USING ATTACHED TEMPLATE AND ATTACHED CASE. 

Name: Pt. Encounter Number:

Date: Age: Sex:

SUBJECTIVE

CC:
Reason given by the patient for seeking medical care “in quotes”

HPI:
Describe the course of the patient’s illness, including when it began, character of symptoms, location

where the symptoms began, aggravating or alleviating factors, pertinent positives and negatives, other

related diseases, past illnesses, and surgeries or past diagnostic testing related to the present illness.

Medications: (List with reason for med )

PMH

Allergies:

Medication Intolerances:

Chronic Illnesses/Major traumas

Hospitalizations/Surgeries

“Have you ever been told that you have diabetes, HTN, peptic ulcer disease, asthma, lung disease, heart

disease, cancer, TB, thyroid problems, kidney problems, or psychiatric diagnosis?”

Family History

Does your mother, father, or siblings have any medical or psychiatric illnesses? Is anyone diagnosed with:

lung disease, heart disease, HTN, cancer, TB, DM, or kidney disease?

Social History

Education level, occupational history, current living situation/partner/marital status, substance use/abuse,

ETOH, tobacco, and marijuana. Safety status

ROS

General

Weight change, fatigue, fever, chills, night sweats,

and energy level

Cardiovascular

Chest pain, palpitations, PND, orthopnea, and

edema

Skin

Delayed healing, rashes, bruising, bleeding or skin

discolorations, and any changes in lesions or moles

Respiratory

Cough, wheezing, hemoptysis, dyspnea, pneumonia

hx, and TB

Eyes

Corrective lenses, blurring, and visual changes of

any kind

Gastrointestinal

Abdominal pain, N/V/D, constipation, hepatitis,

hemorrhoids, eating disorders, ulcers, and black,

tarry stools

Ears
Ear pain, hearing loss, ringing in ears, and

discharge

Genitourinary/Gynecological
Urgency, frequency burning, change in color of

urine.

Contraception, sexual activity, STDs

Female: last pap, breast, mammo, menstrual

complaints, vaginal discharge, pregnancy hx

Male: prostate, PSA, urinary complaints

Nose/Mouth/Throat
Sinus problems, dysphagia, nose bleeds or

discharge, dental disease, hoarseness, and throat

pain

Musculoskeletal
Back pain, joint swelling, stiffness or pain, fracture

hx, and osteoporosis

Breast
SBE, lumps, bumps, or changes

Neurological
Syncope, seizures, transient paralysis, weakness,

paresthesias, and black-out spells

Heme/Lymph/Endo

HIV status, bruising, blood transfusion hx, night

sweats, swollen glands, increase thirst, increase

hunger, and cold or heat intolerance

Psychiatric

Depression, anxiety, sleeping difficulties, suicidal

ideation/attempts, and previous dx

OBJECTIVE

Weight BMI Temp BP

Height Pulse Resp

General Appearance
Healthy-appearing adult female in no acute distress. Alert and oriented; answers questions appropriately.

Slightly somber affect at first and then brighter later.

Skin

Skin is brown, warm, dry, clean, and intact. No rashes or lesions noted.

HEENT
Head is normocephalic, atraumatic, and without lesions; hair evenly distributed. Eyes: PERRLA. EOMs

intact. No conjunctival or scleral injection. Ears: Canals patent. Bilateral TMs pearly gray with positive

light reflex; landmarks easily visualized. Nose: Nasal mucosa pink; normal turbinates. No septal deviation.

Neck: Supple. Full ROM; no cervical lymphadenopathy; no occipital nodes. No thyromegaly or nodules.

Oral mucosa, pink and moist. Pharynx is nonerythematous and without exudate. Teeth are in good repair.

Cardiovascular

S1, S2 with regular rate and rhythm. No extra sounds, clicks, rubs, or murmurs. Capillary refills two

seconds. Pulses 3+ throughout. No edema.

Respiratory
Symmetric chest wall. Respirations regular and easy; lungs clear to auscultation bilaterally.

Gastrointestinal

Abdomen obese; BS active in all the four quadrants. Abdomen soft, nontender. No hepatosplenomegaly.

Breast
Breast is free from masses or tenderness, no discharge, no dimpling, wrinkling, or discoloration of the skin.

Genitourinary

Bladder is nondistended; no CVA tenderness. External genitalia reveals coarse pubic hair in normal

distribution; skin color is consistent with general pigmentation. No vulvar lesions noted. Well estrogenized.

A small speculum was inserted; vaginal walls are pink and well rugated; no lesions noted. Cervix is pink

and nulliparous. Scant clear to cloudy drainage present. On bimanual exam, cervix is firm. No CMT.

Uterus is antevert and positioned behind a slightly distended bladder; no fullness, masses, or tenderness.

No adnexal masses or tenderness. Ovaries are nonpalpable.

(Male: Both testes are palpable, no masses or lesions, no hernia, and no uretheral discharge.)

(Rectal as appropriate: No evidence of hemorrhoids, fissures, bleeding, or masses—Males: Prostrate is

smooth, nontender, and free from nodules, is of normal size, and sphincter tone is firm).

Musculoskeletal
Full ROM seen in all four extremities as the patient moved about the exam room.

Neurological

Speech clear. Good tone. Posture erect. Balance stable; gait normal.

Psychiatric
Alert and oriented. Dressed in clean slacks, shirt, and coat. Maintains eye contact. Speech is soft, though

clear and of normal rate and cadence; answers questions appropriately.

Lab Tests

Urinalysis—pending

Urine culture—pending

Wet prep—pending

Special Tests

Diagnosis

o Include at least three differential diagnosis
o Final diagnosis

 Evidence for final diagnosis should be documented in your Subjective and
Objective exams.

PLAN including education

o Plan:
 Further testing
 Medication
 Education
 Nonmedication treatments
 Follow-up

Internal Medicine 33: 49-year-old female with confusion

User: YULAK LANDA
Email: landayrn17@stu.southuniversity.edu
Date: March 31, 2021 2:49AM

Learning Objectives

The student should be able to:

Compare the pathophysiology of major etiologies of acute renal failure including decreased renal perfusion (pre-renal), intrinsic
renal disease, and acute renal obstruction (post renal).
Calculate fractional excretion of sodium and apply it to distinguish between pre-renal and intrinsic renal disease.
Develop appropriate initial management plan for acute renal failure including volume management, dietary recommendations,
drug dosage alterations, electrolyte monitoring, and indications for dialysis.
Identify risk factors for contrast-induced nephropathy and recommend steps to prevent this complication.
Interpret a urinalysis, including microscopic examination for casts, red blood cells, white blood cells, and crystals.
Calculate the anion gap and generate a differential diagnosis for metabolic acidosis.

Knowledge

Acute Kidney Injury – Definition & Classification

Definition

Acute kidney injury (AKI) is defined by an abrupt (within 48 hours) decrease in glomerular filtration function with a concomitant
elevation in serum creatinine. In this setting, the kidneys are unable to maintain fluid, electrolyte, and acid-base homeostasis.
Classification

Development of consensus definitions for acute kidney injury over the past several years have improved physicians’ ability to
describe acute kidney injury with consistent terminology. This is of benefit for both research and for clinical care prognostication
as it has been demonstrated that categories of worsening acute kidney injury are predictive of morbidity including future chronic
kidney disease and mortality during the acute kidney injury episode. The first consensus definition was called the RIFLE criteria.
Subsequent criteria were developed by the Acute Kidney Injury Network (AKIN). These criteria have been merged and simplified by
the Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Acute Kidney Injury.
In the KDIGO guidelines acute kidney injury is defined as:
1. An increase in serum creatinine ≥ 0.3 mg/dl within 48 hours
– or –
2. Increase in serum creatinine to ≥ 1.5 times baseline, which is known or presumed to have to have occurred within the prior
seven days
– or –
3. Urine volume < 0.5 ml/kg/hr for six hours In the KDIGO guidelines, acute kidney injury is categorized in to three progressively worsening stages:

Stage Serum creatinine Urine output

1
1.5 – 1.9 times baseline

or ≥ 0.3 mg/dl increase
< 0.5ml/kg/hr for 6 - 12 hours

2 2.0 – 2.9 times baseline < 0.5ml/kg/hr for ≥ 12 hours

3

3.0 times baseline

or increase ≥ 4.0 mg/dl

or initiation of renal replacement therapy

or in patients < 18 years, decrease in eGFR < 35 ml/min/1.73m2

< 0.3ml/kg/hr for ≥ 24 hours.

or anuria for ≥ 12 hours

It should be stressed that this definition of acute renal injury is based on the serum creatinine, which is a relatively late biomarker
of acute injury. There are presently several promising biomarkers under investigation that may more rapidly identify patients with

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acute renal injury. The ability to more rapidly identify renal injury after an insult will hopefully lead to earlier recognition and more
effective treatment.

Pathophysiology and Etiology of Acute Renal Failure

Pathophysiology Etiology

Pre-
renal

Tubular and glomerular
function are intact.

Decreased renal
perfusion due to
hypovolemia or
hypotension
compromises renal
function.

Enhanced tubular
absorption of both
sodium and water
increases passive
reabsorption of urea.

Hypovolemia from vomiting, diarrhea, poor fluid intake, diuretics, fever, surgical fluid
losses

Cardiorenal syndrome: decreased cardiac output with decreased renal perfusion (e.g.,
congestive heart failure, myocardial infarction)

Systemic vasodilation with decreased renal perfusion (e.g., sepsis, cirrhosis with
hepatorenal syndrome, anesthesia)

Renal hypoperfusion could be due to atherosclerosis, fibromuscular dysplasia, or from
medications leading to vasoconstriction of the afferent arteriole and impaired glomerular
blood flow

Pre-renal kidney injury is the commonest cause of decreased renal function in hospitalized
patients.

Intrinsic
renal

Dysfunction is due to a
primary intrarenal cause
(damaged tubules,
interstitium, glomeruli or
blood vessels).

Injured nephrons are no
longer able to maintain
homeostasis for
electrolytes, acid-base
balance and water.

Categorized by primary site of injury:

Tubules: Acute tubular necrosis (ATN) accounts for 85% of intrinsic renal failure.

The leading cause of intrinsic injury in hospitalized patients is sepsis. The next most
common cause of ATN is renal ischemia occurring during major heart or vascular
surgery.

Toxins also play a major role (aminoglycosides, radiocontrast, myoglobin, hemoglobin,
chemotherapy, myeloma light chains, etc.).

Ischemia from prolonged prerenal azotemia will progress to ATN if the prerenal insult
cannot be reversed.

Hemorrhagic shock in the setting of bleeding or obstetrical complications may also lead
to ATN.

Interstitium: Acute interstitial nephritis accounts for 10% of cases of intrinsic AKI. Most often
allergic reaction to a drug. Look for fever, drug rash, eosinophilia, and renal dysfunction.
Common causes are fluoroquinolones, sulfa drugs, beta lactams, and NSAIDs. Unlike other
drugs, NSAID-induced interstitial nephritis is frequently associated with nephrotic syndrome.
Less common causes are infections or autoimmune disease.

Glomeruli: Glomerulonephritis or GN accounts for 5% of cases of intrinsic AKI. These diseases
include the the primary and secondary causes of the nephritic syndrome (proliferative lupus,
infection related GN, MPGN, IgA nephropathy and the vascular diseases of the glomerular
capillary bed). Less commonly, nephrotic diseases can present with AKI .

Vascular lesions: Examples include hypertensive emergency, embolic phenomenon,
catastrophic lupus anticoagulant syndrome, scleroderma renal crisis and vasculitides such as
granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA).

It is important to recognize and diagnose these intrinsic renal causes of AKI as many of them
have disease-specific therapies available.

Post-
renal

Due to obstruction of the
urinary outflow tract
that can occur anywhere
from the collecting
tubules to the urethra.

Both urinary outflow tracts are obstructed or there is obstruction of one tract in a patient with
one functional kidney. Anatomically one can think about post-obstructive causes occurring in
the following areas:

Tubules: crystals such as uric acid, acyclovir, indinavir or sulfa drugs.

Ureteral: cancer, calculi, clot, sloughed papillary necrosis, lymphadenopathy, retroperitoneal
fibrosis

Bladder neck: tumors, calculi, benign prostatic hypertrophy (BPH), prostate cancer, cervical
cancer, neurogenic bladder.

Urethral: stricture, tumors, posterior urethral valves in infant males, obstructed in-dwelling
catheter

Post-renal renal failure is important to recognize early because the chance of recovery of renal
function is inversely related to the duration of the obstruction.

Note: Because hypovolemia and obstruction are so readily treatable, they are considered “can’t miss” diagnoses when evaluating

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a patient with acute kidney injury.

Drugs Affecting Glomerular Hemodynamics

Cyclosporine-A, NSAIDs, radiocontrast, and tacrolimus can induce renal dysfunction through vasoconstriction of the afferent
arteriole.
Angiotensin blockers vasodilate the efferent arteriole , which is generally renal protective by causing a decrease in filtration
pressure. However, in a patient with renal artery stenosis with a fixed inflow to the kidney, the addition of an angiotensin blocker
(ARB) or angiotensin converting enzyme inhibitor (ACEI) will result in acute kidney injury due to the sudden release of the efferent
arteriole vasoconstriction. As a general rule, any creatinine increase beyond 30% should be viewed as AKI prompting the
medication to be stopped and an investigation for renal artery stenosis initiated.
NSAIDs

NSAIDs have an anti-prostaglandin effect that leads to vasoconstriction of the afferent arteriole and impaired glomerular
perfusion.
NSAIDs can be particularly harmful in:

older adults
patients with underlying renal dysfunction (estimated GFR < 30-50mL/min) patients on diuretics or ACE inhibitors those exposed to IV contrast

Over-the-counter and herbal medicines

It is important to ask every patient with renal dysfunction if they are taking over-the-counter medications such as NSAIDs and
even herbal medicines.
Two links on herbals and kidney injury:
Herbs and the kidney
Kidney injury from alternative medicines
Note: In addition to vasoconstriction of the afferent arteriole, radiocontrast – induced kidney dysfunction is also related to oxidant
injury.

Potential Nephrotoxins

Aspirin Aspirin leads to renal hypoperfusion through vasoconstriction of the afferent arteriole. Renal toxicity istypically not seen at standard doses of 81-325mg daily.

Valsartan Valsartan indirectly decreases glomerular filtration pressure and blood flow through vasodilation of theefferent arteriole.

Hydrochlorothiazide Hydrochlorothiazide may rarely cause an allergic interstitial nephritis.

Atorvastatin Atorvastatin is not directly nephrotoxic but in rare cases could lead to rhabdomyolysis, which could inducerenal failure.

Metformin is excreted 100% unmetabolized by the kidneys. It is not nephrotoxic but can lead to lactic acidosis in patients with
renal failure or liver disease and should be avoided in these settings.

Relevant Radiological History in the Setting of Acute Kidney Injury

In addition to nephrotoxins, another important historical question is to inquire about radiologic imaging studies using contrast.
Contrast nephropathy is a relatively common cause of acute kidney injury, particularly in patients with diabetes. This would be an
important clue to look for in a patient presenting with acute kidney injury.
Also, if the patient has undergone an invasive angiographic procedure, it would be important to consider cholesterol embolization.
Disruption of atherosclerotic plaques can shower cholesterol crystals to the kidneys, inducing an inflammatory response. Unlike
contrast-induced nephropathy, in which the creatinine almost always rises within 72 hours, with cholesterol embolization the
creatinine does not increase for two to three weeks and may stay elevated. Associated findings are a fine reticular rash (livedo
reticularis), low serum complement levels, and eosinophilia.

Key Physical Exam Findings For Acute Kidney Injury

Absence of
fever Absence of fever makes infection less likely, though not impossible.

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http://www.ncbi.nlm.nih.gov/pubmed/15211432?ordinalpos=13&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSumtarget=

http://www.ncbi.nlm.nih.gov/pubmed/16010641?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1

Normal
bowel
sounds

The presence of normal bowel sounds points away from a surgical emergency that led to renal failure (decreased in
peritonitis, increased in GI bleeding).

Signs of
hypovolemia

Hypovolemia is critical to identify in patients with acute kidney injury, as prompt treatment can lead to rapid
recovery of renal function. The ability of physical examination to diagnose hypovolemia has not been well studied.
The available evidence suggests:

Orthostatic vital signs can help identify patients with hypovolemia. Orthostasis with pulse increase >30
bpm and BP decline of >20mmHg have moderate specificity (75% for HR, 81% for BP) but poor sensitivity
(43% for HR, 29% for BP). Orthostatic vital signs are less reliable in patients who are on medications that may
affect autonomic response (adrenergic blockers, central alpha agonists, psychotropic medications) or who
have underlying autonomic dysregulation from diabetes or other neurological diseases.

Sunken eyes (LR+ 3.4) and dry axilla (LR+ 2.8) are the best predictors of hypovolemia, but their absence
does not exclude the diagnosis.

Dry mucous membranes are not very helpful in ruling in the hypovolemia (LR+ 2), but their absence
suggest hypovolemia is not present (LR- 0.3).

One study suggests that a combination of findings (for example dry mucous membranes and tongue, sunken
eyes, extremity weakness, confusion, nonfluent speech) is highly predictive of hypovolemia.

Skin tenting

Poor skin turgor (skin tenting) refers to the slow return of skin to its normal position after being pinched between
the examiner’s thumb and forefinger. The protein elastin, which is responsible for the recoil of skin, is markedly
affected by moisture content. As little as 3.4% loss in wet weight may prolong the recoil time 40-fold. Elastin
deteriorates with age, suggesting that the recoil of skin normally declines with age, although this has never been
formally studied.

Absence of
signs of
volume
overload

Absence of signs of volume overload argues against CHF as a cause of possible prerenal hypovolemia.

Absence of
palpable
bladder

Absence of a palpable bladder makes an obstructive uropathy slightly less likely, although this finding may be less
reliable in patients with obesity.

Normal
reflexes

Normal reflexes do not help you identify the cause of AKI, but do point against severe derangements in potassium,
magnesium, and calcium that could be present in acute kidney injury.

Altered
mental
status

Altered mental status can lead to hypovolemia by impairing the thirst mechanism.

Hemiparesis Hemiparesis can impair patients’ ability to take fluids.

Key Physical Exam Findings in a Patient with Acute Kidney Injury

In a patient with laboratory findings consistent with acute kidney injury, the main question to answer with the exam is: “Does this
patient have evidence of volume overload or volume depletion?” Either of these could contribute to pre-renal renal failure by
decreasing perfusion to the kidney.
Likewise, identifying a distended bladder or elevated post-void residual urine volume is critical because these are signs of
obstruction that could be causing post-renal renal failure.
Each of these states would be treated very differently, so identifying them would have an impact on which course of therapy is
ultimately chosen.
It is important to note that although we must look for signs and symptoms of fluid overload, such as jugular venous distension
(JVD), the presence of an S3 gallop, crackles, peripheral edema, and ascites — the sensitivity of these signs individually for making
a definitive diagnosis of volume overload is quite low.

Update on Contrast-Induced Nephropathy

Contrast-induced nephropathy (CIN) is defined as an acute decline in renal function within two or three days after the
administration of iodinated contrast agent in the absence of another potential cause.
Iodinated contrast has been recognized as a potential nephrotoxin for many years. The mechanisms of renal injury likely include
both vasoconstriction of the renal vasculature and direct tubular toxicity.
In older studies a number of risk factors for CIN were identified including pre-existing renal insufficiency, diabetes, older age,

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hypovolemia, congestive heart failure, cirrhosis, peripheral vascular disease, NSAID use, high dose or repeated loads of contrast
and intra-arterial injection.
Until recently CIN was attributed to be the third leading cause of AKI in hospitalized patients. However, recent scrutiny of the data
has led to a reconsideration of the prevalence and risk of CIN with the use of low osmotic and isosmotic contrast agents in modern
use. A number of observational studies including studies employing propensity score matching have found that among
hospitalized patients who undergo CT studies, those who receive IV contrast have the same risk of AKI as those who do not receive
contrast. A recent meta-analysis examined the data and found no increased risk for AKI, need for renal replacement therapy or
mortality for patients who received iodinated contrast for CT imaging versus patients who who underwent CT imaging without
contrast.
The 2018 American College of Radiology Manual on Contrast Media concludes that CIN is a real but rare condition. They suggest
that if a renal function threshold is to be used to avoid use of iodinated contrast a cut of < 30 ml/min/1.73m2 is best supported by the available data. In the case of AKI there is a lack of data but it is prudent to avoid iodinated contrast unless the potential benefits outweigh the risk. If iodinated contrast is indicated and the patient has preexisting renal insufficiency IV hydration with normal saline should be administered. Data does not support the use of N-acetylcysteine to reduce the risk of CIN. As for all patients at risk for AKI, other identifiable risks should be eliminated such as exposure to NSAIDS or other renal toxic medications.

Management

Treatment of Acute Kidney Injury

1. Identify and correct pre-renal and post-renal conditions.
2. Volume management: Accurate monitoring of daily weights and fluid balance is critical. A small fluid challenge is not

unreasonable if your diagnostic studies are inconclusive for a pre-renal etiology. Avoid giving large volumes of fluids to
prevent pulmonary edema. Diuretic therapy should be used in patients with clear evidence of volume overload (such as
edema, crackles, jugular venous distension, ascites); however, diuretic therapy has not been shown to improve survival or
renal recovery rate. The medical literature provides little guidance on vasoactive medications for blood pressure support in
the setting of hypotension and acute kidney injury (for example, hypotension in sepsis with ischemic ATN). The use of low
dose or so-called “renal-dose” dopamine has not been shown to improve outcomes in critically ill patients with renal failure
and should not be used.

3. Dietary recommendations: Placing the patient on a renal diet with low potassium, phosphorus, and protein as well as
monitoring fluid intake is necessary to maintain fluid and electrolyte balance. If the patient cannot eat, nutritional support is
necessary. This strategy is particularly important in the setting of critical illness, because marked visceral and muscle
protein wasting can occur. Enteral feeding is preferred over parenteral nutrition.

4. Drug dosage alterations: No drug treatment has been shown to limit the progression or hasten the recovery in the setting
of acute kidney injury due to ATN. For all causes of AKI it is important to stop nonsteroidal anti-inflammatory or other
nephrotoxic agents (in this case, stop losartan, aspirin, metformin, hydrochlorothiazide and furosemide), avoid nephrotoxic
antibiotics (aminoglycosides, amphotericin), and avoid radiocontrast. Renally dose all medications that are given and
monitor drug levels where appropriate.

5. Electrolyte monitoring: Watch for hyperkalemia and hyperphosphatemia. Monitor anion gap and acid-base status. In the
setting of recovery from ATN (diuretic phase of ATN) electrolyte wasting may occur and potassium supplementation for
hypokalemia may be required.

6. Identify and aggressively treat infections: Minimize the use of in-dwelling lines as much as possible. If the patient is
anuric, removal of the Foley catheter is appropriate.

7. Watch for increased risk of bleeding: Uremia can lead to abnormal bleeding through a variety of mechanisms, such as
dysfunctional vWF. Uremia-related bleeding has specific treatment strategies, including DDAVP.

8. Indications for dialysis: Initiate dialysis before uremic complications develop.
9. Consult Nephrology: Nephrologists are underutilized in these cases, even though studies have shown that

early consultation can improve outcomes. Surprisingly, these better outcomes result simply through
meticulous attention to detail regarding supportive care. Nephrologists may also start disease specific
therapy such as steroids, immune modulators or plasmapheresis.

Consultation is mandatory in cases when:

the diagnosis is uncertain despite initial diagnostic workup
renal replacement therapy or dialysis is likely needed
an intrinsic renal cause other than ATN is present

Indications for Acute Dialysis

The mnemonic AEIOU is helpful to remember the indications:
Acidemia that does not respond to bicarbonate therapy and other supportive measures.
Electrolyte derangements that do not respond to supportive measures (for example hyperkalemia).
Ingestion of toxins/medications that are water soluble and easily removed via dialysis.
Volume Overload that does not respond to diuretic therapy or causes cardiopulmonary collapse.
Clinical evidence of Uremia (persistent mental status changes, uremic pericarditis, etc.).
Drugs that can be removed via dialysis

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Toxic alcohols (ethylene glycol, methanol, isopropyl alcohol)
Aspirin or salicylates
Phenobarbital
Lithium
Theophylline

Note: The optimal timing and indication for initiation of dialysis in patients with AKI remains uncertain. Currently, there is not a
strong consensus on timing of initiation of dialysis in acute kidney failure. As mentioned above, early involvement of a
nephrologist has been shown to lead to improved outcomes, however further well designed multi-center clinical trials of early vs
late initiation of renal replacement therapy in patients with AKI including both short and long term outcome data are needed.

Recommended Prevention & Treatment of Contrast-Induced Nephropathy

The prevention of CIN requires identification of patients at risk.
In these individuals the proven treatment options are:

avoidance of high osmolar radiocontrast agents
discontinuation of NSAIDs
intravenous hydration with 0.9% sodium chloride

A large number of studies have explored potential treatments for the prevention of CIN, but have been challenged by
heterogeneity of design and mixed results. The PRESERVE trial, a multinational randomized controlled trial of hydration with
normal saline versus sodium bicarbonate and use of oral n-acetylcysteine versus placebo in patients with CKD undergoing intra-
arterial angiography published in 2018 was halted early due to a lack of additional benefit beyond hydration with IV normal saline
for prevention of death, need for renal replacement therapy, persistent decline in renal function or AKI due to contrast. Hydration
with bicarbonate was not found to be superior to normal saline. Thus normal saline can be viewed as the preferred fluid for
hydration given the standard availability of this fluid. In addition, this study establishes there is no role for n-acetylcysteine for the
prevention of CIN. Further high quality randomized trials of statins are required to fully establish the role of these agents for this
indication.

Studies

Recommended Evaluation of Etiology of Renal Failure

Creatine
kinase

The creatine kinase level is not unreasonable to check if you are concerned about rhabdomyolysis, this is
particularly relevant if the patient has a history of taking a statin.

Lactic acid The serum lactic acid level is important if the patient is taking metformin, you want to ensure that there is no lacticacidosis.

Post-void
residual

The post-void residual is an easy bedside method of detecting obstruction from the bladder neck down. After the
patient maximally voids, either an ultrasound scan of the bladder to calculate residual volume is obtained or in a
more invasive approach, a urinary catheter is inserted. If there is a residual urine volume of >100 mL, this is
consistent with obstruction at the level of the bladder neck or lower. If it is <100 mL, this does not exclude an obstruction higher up in the urinary tract.

Renal
ultrasound

The renal ultrasound is helpful to assess for urinary obstruction. It is 80-85% sensitive at determining if obstruction
is present. It can be falsely negative in early obstruction, severe dehydration, and retroperitoneal fibrosis that will
not allow ureteral dilation. Renal ultrasound is also helpful to determine if there is pre-existing renal disease by
examining kidney size.

Normal-sized kidneys suggest an acute process. Small atrophic kidneys are seen with chronic kidney disease. An
important exception to this rule is diabetic nephropathy as diabetes can cause kidney enlargement even in the
setting of chronic disease. Asymmetric kidneys can suggest an underlying renovascular disease.

Spot urine:
creatinine
ratio

The spot urine : creatinine ratio would be helpful to determine if there is underlying glomerular injury that would
lead to urinary protein loss.

Urine
chemistries

Urine chemistries can be used to calculate the fractional excretion of sodium (FENa) as shown on the next page. One
can also look specifically at Urine Na. Realize that the utility of these measures is compromised in patients taking
diuretics or those who have pre-existing chronic kidney disease. In these patients a fractional excretion of urea
(FEUrea) may be calculated: FEUrea = 100 x (UUrea x SCr)/(SUrea x UCr). A FEUrea < 35% is consistent with a pre- renal state.

The fractional excretion of sodium can help distinguish prerenal from intrinsic AKI. The FENa should be less than 1%
in prerenal AKI, reflecting avid sodium and water reabsorption of intact nephrons. It should be higher than this in
intrinsic AKI when damage to the nephrons impairs the ability of the kidney to absorb sodium and water.

The FENa is most accurate in oliguric states because the kidney does not avidly reabsorb sodium and water in non-

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oliguric states. Note also that the administration of diuretics within 12-24 hours of the time of the test may elevate
the FENa in the setting of prerenal failure because diuretics impair renal sodium and water reabsorption. Therefore,
this test may not be helpful in Mrs. Baxter’s case (although she was not taking her medications). However, in a
patient not taking diuretics, it would be a very important way to distinguish pre-renal from intrinsic renal failure.

Interpereting FENa

There are several caveats to consider when interpreting the FENa:
1) Some intrinsic renal disease conditions can be associated with a low FENa <1%. In these cases, the urine sediment would be abnormal.

Rhabdomyolysis and myoglobin-related ATN
Hemolysis related ATN
Contrast nephropathy and ATN
ATN occurring in a patient with a sodium avid state (CHF, cirrhosis)
Acute glomerulonephritis
Vasculitis

2) Early obstruction is associated with a FENa <1%. The FeNa has no role in determining the diagnosis post-obstructive renal failure. 3) Last, FENa can be elevated in any patient on diuretic therapy because diuretics lead to urinary electrolyte wasting. A fractional excretion of urea can be used in this setting as the urinary excretion of urea is not affected by diuretics.

Diagnostic Studies in Acute Kidney Injury

Prerenal ARF Intrinsic Renal Post Renal*

BUN/Cr > 20 10-20 10-20

Urine Sp Grav >1.020 ≈1.010
E > 1.010

L < 1.010

Urine Osm’s >350 ≈300
E > 400

L < 400

Urine Na < 20 > 30
E > 20

L < 20

FeNa < 1 > 2
E < 1

L > 3

Ucreat / Pcreat ≥ 40 ≤ 20
E ≥ 40

L ≤ 20

Renal U/S reveals hydronephrosis No No Yes

*Urine diagnostic studies are not very helpful in obstruction or post-renal renal failure
E=Early, L=Late

Urine Microscopy Findings in Intrinsic Renal Failure

Cells Casts Other Webpath resources

Acute tubular necrosis
(ATN) renal tubular epithelial cells

Granular casts and muddy
brown casts None

Example of renal muddy
brown casts

Acute
glomerulonephritis
(AGN)

dysmorphic RBCs, RBCs, WBCs,
epithelial cells RBC (WBC can be seen) Protein

Example of

dysmorphic RBC

in RBC casts

Comparison: normal and

© 2021 Aquifer 7/9

http://library.med.utah.edu/WebPath/webpath.html#MENU

http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URIN080.html

http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URIN070.html

https://library.med.utah.edu/WebPath/TUTORIAL/URINE/URIN082.html

dysmorphic RBC

Acute interstitial
nephritis (AIN) eosinophils, WBCs WBC and hyaline None Example of wbc casts

The following link is an excellent resource for both macroscopic and microscopic urinary findings:
http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URINE.html#2

Glomerular vs Nonglomerular Hematuria

Urine microscopy Dipstick

Glomerular
hematuria

Red cell casts, red cells of varying sizes and shapes, acanthocytes
(some red cells appearing to have buds), or so called dysmorphic
red cells.

Urine dipstick will also be positive for protein
as the glomerular basement membrane is
damaged.

Nonglomerular
hematuria All the red cells look the same (monomorphic). Dipstick is negative for protein.

In a symptomatic patient, nonglomerular hematuria may be due to infection, nephrolithiasis, and other causes.
In an asymptomatic patient, you have to be concerned about an urothelial malignancy or cancer.

Clinical Reasoning

Differential of Acute Kidney Injury

Pre-renal AKI

Pre-renal AKI is the most common cause of renal failure and accounts for 40-70% of all cases.
The presence of orthostasis implies that the patient has lost approximately 20% of their intravascular volume and is
suggestive of a pre-renal cause. Supine hypotension and tachycardia in the absence of fever/infection suggest an
approximately 40% loss of intravascular volume.
A BUN:creatinine ratio > 20 is consistent with a pre-renal cause although the BUN:creatinine ratio can also be elevated for
other reasons including a catabolic state (such as that caused by sepsis or glucocorticoid therapy) and gastrointestinal
bleeding.
Urinalysis can be normal in pre-renal AKI.

Intrinsic
AKI

Renal failure develops in 7-15% of inpatients with the most common cause being intrinsic AKI, particularly ATN. In
fact, ATN accounts for 55-60% of all hospital acquired AKI. ATN is less common in the outpatient setting; it
accounts for only 11% of community acquired AKI.

The top three causes of renal failure in hospitalized patients are ATN due to sepsis, post-operative renal ischemia,
and contrast nephropathy.

Intrinsic renal failure can be both non-oliguric or oliguric and patients with intrinsic AKI may be orthostatic.

Urinary casts, cells, and protein are typically seen on urinalysis with intrinsic disease.

Post-
renal
AKI

Complete anuria is highly suggestive of post-renal AKI or obstruction although complete anuria can also be seen
with severe dehydration and aortic dissection through both renal arteries. Note that decreased urine output can be
seen with all three types of renal failure.

The urinalysis is typically normal in post-renal failure.

A palpable bladder would suggest obstruction.

Urine volume may vary from oliguria or anuria to normal urine output.

A note about urine volume:
Oliguria is defined by a urine output of < 400 ml/day. Anuria is defined as < 200 ml/day. Oliguria and anuria may occur with any etiology of AKI.

References

American College of Radiology. ACR Manual on Contrast Media Version 10.3. https://www.acr.org/Clinical-Resources/Contrast-Manual.
Accessed April 11, 2019.

© 2021 Aquifer 8/9

http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URIN071.html

http://library.med.utah.edu/WebPath/TUTORIAL/URINE/URINE.html#2

https://www.acr.org/Clinical-Resources/Contrast-Manual

Aycock RD, Westafer LM, Boxen JL, Majlesi N, Schoenfeld EM, Bannuru RR. Acute kidney injury after computed tomography: a meta-
analysis. Ann Emerg Med. 2018;71(1):44-53. DOI: 10.1016/j.annemergmed.2017.06.041.

Boccardo P, Remuzzi G, Galbusera M. Platelet dysfunction in renal failure. Semin Thromb Hemost. 2004;30(5):579-89.

Davenport MS, Khalatbari S, Cohan RH, Dillman JR, Myles JD, Ellis JH. Contrast material-induced nephrotoxicity and intravenous low-
osmolality iodinated contrast material: risk stratification by using estimated glomerular filtration rate. Radiology. 2013;268(3):719-28.
DOI: 10.1148/radiol.13122276.

Hinson JS, Ehmann MR, Fine DM, Fishman EK, Toerper MF, Rothman RE, Klein EY. Risk of acute kidney injury after intravenous contrast
media administration. Ann Emerg Med. 2017;69(5):577-586. DOI: 10.1016/j.annemergmed.2016.11.021.

Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Acute Kidney Injury. Kidney International
Supplements. 2012;2(2).

Malhotra R, Siew ED. Biomarkers for the early detection and prognosis of acute kidney injury. Clin J Am Soc Nephrol. 2017;12(1):149-
73. DOI: 10.2215/CJN.01300216.

McDonald RJ, McDonald JS, Bida JP, et al. Intravenous contrast material-induced nephropathy: causal or coincident phenomenon?
Radiology. 2013;267(1):106-18. DOI: 10.1148/radiol.12121823.

McGee S, Abernethy WB 3rd, Simel DL. The rational clinical examination. Is this patient hypovolemic? JAMA. 1999;281(11):1022-9.

Mehta AN, Emmett JB, Emmett M. GOLD MARK: an anion gap mnemonic for the 21st century. Lancet. 2008;372(9642):892.

Subramaniam RM, Suarez-Cuervo C, Wilson RF, et al. Effectiveness of prevention strategies for contrast–induced nephropathy: a
systematic review and meta-analysis. Ann Intern Med. 2016;164(6):406-16. DOI: 10.7326/M15-1456.

Thomas ME, Blaine C, Dawnay A, et al. The definition of acute kidney injury and its use in practice. Kidney Int. 2015;87(1):62-73. DOI:
10.1038/ki.2014.328

Wagner B, Drel V, Gorin Y. Pathophysiology of gadolinium-associated systemic fibrosis. Am J Physiol Renal Physiol. 2016;311(1):F1-
F11. DOI: 10.1152/ajprenal.00166.2016.

Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after angiography with sodium bicarbonate and acetylcysteine. N Eng J Med.
2018;378(7):603-14. DOI: 10.1056/NEJMoa1710933.

Wilhelm-Leen E, Montez-Rath ME, Chertow G. Estimating the risk of radiocaontrast-associated nephropathy. J Am Soc Nephrol.
2017;28(2):653-659. DOI: 10.1681/ASN.2016010021.

Zarbock A, Mehta RL. Timing of Kidney Replacement Therapy in Acute Kidney Injury. Clin J Am Soc Nephrol. 2019 Jan 7;14(1):147-149.
DOI: 10.2215/CJN.08810718.

© 2021 Aquifer 9/9

https://www.ncbi.nlm.nih.gov/pubmed/28811122

https://doi.org/10.1016/j.annemergmed.2017.06.041

https://www.ncbi.nlm.nih.gov/pubmed/15497100

https://www.ncbi.nlm.nih.gov/pubmed/23579046

https://doi.org/10.1148/radiol.13122276

https://www.ncbi.nlm.nih.gov/pubmed/28131489

https://doi.org/10.1016/j.annemergmed.2016.11.021

https://www.kisupplements.org/issue/S2157-1716%2812%29X7200-9

https://www.ncbi.nlm.nih.gov/pubmed/27827308

https://doi.org/10.2215/CJN.01300216

https://www.ncbi.nlm.nih.gov/pubmed/23360742

https://doi.org/10.1148/radiol.12121823

https://www.ncbi.nlm.nih.gov/pubmed/10086438

https://doi.org/10.1016/S0140-6736%2808%2961398-7

https://www.ncbi.nlm.nih.gov/pubmed/26830221

https://doi.org/10.7326/M15-1456

https://www.ncbi.nlm.nih.gov/pubmed/25317932

https://doi.org/10.1038/ki.2014.328

https://www.ncbi.nlm.nih.gov/pubmed/27147669

https://doi.org/10.1152/ajprenal.00166.2016

https://www.ncbi.nlm.nih.gov/pubmed/29130810

https://doi.org/10.1056/NEJMoa1710933

https://www.ncbi.nlm.nih.gov/pubmed/27688297

https://doi.org/10.1681/ASN.2016010021

https://www.ncbi.nlm.nih.gov/pubmed/30504248

https://doi.org/10.2215/CJN.08810718

Internal Medicine 33: 49-year-old female with confusion
Learning Objectives
Knowledge
Acute Kidney Injury – Definition & Classification
Pathophysiology and Etiology of Acute Renal Failure
Drugs Affecting Glomerular Hemodynamics
Potential Nephrotoxins
Relevant Radiological History in the Setting of Acute Kidney Injury
Key Physical Exam Findings For Acute Kidney Injury
Key Physical Exam Findings in a Patient with Acute Kidney Injury
Update on Contrast-Induced Nephropathy
Management
Treatment of Acute Kidney Injury
Indications for Acute Dialysis
Recommended Prevention & Treatment of Contrast-Induced Nephropathy
Studies
Recommended Evaluation of Etiology of Renal Failure
Interpereting FENa
Diagnostic Studies in Acute Kidney Injury
Urine Microscopy Findings in Intrinsic Renal Failure
Glomerular vs Nonglomerular Hematuria
Clinical Reasoning
Differential of Acute Kidney Injury
References