Well, I obviously failed to update my blog earlier this week; here's why...
Lt's begin with this weeks' labs.
27 Nov 18 Labs
*Creat: 2.84 (+0.14) Rising (3rd consecutive increase)
*HCT: 33.6 (-0.1) Low, but stable
*Hemo: 10.5 (+0.1) IR and stable
*Lymph: 8.0 (-1.0) Low, but stable
*Lymph ABS: 0.7 (+0.2) Low, but stable
*Neut: 83.8 (+6.5) Very High
*Neut ABS: 6.9 (+2.9) Very High
*RBC: 3.62 (-0.04) Low, but stable
*WBC: 8.3 (+3.1) IR
*BUN: 51 (+6) Extremely High
*CA: 9.8 (-0.1) IR
*GFR: 24 (-1) Extremely Low
*Gluc: 108
*K+: 4.7 (+0.5) IR
*NA+: 144 (+5) IR
*Prot: 6.9 (NC) IR
*MG: 2.2 (-0.2) IR
*Phos: 4.4 (+0.5) IR
*BK: Not Detected
*CMV: Not Checked
NC= No Change IR= In Range
First, the stability of the HCT, Hemo, RBC, Lymph and Lymph ABS are most welcome! Earlier posts had my postulating on hoping the time for fluctuation of all of these labs was drawing to a close. Had one or two of these been stable I would have been pleased; but having all five stable was terrific news! Let's now hope that the stabilization continues.
The big news though, is why I have been delayed getting this post written.
With the 3rd consecutive increase of the Creatinine, I received a call on Wednesday from one of the Kidney Clinic doctors who wanted me to get another Renal Biopsy, just to rule out any possible rejection. The test was set up for Thursday morning.
As I have gone in-depth about previous biopsies, I will skip the details about the procedure aside from a few items. First, I had no negative or untoward reactions during this latest test. (Excellent news!) Second, the first kidney tissue sample that was aspirated (drawn) was the only sample needed, which was nice. Last...and this is one my wife wanted on here...I slept well afterwards...
Following the usual 4+ hour post-biopsy wait time to check for any bleeding, we were on the way home. I then spent yesterday recovering from what is always a painful test. I am still very sore today, but it is improved.
Also, the Clinic doctor called yesterday to state that there is no apparent rejection happening! This is fantastic news!
(I am posting the official biopsy report at the end of this entry.)
In other news: I had my latest Belatacept Infusion on Tuesday. The stick was good, the infusion was uneventful and I have had zero side effects from the med.
On Wednesday I met with my local Nephrologist to update him on how everything is progressing. Aside from the while Creatinine thing he is very pleased with my current progress; especially with my electrolyte levels. Also, I asked him why my Blood Glucose reading is always high on my labs (80-100 is normal). He told me that with all the meds, the body responds by releasing extra sugar from the liver to compensate for the toxicity of the meds themselves. (It's a very simple explanation of the why.) So, now I understand why the Blood Sugar is high despite not eating prior to having my labs drawn.
That's all I have for today. There just wasn't much happening other than what I've already discussed. So, remember to read the post-biopsy report below, if it interests you.
Until next time...
Good Health to All!
ScottW
Surgical Pathology Report
THIS IS AN ADDENDUM REPORT, PLEASE SEE THE END OF THE REPORT FOR ADDENDUM DATA REPORT STATUS:
Addendum Final REASON FOR ADDENDUM: Ancillary Test Result(s) Addenda listed at the end of the original report
PHYSICIAN: NP ACCESSION DATE: 11/29/2018 REPORT DATE: 11/30/2018
**** THIS IS AN ADDENDUM REPORT **** PATIENT: SCOTT W
Clinical History: 55yo M with DDKT 5/4/17 for PCKD; h/o ACR type 2A in Sept 2017, type 1B in Mar 2018; now with Creat 2.8 (has been stable at 2.2). Special Exams Requested:
FINAL DIAGNOSIS:
LEFT RENAL ALLOGRAFT, BIOPSY:
- FEATURES SUGGESTIVE OF CHRONIC CALCINEURIN INHIBITOR TOXICITY. - NEGATIVE FOR ACUTE CELLULAR AND ANTIBODY-MEDIATED REJECTION. - SEE COMMENT.
COMMENT:
The biopsy is adequate for interpretation and shows frequent arteriolar hyalinosis, striped interstitial fibrosis/ tubular atrophy (about 20% overall), and mild-moderate arteriosclerosis. While donor- or recipient-derived diabetic or hypertensive disease might show some of these morphologic features, the glomeruli in this case are very well-preserved and do not show any of the changes typically associated with such disease. In this context, the features are suggestive of chronic calcineurin inhibitor (CNI) toxicity.
There is no evidence of active thrombotic microangiopathy. There is also no significant interstitial inflammation, tubulitis, glomerulitis, or peritubular capillaritis, and C4d staining is negative, helping to exclude acute rejection. No viral cytopathic effect is seen, although staining for BK virus will be performed and reported as an addendum.
Intermountain Medical Center, ScottW, Surgical Pathology Report, 12/01/2018 11:22:17 AM
Page 2 of 3
Banff classification: g0, t0, i0, v0, cg0, ct1, ci1, cv1, ah3, mm0, ptc0
GROSS EXAMINATION:
The specimen consists of 1 fragments of renal tissue, measuring 2.5 cm, submitted for light microscopic examination. In addition, small fragments of renal tissue are submitted for immunofluorescence studies and electron microscopy.
MICROSCOPIC EXAMINATION:
LIGHT MICROSCOPY:
One H+E-, one PAS-, one trichrome-, and one Jones silver-stained slide is reviewed. Serial sections through the biopsy show 1 fragments of renal cortex containing up to 24 glomeruli, 6 of which are globally sclerosed with associated features of ischemia and obsolescence (periglomerular fibrosis and collapse with PAS-negative material in Bowman's space). The glomeruli otherwise do not show increase in mesangial matrix nor increase in mesangial cellularity. The capillary loops appear smooth, patent, and do not contain holes, spikes, or splitting.
Endocapillary proliferation, segmental sclerosis, and crescents are not identified. There is a noticeably striped pattern of interstitial fibrosis and tubular atrophy involving about 20% of the tissue and associated with minimal chronic inflammation including a rare eosinophil and a few neutrophils. There are also very focal areas of tubules with isometric vacuolization and a few with dilated lumina. Scattered luminal calcifications are also seen. The majority of the arterioles present for evaluation show medial hyalinosis in a fairly symmetric circumferential distribution. The interlobular arteries demonstrate mild to moderate intimal fibrosis.
IMMUNOFLUORESCENCE:
A C4d immunofluorescent stain is performed with appropriately reactive internal controls and is negative. Three glomeruli are present in the IF sample.
ADDENDUM:
This addendum is issued to report the results of an immunohistochemical stain* for BK virus (Polyoma), performed with appropriately reactive controls. The result is negative.
The final diagnosis is unchanged.
*This test was developed and its performance characteristics were determined by Intermountain Central Laboratory. It has not been cleared or approved by the U.S. Food and Drug Administration. The FDA has determined that such clearance or approval is not necessary. This test is used for clinical purposes. It should not be regarded as investigational or for research. This laboratory is certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA-88) as qualified to perform high complexity clinical laboratory testing.
Intermountain Medical Center, ScottW63, Surgical Pathology Report, 12/01/2018 11:22:17 AM
Page 3 of 3
Immunoperoxidase procedures are done using a standard autostainer. DAB, AEC, or Fast Red reagent is used as detection. Procedure and dilutions of antibodies are on file. The standard immunoperoxidase protocol was followed. Laboratory extrinsic controls for the antibodies tested exhibited appropriate staining. All immunohistochemical/cytochemical stains (IHC) are performed on separate slides per different antibody.
REPORT STATUS: Addendum Final
