ACUTE RENAL FAILURE Flashcards
1
Q
define acute kidney injury
A
- is a rapid rise in blood urea nitrogen (BUN) and creatinine over several hours to days
- a rise in creatinine and a decrease in renal function or glomerular filtration rate.
2
Q
In rhabdomyolysis or contrast-induced renal failure, it may develop IN ………….
A
several hours.
3
Q
In aminoglycoside toxicity or poststreptococcal glomerulonephritis, it may develop in
A
several weeks.
4
Q
Renal insufficiency means renal failure, but not to
A
the point of needing dialysis
5
Q
azotemia means
A
buildup of azole groups or nitrogen in the blood
6
Q
Uremia (which means urea in the blood) describes
A
very severe renal failure in which dialysis is needed to save life
7
Q
Clinical presentation of ACUTE RENAL FAILURE
A
1– Severe acidosis, mental status changes, hyperkalemia, and fluid overload
2– Anemia, hypocalcemia, and possible pericarditis
3– Bleeding diathesis due to platelet dysfunction
8
Q
Uremia does not necessarily mean
A
chronic renal failure as from diabetes
or hypertension,
9
Q
it is possible to become uremic in as little as 1–2 weeks with a severe illness such as
A
tumor lysis syndrome or rhabdomyolysis
10
Q
AKI is also classified as
A
prerenal, postrenal, or intrarenal to determine the site of the defect.
11
Q
Prerenal azotemia means
A
decreased perfusion of the kidney
12
Q
Postrenal azotemia means
A
decreased drainage from the kidney or decreased forward flow of urine.
13
Q
Intrarenal azotemia means
A
a tubular or glomerular problem, and the kidney itself is defective.
14
Q
Diagnostic Tests of ACUTE RENAL FAILURE
A
- BUN becomes abnormally elevated.
- can be falsely elevated even when renal function is normal, in response to increased protein load in the diet or GI bleed. This is also from increased catabolism. The BUN is derived from protein waste products; blood in the gut acts like a big protein meal
15
Q
BUN will improve after
A
a session of dialysis
16
Q
The BUN can be falsely low when there is
A
liver disease, malnutrition, or SIADH.
17
Q
The BUN level corresponds to the degree of
A
renal failure, the higher the BUN, the worse the kidney function.
18
Q
what is Creatinine ?
A
a metabolic product of skeletal muscle, is our main measure of renal function.
19
Q
Creatinine clearance is our closest approximation of
A
glomerular filtration rate (GFR)
20
Q
Creatinine clearance slightly overestimates GFR because
A
there is some tubular secretion of creatinine.
21
Q
Creatinine can be falsely low because of
A
decreased muscle mass
22
Q
Creatinine needs some time to
A
rise.
23
Q
if the patient becomes anuric, the creatinine will rise only at a rate of
A
0.5–1.0 point per day
24
Q
This rise will be faster if the body muscle mass
A
is greater
25
if the creatinine goes from 1 to 3 over 2 days in a patient with renal injury, this is consistent with
nonfunctioning kidneys
26
define Prerenal Azotemia
- a form of renal insufficiency caused by diminished perfusion of the kidney
- The kidney itself is normal
27
If the kidney could receive adequate perfusion,
| the BUN and creatinine would
normalize.
28
The causes of prerenal azotemia include
1- hypovolemia on any basis (dehydration, burns, poor oral intake, diuretic, vomiting, diarrhea, sweating, hemorrhage),
2-hypotension on any basis (septic shock, cardiogenic shock, anaphylactic shock),
3-and third spacing of fluids such as peritonitis, osmotic diuresis, or low aldosterone states such as Addison disease
29
Addison disease results in
intravascular volume depletion, leading to diminished tissue perfusion.
30
Diminished perfusion from a decrease in cardiac output also results in
prerenal azotemia
31
Although there may be total body fluid overload with significant edema, all that matters in terms of renal function is
1-how much fluid is still in the vascular space and
| 2-how much can provide meaningful perfusion of the kidney
32
With severe CHF, constrictive pericarditis, or coarctation of the aorta, there may be
edema and fluid overload
33
The first clue to the diagnosis of prerenal azotemia is
BUN:creatinine ratio of 20:1
34
what are the other clues to the diagnosis of prerenal azotemia?
low urine sodium and low fractional excretion of sodium (FeNa <1%)
- because the kidney perceives the body as being volume-depleted (hence, there will be a vigorous sodium and water reabsorption by the kidney).
35
low urine sodium and low fractional excretion of sodium results in
a very high urine osmolality, because the kidney attempts to retain all the water it can in the kidney, and therefore excretes very concentrated urine
36
Concentrated urine has
a high specific gravity (>1.010) and high urine osmolality (>500).
37
Low albumin states also lead to
decreased renal perfusion
38
diagnosis of prerenal azotemia is
BUN:creatinine ratio rises to 20:1, urine sodium is low, and the urine osmolality is high
39
Renal artery stenosis, especially if bilateral, results in
high BUN and creatinine with a high BUN:creatinine ratio
40
Although systemic BP may be markedly elevated, the result is still a form of
prerenal azotemia.
41
There is markedly diminished renal perfusion because of the obstruction
in the renal artery
42
The systemic BP does not matter; all that matters is
how much is getting to the kidney
43
renal artery stenosis functions like
hypotension
44
renal artery stenosis effect is greatly exaggerated with the use of
ACE inhibitors, which markedly diminish renal perfusion. because of the extremely high aldosterone state
45
define Hepatorenal syndrome
renal failure based entirely on the presence of hepatic failure. The kidneys are normal
46
The rise in BUN and creatinine is believed to be due to an
intense vasoconstriction of the afferent arteriole, causing decreased renal perfusion
47
Because the defect is at the afferent arteriole, lab numbers are consistent with prerenal azotemia like
1-high BUN:creatinine ratio >20:1.
2-Urine sodium is low (<10) and fractional excretion of sodium <1%
3-Intrinsic renal disease should be excluded to make a diagnosis.
4-No improvement in renal failure after 1.5 L of colloid, like albumin, is diagnostic of hepatorenal syndrome
48
Treatment of Hepatorenal syndrome is
1-correction of the underlying liver disease.
2-Midodrine, an alpha agonist,
3-and octreotide may be beneficial,
4-but the best treatment is liver transplantation
49
ACE inhibitor–induced renal failure is caused by
vasodilation of the efferent arteriole.
50
Angiotensin has a significant vasoconstrictive effect on
the efferent arteriole
51
ACE inhibitors block this vasoconstrictive effect, causing
a decreased GFR that is usually transient
52
in the elderly, diabetics, hypertensives, or patients with baseline renal disease such as from myeloma, an ACE inhibitor can produce
a marked decrease in renal function.
53
if there is underlying renal insufficiency, there can be a
| rise in
BUN and creatinine after initiating an ACE inhibitor
54
In patients with bilateral renal artery stenosis, observe for
severe decline in renal function after an ACE inhibitor has been initiated.
55
Despite the ability of ACE inhibitors to potentially worsen renal function, their overall effect on the kidney is to
diminish the rate of progression to uremia and renal failure
56
This beneficial effect is most likely secondary to the decrease in
intraglomerular hypertension
57
ACE inhibitors and angiotensin receptor blockers decrease
hypertension inside the glomerulus
58
ACE inhibitors decrease proteinuria by
35–45%.
59
ACE inhibitors produce a brief decrease in
GFR in the short-term
60
with a long-term beneficial effect on decreasing
proteinuria and the rate of progression of renal failure. This is particularly true in patients with diabetes.
61
Postrenal azotemia is caused by any decrease in
the outflow of urine
62
One cannot get renal failure by the obstruction of a single kidney if a patient has both kidneys in place, i.e., a large stone in one ureter cannot cause
renal failure because creatinine does not rise if there is loss of only one kidney.
63
A small stone or clot in the bladder can obstruct both ............, and this can cause ............
kidneys
| postrenal azotemia.
64
Other causes of postrenal azotemia include
-bladder cancer, prostate hypertrophy/cancer, bilateral ureteral disease e.g., retroperitoneal fibrosis, neurogenic bladder, or any other cause of bilateral obstructive disease.
65
Strictures can cause this problem but only if they are ................ in location.
bilateral
66
The complete obstruction of a single kidney does not cause renal failure because
only 35% of one kidney is needed in order to live
67
Creatinine will begin to rise only 70–80% if renal function has been
lost
68
Thus, more renal function is lost as one goes from
| creatinine...............than from creatinine.............
1 to 2
| 2 to 10.
69
Patients usually have a preceding history of obstructive symptoms followed by
sudden onset of oliguria or anuria.
70
Neurologic causes such as MS, spinal cord lesion, and neuropathy may lead to
poor function of the urinary bladder and obstruction.
71
what is the diagnosis of Postrenal Azotemia
- Initially, BUN and creatinine will elevate in a ratio 20:1 as it does with prerenal azotemia.
- There will also be a low fractional excretion of sodium (FeNa) and low urine sodium.
72
When the obstruction continues for such a long time that there is permanent damage to the kidney and the kidney tubule cells die, then the BUN:creatinine ratio
will
lower to 10:1, as is seen in acute tubular necrosis (ATN). Early diagnosis is, therefore, essential. Complete recovery is possible until 10–14 days of obstruction.
73
ATN is the most common cause of ......... (intrinsic) in hospitalized patients.
AKI
74
The diagnosis of postrenal azotemia is determined by finding
1-a distended bladder on examination,
2-bilateral hydronephrosis on renal sonogram or CT scan,
3-or by finding large volumes of urine in the bladder after passing a Foley urinary catheter
75
After urinating (voiding), there should be no more than .......... of urine left in the bladder. If this post-void residual is markedly elevated, it implies an............... to the flow of urine out of the bladder.
50 mL
| obstruction
76
Treatment is based on relieving the cause of the
obstruction
77
define Acute tubular necrosis
acute renal failure on the basis of tubular damage (as opposed to glomerular damage), or simply decreased perfusion of the kidney or drainage out of the kidney.
78
About 85% of acute renal failure is secondary to intrinsic renal disease such as
ATN
79
ATN is caused by
hypoperfusion of the kidney
leading to such severe ischemia that there is cellular death or by a toxic injury to the kidney such as aminoglycoside toxicity or from amphotericin (caused by sepsis or post-cardiac/aortic surgery).
80
ATN often occurs from a combination of
toxic and ischemic injury.
81
If tissue ischemia seems similar in concept to what was described for prerenal azotemia, that is because
there is overlap. It is like the difference between
myocardial ischemia and a myocardial infarction.
82
If there is modest hypotension or hypovolemia, BUN and creatinine will
rise in a 20:1 ratio consistent with prerenal azotemia. Prerenal azotemia is essentially reversible.
83
If the ischemia becomes more severe, the tubular cells will
necrose and slough off into the urine and become visible as granular, muddy brown, or pigmented casts
84
At the point of necrosis, the renal insufficiency can be ................... In less severe disease and nonoliguric ATN, urinalysis may be relatively .............
permanent
| normal
85
The hypotension causing tubular ischemia can be of any etiology,
surgical or medical. The degree, and especially the duration of hypotension, are extremely important.
86
The longer the duration of hypotension/hypoperfusion, the greater the chance of ..........
ATN
87
the likelihood of rhabdomyolysis causing renal failure is markedly increased when there is
hypoperfusion of the kidney.
88
the likelihood of cisplatin toxicity, tumor lysis syndrome, or injury from hemoglobin toxicity causing renal failure is markedly increased when there is
hypoperfusion of the kidney.
89
There are 3 phases in ATN, although not everyone experiences all phases
* Prodromal: time between the acute injury and onset of renal failure
* Oliguric (<400 mL/24 hrs) or anuric (<100 mL/24 hrs)
* Postoliguric: diuretic phase when all the water not previously excreted will leave the body in a vigorous polyuria
90
Diagnosis of Acute tubular necrosis
The initial clue is a BUN:creatinine ratio close to 10:1; by itself this ratio simply implies the damage is intrarenal (inside the kidney itself),
91
Further clues to the diagnosis of ATN are
high urine sodium (>40), high fractional excretion of sodium (>1%), and low urine osmolality (<350)
92
This is because tubular cells are responsible for forming either ............... or ................. urine
concentrated or
| dilute urine
93
If the tubular cells die from ischemia, then the kidney can neither .................. nor ............. the urine.
concentrate nor dilute the urine
| Dead cells don’t work
94
```
Prerenal
Urine osmolarity ..............
Urine Na+ ..............
FeNa+ ..............
Urine sediment ..............
```
>500
<20
<1%
Scant
95
```
ATN
Urine osmolarity ..............
Urine Na+ ..............
FeNa+ ..............
Urine sediment ..............
```
<350
>40
>1%
Full (brownish pigmented granular casts, epithelial casts may be seen)
96
Treatment of Acute tubular necrosis
1-Treatment focuses on correcting the underlying cause
2-There is no therapy that can reverse the renal failure.
3-Hydration is often given to make sure there is no prerenal component;
4-hydration can prevent contrast-induced renal failure, but it does not reverse it once it occurs, nor can diuretics
97
ATN is a combined ............../............ disease.
ischemic/toxic
98
It is like a ‘sunburn for the kidney.’ Once it occurs, all you can do is
support the patient and wait to see if the renal tubular cells can restore themselves.
99
If the degree of renal failure is severe and life threatening, then ............... is used.
dialysis
100
Allergic interstitial nephritis (AIN) accounts for ............ of intrinsic renal failure
10–15%
101
It can be distinguished from other causes of renal failure by the presence of
fever and rash on physical examination and many WBCs, occasionally eosinophils.
102
The etiology of AIN is usually an adverse immunologic effect to
medication (70% of cases).
103
The medications most likely to be allergenic in general are those medications most likely to cause
AIN
104
```
for example skin rash from an allergic drug reaction can be caused by
1- .............. ,
2-..............,
3-.............. ,
4-..............,
5-..............,
6-and .................
These are the same medications to cause ........... In addition, many of these same drugs cause........................... hemolysis as well.
```
```
1-penicillin,
2-cephalosporin,
3-sulfa drugs,
4-allopurinol,
5-rifampin, and
6-quinolones
```
AIN
drug-induced
105
In other words, 10% of the population is allergic to ................. or ................ drugs
penicillins or sulfa
106
This allergic reaction can take the form of a .............., ............... ............... ............, .............., or ...............
rash, Stevens-Johnson syndrome, hemolysis, or AIN
107
The most common infections to result in AIN are ...................., ..........................., .............., ..................., and ......................
leptospirosis, legionella, CMV, rickettsia, and streptococci.
108
```
The least common causes of AIN are several autoimmune disorders such as
1-...................
2-...................
3-...................
4-...................
```
1-systemic lupus erythematosus (SLE),
2-Sjögren syndrome,
3-sarcoidosis,
4-cryoglobulins.
109
Cryoglobulins can cause renal failure from .................
..................... as well.
membranous glomerulonephritis
110
clinical picture of AIN
1-Fever is present in 80% of those with AIN.
2-Rash is present in 25–50% of patients.
3-Joint pain is common because AIN acts somewhat like serum sickness.
111
Lab abnormalities include the following:
* Eosinophilia, eosinophiluria, hematuria, proteinuria, increased serum IgE
* Hematuria (95% of patients), though this finding is rather nonspecific. More people with AIN have eosinophils in the urine rather than in the blood.
* Mild proteinuria, nearly always <2 grams/24 hrs
112
The best initial test for AIN is a .............................. looking for white cells.
urinalysis (UA)
113
the UA cannot distinguish ................. from other white cells
eosinophils
114
The most accurate test for urine eosinophils is .................... or ..................of the urine.
Hansel or Wright stain
115
The most accurate test for AIN is actually ................. ...................., although that is not needed in the presence of the other findings above
kidney biopsy
116
NSAID-induced injury typically lacks
1-.............,
2-.............,
3-.............
1-fever,
2-rash,
3-and eosinophilia
117
Treatment of Allergic interstitial nephritis
1-There is no specific therapy necessary for AIN in most patients; it should resolve spontaneously after stopping the offending agent.
2-If renal failure persists or worsens, consider a short course of steroids.
118
Rhabdomyolysis is caused by
sudden, severe crush injury; seizures; severe exertion; and sometimes by hypokalemia, hypophosphatemia, or medications such as statins
119
Massive hemoglobinuria severe enough to cause renal failure is generally only caused by an ................ ....................
ABO incompatibility
120
Both of these disorders result in enough pigment release in the bloodstream to cause ........................
nephrotoxicity
121
The toxicity is because the pigment is directly toxic to the .............. ............. as well as from precipitation of the ................. in the tubules.
tubular cells
| pigment
122
The degree of toxicity is related to the duration of
| contact of the tubular cells with the .............. or ..................
hemoglobin or myoglobin.
123
a person who has run a marathon has both .................. release as well as poor kidney perfusion. This is cumulative in the risk of renal failure.
myoglobin
124
The most important test with a severe crush injury or seizure and potentially life-threatening rhabdomyolysis is an
EKG or potassium level
125
Acidosis and hyperkalemia can lead to an ....................
arrhythmia
126
If there are peaked T-waves on the EKG, give ................ ............... or .................
calcium chloride or gluconate.
127
The best initial test for rhabdomyolysis is a ........... , in which you find a dipstick positive for blood but with no red cells visible (that is because ................. can react with the reagent on the dipstick and come out as if there were red cells present)
UA
| myoglobin
128
The dipstick of the UA cannot distinguish among ......................, ....................., and ...............
This is because myoglobin has .............in it.
hemoglobin, myoglobin, and RBCs.
| heme
129
Rhabdomyolysis is confirmed with the following:
* Markedly elevated serum CPK level (a biochemical marker of skeletal muscle neurosis)
* Metabolic acidosis with decreased serum bicarbonate, hyperphosphatemia secondary to muscle breakdown, and hypocalcemia secondary to the deposition of calcium in damaged muscles
* Possible severe hyperuricemia due to release of purines from damaged muscles
* Very rapidly rising creatinine level due to the renal failure and massive release of muscle products; thus, BUN:creatinine ratio may be low (below 10:1)
130
Treatment is
1-In general, therapy is hydration and mannitol used as a diuretic to decrease the duration of contact between the nephrotoxic hemoglobin/myoglobin and the kidney tubule.
2-Alkalinizing the urine with bicarbonate may help prevent the precipitation of the pigment in the tubule.
131
If there are EKG abnormalities from the hyperkalemia, the best initial therapy is ..................... .................. or ....................
calcium chloride or gluconate.
132
Bence-Jones proteins, such as in myeloma, also cause .............. ....................
Myeloma is most prominently a cause of ................... ..................., however, not tubular damage
tubular damage
| nephritic syndrome
133
The most common cause of hyperoxaluria resulting in acute renal failure is ................. .................. ................... in a suicidal person who ingests .................... Look for an intoxicated person with metabolic acidosis and elevated anion gap who is found to have renal insufficiency. Diagnosis is confirmed with ............... ................. seen on urinalysis.
ethylene glycol overdose
antifreeze.
oxalate crystals
134
Look for an intoxicated person with metabolic acidosis and elevated anion gap who is found to have renal insufficiency.
Diagnosis is confirmed with
oxalate crystals seen on urinalysis
135
Treat acute ethylene glycol overdose with .................. .................. to prevent the formation of the toxic metabolite of ethylene glycol,
fomepizole infusion
136
Dialysis must also be used to then remove the ............... .................... Sodium bicarbonate can be given to correct ................
ethylene glycol
| acidosis
137
Chronic hyperoxaluria and kidney stones can be caused by ..................... .................... because of fat and calcium malabsorption.
Crohn’s disease
138
Acute renal failure from uric acid toxicity occurs in the setting of ................... .................... ............. . This is why patients with ................... or ...................... receive vigorous hydration and allopurinol prior to receiving chemotherapy.
tumor lysis syndrome
| leukemia or lymphoma
139
.......................reduces the production of uric acid by inhibiting conversion of xanthine to hypoxanthine to uric acid
Allopurinol
140
Uric acid stones precipitate in an............... ................ , unlike oxalate crystals, which precipitate in ................ ................
acidic urine
| alkaline urine
141
Allopurinol treatment with ................... of urine markedly reduces the risk of uric acid nephropathy
alkalinization
142
Chronically, ............. causes renal impairment through a slower and milder version of the same mechanism.
gout
143
In hypercalcemia, calcium precipitates in the kidney tubule, forming .............
stones
144
The most common cause of hypercalcemia is .................. ...........................
primary hyperparathyroidism
145
If there is no renal damage (or decreased GFR) and no symptoms, i.e., mild hyperparathyroidism.
treatment is ................. ...............
If the hyperparathyroidism is associated with evidence of renal impairment, treatment is ................ .................. .......................
not surgical
| surgical resection of the glands.
146
The most common toxins to be associated with renal insufficiency and ATN are
NSAIDs; aminoglycosides; cephalosporins;
contrast agents; amphotericin;
chemotherapy e.g., cisplatin;
radiation effect;
heavy metals e.g., lead, mercury, gold; and cyclosporine.
147
1-Allergic interstitial nephritis occurs with the .......... ............. , and is associated with .......... , .......... , .......... .......... , and .......... in both blood and urine.
first dose
| fever, rash, joint pain, and eosinophils
148
Direct-acting toxins can take days to weeks to produce enough cumulative toxicity to cause .......... ..........; they are not associated with eosinophils, fever, joint pains, or rash
renal failure
149
There is no test which can confirm a specific toxin as the etiology of the renal failure. Other causes of renal failure must first be ................ , and the toxin must be found in the history.
Regarding treatment, there is no ................ ............ that can reverse the renal insufficiency of any direct-acting toxin.
excluded
| specific therapy
150
..................... toxicity generally takes 5–10 days of administration to result in toxicity
Aminoglycoside
151
Renal failure due to aminoglycosides is
non-oliguric (K+ levels not elevated)
152
Hypokalemia and hypomagnesemia predispose
| the patient to
aminoglycoside toxicity
153
The ability of antibiotics to kill bacteria is associated with the peak level, but the likelihood of toxicity is associated with the .....................
trough level
154
This is most because a low trough allows time for the renal tubular cells and neural cells of the inner ear to
regenerate themselves.
155
Aminoglycosides also exert a bactericidal effect after their level has become low because they enter the bacteria and continue to kill. This ability to exert an effect despite low or absent levels is called
postantibiotic effect
156
Once-a-day dosing allows high bactericidal levels with the same efficacy and very low trough levels. The low trough levels ................. .................
reduce toxicity
157
Aminoglycoside-related nephrotoxicity is estimated to be between 10–20% of all ................................................ and is usually reversible
drug-induced nephrotoxicity
158
Amphotericin B associated with
renal insufficiency and distal renal tubular acidosis.
159
These often revert to normal after the medication is stopped. This form of toxicity is ................. ...................
cumulative dosing
160
It is expected that after several days or weeks of amphotericin use, the patient will develop
a high creatinine as well as a decreased magnesium, bicarbonate, and potassium
level.
161
clinical picture of Atheroembolic Disease.
Look for a patient who undergoes a vascular catheter procedure such as angioplasty who develops renal failure several days later
162
the most accurate test is a ............... ............. to see cholesterol crystals in the skin, this is rarely done.
skin biopsy
163
ttt of Atheroembolic Disease.
There is no therapy for atheroemboli. High doses of statins have been tried.
164
Radiocontrast material for CT scanning can result in renal failure in as little as ............... hours after the use of the agent. This is one of the main ways to distinguish this form of renal failure from aminoglycoside or amphotericin toxicity, which need ............................................ of cumulative exposure.
12–24
| several days to weeks
165
The rise in creatinine peaks at.............. days after the injury.
The BUN and creatinine may be up in a ........... ratio, such as in prerenal azotemia, because the hypertonicity of the agent provokes an intense vasospasm of the ................. ................
3–5
20:1
afferent arteriole
166
The worse the underlying .................................., the more likely the patient is to have renal failure secondary to contrast material.
renal parenchyma
167
If you are elderly, diabetic, and hypertensive with myeloma, you are far more likely to experience
contrast-induced renal insufficiency
168
................... is associated with renal failure in addition to its toxicity on the pancreas.
Pentamidine
169
Vancomycin, cyclosporine, and lithium can all cause renal failure in a ..............................................
dose-dependent fashion
170
....................... is a protease inhibitor that results in renal failure usually from the drug precipitating out in the kidney tubules
Indinavir
171
NSAIDs are a frequent cause of renal failure. NSAIDS cause renal failure by several mechanisms:
```
1-Interstitial nephritis
2-Direct toxic effect on the tubules
3-Papillary necrosis
4-Inhibition of vasodilatory prostaglandins in the afferent arteriole
5-Membranous glomerulonephritis
```
172
A person without underlying renal insufficiency should not experience a rise in
creatinine
| from the use of NSAIDs
173
That only occurs in those with significant impairment such as the
1-elderly or
2-with hypertension
3-or diabetes
174
NSAIDs can also cause ............... by a combination
| of these.
toxicity
175
More than 50% of patients have pyuria, which, if persistently associated with sterile urine, can be an important clue to
diagnosis.
176
There is no specific test to confirm that NSAIDs caused .
the renal failure
177
There will be a rise in
BUN and creatinine and a history of NSAID use
178
There is no specific therapy other than to stop the
NSAID.
179
Acute papillary necrosis occurs in patients with a history of
1-sickle cell disease,
2-diabetes,
3-urinary obstruction,
4-chronic pyelonephritis.
180
It can be brought on acutely by the ingestion of
NSAIDs
181
The presentation of Acute papillary necrosis is
1-the sudden onset of flank pain,
2-hematuria,
3-pyuria,
4-and fever.
182
This can be very similar in presentation to
acute pyelonephritis.
183
In a patient with the risks described, symptoms for ................ ..................... will come on very suddenly
papillary necrosis
184
The findings of ................ and ..................... on urinalysis will not distinguish them. However, papillary necrosis will not grow any organisms on culture. The most accurate diagnostic test for papillary necrosis is ............., which will show .............. contours in the renal pelvis where the papillae have sloughed off. There is no specific therapy for papillary necrosis.
white and red cells
CT scan
“bumpy”
185
In patients with significant underlying renal disease who require a radiologic procedure requiring contrast, what is is required before the procedure.
hydration with 1–2 liters of normal saline over 12 hours
186
Prevention of contrast-induced renal failure
1-Hydration has been shown to decrease the likelihood of contrast-induced renal failure.
2-Bicarbonate and N-acetyl cysteine have been shown to decrease the risk of renal failure.
3-Ineffective preventive measures are diuretics such as furosemide or mannitol.
