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Kalel

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This is an actual patient that I saw in my clinic, but I have altered her original presentation to make her more interesting:

In 11/03; a 52 yo WF presented to an outpatient clinic c/o L flank pain that that she charecterizes as severe and sudden that occurred this morning. She now reports that her pain is now just a L flank soreness and that she now has urinary frequency, urgency, and irritative symptoms in her bladder.

A U/A is performed and reveals microscopic hematuria with a normal pH.

PMHx: IBS/Lactose intolerance
Meds: none
NKDA
SHx: works as a construction worker, smokes 1 ppd X 30 yrs, occasional alcohol use, denies illicit substance use. No recent travel hx, is married with 2 grown children.
FHx: Unremarkable, F had MI at age 70, M is alive and has htn

Physical exam:
Afebrile, P: 110, BP: 130/80, R: 12
CVS: RRR, no m/r/g
Resp: CTA b/l
Abd: diffuse minor L flank tenderness and suprapubic tenderness, no CVA punch tenderness, no rebound/guarding, soft, +BS

Questions:
1. What is the most likely diagnosis? What is your differential?
2. How would you confirm this diagnosis and what would you do to treat the patient?
3. What further laboratory studies does the patient need to prevent this condition from recurring?

More information with labs that were actually done will be posted later.
 

Renovar

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Normally with someone complaining of flank pain, urinary symptoms and microscopic hematuria, I think about nephrolithiasis. The patient may or may not have passed a stone, and if she does, may be causing her bladder symtoms.

That's most likely.

Other less likely items on my ddx would incluce pyelo (much less likely for she is not febrile and no obvious CVAT), other obstructive etiologies (retroperiotoneal abscess, blood, etc - all unlikely), neoplastic processes (always keep in mind in a big smoker - RCC can definitely give the patient's clinical picture, so can transitional cell bladder cancer.)

At any rate, I would do a UA/microscopic to see if there is any signs of infection or crystals. A CT scan is the best for diagnosing a stone, and it can pick up most of the other stuff. Also, would check a BMP, calcium and phos.

Most likely cause of stone is dehydration, so the patient ought to be adequately rehydrated, and pain meds such as MSO4 and toradol are useful in controlling pain. Also treat infxn if it's there. Of course, uro consult if the stone is obstructing. And if the CT scan shows something else, then all bets are off.

That would be my starting point.
 

Kalel

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Nephrolithiasis is the correct dx.

Pyelo is one possibility. It's presentation can be similar to nephrolithiasis with flank pain and hematuria. Patients with pyelo can occasionally be afebrile, but almost all patients with pyelo will have evidence of infection in their urine (WBC's). A CBC may help make dx too (although leukocytosis is common in nephrolithiasis too).

Bladder ca is another possibility. Usually not associated with flank pain, but can have many of the irritative urinary sx with frequency and dysuria (also frequently associated with UTI's). Most common dx in elderly asymptomatic gross hematuria. Our patient would be a little young for bladder ca (mean age 68). It is frequently associated with smoking and other environmental exposures. Dx would be confirmed by urinary cytology and cystoscopy.

Renal cell ca is possible. Classic triad of flank pain, hematuria and palpable mass is only present in 10% of patients (causing the typical confusion over usage of the word "classic). Often associated with metastasis by the time of dx and weight loss too. More of an insidious onset too, patients often not dx until late stage making the ca have a very poor prognosis. Dx is confirmed by CT with contrast and biopsy.

Returning to our case:
CT without contrast is ordered (important not to give IV contrast so you won't obstruct the stone). Read as multiple 1-2 mm radio-opaque stones seen bilaterally, some in the initial stages of forming in the kidney with others in the ureters. No ureter or renal pelvic dilation suggesting obstruction.

Labs:
Chem-7: WNL
Calcium: 11.2 (slightly elevated)
Phosphorous: 2.7 (normal)
LFTs, including albumin are normal

Based on these labs and the patient's presentation, out-patient management of the patient nephrolithiasis with passage of the stones was decided upon. Patient was given analgesics and told to remain well hydrated, also given sieve to try to catch the stones (which she was unsuccessful at doing secondary to difficulty using sieve while using port-a-potty at construction site). Meanwhile, the following labs were ordered:

Ionized Ca: 6.7 (high)
24 hr urinary calcium: high
24 hr urinary oxalate: normal
Plasma intact PTH: 57 (normal ~10-60)

In 12/03, a decision was then made to start the patient on Hctz in addition to recc'ding that the patient remain well hydrated. Hctz was poorly tolerated secondary to patient's complaints of a constipation, lethargy, and leg pain b/l.

Questions:

What do you think about the patient's management?
What is your most likely dx now?
What further steps in management would be appropriate for this patient?
 
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SoCalDreamin'

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Originally posted by Kalel
Questions:

What do you think about the patient's management?
What is your most likely dx now?
What further steps in management would be appropriate for this patient?

1.) Management is appropriate, with the minor exception of not having ordered a couple of imaging studies as part of follow-up.

2.) Assuming no Hx of renal failure: primary hyperparathyroidism most likely secondary to a parathyroid adenoma.

3.) a.) Order a Techemetium-99 Sestamibi scan and obtain an endocrine surgery consult for removal of the gland. Keep in mind that not all parathyroid adenomas light up via this imaging study.

b.) Also obtain a Dexa Scan of the patient's hip and femur to assess for possible osteopenia or osteoperosis.

c.) Order an ultrasound of the thyroid to rule out the possibility of any thyroid nodules / masses that might be present secondary to an underlying Multiple Endocrine Neoplasia (MEN) IIa syndrome. The presence of a thyroid nodule is highly unlikely, given that most MEN syndromes have a documented family Hx and appear much earlier than the patient's stated age.
 

Harrie

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Why would you give a patient with hypercalcemia HCTZ?
 

the END.

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Originally posted by Harrie
Why would you give a patient with hypercalcemia HCTZ?

This is an excellent question. Moreover, why is this patient on a diuretic, period? We have no hx of HTN, only one reading of borderline elevation at a time I'm assuming the pt was in pain, and a clinical situation in which a diuretic is not going to help very much (nephrolithiasis). HCTZ is exactly the wrong diuretic for hypercalcemia because it conserves calcium. Remember, one uses Lasix for hypercalcemia emergencies because of its tendency to waste calcium (and virtually every other ion as well). Thus, don't try to restart HCTZ (which would be better tolerated with potassium supplementation as I believe this was the source of her muscle cramps and fatigue, but that's a moot point anyway).

In addition to current management and the check for primary hyperparathyroidism mentioned by SoCalDreamin', the pt needs to alter her diet. The hyperoxaluria is not helping her stone-forming potential. The problem is it is difficult to alter oxalate in diets because it is still not well known all foods that have high oxalates; however, the majors should be avoided such as spinach, peanuts, colas, tea, and chocolate. Actually, in a type of ironic twist, giving a patient calcium carbonate po can help prevent calcium oxalate stones by forming these deposits in the GI tract rather than the GU. Its also been noted that women with hyperoxaluria more often than male counterparts have hypocitruria that predisposes to stone formation. This can be corrected by giving potassium citrate supplements. Don't forget the standards as well: 2L of water a day, diet low in sodium and protein, and stay away from vitamin C supplements.
 

SoCalDreamin'

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Originally posted by Harrie
Why would you give a patient with hypercalcemia HCTZ?

That's an excellent point that I overlooked. In fact, I believe that the physician in this case was "intending" on giving furosemide, since loop diuretics cause one to lose calcium, in an attempt to lower the serum calcium level. However, such practice, in my opinion, would not be wise for the following two reasons:

1.) You would promote concentration of calcium in the kidney's collecting ducts, thus possibly exacerbating the formation of kidney stones.

2.) Even if such a method were to work (i.e. lower serum calcium levels), it would only act as a band-aid for the problem at hand: a likely parathyroid ademona. The definitive solution would be to remove the adenoma.
 

Surfer75

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Fun case. What about ruling out malignancy as a cause for hypercalcemia via paraneoplastic --> long smoking history noted --> ?sq cell lung ca, or renal cell ca, or any ca secreting PTHrP for that matter? Or.. all the other TB related conversion of 25 to 1,25 OH-Vit D...etc.. MilkAlkali, Vit D toxicity... etc..etc.. sorry, I was presented a similar case, but with an additional past history of non-gallstone/EtOH pancreatitis, and they just raved on about checking all the other possibilities...

but yeah, stick with Lasix and push lotsa fluids.

S
 

the END.

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Originally posted by Surfer75
What about ruling out malignancy as a cause for hypercalcemia via paraneoplastic --> long smoking history noted --> ?sq cell lung ca, or renal cell ca, or any ca secreting PTHrP for that matter? S

I thought about this also and thought with the tobacco hx this was where the case was going, but I didn't mention it because I thought the OP might make this the next question (as in what if you had the same findings only low intact PTH?).

Remember though, as long as your lab is in the realm of the present day, the tests now used for intact PTH are specific without cross-reactivity to PTHrp. If it were hypercalcemia of malignancy, the intact PTH should be low. Thus, elevated ionized and total calcium with high normal intact PTH still warrants a sestamibi scan.

As for other causes (milk-alkali, etc.), you have to explain why the intact PTH has not been down regulated first. Don't violate Occam's Razor until you have no other choice.
 

Kalel

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I will write out what I think about the case now, but recognize that I'm just a med student and this is a real patient, so my thoughts aren't necessarily the correct ones.

As far as why she was managed the way she was managed, I can only give you the thought process of the physicians who managed her according to their notes. They thought that she did not have hyper-PTH because her PTH levels were normal. Measuring intact PTH levels is usually pretty sensitive and specific for PT adenomas. Therefore, once hyper-PTH was thought to have been ruled out, the physicians thought that it would be appropriate to start her on Hctz, which would treat the hypercalciuria, which they believed was the sole etiology of her stone formation.

Nephrolithiasis is most commonly secondary to calcium oxalate crystals, which are most commonly secondary to hypercalciuria. Absortpive hypercalciuria is the most common cause of hypercalciuria; other causes include resorptive hypercalciuria (which our patient actually had, secondary to hyperparathyroidism) and renal hypercalciuria (renal tubule dysfunction). For hypercalciuria secondary to abosrptive hypercalciuria or renal hypercalciuria, thiazide therapy is an appropriate choice of therapy. Thiazides will decrease calcium secretion from the kidneys, causing the potential side effect of hyper-calcinemia. That's why it's important to rule out hyper-PTH, because otherwise, you will worsen the patient's hypercalcinemia. I believe that's what happened in our patient. Her chief complaint causing her to d/c the hctz was b/l pain in the thighs, which I thought might have been secondary to hypokalemia (a known adverse effect of hctz, as a diuretic), but she informed me that her potassium levels were normal at this time. So, I added the stuff with fatigue and constipation to give her a more typical presentation of hypercalcinemia (using my artistic liscense as case writer);) . Remember that hypercalcinemia's mneumonic is bones, stones, abdominal groans, and psychic overtones. 90% of cases of hypercalcinemia are secondary to either hyperPTH or metastatic/malignant disease effecting the bones. Other potential causes can be remmebered by the mneumonic CHIMPANZEES (calcium supplementation, hyper pth, iatrogenic (hctz)/immobility, milk alkali syndrome, paget's disease, adison's disease/acromegaly, neoplasms, zollinger ellison syndrome (MEN I), exces vit A, excess vit D, and sarcoidosis (through vit D synthesis of granuloma). Treatment of hypercalcinemia is with IV hydration and furosemide diuresis to secrete out the excess calcium. Other potential methods include the bisphosphanates, dialysis, calcitonin, and steroids. I failed to mention that our patient actually had a few high normal calcium levels along with a few slightly above normal levels in the interim because I didn't want to confuse the case, and her ca never rose to be all that high, so that, combined with the "normal" pth mislead the physicians responsible for her care to believe that she did not have hyper pth.

Their work-up of the patient was somewhat appropriate. I agree with the 24 hr urinary calcium and oxalate in order to w/u the cause. I would have also drawn uric acid levesl as high uric acid levels can cause calcium nephrolithiasis in addition to the uric acid nephrolithiasis; and I would have measured urinary citrate levels because citrate inhibits calcium stone formation and would be treated differently. Given the size of her stones and the amount of pain she was in at the time (not very much), I agree with their decision to attempt spontaneous passage of the stone. Had that failed, or if the stones had been greater then 6 mm, causing ureter obstruction, or had she been experiencing more intractable pain; extracorpeal shock wave lithotrsy or ureteroscopic stone extraction would have been appropriate. Follow up films would have been appropriate as well. We had not done this yet when the patient came to visit us last week. The patient was also placed on a low calcium diet, which is also appropriate until further w/u is completed, but it's important to recognize that most urinary calcium stones are actually associated with high dietary sodium and not high dietary calcium. Non-medical management of all sotnes includes encouraging the patient to keep over-hydrated (drinking water every second that he or she can, even during the night). Most patients cannnot follow through with such a regimen. Other reccomendations include diet restriction in sodium and protein (which is made into uric acid). Only one specific type of calcium nephrolithiasis patient (type II aborptive hypercalciuria) will benefit from decreasing calcium in their diet.

The user who explained why the patient had hyper-PTH was correct. Given hypercalcinemia, if the PTH gland was functioninge normally, PTH levels would be low normal. PTH is very sensitive to calcium levels. Having a high normal in tact PTH level ruled out the possibility of this being secondary to a paraneoplatic process secreting PTH-rP, which we did not check levels for because it wasn't necessary given the in tact PTH level.

Regarding the Techemetium-99 Sestamibi scan, one was eventuall ordered (in 1/04) and it was read as normal. This does not mean that she does not have a hyper-PTH adenoma though, the sensitivity of this scan is 90% in single adenomas (as is the case 80-90% of the time), but it's sensitivity drops to ~50% in multi-glandular adenomas. I was told by an endocrinologist that we informally consulted that many ENT doc's don't bother with scan for that reason; apparently, there is some nifty way of measuring PTH levels inside the OR which tells them which gland(s) are effected. Surgery is not always indicated for hyper-PTH. Hyper-PTH is a growing diagnosis in the elderly population as we are routinely checking more calcium levels, and since PT adenomas are almost always benign, it's not always worthwhile to go into the OR to offer the definitive treatment. Surgical removal of the PT gland is also associated with bad complications such as persistent hypoPTH, in which case our only therapy is calcium and calcitrol supplementation which doesn't work all that well. Indications for surgery include fractures, pruitis, calciphlaxis, and nephrolithiasis, particularly in our relatively young patient. Bisphosphanates can be used to treat patients medically who you do not want to take to the OR. Bone density studies were done on our patient, examining the hips and lumbar spine. They were read as normal. I suppose that the bone density studies can help you decide what therapy you want the patient to undergo. We did order vitamin D levels, but these levels (except for the one hydroxylated by the kidney, forget which one) should be normal if we are correct about our hyper-PTH dx.

MEN 1 is an excellent thought that I failed to consider. MEN-1 most commonly presents with hyper-PTH with hyperplasia of all four glands (consistent with our scan). A gastrinoma may even account for her "IBS" dx. Most women typicall present in their 30's, but I don't think that her being 51 is too far of a stretch. I will ask the attending whether or not he wants to work her up for this if she comes back while I am still in clinic. We sent our patient to a different endocrinogist and an endocrine surgeon, so hopefully, one of them will think of the diagnosis. Thanks for pointing it out, that's one of the reasons why I like posting interesting cases in here; I always learn something new too.

Anyways, thanks again for participating in my case guys. Keep the comments coming!
 

Docxter

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Originally posted by Kalel

Dx is confirmed by CT with contrast and biopsy.


Actually most urologists and radiologists will not biopsy something highly suggestive of RCC on imaging, fearing seeding of the biopsy tract. Only very few actually biopsy solid renal masses. There is not much in the differential diagnosis of a solid renal mass suspicious for RCC ( Angiomyolipomas and xanthogranulomatous pyelonephritis are almost always distinguishable by imaging +/- clinical features). Cystic RCCs can occasionally be a problem, but Bosniak type III & IV cysts are often treated like RCCs by conservative urologists. Patients usually go from imaging diagnosis straight to partial, total, or radical nephrectomy depending on the tumor.
 

Kalel

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Originally posted by Docxter
Actually most urologists and radiologists will not biopsy something highly suggestive of RCC on imaging, fearing seeding of the biopsy tract. Only very few actually biopsy solid renal masses. There is not much in the differential diagnosis of a solid renal mass suspicious for RCC ( Angiomyolipomas and xanthogranulomatous pyelonephritis are almost always distinguishable by imaging +/- clinical features). Cystic RCCs can occasionally be a problem, but Bosniak type III & IV cysts are often treated like RCCs by conservative urologists. Patients usually go from imaging diagnosis straight to partial, total, or radical nephrectomy depending on the tumor.

Whoops, I stand corrected. I do recall a nephrologist telling me the same thing now that I think about it, how you can make a line full of malignant cells in the abdominal wall if you go in there and try to needle biopsy it. I would just add that the only renal tumor that cannot be distinguished by CT scan is a tumor called oncocytomas, which account for 3-5% of renal tumors. Unfortunately, because we can't distinguish between this supposedly benign tumor and RCC without using histology, these tumors are treated with a partial or complete nephrectomy in the OR. With more and more patients getting CT scans and finding incidentalomas, I suspect that these tumors as well as other benign masses will become more and more of a health care problem in the future. Thanks for the correction!
 

HairlessHeart

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Wow Kalel,

I just wanted to thank you for taking the time to post the case and discussing it, as this is the kind of thing I learn a great deal from...me being a lowly MSII.

:)
 

Kalel

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Originally posted by HairlessHeart
Wow Kalel,

I just wanted to thank you for taking the time to post the case and discussing it, as this is the kind of thing I learn a great deal from...me being a lowly MSII.

:)

Thanks!:)

I learn a lot from the responses that I get and looking stuff up for my cases as a lowly MSIV too!
 

PimplePopperMD

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Originally posted by Docxter
Actually most urologists and radiologists will not biopsy something highly suggestive of RCC on imaging, fearing seeding of the biopsy tract.

Old wives' tale? Certainly, that is the case, that there is hesitation due to the theoretical seeding of surrounding tissue. I haven't found any literature to support this idea of seeding, and have heard the theory debunked by several as unscientific. Has anyone seen any literature/case reports of surgically seeding and extending tumor?
 

Kalel

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Originally posted by PimplePopperMD
Old wives' tale? Certainly, that is the case, that there is hesitation due to the theoretical seeding of surrounding tissue. I haven't found any literature to support this idea of seeding, and have heard the theory debunked by several as unscientific. Has anyone seen any literature/case reports of surgically seeding and extending tumor?

There have been case reports, even though it is considered a "rare occurence".
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8595548&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3773108&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=916121&dopt=Abstract

I spoke with my attending about the possibility of MEN I today, and he said that it was a "great thought!". I gave you guys credit though. ;) I then asked the endocrinologist who I informally spoke with before about this case, and he told me that while MEN was a possibility, usually their PTH levels are much higher then the levels we got on our patient; and MEN is much more rare then parathyroid adenomas (85% of hyperPTH cases are secondary to single PTH adenomas). However, he also said that he did not think that it would be unreasonable to draw a gastrin and prolactin level which we will do the next time we see her.

New labs received today:
Vit D 1,25: 50.2 (wnl)
Vit D 25: 25.7 (wnl)
phos: 2.3 L (previous levels were wnl)
Ionized Ca: 5.9 H
Ca: 10.8: H
PTH level sample not collected correctly

These new lab values are still consistent with hyperPTH, since PTH causes phosphorous to be secreted from the kidneys while retaining Calcium. Vit D levels are actually expected to be normal in hyper PTH too.
 

Docxter

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Originally posted by PimplePopperMD
Old wives' tale? Certainly, that is the case, that there is hesitation due to the theoretical seeding of surrounding tissue. I haven't found any literature to support this idea of seeding, and have heard the theory debunked by several as unscientific. Has anyone seen any literature/case reports of surgically seeding and extending tumor?

It depends on the tumor. Most solid organ tumors are routinely biopsied but things like RCC and most testicular neoplasms and a few others often do not undergo percutaneous biopsy because of multiple case reports of tract seeding for example in the case of RCCs. Most, but not all people, would not biopsy these lesions. If you do seed the tract, you'll increase the staging of tumor and possibly you might prevent the chance of cure. I hear "lawsuit, lawsuit".
 

Whisker Barrel Cortex

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Originally posted by PimplePopperMD
Old wives' tale? Certainly, that is the case, that there is hesitation due to the theoretical seeding of surrounding tissue. I haven't found any literature to support this idea of seeding, and have heard the theory debunked by several as unscientific. Has anyone seen any literature/case reports of surgically seeding and extending tumor?

Not an old wives tale. Six case reports have been published. Yes, that isn't that common, but it happens.

Other factors:

1. Renal cell carcinomas are hypervascular and there is risk of hemhorrage.

2. If there is a large solid renal lesion, it is almost certainly malignant and should be taken out. Although biopsy of larger lesions may yield good sensitivity, since the pre-test probability is so high, even a negative result will likely not settle the issue.

3. If there is a small solid lesion that could be oncytoma or a very unusual complex cyst, biopsy will have a lower sensitivity since it will be harder to get a good sample. Most urologists will not be entirely comfortable with this diagnosis. Thus, it will have to be taken out. Plus oncocytoma (relatively rare by the way) has malignant potential.

4. Not many lesions look like renal cell. Oncocytoma can't be differentiated, but also has malignant potential and should be removed. Metastatic lesions to the kidneys are relatively uncommon, can look like RCC, but the primary is usually found during the met survey. Lymphoma can usually be differentiated (not hypervascular, usually multiple, other lesions are almost always visible). Angiomyolipoma (benign) can be deteremined by presence of fat in the lesion. Transiitional cell rarely cannot be differentiated, but should be removed anyway.

So given all of the above factors, nephrectomy or at least partial nephrectomy is the best answer. Alternatively, for smaller lesions in people with significant co-morbitiy for surgery, radiofrequency ablation could be performed (done by radiologists at many institutions).

Other, "don't biopsy" organs include the ovaries (if you've ever seen a peritoneum full, I mean FULL of mucinous ovarian tumor, you will understand why). Testicles: testicles are in a encapsulated area which is considered to be protective. Violating this is asking for metastases.

Liver lesions, adrenal lesions (except pheo), lymph nodes, lungs are all fair game for biopsy. Colon lesions and stomach lesions can be reached endoscopically.
 

Pheo

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A solid renal mass on CT is malignant 90 - 95% of the time if not more.

The reasons Whisker Barrel Cortex gave are all the reasons we do not biopsy renal masses. I would say the number one reason is the poor sensitivity of the fine needle aspirate.

The only indication for a renal biopsy is if you suspect metastatic disease. Otherwise we just go ahead with the nephrectomy (or partial).

In terms of seeding, that is a possibility although it is much more likely with TCC rather that RCC.

Still, every now and then we'll get a referral for a patient with RCC or TCC diagnosed at an outside hospital with an FNA. This seems to happen more frequently than we would like to see.

Urolap
 

Kalel

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New lab values:

Gastrin: 133 (high, but patient was not fasting; normal: =25-111)
Prolactin: 14.4 (normal)
PTH in tact: 83 (high)

Although a gastrin level of 133 would have been high had the patient been fasting, a radom gastrin level of 133 should be enough to exclude the diagnosis of Zollinger Ellison's Syndrome or the patient having a gastrinoma. The cut-off which produces a fairly good sensitivity and specifity for hypergastrinemia is actually a fasting level of 150; gastrinoma patients have a median gastrin level of 500-700, with 40% of patients having gastrin levels greater then 1,000. Thanks for the thought though! You guys impacted the management of a patient over the internet. Pretty neat stuff.

For our patient's last visit, I strongly wanted to start our patient on bisphosphonate therapy as a way of trying to prevent further stones and to preserve our post-menopausal patient's bone density. My attending disagreed though, because our patient had a new complaintof slow esophageal motility with symptoms of GERD upon further questioning (along with a sister having a "thyroid disorder", which made me think even more about the prospect of MEN), so my attending was worried about pill esophagitis occuring in our patient. Esophageal dysmotility is a contraindication to starting bisphosphonate therapy. He would rather have the patient just receive the "definitive" therapy through surgery. The patient was having difficulty getting an appointment with an ENT doctor (3 mo wait) at the time of her last visit though, so my attending sent her to another endocrinologist with the hopes that he might be able to push her through the system faster

Thanks again for participating! I will keep my eye out for future "interesting" cases to post, I hope that others will post their interesting cases as well.
 

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Docxter said:
Actually most urologists and radiologists will not biopsy something highly suggestive of RCC on imaging, fearing seeding of the biopsy tract. Only very few actually biopsy solid renal masses. There is not much in the differential diagnosis of a solid renal mass suspicious for RCC ( Angiomyolipomas and xanthogranulomatous pyelonephritis are almost always distinguishable by imaging +/- clinical features). Cystic RCCs can occasionally be a problem, but Bosniak type III & IV cysts are often treated like RCCs by conservative urologists. Patients usually go from imaging diagnosis straight to partial, total, or radical nephrectomy depending on the tumor.

Had a 14 yr old patient recently on peds service with fevers and unintentional weight loss of 30 lbs over about 4 mos, scans showed both kidneys (and pancreas) looking alot like swiss cheese b/c there were TNTC lesions....ultrasound indicated they were solid, not cystic, so urology went ahead and did a wedge biopsy b/c it was uncertain as to infectious vs neoplastic nature....turned out to be large-cell lymphoma that had been missed by 2 physicians in the previous months (blood flow cytometry was negative, but the diagnosis was made by the flow of the renal bx). Interesting case, but quite sad -- she was subsequently transferred to St. Jude's.
 
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  6. Your reply has occurred very quickly after a previous reply and likely does not add anything to the thread.
  7. This thread is locked.