Renal Path Flashcards
Bladder cancer and Kidney stones present with:
Hematuria
no casts
acute cystitis
shows what on UA
what type of cast are present, if any?
pyuria (WBCs in pee)
no casts
Hypertensive emergency can precipitate Glomerulonephritis.
What type of casts can be seen?
RBC casts
Tubulo-interstitial inflammation
acute pyelonephritis
transplant rejection
what type of casts form?
WBC casts
Acute tubular necrosis (ATN)
Rhabdomyelosis
what type of casts form?
Granular Casts
Can be “muddy-brown” in appearance
*Tubular epithelial cell debri
NephrOtic syndrome casts
Associated with “Maltese cross” sign
Fatty casts
aka oval fat bodies
(Look like target sign with a dark cross super imposed)
End-stage renal disease/chronic kidney disease/ chronic pyelonephritis
what type of casts form?
Waxy Casts
(Fat/broad rectangles, a little granular/ rough looking
can also be tortuous, but still wide/finely grainy)
Nonspecific, can be a normal finding.
Benign urinary cast
Hyaline casts
(can be long skinny smooth rectangles or tortuous, skinny, smooth cylinders)
*made of Tomm-Horsefall mucoprotein
Form via solidification of Tamm-Horsfall mucoprotein (secreted by renal tubular cells)
Hyaline casts
Thickening of glomerular basement membrane (GBM)
Membranous Nephropathy
Ureteral dilation recurrent flank pain (acute) Hydro-nephrosis Normal RBC morphology \+/– Calyceal dilation
Ureterolithiasis
2 nephritic-nephrotic syndromes
Diffuse proliferative glomerulonephritis (DPGN)
Membrano–proliferative glomerulonephritis (MPGN)
Specific gravity < 1.005 =
Specific gravity > 1.015 =
dilute pee
concentrated pee
normal range for urine specific gravity is 1.005 to 1.015
Specific gravity > 1.015
concentrated pee
NSAIDs, Diuretics, Penicillins, PPIs, Sulfa drugs, Rifampin can all cause
Allergic (Acute) Interstitial Nephritis
Fever, Maculopapular Rash, new/recent Drug taken
eosinophilia in urine
Allergic (Acute) Interstitial Nephritis
Hematuria Flank Pain associated with: chronic NSAIDs Diabetes Sickle Cell Disease, severe Pyelonephritis
Renal Papillary necrosis
Hypoalbuminemia (edema)
Hypogammaglobinemia (infections)
Hypercoagulable (loss of ATIII)
Hyperlipidemia/Hypercholesterolemia (fat casts)
Nephrotic Syndrome
Associated with Hodkins Lymphoma (HY)
Minimal change disease
*Most common cause of NEPHROTIC in kids
Effaced/Flatten podocytes
CYTOKINES fault
Minimal change
H&E: Normal
EM: Effacement of foot processes
IF: Negative
Minimal Change
Selective proteinemia loss of albumin
HYPOalbuminemia (other protein levels ok)
excellent response to steroids
Minimal Change
Hispanics, Blacks, HIV, Heroin, Sickle cell
FSGS
EM: Effacement of foot process
H&E: some glomeruli has parts that have a pink & plain, acellular areas.
Poor response to steroids
FSGS
part of glomeruli is just a flat, empty pink
FSGS
Caucasian white boys
(H&E): Thick/dark outlines on the glomeruli basement
Don’t fuck with steroids
Membranous Nephropathy
LUPUS, HBV, HCV, Syphilis, Solid Tumors, Drugs (NSAIDs/ Penicillins)
Membranous Nephropathy
EM : Spike and Dome
(Ig blobs in the light grey area underneath black podocyte aka subepithelial layer)
IF: Granular (Ig-Immune complex deposits )
H&E: Swollen/puffy , packed pink cells
Membranous Nephropathy
Nephritic & Nephrotic Syndrome:
Mesangial cell proliferation separates the immune complex deposits
creates a tram-track appearance on H&E and PAS
due to BM splitting
Large, Hypercellular Glomeruli
Membranoproliferative Glomerulonephritis (MPGN)
H&E: the hot pink outline of the cells are now 2 separate/ split pink outlines with light pink in the middle)
Granular IF
Tram-Track H&E
Subendothelial deposits on EM
HBV/HCV association
Type 1
Membranoproliferative Glomerulonephritis
Granular IF
Tram-Track H&E
Intramembranous (inside the BM) deposits on EM
Type 2
Membranoproliferative Glomerulonephritis
aka dense deposit disease
associated with C3 nephritic factor
overactivation of complement
low levels of circulating C3
Type 2
Membranoproliferative Glomerulonephritis
Hyaline arteriosclerosis from _______ of vascular basement eventually leading to a HYPERFILTRATION injury of the kidney
(↑ GFR due to ↑permeability despite thickened membrane)
non-enzymatic glycosylation
Diabetic Nephropathy
Hyaline arteriosclerosing has a predilection towards the ____ arteriole thus narrowing the lumen & causing hyper-filtration resulting in _____
efferent
Microalbuminemia
Eosinophilic acellular nodules from glomerular sclerosis.
Kimmelstiel-Wilson Nodules
Diabetic Nephropathy
What can help slow the progression of Diabetic Nephropathy
ACE-I
ARBs
Oliguria and Azotemia
Nephritic syndrome
Hypercellular, inflammed glomeruli
Nephritic syndrome
PERIORBITAL edema
HTN
Nephritic syndrome
Immune complex deposition + C5a attracting neutrophils
Nephritic syndrome
EM: SubEPIthelial (under podocytes) HUMPS IC
IF: Granular (blobs–Starry sky–lumpy bumpy) due to IgG, IgM, and C3 deposits on GBM/ mesangium
H&E: Hypercellular glomeruli with HOT pink outlines
PSGN
Blood → Foot process → subepithelial → GBM (intramembranous) → subendothelium→ Endothelium → Tubular lumen
Periorbital edema
dark urine
recent infection
Kid
PSGN
Crescents in bowman’s space of RPGN made up of (2)
Fibrin and MQs
Nephritic syndrome that may progress to Renal Failure in a few days
RPGN
List 6 RPGNs
Goodpastures PSGN Diffuse Proliferative GN Wegener's Churg-Strauss Microscopic polyangiitis
Linear IF RPGN
Goodpastures
Granular IF RPGN
PSGN
Diffuse Proliferative GN