ICR 2010-2011 Acid-Base Case Study 1
A 77 year old man is brought into the emergency room by a concerned family member because he has been having “the dwindles”. He notes a lack of energy and appetite for several weeks along with a 20-lb weight loss and intermittent vomiting over the past three days. His medical history is significant for hypertension for which he takes a diuretic, and a 150 pack-year smoking history. He also states he was told last year there was a
“spot” on his chest x-ray, but he never scheduled the recommended follow-up CT scan.
On exam he is lethargic-appearing white male. His vitals signs: weight 69 inches, weight 130 lbs, T 99.1 F, BP 88/61, pulse 109, RR 28/min. The skin has increased turgor with normal capillary refill. Cardiopulmonary exam is significant for tachycardia and a prolonged expiratory phase with scattered faint wheezing. ECG is normal.
Laboratories:
Basic metabolic profile
Na = 123 mEq/L
K = 3.7 mEq/L
Arterial blood gas pH=7.06 pCO
2
=40
PO
2
= 65 HCO
3
= 11 mEq/L
BUN = 44 mg/dL
Cr = 1.5 mg/dL
Glucose = 87 mg/dL
Questions:
1.
Construct a problem list for this patient’s presentation
CORRECTION: Cl- = 82 mEq/L (left out of printed material but students were notified)

Symptoms/Signs

Failure to thrive, weight loss, vomiting

Hypotension, tachycardia

Signs of obstructive lung disease

Contributing medical history

Tobacco abuse
 h/o hypertension w/diuretic use

? Chest x-ray abnormality

Lab findings

Hyponatremia

Metabolic acidosis

Elevated creatinine
2.
What is his primary acid-base disorder?
Is there appropriate compensation or does one or more secondary disorder exist? If a secondary disorder exists, what is/are the disorder(s)?

Primary anion-gap metabolic acidosis : AG = 123 – (82+11) = 30

Respiratory compensation: For primary metabolic acidosis, there should be a compensatory respiratory alkalosis. Using Winter’s formula: expected pCO2 = (1.5 x bicarb) + 8 = (1.5 x 11) + 8 = 24.5 (+/-2). This is lower than measured pCO2=40, therefore there is also a secondary respiratory acidosis.
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
AG = 30, delta(AG) = 30-12 = 18; expected HCO
3
= 24-18 = 6, which is < 11. Therefore there is an additional metabolic alkalosis.
3.
List the causes of his primary acid-base disorder? What do you think is the cause of his disorder and what laboratories would you obtain to confirm this? List potential causes of any secondary disorders.

DDx of AG metabolic acidosis:

Lactic: possible from hypoperfusion, dx by checking serum lactate

Ketoacids: possible contribution from starvation but unlikely to be primary cause; dx by checking serum and urine ketones

Ingestions: MeOH, EtOH, ethylene glycol, salicylate, are all unlikely. Dx by checking levels +/- serum osmolality (or ethylene glycol by UV examination of urine or urine sediment)

Renal failure: possibly contributory if chronic, but unlikely to be signficiant in mild CKD

Secondary respiratory acidosis

Most likely due to chronic obstructive lung physiology

Other possibilities are less likely: musculoskeletal dysfunction, central respiratory depression

Secondary metabolic alkalosis:

Chronic compensation from chronic respiratory acidosis. Possible dx through review of previous baseline labs.

Chloride-responsive metabolic alkalosis from vomiting. Dx by checking urine chloride. When alkalosis is due to loss of HCl (vomiting) or loss of NaCl
(diuretics, volume depletion), then kidney will then retain Cl and Urine Cl will be low.
4.
What is the pathogenesis of his low bicarbonate concentration?

Low bicarbonate is due to excess organic anions (lactic acid, ketoacids). These acids are buffered in part by extracellular bicarbonate, causing the levels to drop.
5.
What is the differential diagnosis of his hyponatremia? What additional studies would you obtain?

His risks for hypovolemic hyponatremia:

Vomiting, diuretic use

Risk factors for euvolemic hyponatremia

SIADH from possible malignancy

Adrenal insufficiency from possible metastatic lung disease

Age (reset osmostat)

Studies: urine and serum osmolality, morning cortisol, TSH, FeBUN
6.
What are the potential explanations for his BUN and creatinine? What additional studies would assist in the diagnosis?

Chronic kidney disease (HTN, obstruction being statistically most likely) vs. acute kidney injury (volume depletion)

Most useful information would be previous labs. Renal ultrasound (obstruction, kidney size, cortical thickness). CBC, iPTH also potentially helpful to establish chronicity (CBC less useful with possible malignancy).
7.
What therapeutic measures would you consider at this time?

Gentle volume repletion, consider normal bicarbonate

Hold diuretics
2

ICR 2010-2011 Acid-Base Case Study 2
A 56 year old female presents to your clinic for a routine appointment. She is without specific complaints today, but has not been seen by a physician in two years. She has a history of type 2 diabetes mellitus with proliferative retinopathy, hypertension, and osteoarthritis. She is taking metformin, glipizide, losartan, and hydrochlorothiazide, and has been taking ibuprofen for a few days for knee pains.
On exam, she is an African-American female in no distress. Vital signs: height 54 inches, weight 165 lbs, T 98.7 F, BP 167/91, P 75, R 16. Cotton-wool spots are evident on funduscopic exam. There is trace bilateral pedal edema.
Laboratories:
Basic metabolic profile
Na = 138 mEq/L
K = 6.4 mEq/L
Cl = 108 mEq/L
HCO
3
= 17 mEq/L
Urinalysis sp grav = 1.012 pH = 6.0 protein = 3+ blood/glucose = negative
BUN = 59 mg/dL
Cr = 2.7 mg/dL
Review of her chart shows previous serum creatinines of 1.0 (4 years prior), 1.2 (3 years prior), and 1.4 (2 years prior).
1.
Construct a problem list for this patient’s presentation.

Signs/symptoms

Elevated blood pressure

Retinopathy

Trace edema

Contributing medical history

Diabetes w/proliferative retinopathy

Hypertension

Use of ARB, diuretics, NSAIDs

Metformin use

Lab findings

Hyperkalemia

Progressively elevated BUN/creatinine

Metabolic acidosis with urine pH = 6
 proteinuria
2.
What is the differential diagnosis of her elevated creatinine? What are the preferred treatments for each possible disorder?

Progression of CKD (likely diabetic) vs. acute-on-chronic CKD (from ibuprofen use in combination with ARB/diuretic). Plot of 1/Cr curve suggests progressive CKD is more probable.

Rx for CKD: BP control < 130/80, maximize use of ACEI/ARB for DM nephropathy, glycemic and lipid control, avoidance of nephrotoxins (NSAIDs, intravenous contrast, aminoglycosides). Rx for acute-on-CKD: correction of underlying cause (d/c of NSAID use).
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
Metformin use should be stopped.
3.
What is the primary acid-base disorder?
Using your equations, is there appropriate compensation or does one or more secondary disorder exist? If a secondary disorder exists, what is/are the disorder(s)?

Primary non-AG metabolic acidosis

No blood gas so unable to determine if there is appropriate respiratory compensation

Metformin use would be more likely associated with a lactic acidosis
4.
List the causes of the primary acid-base disorder. What do you think is the cause here and what laboratories would you obtain to confirm this? List potential causes of any secondary disorders.

DDx of normal-AG metabolic acidosis i.
Renal tubular acidosis: possible given elevated urine pH. Diabetic nephropathy and hyperkalemia may be c/w Type IV RTA. Also may be RTA of CKD. ii.
Extrarenal origin: nothing in this case to suggest GI losses
5.
What are the possible causes of her hyperkalemia?

ARB, AKI, Type IV RTA
4

ICR 2010-2011 Acid-Base Case Study 3
An 8-year old boy is brought into the emergency department after being found lying on the floor of the bathroom unresponsive. He has no significant medical history and no known allergies.
On exam he responds to loud noises and sternal rub. He is afebrile, BP 100/55, pulse
112, RR 40. Exam is otherwise unremarkable.
Laboratories:
Basic metabolic profile
Na = 138 mEq/L
K = 5.3 mEq/L
HCO3 = 12 mEq/L
BUN = 8 mg/dL
Cr = 0.7 mg/dL
Glucose = 123 mg/dL
Arterial blood gas (on 100% O pH = 7.50 pCO2 = 16 pO2= 690 mmHg
2
)
1.
What is his primary acid-base disorder?
Is there appropriate compensation or does one or more secondary disorder exist? If a secondary disorder exists, what is/are the disorder(s)?

CORRECTION: Cl- = 102 mEq/L (left out of printed material but students were notified)

Primary disorder = respiratory alkalosis, decrease in pCO2 = 40-16 = 24. Compensation for respiratory alkalosis should be an expected drop in serum bicarbonate (acute) = 0.2
*24 = 4.8 or (chronic) = 0.5*24 = 12. Since this is presumably acute, the expected bicarbonate should be about 19-20. Thus there is an additional metabolic acidosis.

The metabolic acidosis is with an elevated anion gap 138 – (102+12) = 24.
2.
List the causes of each acid-base disorder. What further laboratories or studies are indicated? List potential causes of any secondary disorders.

Ddx for respiratory alkalosis:

CNS stimulation (voluntary hyperventilation, anatomical lesion, sepsis, salicylates)

Pulmonary disease/hypoxemia

Ddx for anion-gap metabolic acidosis as in Case Study 1

Given clinical scenario, should consider salicylate overdose (which may be concomitant with ketoacidosis in children). This case was constructed to emphasize both respiratory and metabolic derangements. In reality, in adults the respiratory alkalosis is usually more prominent and while in children the metabolic acidosis tends to be more prominent.
3.
What is the treatment?

Urine alkalinization; hemodialysis
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ICR 2010-2011 Kidney Failure Case 1
A 31 year old solider comes to the Emergency Department complaining of fatigue and diffuse muscle pain. He was previously healthy on no prescribed medications but notes that he had been less physically active than usual for the past few months, and had gained
5 kg. In an attempt to get back in shape and prepare for his upcoming PT test, five days ago he started running and lifting weights and using some dietary supplements given to him by a friend. Three days ago he notice soreness in his thighs and back for which he has been taking ibuprofen 800 mg three times a day, but the pain has been getting worse over the last day, and he has been unable to eat for over 24 hours due to nausea and two episodes of vomiting, but has been eating saltine crackers, drinking water and fruit juices.
He denies any chest pain, shortness of breath, fever, chill, and lower extremity edema.
He does note that perhaps he is not urinating as frequently.
On examination he looks well but slightly short of breath. Temperature is normal, blood pressure is 165/100, pulse is 86, height is 74 inches and weight is 110 kg (which he notes is 2 kg less than he weighed before he started lifting). Lungs are clear and heart sounds are normal. He has soreness in his biceps, hamstrings and quadriceps, but no firmness, swelling, or erythema and no edema. He is oriented x 3 and has no asterixis.
Serum: Urine:
Na=130 mEq/L
K=6.6 mEq/L
Cl=98mEq/L
Bicarb=10 mEq/L
BUN=98 mg/dL
Cr=9.6 mg/dL
CPK=212,000
WBC=10,000/mm3
Hgb=12.4 gm/dL
Platelets=350,000
Arterial Blood Gas pH=7.26
Specific gravity=1.010 protein=1+, blood 3+
2 RBC/HPF, 2 WBC/HPF, 20-30 “muddy” brown pigmented casts/LPF
Urine electrolytes:
Na= 50 mEq/L
K=15 mEq/L
Cr=68 mg/dL pCO2=22 pO2=100
ECG reveals regular rate and rhythm, normal axis and intervals. Tall peaked T waves are seen.
Case 1 discussion questions :
1. Construct a problem list for this patient’s presentation. Which of these is of most immediate concern?
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
CORRECTION: The paragraph above should read: “He has had nausea and two episodes of vomiting over the past 24 hours, but has been eating saltine crackers, drinking water and fruit juices.”

Signs/symptoms

Muscle pain

Nausea/vomiting

Hypertension

Contributing medical history

Intense exercise after period of deconditioning

Use of dietary supplements and NSAIDs

Lab findings

Hyponatremia

Hyperkalemia with ECG changes (this is of most immediate concern)

Anion-gap metabolic acidosis

Elevated BUN/creatinine with elevated CPK

Abnormal urine sediment with disproportionately positive dipstick for hematuria, and muddy brown casts
2. Is this patient suffering from acute or chronic kidney failure? List history, physical, and ancillary clues to support your opinion.

Odds are acute given precipitating factors and onset of symptoms and lack of significant medical history. However, there is really nothing which definitely proves that this is not chronic.
3. Calculate his CrCl using the Cockcroft Gault equation. Calculate his Fractional excretion of sodium (FeNa).

CrCl = (140-31) x 110 /9.6/72 = 17 ml/min. This assumes that his current function is at steady-state.

FeNa = (50/130)/(68/9.6) = 5.4%
4. How does the kidney become involved in muscle injury?

Pathological muscle breakdown releases myoglobin, which is freely filtered through the glomerulus and has direct toxic effects on the proximal tubules. Acute tubular necrosis results.
5. How do the following impact the development and/or course of acute renal failure? i) exercise

See answer to #4. ii) dietary supplements

May have direct renal toxicity, cause changes in intravascular volume, or have cardiovascular activity. iii) NSAID use

Cause hemodynamically-mediated dysfunction;iImpair renal blood flow by inhibition of prostaglandin vasodilitation iv) content of oral intake

Caffeine may have diuretic effect causing intravascular volume depletion. Alcohol inhibits anti-diuretic hormone, leading to volume depletion, and also may be directly myotoxic.
6. What other common classes of medications should you inquire about when evaluating renal failure?

Antibiotics, antihypertensives. Also alcohol intake and recreational drug use.
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7. List values in the below table which can help differentiate pre-renal from intra-renal acute kidney failure.
Serum :
Pre-renal Intra-renal
BUN/Cr ratio > 20
Uric acid may be elevated ratio ~10 normal
Urine :
Na < 20 mEq/L
Specific gravity >1.030
Sediment unremarkable
> 40 mEq/L
1.010 (isosthaneuric) muddy brown granular casts, RTE cells
FeNa < 1% > 2%
8. What is this patient’s acid base status at this time?

Primary elevated AG metabolic acidosis, AG = 130-(98+10) = 22

Respiratory compensation: For primary metabolic acidosis, there should be a compensatory respiratory alkalosis. Using Winter’s formula: expected pCO2 = (1.5 x bicarb) + 8 = (1.5 x
10) + 8 = 23 (+/-2). The measured pCO2 = 22.

AG = 22, delta(AG) = 22-12 = 10; expected HCO
3
= 24-10 = 14, which is > 10. Therefore there is an additional NAGMA.
9. What is the treatment for his hyperkalemia? What is the treatment for his renal failure?

Hyperkalemia: cardiac stabilization with calcium; facilitate intracellular shifts with insulin/glucose and beta-agonists; possibly consider bicarbonate. Potassium clearance through Kayexalate or dialysis.

Renal failure: supportive care, volume resuscitation as indicated, avoidance of nephrotoxins. May consider alkaline/mannitol dieresis but risk/benefit ratio unclear.
10. What is your differential diagnosis for this patient’s kidney failure? How might the diagnosis change if the urine sediment was bland and the urine sodium was 8?

DDx includes nephrotoxic acute tubular necrosis from rhabdomyolysis +/- supplements/NSAID use. NSAID use could add an ischemic/prerenal component to the insult.

With bland sediment and low urine sodium, one could consider prerenal azotemia, although this degree of lab abnormalities would be unusual in an otherwise healthy young person.
11. List the acute indications for dialysis. Is there a role for dialysis in this case?

Volume overload refractory to medical management, electrolyte changes refractory to medical management (potassium, acidosis), toxic ingestions otherwise refractory to medical management, uremia (encephalopathy, serositis, coagulopathy)

At this point, if hyperkalemia can be managed, probably no acute indications. Will need to be monitored carefully for a response to volume repletion.
8

Kidney Failure Case 2
Initial Presentation
A 45-year-old African-American Lieutenant Commander presents with a several week history of generalized fatigue, diffuse arthralgias, and “low grade” fever. She also reports malaise and a decreased appetite during this time, though she has gained 7 lbs since symptom onset. She denies chills, night sweats, nausea, vomiting, diarrhea, alopecia, or skin rashes. She also denies chest pain, shortness of breath, PND, or orthopnea.
Medications: acetaminophen as needed, low estrogen birth control pill
Social history: No tobacco, alcohol, history of IVDA or other illicit drug use
Family history: Hypertension-father; Type 2 diabetes-mother
PE : Was essentially normal with the following findings:
BP=160/85, HR=90, RR=18, weight=60 kg
HEENT: pale conjunctivae without scleral icterus
Cardiac: 4ht heart sound, Extremities: 2+ ankle and pretibial edema.
Laboratories :
Na=134 mEq/L
K=4.9mEq/L
Cl=105 mEq/L
WBC=3.0
Hgb=8.2g/L (MCV=82, RDW=16)
Platelets=200,000
CO2=19mEq/L
BUN=42 mg/dL
Creatinine=2.8.mg/dL (creatinine noted to be 0.8mg/dL at a pre-deployment physical 6 months ago)
Glucose = 104mg/dL (not fasting)
Calcium=8.1mg/dL
Phos = 6.2mg/dL
Albumin= 2.8 mg/dL
Urinalysis: specific gravity=1.018, pH=6, 4+ protein, 2+ blood, glucose neg, esterase slightly positive, nitrate neg; sediment: 5-10 dysmorphic RBCs/hpf, 2-4 WBCs/hpf, 0-2
RBC cast/lpf, 1-2 granular casts with RTE inclusions/lpf
Case 2 Initial Presentation Discussion Questions:
1. Construct a problem list for this patient’s presentation

Symptoms/Signs

Fatigue, arthralgias, fever, malaise

Weight gain

Hypertension

S4

Edema

Contributing medical history

Normal creatinine six months prior

Family history of HTN/DM
9


Lab findings

Elevated creatinine

Metabolic acidosis

Hypoalbuminemia

Hyperphosphatemia/hypocalcemia

Anemia and leukopenia

Proteinuria and hematuria with active urine sediment
2. Calculate her CrCl using the Cockcroft-Gault equation. What is her estimated GFR?

CrCl = (140-45) x 60/2.8/72 *0.85= 24 ml/min. This assumes that his current function is at steady-state.
 eGFR = 23.5 ml/min/1.73 m 2 (4-variable MDRD), = 20.6 ml/min/1.73 m 2
3. Would you characterize her kidney failure is acute or chronic? Provide supporting data: history, physical exam, and/or laboratory data for your answer.

Most likely acute based on recent labs showing normal creatinine and presuming constitutional symptoms are part of kidney disease.

Anemia normally suggests chronic disease but here may be c/w autoimmune process.

S4 may be more c/w chronic hypertension
4. What is the differential diagnosis for her kidney failure?

Ddx includes acute GNs (idiopathic vs. SLE/vasculitis vs. infection-related).
Less likely includes rhabdo, paraproteinemia. No evidence of pre/post-renal physiology.
5. What additional tests should be considered and why?

Proteinuria quantification. Lipid panel

Consider ANA/dsDNA, complements, ANCAs, anti-GBM, Hepatitis B/C,
SPEP/UPEP, anti-streptolysin, DNAse B, CPK
6. Is there a role for a renal biopsy in this case? If so, what are possible findings?

Indications for biopsy: nephrotic-range proteinuria, RPGN, unexplained renal failure, SLE for classification, parproteinemia
7. What treatments might be considered empirically before a final diagnosis is known?
What treatments might be considered after a final diagnosis is known?

Empirically: ACEI/ARB, other antihypertensives, statins

Post-biopsy: Immunosuppression: steroids, cytotoxics
Renal Failure Case 2
Clinic Presentation 6 Years Post Diagnosis
After the initial diagnosis and treatment the patient is followed by multiple specialialties including nephrology for six year. She comes to see you in the nephrology clinic for a routine follow-up appointment with a history of chronic kidney disease, diabetes,
10

hypertension, and a collagen vascular disease. About one week ago, she developed slight burning when she urinated but this resolved in two days. Three days prior to the clinic visit the burning returned along with a low-grade fever and mild lower abdominal pain.
She may have had one chill after taking tylenol the night before the clinic visit but is not sure.
Her current medications include tylenol 325mg prn, oral vitamin D, ramipril 10 mg/d, metoprolol 50 mg twice/day, furosemide 40 mg day, and daily insulin.
On exam, blood pressure is 155/85, pulse 68, weight 62 kg temp 100.8
o
otic. Exam shows no jugular venous distention, clear lungs, a fourth heart sound, and no bilateral edema. She has supra-pubic tenderness to deep palpation and mild bilateral CVA tenderness to percussion.
Laboratories :
Na=136 mEq/L
K=4.3 mEq/L
Cl=100 mEq/L
CO2=20 mEq/L
BUN= 44 mg/dL
Creatinine=3.8 mg/dL
Glucose = 143 mg/dL
Calcium=9.1 mg/dL
Phos = 5.6 mg/dL
Albumin= 3.5 mg/dL
1.2 (post 6 months therapy with corticosteroids-prednisone)
1.6
1.9
2.0
3.8
WBC=11.8
Hgb=10.2g/L
Platelets=296,000
Urinalysis: specific gravity=1.013, pH=7, 3+ protein, 3-5 hyaline casts/lpf, 10-15 WBCs hpf, 2 WBC casts seen, esterase positive, nitate positive, numerous bacteria noted
Urine electrolytes = Na = 38 mEq/L, Creatinine = 68 mg/dL, urea = 245 mg/dL
Review of her labs shows the following:
Date Serum creatinine
5.5 years ago
5.5 years ago
0.8
2.8 (time of hospitalization)
5 years ago
3 years ago
1 year ago
6 months ago
Today
11

Case 2 Clinic Visit Discussion Questions:
 Construct a problem list for this patient’s presentation

Symptoms/Signs o Dysuria, fever, abdominal pain o Hypertension o
S4 o
Suprapubic and CVA tenderness

Contributing medical history o Hypertension o CKD/GN related to “collagen vascular disease” o Diabetes mellitus o Medications: ACEI, diuretic, beta-blocker

Lab findings o
Elevated creatinine o Metabolic acidosis o Hypoalbuminemia o
Hyperphosphatemia o
Anemia o Possible leukocytosis o
Abnormal urine sediment: proteinuria, pyruia, bacteria

How would you characterize the kidney failure in terms of acute vs. chronic. Provide supporting data for your answer. Construct a plot of 1/Creatinine vs. time.

CORRECTION to creatinine history: Cr=0.8 six years ago

1/Cr plot suggests acute-on-chronic kidney disease

Does the FENa help in this case? Why or why not? What other data may be considered in place of the FENa?

FeNa = 1.6%, but unreliable because of diuretic use

FeBUN = 31%, which is consistent with prerenal disease. Recent studies, however, suggest that reliability of FeBUN compared to FeNa may be overstated.

Why has her creatinine continued to rise through the 5 years since her initial diagnosis?

The hypothesis that CKD may progress through a hyperfiltration/hypertrophy/sclerosis cycle independent of the nature of the initial insult/underlying disease

What is the differential diagnosis for her acute renal failure?

Prerenal azotemia from diuretic use + underlying infection

Post-renal obstruction from mass

Intrinisic renal disease: consider new flare of collagen vascular disease, but sediment not active.
UTI/pyelonephritis by itself unlikely cause of AKI (more likely associated with volume/antibiotics)

What additional tests would you consider based on your differential diagnosis?

Urine culture, Renal ultrasound. Consider repeat of serologies for previous CVD.

Would your concerns be different if this patient was male?
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
UTI/pyelonephritis is much less frequent in males and is an indication for evaluation of anatomical/functional abnormality (prostatism, prostatitis, nephrolithiasis, other obstructing problem).

Does the urine pH help in your differential diagnosis?

Alkaline urine pH suggests the possibility urease-secreting microbacterial infection. Urease hydrolyzes (“splits”) urea, which alkalinizes urine and can lead to formation of struvite stones.
The most common organisms which do this are Proteus and Ureaplasma,. Staphylococcus,
Klebsiella, and Pseudomonas can also split urea.

What would be your initial therapy and why could this change with time?

Volume resuscitation with normal saline. May need change to bicarbonate solution if a NAGMA is exacerbated.

Treatment of UTI with empiric antibiotic coverage and wait for sensitivities from cultures.
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