Katrina Booth Dr. Suneel Udani December 8, 2010

Katrina Booth
Dr. Suneel Udani
December 8, 2010

A 47-year-old man with a long-standing history of
alcoholism is hospitalized for abdominal pain, nausea, and
vomiting omiting of 7 days’ da s’ duration. d ration His last drink was as 6 days da s ago. ago
He has lost approximately 10% of his body weight over the
past 4 months; he states that his weight loss was caused by
drinking alcohol and not eating eating.
On physical examination, he appears cachectic. Temperature
is 37.1 °C (98.8 °F), blood pressure is 100/70 mm Hg, pulse
rate is 110/min, 110/min and respiration rate is 18/min 18/min. BMI is 17 17. He
is not confused or tremulous. There is midepigastric
tenderness without rebound. Bowel sounds are present.
Neurologic g
examination is normal.

Laboratory studies:
Amylase 300 U/L
Lipase 150 U/L
Sodium 130 meq/L (130 mmol/L)
Potassium 3.4 meq/L (3.4 mmol/L)
Chloride 90 meq/L (90 mmol/L)
Bicarbonate 20 meq/L (20 mmol/L)
Phosphorus 3.5 mg/dL (1.1 mmol/L)
Calcium 9.0 mg/dL (2.2 mmol/L)
Urinalysis Positive for ketones

The patient receives immediate thiamine
replacement, folic acid supplementation, and a
multivitamin followed by vigorous intravenous fluid
replacement with 5% dextrose and normal saline
with aggressive potassium replacement. replacement Morphine
is used to control pain.
Eighteen hours later, the patient’s abdominal pain
has improved but he becomes restless, agitated,
and extremely weak and is barely able to raise his
extremities against gravity gravity.

Which of the following is the most likely
cause of this patient’s new findings?
A. Hypercalcemia
BB. HHypokalemia k l i
C. Hyponatremia
DD. Hypophosphatemia

A. Hypercalcemia
yp
B. Hypokalemia
C. Hyponatremia
D. Hypophosphatemia

Which of the following is the most likely
cause of this patient’s new findings?
A. Hypercalcemia
BB. HHypokalemia k l i
C. Hyponatremia
DD. Hypophosphatemia

Severe hypophosphatemia develops in patients with
chronic alcoholism due to:
◦ Poor oral intake
◦ Decreased intestinal absorption due to NV
◦ Increased kidney excretion due to effects of etoh on
tubule
Despite total body depletion of phos, may have normal
lab values on admission
Sudden severe hypophosphatemia can cause confusion,
rhabdomyolysis, hemolytic anemia, severe muscle
weakness k lleading di tto respiratory i t ffailure il

78 yom presents with fatigue, n/v

130
8.8 88
105
13 113
3.9 39
79
9.5
2.5
6.1
26.8
9.7
229
8.3
0.2
3.7
0.1/0.2
N72 L13 M5 47 26
2233
UA: 1.018/5.0/+LE/-- nit/-- prot/2+bld/3-5WBC/occ. RBC
U Na 71 Uosm 483
U K 19 S osm 325
U Cl 25 TTKG 1.45
U Cr 82
U eos 0
FeNA 2.6%

Urine anion gap
◦ UN UNa + UK – UCl
+ gap renal
- gap GI
TTKG
◦ (UK/PK)/(Uosm/Posm)
With hypokalemia
4 = Renal loss; excess aldo
With hyperkalemia
10 = non-renal non renal hyperkalemia (normal aldo)

Proximal
(Type 2)
Classical
Distal
Prevalence Rare Rare Very
common
Type 4 Hyperkalemic
Distal
Common
Plasma K Low Low High High
Urine pH 6

136
104 46
5.2 19 2.0
LDH 1383
82
9.2
1.8
3.9
19.3
ABG: 7.33/36/65/18/90 7 33/36/65/18/90 on RA
10.2 196
N37 Bands16
L17 M12 E6
9.1 3.6
0.4
56
239 39
0.1/0.3
33

78 yoM with h/o HIV p/w cough and fatigue
Cough productive of occ. yellow sputum
Subjective fevers
Night sweats
No GI symptoms
RRecently tl stopped t d HAART th therapy
Last CD4 count 157, May 2010
Recently stopped PCP ppx

PMHx
◦ HIV since i 1999
◦ TB 1999, s/p treatment
◦ Shingles
◦ Suicide attempt 2009
◦ CKD 2/2 HIV
nephropathy, p p y, BL Cr 1.8
PSurgHx
◦ None
Meds
◦ None
Social Hx
◦ Lives Li alone l in i senior i
building, no tobacco,
no EtOH, retired
professor f
Fam Hx
◦ Non-contributoryy
Allg: None

2-10% of HIV patients
Associated with high viral load
Pathogenesis
◦ HIV can infect glomerular epithelial and tubular cells
◦ More common in AA than white
Collapsing FSGS
◦ Most common form (60% of renal biopsies)
◦ NNephrotic h i syndrome d picture i
◦ Before HAART, progressed to ESRD in months
Membranoproliferative GN—seen in coinfection
with Hep C
Immune complex GN—IgA deposits against HIV

Screening
◦ HIV patients that are high risk (high viral load, AA)
◦ Biopsy indicated if > 1 g protein/day
Treatment
Treatment
◦ HAART
◦ ACEI/ARB
◦ ? Prednisone or cyclosporine

Concern for PCP PNA
Started on prednisone and bactrim
Feeling better, sat ok on RA
CD 4 count 127
Discharged on bactrim and prednisone

78 yom with h/o HIV, HIV nephropathy
recently treated for PCP p/w n/v and fatigue

130
8.8 88
105
13 113
3.9 39
79
9.5
2.5
6.1
26.8
9.7
229
8.3
0.2
3.7
0.1/0.2
47 26
UA: 1.018/5.0/+LE/-- nit/-- prot/2+bld/3-5WBC/occ. RBC
U Na 71 Uosm 483
U K 19 S osm 325
U Cl 25
U Cr 82
U eos 0
FeNA 2.6%
2233

EKG changes:
◦ Peaked T waves (B)
◦ Lengthening of PR and QRS (C)
◦ P waves disappear (C)
◦ Sine wave (D)

Given Calcium, D50, insulin, kayexalate

Dysphagia with solids and liquids
Constipation, no BM x 6 days
No F/C
Urinary frequency
Unable to empty bladder
NNo cough, h SOB

VS: T 36.5 BP 138/73 HR 70 RR 13 Sat 94%
Gen: NAD
HEENT: bilateral parotid swelling, L>R, oral
thrush
CV: RRR, no murmurs, no LE edema
Lungs: g CTAB
Abd: NT/ND, +BS, no HSM, suprapubic fullness
Neuro: no focal deficits
Skin: no rashes
Psych: pleasant, AxOx3

Can cause hyperkalemia in any pt
Higher risk in HIV pts
◦ High doses to treat PCP
◦ Frequent underlying kidney disease
◦ HIV pts may also have adrenal insufficiency
Avg g rise of 0.5 0 5 to 1.0 0 meq/L q/
Acts like K-sparing diuretic

Patrick Hallak said... The increase in creatinine associated with TMP
is mild: 10% and reversible with drug discontinuation.
The mechanism of Bactrim induced hyperkalemia is via
TTrimethoprim i th i inhibition i hibiti of f th the sodium di channel h l llocated t d on th the
luminal surface of the principal cells, independent of aldosterone
blockade. ( Same site of action of amiloride , triameterene and
pentamidine). p ) This will decrease sodium reabsorption p and the
electro negativity in the lumen thus decreasing the driving force for
the secretion of potassium through an apically located potassium
channel on the same principal cells. This side effect is most common
in HIV infected patients who are treated with high doses of TMP TMP-
SMX. However hyperkalemia can occur with lower doses used to
treat routine infections. Be cautious thus when using TMP-SMX in
patients with preexisting renal dysfunction or in those taking
concurrent medications (such as angiotensin-converting enzyme
inhibitors and potassium-sparing diuretics) that may exacerbate this
hyperkalemic effect to potentially dangerous levels.
December 9, 9 2008 10:43 AM

Further history obtained—h/o BPH requiring
self cath at home. Pt hasn’t been doing this x
several months
What next?

Licurse A et al Renal Ultrasonography in the Evaluation of Acute Kidney
Licurse, A., et al. Renal Ultrasonography in the Evaluation of Acute Kidney
Injury. Arch Intern Med. 2010; 170(21)1900-1907

Bilateral hydronephrosis (right greater than
left). The right kidney is small in size (9 cm)
with cortical thinning suggesting obstruction
may be chronic in nature nature.

Causes Type 1 distal RTA
Tubular injury reduces activity of Na-K
j y y
ATPase, leading to hyperkalemia
Inability to reabsorb Na leads to higher FeNA
Similar to Type 4 RTA (hypoaldo effect)

Decompression and IVF (usually in chronic)
Treatment for BPH
◦ Alpha blockers
◦ 55-alpha alpha reductase inhibitors
Trial without catheter after 2-3 days
◦ Initial success rate 20-40%
Initial success rate 20 40%
◦ Recurrence is common
Surgical treatment
◦ TURP

Foley inserted—1 L urine returned
Foley catheter left in place
IVF replacement given
Started on Tamsulosin
3 days later, Cr 1.8, Na 138, K 4.2
Di Discharged h d hhome with ith catheter th t and d uro f/u f/
Bactrim changed to Atovaquone

138
99 43
4.3 21 4.5
59
10.0
1.6
4.5
144
6.0
108 88
13
Uric acid 18.514.09.9

Can get much information from renal labs
HIV nephropathy common in HIV pts
Bactrim increases risk of hyperkalemia in HIV
pts, esp pts with ihHIV HIV nephropathy h h
Treatment of acute urinary retention-foley,
alpha blocker and fluids