Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
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Renal and urinary tract disease

Kidney medical disease:

  1. Renal function:

    • routine urinalysis: this test (U/A) inexpensively screens for all parameters but in only a semi-quantitative way. The sediment exam gives an idea of presence or absence of...and types of...casts. An obsolete (as of about 1965) attempt to quantitate the sediment exam was the Addis count from a bladder specimen accumulated during about 12 hours overnight; and it was serially tested in cases of renal disease as an attempt to discern worsening or betterment of the disease course.
    • National Kidney Disease Education Program glomerular filtration rate (GFR) on-line calculator
    • microalbumin screen ("dipstick") test: very sensitive screen for onset of early albuminuria in suspected diabetics or persons with such as autoimmune disease who are likely to develope renal disease.
    • microalbumin quantitative test thru LMC lab
    • albumin testing for proteinuria in LMC lab
    • hematuria & hemoglobinuria testing
    • Nephron Website
  2. Urine testing, other:
  3. Percutaneous medical biopsies of kidney: our pathologists work with the radiologist or nephrologist in one of the hospital ultrasound rooms to help be sure to obtain adequate biopsies. Most of sample is sent to expert nephropathologists for processing & interpretation @ NephroPath in Arkansas (after our pathologist divides the specimen by low-power microscopic dissection so that glomeruli are preserved for 3 different modes of study [LM, FM, & EM], final reporting taking a week or less by the end of 2010). If an acute case workup, we may attempt local initial diagnosis [L11-1]. A lengthy, one page info site HERE:
    • polarized light microscopy: this can be done while cores in saline dish and prior to sendout; look for crystalline tubulo-obstructive nephropathy (such as by ethylene glycol [antifreeze] poisoning converted to oxalate crystals [L09-553]; or post-gastric bypass; or ascorbic acid excess; or non-renal post-solid-organ transplant).
    • glomerular component diagnosis: glomeruli are thrombotic (also look for thrombocytopenia, RBC fragments on blood smear, elevated LDH & elevated bilirubin) from a microangiopathy or TTP/HUS? vs. necrotizing? vs. crescentic? vs. hypercellular? vs. deposits? [LMC-04-3013]; don't forget "minimal change" nephropathy.
      1. light:
      2. fluorescent:
      3. electron micro: endothelial tubuloreticular inclusions (TRIs) hint at auto-immune or viral etiology1.
    • interstitial component diagnosis: obvious...especially polys & eos?...due to meds? Lymhoid & lupus [L11-1]?
      1. light:
      2. fluorescent:
      3. electron micro:
    • tubular component diagnosis: We may need to look at prox. tubular epithelium for signs of injury...such as brush border loss (CD10 stains brush border), epithelial disorder, epithelial drop-out, epithelial "simplification"...because that could indicate tubulo-interstitial nephritis or even "adult minimal change glomerulopathy with acute renal failure syndrome" [LMC-04-5045].
      1. light:
      2. fluorescent:
      3. electron micro:
    • vascular component diagnosis: is there any siggestion of vasculitis, hyalinosis, amyloid, thrombophilic obstruction, etc?
      1. light:
      2. fluorescent:
      3. electron micro:
Kidney tumors:
  1. types
  2. IHC findings:
  3. grade
  4. stage

References:

  1. Yang AH, et. al., "The clinicopathological implications of endothelial tubuloreticular inclusions found in glomeruli having histopathology of idiopathic membranous nephropathy. " HERE.

(posted 2002; lasted addition 10 January 2011)

 
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