MEDICINE 2 – [NEPHRO]: CLINICAL CASE DISCUSSION AY 21-22

CCD 4: WHEN ACUTE IS NOT CUTE 1.04

14 SEP 21
Porshia Comes-Natividad, MD; Maria Stella Navarro, MD; Dexter Clifton Pe, MD 16 NOV 21
TABLE OF CONTENTS B. REVIEW OF SYSTEMS
I. CASE ................................................................................ 1 ● Denies blurring of vision
A. HISTORY OF PRESENT ILLNESS............................... 1 ● Denies ear discharge, hearing loss
B. REVIEW OF SYSTEMS ................................................ 1 ● No dysphagia
C. PAST MEDICAL HISTORY ........................................... 1 ● No dyspnea, no nasal discharge
D. CURRENT HEALTH STATUS ...................................... 1 ● No chest pain, no palpitations
II. IS THERE A RENAL SYNDROME PRESENT? ................ 1 ● No jaundice, no hematochezia, no hematemesis
III. CAN WE SAY THAT THIS PATIENT HAS AKI?................ 2
C. PAST MEDICAL HISTORY
A. DIAGNOSIS OF AKI ..................................................... 2
B. PHYSICAL EXAMINATION........................................... 2 ● Non-Hypertensive
C. WHAT TYPE OF AKI DOES THE PATIENT HAVE?..... 2 ● Non-Diabetic
IV. INITIAL IMPRESSION ....................................................... 3 ● Non-Asthmatic
A. AUTOREGULATION..................................................... 3 ● No previous surgeries
B. WHAT HAPPENED TO AUTOREGULATION? ............. 3 D. CURRENT HEALTH STATUS
V. WHAT WOULD YOU LIKE TO REQUEST? ...................... 4
● Non-smoker
VI. WORKING DIAGNOSIS ........................................................ 5
● Non-alcoholic beverage drinker
VII. MANAGEMENT.................................................................... 5
● High protein diet – ingestion of whey protein which patient
VIII. INDICATIONS FOR DIALYSIS ............................................ 6
stopped 1 month ago
A. RRT Modality (Hemodialysis vs. Peritoneal Dialysis) ......... 7
→ Whey protein is seemingly harmless but can also be harmful
END OF TRANSCRIPT .............................................................. 9
to the kidneys to a degree, especially in high doses
REFERENCES ........................................................................... 9
→ Whey protein itself can cause interstitial nephritis to those
MUST KNOW BOOK PREVIOUS TRANS allergic to it
   → Can also cause hyperfiltration, presenting with elevated
creatinine
I. CASE ● No herbal intake
● Juan Macho “J.M.,” single, 36-year-old male, body builder/gym ● 1st COVID 19 vaccine (July 15, 2021)
instructor, was rushed to the ER due to alteration in sensorium. II. IS THERE A RENAL SYNDROME PRESENT?
A. HISTORY OF PRESENT ILLNESS ● Yes.
● Seven (7) days prior to admission (PTA), after his usual workout, → Dr. Navarro:
he drank 2 glasses of root beer with 4 raw eggs after a 4-hour ■ We think that this renal syndrome is acute because the
work out. Six hours later, he had vague abdominal pain. history that was provided happened within a week’s time
● Six (6) days PTA, he started to have loose bowel movement (acute onset).
described as watery, non-bloody, amounting to ~1 cup per ■ There are two criteria to diagnose AKI: urine output
episode, which occurred 7 times. It was accompanied by low-to- (oliguria) and serum creatinine. Although his serum
moderate fever (with fever max of 38ºC). He self-medicated with creatinine is not yet available at this point, there is already
Ibuprofen 200 mg/1 tab every 4 hours, for 5 doses. He had no a very minimal urine output in this patient.
vomiting, no cough, no anosmia during this time. → Dr. Natividad:
● Four (4) days PTA, still with persistent watery stools now ■ We do not need the laboratory in identifying a specific renal
amounting to 2-3 cups, 10-12 times per day. This was syndrome like AKI.
accompanied by 5 episodes of vomiting and low-grade fever with ■ 80% of our initial impression is based on the history and
(fever max of 37.5ºC). He then self-medicated with Loperamide physical examination.
(Imodium) with minimal resolution of loose bowel movement. He ● Aside from this, the patient has a clear setting (risk factors) to
was able to take Gatorade occasionally. have a renal injury.
● Two (2) days PTA, there was persistent watery stools occurring → Several causes of volume loss
8x to 10x a day and still with 4 episodes of vomiting. He was ■ Profuse or massive diarrhea, probably losing more than
afebrile, but he felt weak. He had teleconsult and was advised around 10L in the last 7 days.
admission by his doctor, but he refused due to fear of catching ■ Vomiting
COVID. During this time, he had decreased appetite and noticed ■ Poor intake/replacement – patient was probably not eating
decreasing frequency in urination. He denied dysuria, gross well
hematuria, flank pain, passage of sandy and/or bubbly urine, ■ Fever – increase in insensible water losses
edema. → Intake of Ibuprofen (NSAID) due to myalgia
● One (1) day PTA, still with persistent watery stool, non-bloody, at ■ NSAIDs can affect renal perfusion by affecting the afferent
8x to 10x a day, and vomiting (2x), and decreased appetite; he arteriole
was noted be lethargic. According to the mother, his last urine ■ Remember: NSAIDs block PGE synthesis → constrict
output was at 3 AM ~ 1/2 cup, dark brown urine. The parents afferent arterioles → decrease GFR
decided to bring their son to the hospital, but the ER was full. He → Low blood pressure (85/50 mmHg)
was attended to only at the parking lot. The vital signs at the tent ■ Probably reflective of all the volume losses that he
at the parking lot are as follows: BP 85/50 mmHg; PR 110 bpm; sustained
T: 37.5 ºC. ■ Can also affect renal perfusion
● He was eventually admitted into the ER at UST, 6 hours prior
(8PM).

DE JESUS H.K., DULFO J.P., DY J., ELGAR C.Y., EXCONDE M.E., GONZALES C. Page 1 of 9
A-TG18 | Chan | Chen, Cheng, Ching, Chua B., Chua E.
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III. CAN WE SAY THAT THIS PATIENT HAS AKI? ● VS: BP 80/50 mmHg; PR 112 bpm, regular, thready; RR 26 cpm;
● Dr. Pe: T 37.5ºC; Weight 70 kg
→ The patient has AKI based on the amount of losses from the ● Dry skin, dry mouth, and buccal mucosa
vomiting, frequent diarrhea, and insensible losses. ● Sunken eyeballs, pink palpebral conjunctivae, anicteric sclerae,
→ The patient’s self-medication with ibuprofen is to be pupil 2mm to 3mm ERTL (equally reactive to light)
considered as well. → Sunken eyeballs due to prolonged history of dehydration
→ How was the patient able to get hold of ibuprofen? Has the ● Flat neck veins
patient been taking ibuprofen ever since? How frequent does ● Symmetrical chest expansion, no retractions, normal breath
he take ibuprofen? sounds
→ Dr. Natividad responded: “The patient has no history of ● Apex Beat 5th LICS MCL, no murmurs
chronic ibuprofen intake.” ● Flat abdomen, hyperactive bowel sounds, non-tender, no
● Dr. Laguesma palpable masses, non-distended hypogastric area,
→ The patient has oliguria ● DRE (digital rectal exam): no stools, no palpable masses
→ Not all history of NSAID use can be associated with AKI ● No bipedal edema, (+) asterixis
■ In this patient, he presented with dehydration, along with ● (-) Babinski
NSAID use, will cause obliteration of autoregulation that is ● Dr. Navarro: What is the O2 saturation of the patient?
why he had AKI. → The patient presented with fever and myalgia, which are
symptoms of COVID as well. At the ER, having a patient who
A. DIAGNOSIS OF AKI is exhibiting signs of systemic inflammatory response
Table 1. Diagnosis of Acute Kidney Injury
syndrome (SIRS), we need to find out whether the symptoms
Stage Serum Creatinine Urine Output that the patient exhibited is due to COVID-19.
1 1.5x to 1.9x > < 0.5ml/kg/h for 6- ● Dr. Navarro: Patient’s O2 saturation is 97% at room air.
baseline 12 hours C. WHAT TYPE OF AKI DOES THE PATIENT HAVE?
OR ≥ 0.3 mg/dl
● Dr. Pe: Because of the presentation of the patient (several
(≥26.5 μmol/L) episodes of diarrhea, vomiting, insensible losses), there is a
increase setting for a pre-renal AKI.
2 2.0x to 2.9x > < 0.5ml/kg/h for ≥ 12 → A pre-renal AKI that is not properly addressed may lead to
baseline hours intrinsic AKI later on.
3 3.0x > baseline OR <0.3 ml/kg/h for ≥ 24 → Sepsis or an ongoing infection with a manifestation of volume
Increase in serum hours losses may cause intrinsic AKI.
creatinine to ≥ 4.0 OR
● Dr. Roasa:
mg/dl (≥353.6 Anuria for ≥ 12
μmol/L) hours → “Postrenal is not a good choice here. Those who answered
OR prerenal or intrinsic would be on the right track; since, those
Initiation of renal two conditions can come about from ischemia.”
replacement therapy → “Whether there is enough renal damage so that the patient
OR already has necrosis of the tubules brought about by the
In patients <18 hypovolemia will be in question. You’re going to be using
years, decrease in diagnostics to try and find out based on some urinary indices.”
eGFR to <35 ml/min → “You don’t have creatinine yet; you have to look into that. You
per 1.73m2 have a patient who is uremic. Dr. Marcial alluded to
● Dr. Navarro: something about the breath (uremic breath). You have to
→ Based on the history provided, he came in the ER at 8PM and find out how badly the kidney is failing. If it is really bad,
the last urine output was at 3am. The amount was noted to be you’re probably in a situation where the kidney is not
a half cup or 100 ml in 17 hours. (Dr. Kho: in gold standard, 1 compensating anymore. In prerenal, the kidneys still
cup is 236 ml) manage to compensate.”
→ Stage AKI according to severity (from stage 1 to 3).
→ If you look at stage 3, it is 0.3ml/kg/hr for more than 24 hours,
it is hard to tell because 17 hours is not within 24 hours, but
then there is another criterion under stage 3, which is anuria
for more than 12 hours. Anuria is urine output of less than 100
ml in a 24 hour period. Probably, the patient will fit this
particular stage of AKI.
→ Ideally, we should have asked what the urine output was prior
to 3 am to be able to compute for the 24-hour period AKI.
→ Stage AKI according to the more severe criteria (urine output).
● Dr. Natividad: Why did they come up with a staging of AKI?
● Dr. Pe: Staging of AKI would tell you the severity of the condition,
and it would have a bearing on the prognostication later on.
Probably, this would also tell how aggressive in identifying and in
treating or addressing the causes of AKI, also to prevent its Figure 1. Classification of the major causes of acute kidney injury. Harrison’s 20th
consequences or sequelae. edition, page 2099.
→ The higher the stage, the poorer the prognosis. ● Causes of acute kidney injury:
→ AKI was found to be associated with 80% mortality → Prerenal
● Dr. Laguesma: Diagnosis of AKI is not only based on elevation ■ Hypovolemia
creatinine, but we also have to take note of the urine output of ■ Decreased cardiac output
the patient. This will also help with the staging of AKI, which in ■ Decreased effective circulating volume
turn helps us know how aggressive treatment must be − Congestive heart failure
B. PHYSICAL EXAMINATION − Liver failure
● Lethargic ■ Impaired renal autoregulation
● GCS 12 - opens eyes to verbal stimuli, confused, localize to pain − NSAIDs, ACE-I/ARB, Cyclosporine
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→ Intrinsic A. AUTOREGULATION
■ Glomerular (acute glomerulonephritis)
● Mild degrees of hypovolemia and reductions in cardiac output
■ Tubules and interstitium
elicit compensatory renal physiologic changes
− Ischemia
● Renal vasoconstriction and salt and water reabsorption
− Sepsis/Infection occurs as homeostatic responses to decreased effective
− Nephrotoxins circulating volume or cardiac output
○ Exogenous: → Goal: to maintain blood pressure and increase
= Iodinated contrast intravascular volume to sustain perfusion to the brain and
= Aminoglycosides coronary vessels
= Cisplatin → Goal: to maintain a normal GFR and RBF
= Amphotericin B ● Myogenic reflex within the afferent arteriole leading to dilation in
= PPI the setting of low perfusion pressure → maintaining glomerular
= NSAID perfusion
○ Endogenous: → Production of vasodilatory prostaglandins contribute to the
= Hemolysis maintenance of perfusion, but since our patient took NSAIDs,
= Rhabdomyolysis vasodilation is prevented
= Myeloma ● Tubuloglomerular Feedback: hypovolemia, decreases in
= Intratubular crystals solute delivery to the macula densa elicits dilation of the
→ Postrenal juxtaposed afferent arteriole
■ Bladder outlet obstruction → Mediated by nitric oxide (NO)
■ Bilateral pelvoureteral obstruction (or unilateral obstruction ● Limits:
in cases of solitary functioning kidney) → Autoregulation fails to occur when SBP < 80 mmHg
● Dr. Natividad: Do you think that postrenal AKI is a possibility in → OR when there are prolonged GI losses, and the intake of
this case? NSAIDs and ARBs/ACEIs
● Dr.Navarro: In a patient who presents with acute anuria, ■ Must discontinue the ARBs/ACEI temporarily since they
postrenal would always be a possibility. Correlate the history and inhibit the production of angiotensin II, which is important in
consider the physical exam. A patient presenting with a postrenal cases of volume depletion
obstruction causing AKI, you note any signs of urinary retention. − Angiotensin II vasoconstricts the efferent arteriole and
In the history, elicit for any possible obstruction, history of kidney will maintain glomerular blood flow
stones, radiation, or malignancy. But in this case, the inciting ■ But if they keep taking the ARBs/ACEI that inhibit
events that led to anuria was obviously pre-renal. angiotensin II, it will dilate the efferent arteriole, causing
→ A patient can have several types of AKI. In our case, he has blood to leave the glomerulus and further decrease the
pre-renal and intrinsic AKI, but we don’t know which came pressure
first.
→ “DRE PE finding of no masses in the hypogastric area is B. WHAT HAPPENED TO AUTOREGULATION?
to rule out obstruction. Postrenal is out of the question.” ● Dr. Navarro: It is hard to tell if autoregulation did not happen in
● Dr. Navarro: There is prolonged hypovolemia in this patient. If our patient since there are several possible causes
volume is not restored immediately, this pre-renal AKI can compromising the kidneys such as the intake of NSAIDs, volume
progress to ischemic tubular necrosis. depletion, patient not going to the ER immediately, and vomiting.
→ Due to fever, abdominal pain, vomiting, diarrhea, and altered ● Dr. Pe: The fact that our patient has anuria, it means that the
sensorium, we are thinking that there might be an infection or nephrons are failing to autoregulate.
sepsis, which may affect the renal parenchyma and cause → This happens due to too much volume losses (though the
intrinsic AKI. patient’s BP is still acceptable for autoregulation to occur).
→ NSAIDs can cause both pre-renal AKI and acute → Additionally, the patient took NSAIDs, which may have
tubulointerstitial nephritis. affected the afferent and efferent arterioles to autoregulate.
IV. INITIAL IMPRESSION ● Was there an attempt to restore renal perfusion?
→ Possibly, since the thirst mechanism was intact for him to
● Acute Kidney Injury Stage 3, intrinsic renal cause, secondary voluntarily drink Gatorade.
to hypovolemic shock (that has progressed to ischemic acute → The inability to go to the doctor and be seen medically for early
tubular necrosis) secondary to bacterial gastroenteritis, in intervention could have been detrimental and prevented
uremia autoregulation from happening.
→ Uremia → It is difficult to restore volume to replete losses if the patient is
■ As indicated by altered sensorium (GCS 12) and asterixis vomiting.
on PE → There was an attempt at autoregulation BUT the prolonged
■ Dr. Pe: Very non-specific symptoms/signs: lethargy, period of volume depletion and vomiting took a toll on his
anorexia, asterixis. These non-specific signs are supported kidneys.
by a clinical setting for a renal disease. → It is important to educate our patient that once vomiting and
− Asterixis – can also be seen in hepatic encephalopathy, diarrhea start occurring, they must be admitted right away.
but since there is no history of liver problems, most likely
due to renal causes
■ Uremic breath – retained toxins in the body which presents
itself as a fishy odor.
● Predominantly in Intrinsic type
→ Initially the patient was in pre-renal state, with hypovolemia
with NSAIDS use
→ Infection and ischemia pointing to intrinsic type of kidney injury
● To consider: non-typhoidal salmonellosis
→ For diarrhea
● COVID-19 suspect
→ Fever and diarrhea
→
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Table 2. CBC Results

NICE TO KNOW INFORMATION
Complete Blood Count
How much NSAIDs need to be taken for it to be significant Hemoglobin 101 137-175 g/L
enough to cause a renal injury? Hematocrit 0.33 0.4-0.51
● For acute settings, there is no quantifiable dose of NSAIDs to WBC 14.9 4-10 x 109/L
tell us that it can cause AKI and prevent autoregulation from Seg 90 34-68%
occurring Lymph 10 22-53%
→ There is currently no literature about this Plt 202 150-450x109/L
→ Difficult to quantify how much Table 3. Blood Chemistry Results
● BUT you must consider the setting and comorbidities of the Blood Chemistry
patient along with the NSAID intake Creatinine 9.75 0.51-0.95 mg/dL
● Since there was a setting of volume depletion in our patient, BUN 80.6 6.10-23.32 mg/dL
that puts the patient at a higher risk for AKI Na 135 135-148 mEq/L
● If a patient took NSAIDs not in a setting of volume depletion, K 6.6 3.5-5.3 mEq/L
then the patient will probably not have AKI since the kidneys iCa 1.12 1.10-1.35 mmol/L
are functioning properly iPO4 6.56 2.76-4.46 mg/dL
● Once you can elicit that the patient took drugs such as NSAIDs Cl 86 96-106 meq/L
to block compensation of the afferent and efferent arterioles, ● BUN:Creatinine ratio – 8.3
that becomes a caveat and contributes to the compromised → Result is less than 20, more likely AKI, intrinsic (renal) cause
renal function
Table 4. ABG Results
V. WHAT WOULD YOU LIKE TO REQUEST? Arterial Blood Gas
● Urinalysis (basic test) pH 7.25
→ Specific gravity pCO2 26.5
→ Casts, are they present? HCO3 12.5
→ Very helpful test and commonly requested (so don’t forget!) O2 98
● CBC with Platelet Count ● ABG results: metabolic acidosis
→ To rule out infection Table 5. Chest Xray Results
→ Expected results if infection is present: CXR PA Lat
■ Leukocytosis: Increased WBC with neutrophil Normal
predominance (if bacterial) RT-PCR: negative for SARS-COV 2
■ Allergic interstitial nephritis: eosinophilia and eosinophiluria
Table 6. Urinalysis
− But not usually seen in urinalysis or Gram’s Urinalysis
− Special stain used: Hansel’s Stain Color Dark yellow
● Serum Creatinine and BUN Transparency Turbid
→ Expect these analytes to be increased pH 7.1
→ Then obtain the BUN:creatinine ratio Specific gravity 1.010
■ Pre-renal B:C ratio = >20:1 Protein ++
■ Renal B:C ratio = 10-15:1 Blood +
● Urine Chemistries WBC 5-7/hpf
→ Fractional Excretion of Urine Sodium (FeNa) RBC 2-3/hpf
■ To differentiate between pre-renal and renal AKI Epithelial cells Few
− Pre-renal AKI: <1% Bacteria Few
− Renal (Intrinsic) AKI: >1% Casts Muddy brown granular
● Serum Electrolytes ● Interpret the results
→ Hyponatremia, hyperkalemia → Dr. Natividad: BUN:Creatinine ratio – 8.3, this is more likely
■ Hyperkalemia due to metabolic acidosis and high anion gap intrinsic AKI since the ratio is <20, not pre-renal because
● ABG BUN:Cr ratio must be >20.
→ Metabolic acidosis (a complication of AKI) → Na is low normal; K is high but even though the patient has
■ On PE: RR is rapid and deep, indicating Kussmaul’s diarrhea and GI losses, we expect it to be hypokalemia, but
breathing the patient has oliguria and very low GFR
● GFR → We estimate the GFRwhen the patient’s serum creatinine is
→ Expect this to be decreased in pre-renal AKI stable so patients with AKI, the GFR is <10. K starts to rise in
→ Can be computed; no need for nuclear GFR patients with GFR <30
● Urine Osmolality → Hyperphosphatemia is due to impaired excretion of
● Ultrasound of KUB phosphorus
● Fecalysis → Dr: Marcial: ideally, for this patient we should use the kinetic
→ Diarrhea eGFR. It is the computation of eGFR, usually used in AKI,
● Blood Culture and Sensitivity comparison of previous creatinine (after 24 hrs or 2 days) in
→ Sepsis an app to get the kinetic estimated GFR.
Diagnostics → For this patient, it is expected to have low hemoglobin
● CBC with platelets because in AKI and CKD, there will be decrease production of
● Urinalysis ABO which may lead to anemia.
● BUN, creatinine → WBC is also elevated → sepsis and infection confirmed with
● Electrolytes: Na, K, Cl, iCa, iPO4 CBC
● ABG → Dr. Navarro: for ABG, low pH, low HCO3 and lowpCO2
● Fecalysis → Compute for compensated respiratory response
● Blood culture and sensitivity ■ Shortcut method: HCO3+15= 278.5
● Ultrasound of KUB ■ Using the formula: 1.5x HCO3+8= 26.75-/+2= 24.75-28.75
● In renal failure, always find the cause; because the treatment is
to treat the cause.
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→ The measured pCO2 (26.5) is within the expected Table 8. Fecalysis

compensated response therefore there is simple acid base, Fecalysis
metabolic acidosis Color Brown
→ Next is to compute for anion gap, Na (135) – Cl(86)=49- Consistency Watery, mucoid
HCO3(12.5)= 37.5 (NV: 8-12) RBC 9-10/hpf
→ High anion gap metabolic acidosis in the presence of AKI- this WBC 40/hpf
is expected for our patient No ova/parasites
● Urine pH is 7.1, it is high in the presence of metabolic acidosis
● Specific gravity is 1.010, correlating it to PE findings of Table 9. Culture Results
hypovolemia and low BP Blood Culture on Two Sites Stool Culture
● Are the urinalysis findings compatible with the working Negative Salmonella choleraesuis
impression? • Sensitive:
→ Dr. Navarro: our patient suffered from volume losses, • Ceftriaxone
normally, if prerenal AKI, the kidney will reabsorb water and • Ciprofloxacin
sodium therefore we expect that the urine will be concentrated • Piperacillin-
tazobactam
to compensate for the volume loss. However, the specific
• Meropenem
gravity (1.010) is relatively low compared to the volume losses
of the patient. pH is a little alkalotic (usual is 5.5-6.5). ● Negative blood culture indicates no sepsis
Sometimes, depending on our diet we can have a urinalysis ● Infection is isolated to the GI tract
higher than usual pH but, in this case, there is metabolic ● The primary clinical impression of acute gastroenteritis was
acidosis, we would think that the kidney will compensate confirmed by the stool culture
appropriately and secrete the excess acid. Muddy brown ● At the ER, start IV empiric antibiotics within an hour if suspecting
granular seen in AKI that is renal, intrinsic or ATN. This infection or sepsis
urinalysis is consistent with renal AKI. → Do not need to wait for stool culture results since these are
→ If pre-renal AKI is suspected, normally, we expect the released after 2 to 3 days
nephrons to try to concentrate the urine → If you do not start right away, the patient might die by the time
→ Specific gravity: the nephron has lost the ability to the culture results are released
concentrate urine, since it is not properly responding to the ● To summarize, AKI has been identified as the renal syndrome
hypovolemia of the patient present in the case but when lab results came in another renal
→ pH: Acidic pH (7.1) means there are bicarbonate losses or syndrome also presented
kidney cannot acidify the urine well → Recall the 10 renal syndromes: renal tubular disorder is one
■ Since patient is in metabolic acidosis, bicarbonate disease in this case.
reabsorption by the tubules is expected to compensate for → Lab results of metabolic acidosis, inability to concentrate,
the metabolic acidosis inappropriately dilute urine, and granular casts all point to the
→ Proteinuria: a sign of glomerular damage or pathology and additional renal syndrome (renal tubular disorder)
tubular diseases
VI. WORKING DIAGNOSIS
■ But a glomerular pathology usually presents with more
proteinuria ● Acute Kidney Injury, Stage 3, due to Renal (intrinsic) cause
→ RBC: no dysmorphic RBCs, quantification was approximately (Ischemic Acute Tubular Necrosis) secondary to hypovolemic
< 500mg → unlikely glomerular diseases, more of a tubular shock secondary to bacterial gastroenteritis, in uremia
disease ● COVID-19 negative
→ WBC/pyuria & RBC: not indicative of UTI but of an ongoing ● Non-typhoidal salmonellosis
inflammatory process in the renal tubules
■ WBC in the urine is not always equivalent to UTI VII. MANAGEMENT
→ Muddy brown granular casts: necrosis might already be ● What is the best initial management in this case?
happening in the tubules → Choices:
→ The urinalysis results show that there is a problem in the ■ Dialyze the patient at once
renal tubules → unable to acidify urine, loss of ability to ■ Cautious hydration with PNSS
concentrate urine, necrotic tissues present ■ Start bicarbonate drip
Table 7. Ultrasound of KUB ■ Start antibiotics
Ultrasound of KUB → Dr. Pe: Dialyze the patient at once because based on clinical
Right Kidney: 10.45cm X 4.67 cm CT 1.3 manifestations the patient is already uremic, has anuria,
Left Kidney: 10.20 cm X 4.85 cm CT 1.4 hyperkalemia, and acidotic
No lithiasis, no hydronephrosis ■ If dialysis can be done immediately, choose to dialyze the
Bladder: underfilled patient because this will address the uremia, the volume
Prostate: no enlargement overload if it is present due to the anuria, the hyperkalemia,
● Based on the ultrasound, have we ruled out post-renal cause and the metabolic acidosis.
of AKI? → Dr. Navarro: At the outset, when you see a lethargic patient
→ No obstructing stones, masses, hydronephrosis who is volume depleted with a BP of 80/50, your first instinct
→ Bladder is underfilled → kidneys not forming urine at this time is to insert an IV line to try to restore hemodynamic stability.
→ Anuria is most likely secondary to the kidneys not being able ■ During assessment, wait for confirmation from lab results
to produce urine, rather than an obstructing disease to identify the possibility of uremia
■ Post-renal AKI is ruled out ■ Chief complaint of altered sensorium is non-specific since
→ Probably, the patient started with pre-renal but with prolonged this can be present in septic encephalopathy
hypovolemia developed ischemic acute tubular necrosis − It could not be explained by uremia alone, so you really
(ATN), which is an intrinsic renal cause of AKI have to wait for the lab results
■ Before the lab results arrive, you should have started
already with the resuscitation effort including hydration
with PNSS and started with antibiotics
 MED 2-NEPHRO 1.04 – CCD 4: When Acute is not Cute (14 SEPTEMBER 2021, edited 16 NOVEMBER 2021)
■ Because there is uremia, start the process of emergency
dialysis. The earliest we can dialyze the patient is within
1-2 hours
■ Hydrate right away because patient will die of
hemodynamic instability earlier than dying of uremia
■ The steps in management does not have to be sequential.
You must IDENTIFY all the problems in the patient, then
PRIORITIZE and address all of these
→ Dr. Natividad: Difficult to choose one initial management
since you really must do all of these
■ Once the patient arrives at the ER, hydrate with PNSS.
When hydrating, do PE, check VS, urine output, if JVP is
increasing, and development of fine crackles
− Fine crackles due to fluid overload from hydration yet
patient is not urinating
■ Patient might develop congestion if not monitored properly
■ Start antibiotics right away
■ Decide if for dialysis due to the following indications:
uremia, presence of asterixis, hyperkalemia, and metabolic
acidosis
→ Dr. Natividad: Actually, 1, 2, and 4 should be given at the
emergency room. Because we have to give cautious
hydration but since patient is uremic, we already have to
decide that the patient must undergo dialysis.
■ The patient has an infection, so we must give antibiotics
■ The pH is 7.2, Bicarbonate is not necessary because
dialysis will take care of that.
■ Best initial management for DR. NATIVIDAD: Start
antibiotics
→ Dr: Marla: Dialysis cannot be easily done even if we already
identified that the patient is uremic. Minimum of 2 hours to
have an access and to get everything ready for dialysis.
■ Patient at the ER is hypotensive – Hydrate First
■ Address first hemodynamic stability with cautious hydration
of PNSS
■ While running the fluids we can at the same time order the
nurse to prepare initial bolus of IV antibiotics for the patient.
− It will take around 2 minutes to start an IV line and run
plain NSS
− 5-10 minutes to prepare the antibiotics
■ Prime the patient and relatives the need for dialysis.
■ Bicarbonate therapy is not indicated since addressing the
main reason for acidosis, which is partly because of the
infection and volume depletion, is not yet done
→ IF THIS QUESTION IS GIVEN ON THE QUIZ, CHOOSE
CAUTIOUS HYDRATION WITH PNSS.
● Do we need to start bicarbonate drip?
→ Dr. Navarro: Metabolic acidosis can cause hypotension. For
Dr. Navarro, hydrate and see whether the BP goes up and see
whether the patient urinates since there is no urinalysis yet, so
the presence of granular casts is still unknown.
■ At the moment, we are still entertaining pre-renal cause of
AKI. So, if management is started early, the condition may
be reversible.
■ We start bicarbonate if pH is less than 7.2 (pH indicated in
patients with renal failure) and bicarbonate level of <12.
■ Metabolic acidosis is multifactorial since it could be due to
lactic acidosis or sepsis and a lot of these other causes
could be addressed by initial hydration already.
■ If patient is persistently hypotensive despite adequate
hydration, Dr. might give bicarbonate if you cannot dialyze
right away
→ Dr. PE: With the ABG of the patient and the renal failure
already happening, most likely Dr. Pe will start the patient on
bicarbonate drip while waiting for the other management to
take place or while waiting for dialysis
Page 6 of 9
VIII. INDICATIONS FOR DIALYSIS
● Is there an indication for dialysis? → YES. Uremia.
→ Choices:
■ Yes
■ Repeat BUN and creatinine
● A – Metabolic Acidosis (Intractable)
→ NOT the indication in this case because patient has not yet
been treated for metabolic acidosis (should be intractable)
→ HCO3- is given in cases of metabolic acidosis
● E – Electrolyte Imbalance (Intractable hyperkalemia)
→ NOT the indication in this case because patient has not yet
been treated for hyperkalemia (should be intractable)
→ Calcium gluconate is given in cases of hyperkalemia
→ D50 water plus 10 units HR insulin may also be given to
promote shifting of K+ from extracellular to intracellular
compartments
■ NaHCO3 also promotes shift of K+ to intracellular
compartments
→ Nebulization but if COVID suspect, nebulization is not done
● I – Intoxication of Drugs/ Poisoning
● O – Overload (Intractable)
● U – Uremia
→ This is the indication for this case since patient has altered
sensorium and asterixis
● If we will wait for the repeat BUN and Creatinine
→ It will be detrimental to the patient
→ Uremic toxin
■ increased risk for bleeding
■ high indoles
■ patient may become more acidotic
Figure 2. KDIGO Consensus Guideline for AKI. A screenshot from the lecture.
● At all stages of AKI, including those at high risk:
→ Discontinue all nephrotoxic agents when possible
■ NSAIDs, herbal supplements
→ Ensure volume status and perfusion pressure
→ Consider functional hemodynamic monitoring
→ Monitor serum creatinine and urine output
→ Avoid hyperglycemia
→ Consider alternatives to radiocontrast procedures
■ CT scan contrast
● For AKI stages 1, 2, and 3:
→ Non-invasive diagnostic workup
→ Consider invasive diagnostic workup (if needed)
● For AKI stages 2 and 3 only:
→ Check for changes in drug dosing based on renal function
→ Consider renal replacement therapy
■ Patient in the case needs dialysis
→ Consider ICU admission
■ Doc Navarro: if ICU room is available, admit the patient for
close monitoring
− Patient in the case is hypotensive (hemodynamically
unstable)
● Strictly for AKI stage 3:
→ Avoid subclavian catheters if possible as preparation for renal
replacement therapy
■ It will cause stenosis of the vessels eventually
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Diagnosis Hemodialysis in AKI: Intermittent vs Continuous Therapies

● Acute Kidney Injury, stage 3, due to renal cause (Acute Tubular ● Intermittent
Necrosis) secondary to hypovolemic shock secondary to → Conventional hemodialysis
bacterial gastroenteritis, in uremia ■ HD
Table 10. Goals of Care and Management ■ HDF
GOALS OF CARE MANAGEMENT → Sustained low-efficacy dialysis (SLED)
Achieve hemodynamic stability Isotonic fluid hydration → Usually done for 48 hours
● If not responsive to hydration, ● Continuous
such as in septic shock, give → Addressed for patients who are hemodynamically unstable
vasopressors → Continuous renal replacement therapy (CRRT)
Provision of maintenance and Diet ■ HD
replacement fluid requirements ● through NGT since patient has ■ HDF
altered sensorium → Advantages:
Intravenous Fluid ■ Enhanced hemodynamic stability and consistent solute and
● isotonic fluid so there will be no water removal in hemodynamically unstable patients
shift between compartments − Able to remove 50 mL to 100 mL/hour for 24 hours
Oral replacement solution (once ■ Enhanced inflammatory mediator clearance in septic
vomiting is resolved) patients especially when using the convective modes
Treat underlying cause (Acute Empiric antibiotics, then shift to ■ Better cerebral perfusion:
gastroenteritis) targeted therapy once culture − Better for patients with cerebral edema
results are available
− For patients with acute brain injury
● Salmonella choleraesuis in our
case − Patients with fulminant hepatic failure
Address uremia Emergency Dialysis → Being hypotensive does not necessarily contraindicate
hemodialysis. There are forms of hemodialysis that we can do
A. RRT Modality (Hemodialysis vs. Peritoneal Dialysis) for patients who are unstable
● Dr. Navarro: Both of these modalities have their pros and cons, ● No significant difference in kidney function recovery, mortality,
but given that this patient’s K+ level is 6.6, my choice would survival when both therapies are compared (Mehta et al, 2001)
definitely be hemodialysis ● Dr. Navarro: Both therapies use dialysis (concepts of diffusion,
→ Faster solute clearance ultrafiltration), but the advantage of continuous therapies is that
→ But in cases of unavailability, Peritoneal Dialysis is a viable because it’s continuous, we can do it at infinitum (Pwedeng dere-
option and has its advantages as well dere-dere-dere-derecho hanggang kailangan ng pasyente)
→ We are also entertaining acute gastroenteritis so in that setting → Advantage of using continuous therapy, you can divide the
Peritoneal Dialysis is totally NOT indicated amount of fluid that you will take out of the patient so you can
● Dr. Pe: Hemodialysis for more rapid solute clearance because do it very slowly because you are doing it continuously
patient is acidotic and hyperkalemic → Studies have shown that for septic patients, continuous RRT
● Dr. Marla may have an advantage over intermittent therapy
→ For a patient who is hypercatabolic, has acute volume loses, → However, continuous therapies are not readily available
ischemic acute tubular necrosis, sepsis, the faster modality to → Very expensive
address all these complications of uremia is HEMODIALYSIS ● Dr. Navarro: While intermittent therapies are usually done for 4-
→ CAVEAT: the patient was hemodynamically unstable when he 8 hours (can be done daily if needed - SLED)
got admitted. The first order of treatment is to stabilize the → Can also be done 3x to 4x a week depending on the
patient hemodynamically because one of the disadvantages hemodynamic status of the patient
of hemodialysis is that it will further aggravate the → More readily available
hemodynamic instability. → Using conventional hemodialysis, we can alter the mechanics
→ In terms of correcting the complications, the advantages favor to make it “friendly” for patients who are hemodynamically
hemodialysis over peritoneal dialysis because the latter entails unstable
using the peritoneum as a membrane to remove the toxins that ● Dr. Natividad: Since continuous RRT is not readily available,
have accumulated. Hence, in somebody who has an acute intermittent SLED will be done for the patient
abdominal infection or intraabdominal sepsis, you cannot ● In the patient: “They inserted an IJ and intermittent HD SLED was
administer peritoneal dialysis. done”
● Dr. Pe: With regards to morbidity and mortality, there isn’t much
Peritoneal Dialysis in AKI
significant difference in both continuous vs. intermittent
● Advantages: → Whichever will maintain the patient’s hemodynamic status will
→ Superior hemodynamic tolerance be the one done in this patient
→ Lower risk of dialysis disequilibrium syndrome
→ Anticoagulation not required Acute Complications of Hemodialysis
→ Hyperalimentation for malnourished patients ● Hypotension (most common)
→ Can be done in resource-limited settings → In this case, we do not do the conventional/regular 300 blood
■ Lack of water supply, electricity, personnel flow and 500 dialysate flow
● Disadvantages: → We do it slow (6 hours instead of 4 hours) and low (150
→ Risk of infection instead of 300 blood flow)
→ Increased protein losses ● Dialysis disequilibrium syndrome
→ Avoided in patients with: → Due to abrupt changes in shifting of solutes and electrolytes
■ Abdominal surgery ● Hemolysis
■ Diaphragmatic pleuroperitoneal connections ● Air embolism
■ Impending respiratory failure ● Arrhythmias
■ Severe hyperkalemia ● Dialyzer reactions
■ Intraabdominal sepsis or abdominal wall cellulitis ● Access infection
→ i.e. via femoral catheter
● Clotting
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Phases of Intrinsic AKI ● Serum creatinine (brown line) elevated at time of admission with
● Initiation and extension phases: low urine output
→ Damage to renal tissue (minutes to days) ● 48 hours after start of antibiotics, patient started to have urine
→ In our patient, it occurred within a 1 week period output, but still below 500 mL
→ Urine is still present with normal serum creatinine levels → Creatinine was still high
● Maintenance phase: (Where patient was during admission) → 2 sessions of dialysis (day 1 and day 2)
→ Oliguria/anuria ● After 48 more hours, urine output started to increase and
→ Complete loss of renal function creatinine went down even without dialysis (inverse
→ Stage with lowest GFR proportionality)
→ Creatinine elevates (pink line) → Dialysis was discontinued
→ Urine volume decreasing progressively (yellow bars) ● On the 10th hospital day, creatinine level was down to 2 mg/dL
→ Uremia can set in from 9.75 mg/dL (day of admission) and urine output increased
→ RRT may be indicated if condition is not reversed from almost 0 to >2.5L/day at the time of discharge
● Recovery phase: When to Stop: Management During Recovery of Kidney
→ If able to reverse renal injury Function
→ Increase in urine output and decrease in creatinine ● No accepted standards for discontinuation of dialysis
→ Glomerular function recovers prior to tubular recovery ● Indicators of renal recovery:
→ Creatinine goes down but still can’t concentrate urine which → Increasing urine output
will manifest as polyuria (renal tubular injury) ■ Sign of recovery of renal function and that dialysis might
■ Concentration of urine is a function of the renal tubules not be needed anymore
■ If volume is not replaced through hydration, AKI may → Decreasing pre-dialysis serum creatinine and/or BUN
occur again ■ If there is increasing urine volume, repeat serum
→ Uncontrolled urine quantities creatinine prior to initiating another dialysis session to
● Continued slow recovery of renal function (weeks to several check if renal function is improving
months) ● Other considerations for when to stop management:
→ Increased catabolism
→ Fluid overload
■ Even if patient is urinating, but is volume overloaded,
amount of urine excreted may not be sufficient to
overcome volume overload
− Continue dialysis
→ Ongoing hemodynamic instability
■ Renal perfusion is very important for renal recovery to
occur
→ Ongoing requirement for nephrotoxic drugs
■ Aminoglycoside antibiotics may be needed (based on
culture results) in some patients which may affect renal
recovery
→ Large volumes of obligate fluids
Figure 3. Phases of Intrinsic AKI. A screenshot from the lecture. Yellow bars ■ Critically ill patients may need massive amounts of volume
signify the urine output. Pink line is the serum creatinine. Arrows are the dialysis (5-6 L a day) and urine output is 500 mL – 1L
treatment − Need support with dialysis
● Y-axis: → Electrolyte and acid-base imbalance
→ Left side: urine volume ■ Hyperkalemia, metabolic acidosis
→ Right side: serum creatinine − Need to continue RRT as support until kidney can
● X-axis: function properly
→ Time/days ● Our patient, “J.M.,” was noted to have increasing urine output
● Our patient was in the maintenance phase upon admission → 48 hours after, he became conscious, coherent
→ Low urine output, high serum creatinine, and uremic ■ From GCS 12 to 15
→ Decreasing serum creatinine and BUN
→ Euvolemia from hypovolemia
■ No fluid overload
→ Hemodialysis was discontinued after 2nd session
→ Patient went home with a creatinine of 2 mg/dL
Prognosis for Patient “J.M.”
● Survivors of dialysis-requiring AKI at high risk for progressive
CKD (⁓10% may have End Stage Renal Disease)
● Close follow-up with a nephrologist
→ For aggressive secondary prevention of kidney disease
● Patient was followed up at outpatient
→ Creatinine went down from 2 mg/dL to 1 mg/dL
→ Dr. Pe: Of course, doctors would prefer AKI be identified
early and addressed properly because 80% to 85% of the
time, patients with AKI would recover their renal function
Figure 4. Course of the patient. A screenshot from the lecture. ■ 10-15% of AKI patients especially those who needed RRT
may still progress to CKD later on
● At the ER, patient was hydrated with NSS, but urine output is ■ History of AKI would be a risk factor for CKD development
still very minimal ■ As a general rule, patients with AKI when properly
→ IV ceftriaxone 2 grams every 24 hours was started addressed, would recover 80% of the time
→ IJ catheter insertion
→ Underwent dialysis
 MED 2-NEPHRO 1.04 – CCD 4: When Acute is not Cute (14 SEPTEMBER 2021, edited 16 NOVEMBER 2021) Page 9 of 9

→ Dr. Porsha: The prognosis is good since the patient’s kidney

function recovered but remember that survivors of dialysis
that have AKI are at high risk for progressive CKD. Education
is crucial that the patient should learn how to closely follow
up on a nephrologist because an episode of AKI, especially
the ones requiring dialysis, is a risk factor for a patient to
develop CKD.
Risk Factors for Development of CKD after AKI
● Albuminuria
● Lower baseline estimated GFR (eGFR)
● Older age
● Female
● Greater severity of AKI
→ Our patient, “J.M.,” is AKI stage 3
● Higher creatinine at discharge
● Multiple comorbidities such as heart failure, diabetes, or
hypertension
END OF TRANSCRIPT
Original Transcribers: De Guzman JAMO, Estrada MPAD, Estrella AV | Diwa, Domingo J, Domingo N, Dumala og, Dumo, Dnriquez, Escuadro, Espaldon, Espino, Esteban, Fernandez JG, Fernando S

REFERENCES
CCD4: When Acute is Not Cute, last September 14, 2021, at 7am to 9am