chest pain, back pain, and rarely, anaphylaxis may occur immediately after a patient uses a new dialysis machine 4) Complications associated with anticoagulation - hemorrhage, hematoma, etc. 5) Infection of vascular access site - may lead to sepsis 6) Hemodialysis-associated amyloidosis of Beta2-microglobulin in bones and joints

Question 130

What are 4 complications associated with peritoneal dialysis?

Answer 130

1) Peritonitis, often accompanied by fever and abdominal pain - usually can be reated with intraperitoneal antibiotics; cloudy peritoneal fluid is key sign 2) Abdominal/inguinal hernia - increased risk due to elevated intra-abdominal pressures 3) Hyperglycemia - especially with diabetic patients 4) Protein malnutrition