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Case
Report - A 47-year-old Female with Flank Pain
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Hina
Abbas Naqvi, MD
HISTORY
A
late forty year old white female presented to the emergency
department with a chief complaint of a ten day history of
dry heaves. The patient also reported nausea, vomiting,
anorexia, chills, generalized myalgias, arthralgias and
headache of equal duration. She denied fever, cough, skin
rash, diarrhea, hematuria or dysuria. On further questioning,
the patient reported sharp left flank pain that awoke her
from sleep approximately two weeks prior to presentation.
The pain was episodic, occurring every thirty seconds, was
not relieved by Excedrin, Bengay or a heating pad, and radiated
to her neck, shoulders and chest. This pain only occurred
at night for three consecutive nights and then spontaneously
resolved. The day prior to presentation, the patient reported
abdominal distention and a decrease in the frequency and
quantity of urination.
The
patient's past medical history included hypertension, Grave's
disease status post thyroidectomy, iatrogenic hypoparathyroidism,
mitral valve prolapse and gastric bypass surgery. She also
reported that though her myalgias and arthralgias had recently
worsened, they have been present for approximately four
years. Her medications included celecoxib, irbesartan, Excedrin,
calcitriol, levothyroxine, cyclobenzaprine and a multivitamin.
PHYSICAL
EXAM
On
examination, the patient was afebrile, blood pressure was
149/82, pulse was 65, and respirations were 16 with an oxygen
saturation of 100% on room air. The patient appeared nontoxic
and was in no apparent distress. Oral mucosa was moist without
lesions. Neck was supple without lymphadenopathy. Heart
exam revealed an S1, S2 and a systolic murmur graded II/VI.
Lungs were clear to auscultation bilaterally. Abdomen had
normal active bowel sounds, mild epigastric tenderness and
was not distended. No costovertebral angle tenderness was
elicited. Musculoskeletal exam revealed no joint erythema
or tenderness and normal range of motion of all joints.
Neurological exam was without focal deficits.
DIFFERENTIAL
DIAGNOSiS
Initial
differential diagnosis included nephrolithiasis as the patient
had reported flank pain and a recent decrease in urination.
Dehydration secondary to anorexia and nausea was also a
possibility. Bacterial infection causing chills or a viral
illness causing systemic symptoms was also considered although
could not fully explain all of the patient's symptoms. Vasculitis
causing the patient's arthralgias and myalgias was also
considered.
Initial
laboratory values were as follows:
Table
1. Admission Laboratory Data.*
| Sodium |
131
meq/L (L) |
| Potassium |
5.2
meq/L |
| Chloride |
100
meq/L |
| CO2 |
11
mmol/L (L) |
| BUN |
135
mg/dL (H) |
| Creatinine |
13.0
mg/dL (H) |
| Calcium |
11.8
mg/dL (H) |
*Note:
(H) indicates high. (L) indicates low.
As
the patient had no history of renal insufficiency, investigation
into her acute renal failure was initiated. Although the
patient had reported nausea and anorexia, she was not tachycardic
or hypotensive and the urine sodium was 45; thus a prerenal
etiology was deemed less likely. The urine microscopy revealed
many white and red blood cells without casts. The absence
of casts implied acute tubular necrosis was less likely.
Vasculitis causing an intrarenal acute renal failure remained
on the differential although the arthralgias and myalgias
were the only systemic symptoms suggestive of this etiology.
The patient had no rash or new medication use that could
suggest acute interstitial nephritis. A postrenal or obstructive
lesion remained the most likely reason for the patient’s
acute renal failure.
A
computerized tomography of the abdomen and pelvis was performed
and revealed a right kidney with moderate to severe hydronephrosis
with a 1cm stone at the pelvic inlet and left moderate hydronephrosis
with several calculi including an 8 mm stone and a 1.3x0.5cm
stone. This established the diagnosis of bilateral ureteral
obstruction resulting in acute renal failure.
HOSPITAL
COURSE
The
patient was placed on intravenous fluids with sodium bicarbonate.
She was not emergently dialyzed as her electrolytes remained
stable. Blood cultures were obtained and she was placed
on Gatifloxacin empirically. The urology service was consulted
and the patient underwent cystoscopy, bilateral retrograde
pyelogram and bilateral ureteral stent placement.
Table
2. Further laboratory data.*
| PTH |
<4
pg/ml (L) |
| PTH-related
protein |
<0.7
pmol/L |
| 1,25-dihydroxyvitamin
D |
102.0
pg/ml (H) |
| Urine
calcium |
234
mg/24 hours |
| Urine
oxalate |
55
mg/24 hours (H) |
*Note:
(H) indicates high. (L) indicates low.
Further
studies revealed an elevated urine oxalate level. Serology
was negative for autoimmune diseases. It was determined
that the likely cause of her nephrolithiasis was a combination
of hypercalcemia secondary to calcitriol and increased oxalate
in the urine due to her gastric bypass surgery. The patient's
renal function improved following surgery and she was discharged
home to be followed up in renal clinic. Laboratory values
one month later were as follows:
Table
3. Laboratory Data One Month after Admission.*
| Sodium |
142
meq/L |
| Potassium |
3.9
meq/L |
| Chloride |
103
meq/L |
| CO2 |
29
mmol/L |
| BUN |
33
mg/dL (H) |
| Creatinine |
2.2
mg/dL (H) |
| Calcium |
9.6
mg/dL |
*Note:
(H) indicates high. (L) indicates low.
DISCUSSION
Nephrolithiasis
is a common issue which accounts for seven to ten of every
one thousand hospital admissions(1). The incidence of nephrolithiasis
increases with age and is higher in men than women and in
Caucasians than African Americans. Estimates suggest that
twelve percent of men and five percent of women will develop
a symptomatic stone by the age of seventy.(2)
The
presentation of nephrolithiasis is varied. Occasionally,
patients can be asymptomatic and be diagnosed incidentally
during radiological workup for another condition. Symptomatic
patients will often present with pain, hematuria, urgency,
nausea and vomiting. Pain due to nephrolithiasis classically
presents in paroxysms due to ureteral muscular contraction
that occurs in response to movement of the calculus through
the ureter. The associated pain can vary from a mild ache
to severe pain which requires hospitalization for intravenous
analgesics. The location of pain is determined by the anatomical
site of obstruction. Obstruction at the upper ureters or
renal pelvis will cause flank tenderness whereas lower ureteral
obstruction causes pain that radiates to the groin. As a
result, stone migration can cause a change in pain location.
Gross or microscopic hematuria is present in the majority
of patients with nephrolithiasis. With nephrolithiasis that
is bilateral, the patient may present with symptoms associated
with postrenal obstructive acute renal failure.
Once
nephrolithiasis is suspected, radiological studies can confirm
the diagnosis. The gold standard for radiological diagnosis
is a non-contrast helical computerized tomography scan.
One study concluded that computerized tomography is ninety-five
percent sensitive, ninety-eight percent specific and ninety-seven
percent accurate in detecting ureteral stones(3). In patients
who should avoid radiation such as pregnant women, ultrasonography
is the modality of choice.
The
acute management of patients with nephrolithiasis includes
analgesics and hydration until the stone passes. Stones
that are too large to pass can be treated with extracorporeal
shock wave lithotripsy, open pyelolithotomy or percutaneous
nephrolithotomy. Since an important aspect to management
is evaluation of the stone, patients should be instructed
to strain their urine if the stone has not yet passed.
In
order to prevent recurrent nephrolithiasis, the type of
stone and possible biochemical abnormalities that predisposed
the patient to stone formation must be determined. Calcium
oxalate is the most common type of renal calculus in industrialized
nations with hypercalciuria being absorptive, renal or resorptive.
Hypercalciuria is defined by the excretion of urinary calcium
exceeding 200mg in a 24 hour collection. Absorptive hypercalciuria
is caused by intestinal hyperabsorption of calcium of which
the exact mechanism is unknown. This hyperabsorption increases
the circulating concentration of calcium, increases the
renally filtered load of calcium and suppresses parathyroid
function. The suppression of parathyroid function contributes
to hypercalciuria by decreasing renal tubular calcium reabsorption.
In renal hypercalciuria, the main abnormality is impaired
renal calcium reabsorption which decreases serum calcium
and stimulates parathyroid function. Increased parathyroid
function in turn causes increased circulating calcium and
an increased renally filtered load of calcium. Renal hypercalciuria
can be treated with thiazide which increases proximal tubule
reabsorption of calcium. Resorptive hypercalciuria is caused
by excessive bone resorption stimulated by hyperparathyroidism(4).
Hyperoxaluria
is defined by urinary oxalate excretion greater than 45mg
in a 24 hour collection(4). Increased intestinal oxalate
absorption and hyperoxaluria occurs when less calcium is
available to bind oxalate which occurs in three settings.
These settings include low calcium diet, hypercalciuria
secondary to increased intestinal calcium absorption and
enteric hyperoxaluria which occurs after surgical resection.
Enteric hyperoxaluria occurs when free calcium binds to
fatty acids and colonic permeability to oxalate is increased
through a higher colonic exposure to nonabsorbed bile salts(5-7).
It has been noted that patients with bowel disease have
a higher prevalence of nephrolithiasis. Urine volume and
pH are lower in these patients and these are the main reasons
for this increased prevalence. Patients with small bowel
resection or gastric bypass also have higher urine oxalate
excretion and this is more significant in patients with
bypass(8).
This
patient was hypoparathyroid and thus lacked the parathyroid
hormone dependent renal production of 1,25-dihyroxyvitamin
D. Her supplemental Vitamin D caused hypercalcemia and since
she lacked the hypocalciuric action of parathyroid hormone,
she became hypercalciuric(9). In addition, she had undergone
gastric bypass surgery which caused her hyperoxaluria. For
these reasons, she was at an increased risk for nephrolithiasis.
To
prevent stone recurrence the most important step is to increase
fluid intake to maintain a urine output of 2000 ml/day as
low urine volume is the most common additional abnormality
that predisposes to stone formation(4). Dietary adjustments
are also important and in patients with calcium oxalate
stones restricted intake of protein and salt in addition
to a normal calcium intake has been found to provide protection.
REFERENCES
- Kreutzer
ER, Folkert VW. Current Opinion in Nephrology
and Hypertension 1993; 2:949-55.
- Johnson
CM, Wilson DM, O'Fallon WM, Malek RS, Kurland LT.
Kidney International 1979; 16(5):624-31.
- Dalrymple
NC, Verga M, Anderson KR, Bove P, Covey AM, Rosenfield
AT, Smith RC. The value of unenhanced helical
computerized tomography in the management of acute flank
pain. Journal of Urology 1998; 159(3):735-40.
- Delvecchio
FC, Preminger GM. Medical management of stone
disease. Current Opinion in Urology 2003; 13:229-233.
- William
HE. Oxalic acid and the hyperoxaluric syndromes.
Kidney International 1978; 13:410.
- Kathpalia
SC, Favus MJ, Coe FL. Evidence for size and charge
permselectivity of rat ascending colon. Effects of ricinoleate
and bile salts on oxalic acid and neutral sugar transport.
Journal of Clinical Investigation 1984; 74:805-811.
- Obialo
CI, Clayman RV, Matts JP, Fitch LL, Buchwald H, Gillis
M, Hruska KA. Pathogenesis of nephrolithiasis
post-partial ilea bypass surgery: case-control study.
Kidney International 1991; 39:1249-1254.
- Parks
JH, Worcester EM, O'Connor RC, Coe FL. Urine
stone risk factors in nephrolithiasis patients with and
without bowel disease. Kidney International 2003;
63:255-265.
- Marx
SJ. Hyperparathyroid and hypoparathyroid disorders.
New England Journal of Medicine 2000; 343:1863-1875.
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