CASE

PRESENTATI
ON
AZOTEMIA
 Case
You are called by the surgical intern to see a 68 year old man in the surgical ICU because of new onset azotemia. He
has a history of smoking, hypertension, osteoarthritis, and peripheral vascular disease, and was admitted 3 days
earlier for unstable angina. His pain was refractory to maximal medical therapy, so he underwent cardiac cath and
subsequently 3 vessel coronary bypass grafting 48 hours prior to your call from the intern. His post-operative
course was complicated by a non-ST segment elevation myocardial infarction (NSTEMI)but was otherwise
unremarkable until yesterday when his urine output began to diminish (total of 150 cc over 24 hrs.), and his serum
creatinine was noted to be 3.5 mg/dl (previous creatinine was 1.2 on admission). The patient is intubated and can
give no history. Medications include furosemide, lisinopril, intravenous nitroglycerin, ibuprofen, and perioperative
cefazolin. PE reveals an intubated alert man in no acute distress. T 97.3, P 96, R 12, BP 110/66. SKIN - no rash or
lesions noted; normal turgor. LN - none palp. No jugular venous distension. HEENT - conjunctivae are benign;
Fundi reveal grade 2 arteriosclerotic hypertensive changes; oropharynx is intubated and poorly visualized. CHEST
- clear on the ventilator; sternotomy incision looks normal; COR - RRR with distant heart sounds; no murmurs or
rubs. ABD - soft nontender, without organomegaly; no flank tenderness; bowel sounds are diminished. G/R - Foley
catheter in place; rectal normal; heme negative. NEURO - nonfocal. EXT - saphenous vein harvest site benign; no
edema. LABS Na 133, K 4.5, Cl 100, HCO3 20, BUN 49, Cr 3.5, glu 132 Hb 13.6, Hct 40.2, WBC 8.6, plts 400K UA:
clear/1.015/no protein, glucose or ketones/sediment reveals occasional hyaline casts, moderate pigmented granular
casts and many renal epithelial cells. There are few RBC and rare WBC. EKG: NSR 90/nl axis and intervals;
inverted T waves are noted in the anterior leads. CXR: normal heart size; no CHF or infiltrates noted.
 CHIEF COMPLAINT

New onset of azotemia on post-

coronary artery bypass graft surgery
 Present Illness

 68-year-old man post-CABG complicated by

NSTEMI and new onset azotemia.
 Developed oliguria (150 cc/24 hrs) and elevated
creatinine (3.5 mg/dl from 1.2 mg/dl).
 Past Medical History
0 Peripheral vascular 0
1  Hypertension
disease 2

0 Admission for unstable 0

Osteoarthritis angina
3 4
 Social History

Smoking history
 Laboratory Report
 Serum Creatinine: 3.5 mg/dL (elevated from 1.2 mg/dL)

 BUN: 49 mg/dL

 Electrolytes: Na 133, K 4.5, Cl 100, HCO3 20

 Glucose: 132 mg/dL

 CBC: Hb 13.6, Hct 40.2, WBC 8.6, Plts 400K

 Urinalysis: Specific gravity 1.015, no protein, glucose, or
ketones, sediment with occasional hyaline casts,
moderate pigmented granular casts, many renal epithelial
cells, few RBCs, rare WBCs

 EKG: NSR, 90 bpm, inverted T waves in anterior leads

 CXR: Normal heart size, no CHF or infiltrates

 Physical Examination
:
 Alert intubated man in no acute distress
 Vital signs stable: T 97.3, P 96, R 12, BP 110/66
 Skin: Normal turgor, no rash or lesions
 Lymph nodes: None palpable
 HEENT: Conjunctivae benign, Fundi with arteriosclerotic changes, oropharynx intubated
 Chest: Clear on ventilator, normal sternotomy incision
 Cardiovascular: Regular rate and rhythm, distant heart sounds, no murmurs or rubs
 Abdomen: Soft, nontender, no organomegaly, diminished bowel sounds
 Genitourinary/Rectal: Foley catheter in place, normal rectal exam, heme negative
 Extremities: Benign saphenous vein harvest site, no edema.
 Initial Thoughts
1) New onset azotemia post-CABG and NSTEMI
2) Possible causes include acute kidney injury (AKI) from
hypoperfusion, nephrotoxic medications (NSAIDs, contrast), or
sepsis
3) Monitor fluid balance, consider renal protective strategies, and
investigate for underlying etiology (e.g., hypovolemia,
nephrotoxicity, sepsis).
1. Acute kidney injury
(AKI):
Acute kidney injury is defined as an abrupt (within 48 hours)
decrease in kidney function, manifested by an increase in serum
creatinine level by ≥0.3 mg/dL within 48 hours; or an increase in
serum creatinine to ≥1.5 times baseline, which is known or
presumed to have occurred within the prior 7 days; or urine
volume <0.5 mL/kg/hour for 6 hours.
 2. Broad categories of diagnostic
possibilities for AKI:
AKI can be categorized into three main etiologies

1. Prerenal: Decreased renal perfusion due to volume depletion (e.g., from

hemorrhage, dehydration), decreased cardiac output (e.g., heart failure), or renal artery
:
stenosis
o .
2. Intrinsic renal: Damage directly to kidney tissue, such as acute tubular
necrosis (ATN) due to ischemia (e.g., post-surgery), nephrotoxins (e.g., contrast
agents, medications),
o or . acute glomerulonephritis.

3. Postrenal: Obstruction of urinary outflow, typically by kidney stones, tumors,

or prostatic hypertrophy.
 3.Unique aspects placing this patient
at risk for various etiologies
Prerenal Intrinsic renal Postrenal
History of unstable angina, Exposure to nephrotoxic agents Exposure to nephrotoxic agents
recent cardiac catheterization, (e.g., contrast, medications like (e.g., contrast, medications like
and coronary artery bypass NSAIDs and possibly antibiotics NSAIDs and possibly antibiotics
grafting (increased risk of like cefazolin), as well as like cefazolin), as well as
volume depletion and decreased potential ischemic injury related potential ischemic injury related
renal perfusion). to cardiac surgery. to cardiac surgery.
4. Role of urinalysis and additional
diagnostic information:
Urinalysis findings: Occasional hyaline casts, moderate pigmented
granular casts, and many renal epithelial cells suggest tubular injury
(consistent with intrinsic renal causes like ATN). The absence of protein,
glucose, or significant cellular casts makes glomerulonephritis less likely.
Additional diagnostic tests: Serial measurements of creatinine to
assess trend, review of medication history (including recent contrast
exposure and nephrotoxic medications), and possibly renal ultrasound to
rule out postrenal causes or assess kidney size and vascularity.
5. Need for renal biopsy:

Renal biopsy: Typically, not indicated in the acute setting

unless there is diagnostic uncertainty or suspicion of a
specific glomerular disease not explained by clinical findings.
In this case, the urinalysis and clinical context strongly
suggest ATN secondary to ischemic injury or nephrotoxicity
rather than a glomerular disease.
 6. Complications and
indications for dialysis:
Complications of AKI: Fluid overload, electrolyte imbalances
(hyperkalemia, metabolic acidosis), and uremia (symptoms like nausea,
confusion, pericarditis).
Indications for dialysis: Severe AKI with refractory fluid overload,
severe hyperkalemia, metabolic acidosis, or uremic symptoms that are
not responsive to medical management. In this patient, ongoing oliguria
(150 cc/24 hours) despite fluid resuscitation raises concern for fluid
overload and electrolyte disturbances, potentially warranting dialysis if
these conditions worsen.
 Treatment and Management:
Fluid resuscitation with intravenous crystalloids is the mainstay of therapy.
 Monitoring vital signs, urine output, and electrolytes closely.
An Assessing for potential sources of infection or sepsis.
Considering discontinuing Lisinopril temporarily if volume status improves.
Serial monitoring of renal function and electrolytes.
Identifying and treating the underlying cause of dehydration (e.g., gastroenteritis).
Close observation for potential complications like electrolyte imbalances, arrhythmias, and
progression to intrinsic renal injury.
- JAISANKAR,PRAVIN