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Old 11-10-2012
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Kidney The cause of acute kidney injury!

A 65-year-old man with a history of stage 4 chronic kidney disease and hypertension comes for a follow-up examination. Two days ago, he was discharged from the hospital after a 4-day stay for pneumonia. During his hospitalization, his blood pressure averaged 130/70 mm Hg and he was not exposed to radiocontrast agents. He was treated with ceftriaxone and azithromycin; on discharge, these agents were discontinued and he began oral levofloxacin. Since his discharge, he has had nausea, vomiting, and anorexia. He believes that his urine output over the past day has been less than 500 mL. Additional medications are lisinopril, calcium carbonate, and low-dose aspirin.
On physical examination, temperature is 35.8°C (96.4°F), blood pressure is 110/50 mm Hg standing and 100/80 mm Hg supine, pulse rate is 108/min standing and 96/min supine, and respiration rate is 16/min. The remainder of the examination is normal except for crackles heard at the base of the lungs bilaterally.
Serum creatinine 6.0 mg/dL (530.4 μmol/L) (2.5 mg/dL [221.0 μmol/L] in the hospital) Urinalysis Specific gravity 1.016; no protein or blood; occasional hyaline casts.

Which of the following is the most likely cause of this patient's acute kidney injury?

(A) Acute interstitial nephritis
(B) Acute tubular necrosis
(C) Prerenal azotemia
(D) Renal vein thrombosis
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Old 11-10-2012
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? Acute tubular necrosis ACE inhibitor induced..
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Quote:
Originally Posted by tyagee View Post
(B) Acute tubular necrosis
Its the only one that could make a little bit of sense.. The patient constant BP after changing position rules out C, Acute interstitial nephritis is not caused by any of the drugs that you listed, eventho cephalosporins are linked to AIN, Ceftriaxone is metabolized and excreted by the liver, so it wouldnt even get into contact with the kidney...
The weird thing here is that we are not given the BUN nor the FeNa and also we dont have the Muddy Brown casts... which are pathognomonic of the disease, but i would still pick B.

D cannot be because it is more common with Nephrotic syndrome and anticoagulant wasting such as ATIII
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Old 11-10-2012
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Help This post did wonders for my OCD.. Can't ****ing sleep

Ok so this guy was a old guy who was in hospital. During his stay in the hospital, his BP was normal (-ish). Since no contrast was used, maybe I can exclude the toxic type of ATN? Urine output of less than 500 ml. sounds a lot like kidneys shutting down. It is interesting to note here however how the OP's question stem has one thing standing out like a sore thumb which is the change in blood pressure (did I hear someone in the crowd say "Tilt test" ? ) and pulse. And I am assuming the nausea and vomiting that this poor guy has been having is not midgets wreaking havoc in his brain. My guess that it's urea. As much incoherent this post sounds, and as much tempted I am to select either A or B, my choice is answer C.
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Quote:
Originally Posted by tyagee View Post
A 65-year-old man with a history of stage 4 chronic kidney disease and hypertension comes for a follow-up examination. Two days ago, he was discharged from the hospital after a 4-day stay for pneumonia. During his hospitalization, his blood pressure averaged 130/70 mm Hg and he was not exposed to radiocontrast agents. He was treated with ceftriaxone and azithromycin; on discharge, these agents were discontinued and he began oral levofloxacin. Since his discharge, he has had nausea, vomiting, and anorexia. He believes that his urine output over the past day has been less than 500 mL. Additional medications are lisinopril, calcium carbonate, and low-dose aspirin.
On physical examination, temperature is 35.8°C (96.4°F), blood pressure is 110/50 mm Hg standing and 100/80 mm Hg supine, pulse rate is 108/min standing and 96/min supine, and respiration rate is 16/min. The remainder of the examination is normal except for crackles heard at the base of the lungs bilaterally.
Serum creatinine 6.0 mg/dL (530.4 μmol/L) (2.5 mg/dL [221.0 μmol/L] in the hospital) Urinalysis Specific gravity 1.016; no protein or blood; occasional hyaline casts.

Which of the following is the most likely cause of this patient's acute kidney injury?

(A) Acute interstitial nephritis >>no WBC
(B) Acute tubular necrosis >>no muddy cast, protein
(C) Prerenal azotemia
(D) Renal vein thrombosis >>>no blood
This patient is clearly showing features of Gram -ve sepsis (hypothermia) and hypovolemia (orthostasis).

There is a difference of 30 mm Hg in diastolic pressure highly suggestive of sepsis and his Urinalysis Specific gravity is 1.016 which is normal.
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Last edited by Novobiocin; 11-10-2012 at 03:55 PM.
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c....prerenal azotemia low BP...leading to decreased perfusion
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ans is C
B not because ATN caused by drugs atleast need 5 days ... simple clue ...
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Originally Posted by tyagee View Post
ans is C
B not because ATN caused by drugs atleast need 5 days ... simple clue ...
How can that be a clue ?
He was in hospital for 4 days and it's been 2 days since discharge from hospital making a total of 6 days!
The real clue is absence of muddy brown casts and WBCs as well as normal specific gravity which goes against B & A
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Last edited by Novobiocin; 11-10-2012 at 06:01 PM.
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Originally Posted by Novobiocin View Post
How can that be a clue ?
He was in hospital for 4 days and it's been 2 days since discharge from hospital making a total of 6 days!
The real clue is absence of muddy brown casts and WBCs which goes against B & A
i cant just bank on that. if its present, i can say ATN, if not, then ans can still be ATN if clinical picture says so. isnt ?
but drug induced ATN needs time ! cumulative...

can u list drugs ? ...what i can remember ... drugs causing ATN are

vancomycin
gentamicin
acyclovir
amphotericinB
cyclophosphamide
cisplatin
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Nephrotoxicity can result from various drugs, such as aminoglycosides, amphotericin, calcineurin inhibitors, foscarnet, ifosfamide, cisplatin, and crystal-forming drugs. Additionally, conditions such as multiple myeloma and rhabdomyolysis can cause nephrotoxicity.

Quote:
Causes of ischemic acute tubular necrosis

Ischemic ATN may be considered part of the spectrum of prerenal azotemia, and indeed, ischemic ATN and prerenal azotemia have the same causes and risk factors. Ischemic ATN results when hypoperfusion overwhelms the kidney’s autoregulatory defenses. Under these conditions, hypoperfusion initiates cell injury that often, but not always, leads to cell death.
Specifically, these include the following:
  • Hypovolemic states: hemorrhage, volume depletion from gastrointestinal (GI) or renal losses, burns, fluid sequestration
  • Low cardiac output states: heart failure and other diseases of myocardium, valvulopathy, arrhythmia, pericardial diseases, tamponade
  • Systemic vasodilation: sepsis, anaphylaxis
  • Disseminated intravascular coagulation
  • Renal vasoconstriction: cyclosporine, amphotericin B, norepinephrine, epinephrine, hypercalcemia
  • Impaired renal autoregulatory responses: cyclooxygenase (COX) inhibitors, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs)
Quote:
Exogenous nephrotoxins that cause ATN include the following:
  • Aminoglycoside-related toxicity occurs in 10-30% of patients receiving aminoglycosides, even when blood levels are in apparently therapeutic ranges (risk factors for ATN include preexisting liver disease, preexisting renal disease, concomitant use of other nephrotoxins [eg, amphotericin B, radiocontrast media, cisplatin], advanced age, shock, female sex, and a higher aminoglycoside level 1 hour after dose; a high trough level has not been shown to be an independent risk factor)
  • Amphotericin B nephrotoxicity risk factors include male sex, maximum daily dose (nephrotoxicity is more likely to occur if >3 g is administered) and duration of therapy, hospitalization in the critical care unit at the initiation of therapy, and concomitant use of cyclosporine
  • Radiographic contrast media can cause contrast-induced nephropathy (CIN) or radiocontrast nephropathy (RCN) (commonly occurs in patients with several risk factors, such as elevated baseline serum creatinine, preexisting renal insufficiency, underlying diabetic nephropathy, congestive heart failure [CHF], or high or repetitive doses of contrast media, as well as volume depletion and concomitant use of diuretics, ACE inhibitors, or ARBs). The 2011 UKRA guidelines recommend that patients at risk of CIN should have a careful evaluation of volume status and receive volume expansion with 0.9% sodium chloride or isotonic sodium bicarbonate before the procedure.[2]
  • Cyclosporine and tacrolimus (calcineurin inhibitors)
  • Cisplatin
  • Ifosfamide
  • Foscarnet
  • Pentamidine, which is used to treat Pneumocystis carinii infection in individuals who are immunocompromised (risk factors for nephrotoxicity include volume depletion and concomitant use of other nephrotoxic antibiotic agents, such as aminoglycosides, which is common practice in the immunosuppressed)
  • Sulfa drugs, acyclovir, and indinavir
Quote:
In patients with contrast-induced nephropathy (CIN), FENa tends to be less than 1%. This is an exception to the rule that FENa below 1% usually indicates prerenal failure.
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