Mar 25, 2022
In this
podcast, Dr. Kim Thielen, a nephrologist/kidney specialist with
Minnesota Kidney Specialists joins us today to continue part 2 of
our discussion on acute kidney injury, as we wade further
"into the weeds"
discuss intrinsic renal disease. This episode will break down
hallmark urinary findings and
further subdivide intrinsic concerns into bland, nephrotic and
nephritic, various causes, and
treatment.
Enjoy the podcast!
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SHOW
NOTES:
*See the attachment for
additional show information.
Intrinsic Kidney Injuries:
Urinary analysis findings
- Bland Urine: no protein
- Nephrotic: protein
- Nephritic: protein and blood
Hallmark Urinary Findings:
Casts
- Tamm Horsfall Protein : Mucoprotein made by tubular epithelial
cells that precipitate out and congeal
to form casts on whatever is in the cells at the
time. (i.e. RBCs, WBCs, tubular debris)
Bland Urine
States
-
Crystalline Induced Renal Injury: obstruction and infllamatory
response
- Uric Acid Neuropathy (Most common)
- Cancers,
lymphomas, etc.
- Drugs: acyclovir,
methotrexate, protease inhibitors, etc.
- Toxins: Ethylene
glycol
- Bland Urine Disease states: results from injury to tubules,
instertim or pre glomerular blodd vessels, not
the filters of the kidney
- Interstital Nephritis
- Hallmark: pyuria
and WBC casts
- Biopsy: inflammatory infiltrate
- Causes:
viral, PPIs, Adenover, mizalamin, etc., Checkpoint inhibitors
- Acute Tubular Necrosis
- Hallmark: tubular
epithelial cell cast
- Granular: (course or fine) diagnostic of ATN
- Biopsy: denuded
dilated tubular cells
- Causes: #1:
Ischemia; toxins, drugs, contrast dye; pigment injury.
myoglobin
- What about
contrast dye?
- Categorized under ATN
- Per Dr. Thielen, plays a role, but injury is not
solely dependent on dye alone.
- Hepatorenal Syndrome: ischemic injury to the
kidney due to unopposed vasocontstriction
- Ace inhibitors
cause unopposed efferent vasoconstriction + nonsteroidals cause
unposed
afferent vasoconstriction = no glomerular perfusion pressure
- Multiple Myeloma
- Hallmark: Light
chain cast nephropathy or myeloma kidney
- Light chains precipitate out causing obstruction,
inflammatory response and causes
tubular damage
- Presentation:
older possibly with anemia, bone pain and elevated creatinine with
a bland urine.
- Protein to
creatinine ratio: + for protein (non albumin)
- Dipstick: (which
measures for albumin and not light chains) will be negative for
protein aka
bland
urine
- Hypertensive Nephrosclerosis
- Small vessel
vascular disease
- Blood vessels prematurely atherosclerosis causing
glomerular drop out and scarring of the
interstim
- Scleroderma
- Limited
cutaneous systemic sclerosis
- Diffuse
cutaneous systemic sclerosis: 60-80% have renal injury from disease
state itself
- FANA positive
- Concern for Scleroderma Renal Crisis
= medical emergency
- AKI,
moderate to severe HTN and bland urine
-
Uncontrolled accumulation of collage, thickens vascular walls,
narrowing and renal
ischemia
- Occurs in 10-15% of those with Diffuse
Cutaneous Systemic sclerosis and happens early
in disease
-
Left untreated: renal failure in 1-2 months and death in 1 year
- Treatment: ACE Inhibitor
Nephrotic Urine
States
- Urine protein: albumin excretion greater than 3.5g in 24
hours
- Nephrotic Syndrome:
- Present with 3 things (nephrotic range
protein, hypoalbuminemia, peripheral edema)
- Hyperlipidemia: due to increased hepatic
lipogenesis
- Increased
risk of renal disease and arthroscleratic
- Venous thrombotic disease:
- Loose
proteins other than albumin and develop a hypercoagulale state
- Renal and
peripheral venous thrombosis
- Lipiduria (forms fatty
casts, looks like a latese cross under microscope)
-Pathophysiology or nephrotic syndrome
- Glomerular capillary wall
- 3 layers that work as a
glomerular filtration and responsible in the filtration between
blood and
urine
-
Fenestrated Capillary Enothelial cells (fenestrations allow plasma
through to the basement
membrane)
-
Glomerular Basement Membrane (maintains glomerular filtration
barrier; negatively charged,
repels albumin)
-
Epithelium: Podocytes (Have highly specialized foot processes that
connect and form slit
diaphragms; Slit diaphragm important for the efficient flow
of small solute and water)
- Anything that messes with any
of these layers: nephrotic proteinuria
- Nephrotic Disease States:
- Biopsy: anyone with nephrotic proteinuria (besides
diabetics)
1) Light microscopy: high
overview
2) Immunofluorescens: looks for
nephritic component and identif immunce complexes
3) Electron microscopy: (EM)
helps look at the ultrastructure and better identify immune
deposits
-
Diabetic nephropathy
- Leading cause of kidney
disease in U.S. and western society
- Responsible for 30-40% of all
ESRD causes
- Hyperglycemia: produces
inflammatory responses, oxidative stress, and injures the podocytes
and
deposits that charge and
affect the ability of the kidney to filter.
- Amyoidosis
- Organize into betapleted
sheets and produce spikes of the capillary uniion and poke through
the
GF membrane
- Easily identified by
apple green birefringence on congo red
- Terminal illness
- Present with HTN,
cardiac effects and elevated creatine
- Nephrotic Disease states based of histologic
appearance
- Diagnosed by histologic appearance but does
not determine the etiology
- Minimal Change Disease
- Fairly common
- Minimal change
under light microscope
- EM: podocytes are
abnormal, fused, no unique cell-cell junction
- Primary: Immune
generated circulating facture; alters the cytoskeleton of the
podocytes
- Secondary
- Nonsteriodal -
most common cause of secondary minimal change disease
- Gama
interferon
- Hodgkin's
lymphoma
- Allergy: 30% of
minimal change have associate allergy (mechanism
unknown)
- Presentation
- Sudden onset
(days to weeks)
- Marked edema and
hypoablbuminemia
- 60% have normal
blood pressure, 82% have normal creatinine
- Focal Segmental Glomerulosclerosis (FSGS) - primary and
secondary
- Most common cause idopathic nephrotic
syndrome in adults
- Primary glomerulonephritis in the US
that causes ESRD
- Widespread podocyte injury
- Primary: circulating factor that messes with
regulation of foot process and adhesion to the
glomerular basement membrane (afffect
all podocytes)
- Present with nephrotic syndrome
and rapid progression
- HTN and elevated creatinine
- Secondary: the visceral epithelial cells don't
replicate
- Nephron loss or obesity or
direct foot process injury
- Cannot replicate (podocytes),
leads to decreased to podo denisty at specific areas (focal
injury)
- 2/3 of all cases FSGS
- Present: with slowly increasing
proteinuria and kidney impairment over time
- Causes: interferon,
bisphosphonates, talc, anabolic steroids
- Genetics: gene mutations that encode for the slit
diaphragms of the podocytes (affect all podocytes)
- Present in Childhood:
full blown nephrotic and progress rapidly to ESRD
Membranous
Nephropathy
- Most common cause of nephrotic syndrome in caucasion adults
- 80% present with nephrotic but develops more slowly to ESRD
- Primary: Major antigen identified
- antibody to trans-membrane receptor that is
highly expressed on the glomerular podocyte
- Secondary: Cancers (lung, breast, GI), Lupus, Thyroiditis, Hep B,
Syphilis, Nonsteroidals, Monoclonal
Antibodies
Nephritic
Syndrome
- Hematuria and proteinuria
- Hematuria: blood from kidney or outside the
kidney
- Outside the kidney:
look the same
- Inside the kidney:
dysmorphic red cells
- Present:
- Renal impairment for
days to weeks
- Edmatous, HTN and look
critically ill
- Vasculitis, sinusitis,
oral ulcers
- Pulmonary renal
syndrome: short of breath or hemoptysis
- Skin changes: bruising
, bleeding, purpura
- Myalgias and
arthritis
- Urine:
- Hallmark: red blood
cell casts (polymorphic red cells)
- dipstick + for
blood
- elevated
proteinuria
- Biopsy: nephritic and + urine
Nephritic Disease States
(based on immunofluorescence staining)
- Pauci Immune Disease
- Ankle vasculitis, common
- A paucity (little amount) of immune
complexes
- See black on imaging
- Lab work: check on ANCA and
peripheral eosinophils
- Anti-GBM Disease
- Renal limited, or classic pulmonary
renal: Good Pasture's
- linear staining of the
glomerular basement with anti IGG (looks like a ribbon on a
package)
- Treat with cytotoxic
agents
- Immune
Complex
- Starry sky pattern
- Glomerulus looks dotted with
stars
- Stars =
immune complex definition
- Diseases: Lupus (FANA),
Post Infectious GN, Membranous Proliferative GN
- IGA Nephropathy
- Most common cause of
glomerulonephritis in the world
- Presentation:
- Peak
incidence is the 2nd and 3rd decades of life
- 40-50%
gross hematuria with upper respiratory and GI illness
- Risk Factors for
Progression:
- younger
age or hypertension at time of presentation
- > 1g
proteinuria
- Elevated
creatinine at time of presentation
Thanks for listening.