Latest revision as of 03:21, 22 February 2017

Micrograph showing a glomerulus with an acute thrombotic microangiopathy. PAS stain.

This article describes medical renal disease or the medical kidney. Much in medical kidney depends on the clinical information. Most of the disease seen by pathologists is... glomerular disease. It is one of the few areas that routinely requires electron microscopy.

Medical kidney is niche area in pathology. In the context of exams for general pathologists, if in doubt... the answer to most questions is diabetes mellitus or systemic lupus erythematosus.

Kidney tumours are dealt with in the kidney tumours article, and pediatric kidney tumours article.

Clinical

Creatinine

The standard screening test for renal function.
300 mmol/L is the general cut-point for referral to a nephrologist.^[1]

Notes:

In some parts of the world they use the units mg/dL; normal with these units is: 0.8 to 1.4 mg/dL.^[2]
Conversion: 1.0 mg/dL = 88.4 umol/L.^[3]^[4]

Glomerular filtration rate

Abbreviated GFR.
Ultimate measure of renal function - usually estimated from the serum creatinine using a formula.
Declines with age.
Normal range (dependent on age): 116-75 mL/min/1.73m².^[5]

Urine protein to creatinine ratio

Indicator of proteinuria.
Predictor of glomerular filtration rate.^[6]

Cut points:^[7]

Normal (2 years and older): <0.2 g protein / g Creatinine
Nephrotic range: >3.5 g protein / g Creatinine.

Complement

C3, C4 levels:^[8]

Changed:
- Systemic lupus erythematosus (SLE); levels decreased = increased disease activity.
- Post-infectious GN - decreased.
- MPGN - decreased. (???)
- Infection.^[9]^[10]
- Hemolytic anemia.^[9]^[11]
Normal:
- Minimal change disease.
- Chronic pyelonephritis.
- Renal vein thrombosis.
- Amyloidosis.

ANCA

Types:^[12]

MPO-ANCA (myeloperoxidase antineutrophil cytoplasmic autoantibody).
- Previously p-ANCA.
- Seen in ANCA-vasculitides, esp. microscopic polyangiitis.
PR3-ANCA (proteinase 3 antineutrophil cytoplasmic autoantibody).
- Previously c-ANCA.
- Seen in ANCA-vasculitides, esp. granulomatosis with polyangiitis (Wegener granulomatosis).

C4d

Suggests humoral immunity (antibody-mediated immunity) at play.
Important in monitoring of renal transplant recipients.
Immunostain also available - see below.

Other blood work

ANA, dsDNA -- to screen for systemic lupus erythematosus.
Hepatitis B.
Hepatitis C.
HIV.
Serum protein electrophoresis (SPEP) -- to screen for plasma cell neoplasms.
- Often done together with urine protein electrophoresis (UPEP).

Renal ultrasound

Normal adult kidney size ~10.8+/-0.8 cm.^[13]
Good for assessing the major vessels, drainage system and parenchymal lesions.
- Renal artery stenosis?
- Hydronephrosis?
- Pelviectasis?
- Renal cyst?
- Renal mass?

Urine dip

Findings:^[14]

RBC casts = acute bleed, e.g. nephritic syndrome.
WBC casts = interstitial nephritis, e.g. pylonephritis, parenchymal infection.
Hemegranular casts = acute tubular necrosis, transplant rejection.

Notes:

"Active sediment" = RBCs, RBC casts;^[15] implies glomerulonephritis.
- Some include the above (RBCs, RBC casts) + WBCs & protein.^[16]

Urine crystals

Main article: Crystals in body fluids

Clinical presentations

Nephrotic syndrome

Features:

Anasarca (whole body - edema).
Proteinuria (>3.5 g/24h).
Hypercholesterolemia.
Hypoalbuminemia.

Nephritic syndrome

Features - mnemonic PHAROH:^[17]

Proteinuria.
Hypertension.
Azotemia.
RBC casts.
Oliguria.
Hematuria.

Mixed

Features of nephritic syndrome and nephrotic syndrome.

Clinical DDx

Renal failure 101

Prerenal.
- Shock - cardiogenic, hypovolemic, neurogenic, septic, anaphylatic.
Renal.
- What this article deals with.
Postrenal.
- Outflow obstruction, e.g. prostatic nodular hyperplasia (AKA BPH).

Renal causes

Isolated hematuria.
Isolated proteinuria.
Nephrotic syndrome.
Nephritis syndrome.
Rapidly progressive glomerulonephritis.
Chronic renal failure.
A combination of any of the above.

The clinical presentations suggest a pathologic DDx.^[18]

Isolated hematuria

Proteinuria

Diabetic nephropathy.
Classic causes of nephrotic syndrome:
- FSGS.
- MCD.
- MN.
Paraprotein-related:
- Renal amyloidosis.
- Monoclonal immunoglobulin deposition disease (MIDD).
Weird stuff:
- Fibrillary glomerulopathy.
- Immunotactoid glomerulopathy.

Nephritic syndrome

Classic:

Post-infectious glomerulonephritis.
- Classically streptococcal.
Crescentic glomerulonephritis (AKA rapidly progressive glomerulonephritis (RPGN)).

Others:

Rapidly progressive glomerulonephritis

Classification:^[20]

Linear immune deposits.
- Antiglomerular basement membrane disease & Goodpasture's syndrome.
Granular immune deposits.
- Immune complex diseases.
  - Systemic lupus erythematosus.
  - IgA nephropathy.
  - Others.
Pauci-immune.
- ANCA vasculitides.
  - Wegener's granulomatosis.
  - Microscopic polyangiitis.

Nephrotic syndrome

Minimal segmental disease (MSD) - AKA minimal change disease (MCD).
Focal segmental glomerulosclerosis (FSGS).
Membranous nephropathy.

Mixed presentation

IgA nephropathy.
Focal proliferative glomerulosclerosis (FPGS).
Membranoproliferative glomerulonephritis (MPGN).

Normal kidney

Cells of the glomerulus

Podocytes.
Mesangial cells.
Endothelium.

Epithelium

Features:^[21]

The glomeruli visceral epithelium is part of the capillary wall (part of the glomerular tuft).
The parietal epithelium is part of Bowman's capsule.

Remember: visceral has vessels.

Glomerulus

A large autopsy series suggest it is: 223-292 micrometers.^[22]
- Another autopsy series suggests the mean diameter is: 225 micrometers.^[23]

Note:

If the glomerulus fills half the field at 40x on a microscope with 22 mm diameter eye pieces it is ~ 0.275 mm or 275 micrometers.

Glomerular basement membrane

The glomerular basement membrane (GBM) should be thinner than the tubular basement membrane.

Images

Benign kidney - very low mag.
Benign kidney - low mag.
Benign kidney - low mag.
Benign kidney - intermed. mag.

Basic approach to renal biopsy

Basic components

Glomeruli.
Tubules.
Interstitium.
Vessels.

Memory device GI TV: glomeruli, interstitium, tubules, vessels.

Glomeruli

Mesangium
- Matrix should be: "one cell thick" (expanded in diabetes mellitus).
- Cellularity of the mesangium - normal = upto 3 cells (don't count cell abutting the capillary lumen, don't count at the hilum).
Capillary loops "open"
- Lumina patent? If not patent is it due to matrix or cells (endocapillary hypercellularity).
- Capillary wall morphology - wavy thin is normal; hulla-hoop/wire-like abnormal (suggestive of immune complex deposition).
Bowman's space (urinary space) - crescents present?

Count the number of glomeruli.
Count number of the obsolete glomeruli.

Notes:

Endocapillary hypercellularity has a DDx - it includes: IgA nephropathy,^[24] and lupus nephritis.^[25]

Components of the glomeruli (anatomical)

Podocyte - rarely affect by disease
- One notable disease is collapsing glomerulopathy in HIV.^[26]
Endothelial cell.
Mesangial cell.

Obsolete glomeruli

Completely sclerosed glomeruli are not important - unless present in larger numbers than expected for the age of the patient.

Percent of sclerosed glomeruli = (age in years)/2 - 10%.^[27]

Example:

It is normal for an 80 year-old to have 30% sclerosed glomeruli.

Glomerular disease terms

Number of glomeruli involved:^[28]

Focal = some of the glomeruli.
- In practical terms, defined as: <50% of glomeruli.
Diffuse = most of glomeruli.

How much of the glomerulus is involved:^[28]

Global = most of the glomerulus.
- In practical terms, defined as: >80% of glomerulus.^[29]
Segmental = part of the glomerulus.

Vessels

Arteriolar hyalinosis - too much glassy pink stuff?
Intimal hyperplasia (atherosclerosis).

Consider:

Vasculitis? - inflammatory cells in vessel wall.
Amyloid? - pink.
Rejection? - PMNs.
Cholesterol emboli?

Arteriolar hyalinosis

Microscopic:

Small vessels (afferent +/- efferent arteriole) with:
- Glassy eosinophilic material in arteriolar wall.
  - PAS stain +ve.

DDx:

Aging.
Diabetes mellitus.
Hypertension.
Drugs - calcineurin inhibitors (tacrolimus, cyclosporine).

Note:

Arteriolar hyalinosis - involves afferent and efferent arterioles in diabetes, in others it is only the afferent.

Memory device ADHD:

Aging, Diabetes, Hypertension, Drugs.

Image

Arterial hyaline - HE - very high mag. (WC/Nephron)
Arterial hyaline - PAS - very high mag. (WC/Nephron)
Arterial hyaline - HPS - very high mag. (WC/Nephron)

Atherosclerosis

Main article: Atherosclerosis

Microscopic:

Intimal thickening of medium-sized vessels.
- Where is the intima/media interface?
  - Internal elastic lamina - wavy band of eosinophilic material on H&E that is 1-2 micrometres thick.

Grading - based on the thickness of the media and intima:

Mild: (tunica) media > (tunica) intima.
Moderate: media = intima.
Severe: media < intima.

Tubules

Tubules - proximal portion is the most important.

Consider:

Casts?
Degeneration, i.e. apoptosis.
Necrosis?
Regeneration, e.g. mitoses.

Interstitium

Fibrosis - prognostically important.
- Grading: mild = <25%, moderate 25-50%, severe >50%.
Inflammation?

Important terms/process related

Staining

The standard stain in kidney pathology is PAS. Section are usually 1-2 micrometers, as opposed to 4-5 micrometers seen in rountine section of other organs.

Interpretation of medical renal disease more difficult or even impossible if the sections are thicker, as one does not see the glomerular structures well.

In kidney that is cut thick the glomeruli look more nodular and it is more difficult to find open capillary loops.

Immunofluorescence

Routinue (mnemonic GAM CF):

IgG.
IgA.
IgM.
C1q
C3.
Fibrinogen.
Albumin.

Optional:

Kappa.
Lambda.
C4d.
- Positive staining = peri-tubular capillaries stain.

Negative immunofluorescence

Excludes all immune complex associated disease.

Seen in:

Positive immunofluorescence

Positive immunofluorescence is usually diagnostic.

Basic patterns:

Linear.
Granular.
Ring-like.

Examples:

Linear IgG:
- Antiglomerular basement membrane disease.
- Goodpasture syndrome.
Granular deposits:
- "Full house" - all present.
  - Lupus nephritis.
- Branching IgA.
  - IgA nephropathy.
- IgG, C3, kappa, lambda.
  - Membranous glomerulonephritis.
Linear C3 with mesangial rings; IgG -ve, IgA -ve.
- Dense deposit disease (DDD).

Notes:

Nonspecific linear IgG staining may be seen in diabetic nephropathy.

Immune complex-related disease

Can be:

Subepithelial - distal to basement membrane (BM), closer to the urinary space.
- Membranous nephropathy, Post-infectious glomerulonephritis (hump-like), MPGN.
Subendothelial - proximal to BM, closer to the glomerular capillary.
- MPGN - classic location.

Pathologic differential diagnosis

Tram-tracking of BM

DDx:^[30]

Mesangial hypercellularity

DDx:

Mesangial expansion

A patch of matrix can contain more than three mesangial cell nuclei.
- Highly subjective.

DDx:

Diabetes mellitus.^[31]
MPGN:
Fibrillary glomerulopathy.
Immunotactoid glomerulopathy.
Renal amyloidosis.
Monoclonal immunoglobulin deposition disease.

Glomerular crescents

AKA crescents.

General

Indicates a rapidly progressive disease.
Etiology/definition: break in the glomerular basement membrane (GBM).

Microscopic

Features:

Crescentic-shaped lesion in the urinary space of a glomerulus.
- Crescent = looks like the moon shortly after new moon.
- Cells & cellular debris in the urinary space.
  - Crescents lack GBM -- thus PAS -ve and MPAS -ve.
Break in the glomerular basement membrane - key feature.
- Best seen on a silver stain (e.g. Jones stain).
Fibrin.
- Orange on HPS.
- Pink on H&E.

Inflammatory cells (lymphocytes, plasma cells, eosinophils, macrophages) - extravascular - low power feature.

DDx:

Glomerular sclerosis:
- GBM visible through-out glomerulus.
- No fibrin.
- Collagen deposition within the glomerular tuft.
  - Seen with trichrome stain.
- +/-Glomerular tuft-capsule adhesions.
- +/-Glomerular enlargement.
- Usu. no significant inflammation.

Bland necrotic crescents

DDx:

ANCA-related glomerulonephritis.
Anti-GBM disease.

Diseases with crescents - is a long list.^[32]

Primary light microscopy patterns

Pattern	Key feature	Other findings	DDx of the pattern	DDx	Image
Normal light microscopy	Normal histology	none or few glomeruli in a biopsy of an under sampled FSGS	membranous nephropathy, focal segmental glomerulosclerosis (FSGS)	normal kidney, minimal change disease, thin glomerular basement membrane disease, Alport syndrome, early membranous nephropathy	Benign kidney (WC)
Nodular mesangial expansion	nodular mesangial matrix expansion, no mesangial hypercellularity	GBM thickening, both afferent and efferent arteriole hyalinized	diffuse proliferative GN, membranous nephropathy	diabetic nephropathy, idiopathic nodular glomerulosclerosis, renal amyloidosis, light chain deposition disease, fibrillary glomerulopathy, immunotactoid glomerulopathy	Nodular GS (WC)
Membranous nephropathy (MN)	GBM spikes or pinholes with silver stain, GBM thickening on PAS	+/-mesangial hypercellularity +/-tram-tracking/wireloop GBM	normal light microscopy, light chain deposition disease	hepatitis B, hepatitis C, carcinoma, NSAID toxicity, SLE, idiopathic (MN); light chain deposition disease (plasma cell neoplasm)	MN (WC)
Focal segmental glomerulosclerosis	sclerosed glomeruli = mesangial expansion with collagen	+/-glomerular enlargement, +/- tuft-capsule adhesions	rapidly progressive glomerulonephritis, nodular mesangial expansion	primary FSGS, secondary FSGS (HIV, IVDU, obesity, parvovirus B19, Alport syndrome	FSGS (WC)
Diffuse proliferative glomerulonephritis	mesangial hypercellularity	+/-mesangial expansion, +/-interstitial inflammation	nodular glomerulosclerosis	post-infectious glomerulonephritis, MPGN, dense deposit disease, diffuse proliferative lupus nephritis (class IV), cryoglobulinemic GN	MPGN (WC)
Rapidly progressive glomerulonephritis	glomerular crescents	+/-inflammation, +/-vasculitis	FSGS, diffuse proliferative glomerulonephritis	AGBM, post-infectious glomerulonephritis, pauci-immune GN, immune complex diseases (lupus nephritis, IgA nephropathy, others)	Crescentic GN (WC)
Tubular injury	tubular degeneration (loss of cilia in proximal tubule, apoptosis, necrosis), regeneration (mitosis, nucleoli)	+/-interstitial fibrosis	normal light microscopy	acute tubular necrosis, chronic allograft nephropathy	CAN (WC)
Small vessel pathology	luminal narrowing; +/-thrombosis, +/-hyalinosis	+/-onion-skinning	none	thrombotic microangiopathy (malignant hypertension, scleroderma renal crisis, DIC, HUS, TTP,	Hyalinosis (WC) TMA (WC)
Large vessel pathology	luminal narrowing or obstruction; +/-intimal thickening; +/-embolization	+/-medial thinning	none	atherosclerosis, cholesterol embolism, other types of embolism, thrombosis	Cholesterol embolus (WC)

Diagnoses - Table

Pattern	Key feature	Other findings	IF & EM	Presentation	Clinical	Pathol. DDx	Image
Nodular glomerulosclerosis	nodular mesangial matrix expansion	GBM thickening, both afferent and efferent arteriole hyalinized	EM?	proteinuria - typical presentation, nephrotic syndrome^{[citation needed]}	diabetes mellitus (DM)	amyloidosis, idiopathic nodular glomerulosclerosis (nodular GS without DM)	Nodular GS (WC)
Focal segmental glomerulosclerosis (FSGS)	focal sclerosis of gloms	+/-interstitial fibrosis	IF: negative; EM: foot process loss	nephrotic syndrome	primary FSGS, secondary FSGS (HIV, IVDU, obesity, parvovirus B19, Alport syndrome); unresponsive to steroids, worse prognosis than MCD	minimal change disease	FSGS (WC)
Membranous nephropathy (AKA membranous GN)	spikes or pinholes with silver stain	mesangial hypercellularity; +/-tram-tracking/wireloop GBM	IF: diffuse granular capillary loop IgG, C3, kappa, lambda; EM: diffuse subepithelial deposits - spike forming	nephrotic syndrome	hepatitis B, hepatitis C, carcinoma, NSAID toxicity, SLE, idiopathic	Nodular glomerulosclerosis (?)	MN (WC)
Minimal change disease (MCD)	foot process loss on EM	usu. none	EM: foot process loss	nephrotic syndrome	primary vs. secondary (lymphoproliferative disorder, NSAIDs); idiopathic responds to steroids	FSGS, thin glomerular basement membrane disease (histologic DDx)	Image?
IgA nephropathy	IgA branching pattern	+/-mesangial hypercellularity, +/-crescents	IF: IgA +ve (branching pattern); EM: dense mesangial deposits	mixed nephrotic/nephritic	primary vs. secondary (Henoch-Schoenlein purpura)	RPGN	HSN - IgA IHC (WC)
Membranoproliferative glomerulonephritis (MPGN)	thick GBM	Other findings?	subepithelial deposits	mixed nephrotic/nephritic	SLE, cryoglobulinemia, hepatitis B, hepatitis C	Pathol. DDx?	MPGN (WC)
Focal proliferative glomerosclerosis (FPGS)	<50% of glomeruli partially sclerosis	Other findings?	EM?	mixed nephrotic/nephritic	Clinical?	Pathol. DDx?	Image?
Rapidly progressive GN (RPGN)	crescents	Other findings?	EM?	nephritic syndrome	AGBM, ANCA-vasculitis	IgA nephropathy with crescents	Image?
Dense deposit disease	IF: linear C3 with rings	+/-thick GBM	EM: GBM lamina densa thickening	Presentation?	mixed nephrotic/nephritic (???)	MPGN	(nature.com)

Diffuse proliferative glomerulonephritis

Pattern	Key feature	Clinical
Post-infectious glomerulonephritis	IF: capillary loop +/- mesangial IgG/C3; EM: large infreq. hump-like subepithelial deposits	post-infection
Membranoproliferative glomerulonephritis (MPGN)	mesangial proliferation with thickening of the glomerular capillary loops^[33]	low C3, normal C4; primary vs. secondary (often hepatitis C)
Dense deposit disease	IF: linear C3 with rings
Cryoglobulinemic glomerulonephritis
Diffuse proliferative lupus glomerulonephritis		systemic lupus erythematosus; low C3, low C4
Diffuse proliferative IgA nephropathy	IF: IgA +ve (branching pattern)

Common diseases

Diabetic nephropathy

General

Due to diabetes mellitus - key feature.
- If there is no history of diabetes... it is idiopathic nodular glomerulosclerosis.
Most common cause of end-stage renal disease (ESRD).
Biopsied only if the (clinical) features are atypical.

Microscopic

Features:^[34]

Thick glomerular basement membrane (GBM).
Thickened (eosinophilic) tunica media in both the afferent and efferent arterioles.^[35]
Mesangial matrix expansion - leads to nodule formation Kimmelstiel-Wilson nodules (nodular glomerulosclerosis).

Others:

Armanni-Ebstein change = cytoplasmic vacuolization of tubular cells (usu. loop of Henle) -- innermost cortex, outer medulla;^[36] not specific to diabetes mellitus.^[37]
Capsular drop = hyaline material deposited in the Bowman's capsule.^[38]
Fibrin cap = subendothelial deposition of hyaline material.^[38]

Other - with weak evidence:

Extra efferent vessels.^[39]

Memory device:

GBM = thick GBM, both afferent & efferent arterioles thickened, mesangial matrix expansion.

Images

Diabetic glomerulosclerosis. (WC/KGH)
Diabetic glomerulosclerosis. (WC/KGH)
Diabetic glomerulosclerosis. (WC/KGH)
Nodular glomerulosclerosis. (WC)

www:

Notes:

Hypertensive kidneys have changes only in the afferent arteriole, i.e. the efferent arteriole is spared (see hypertension).

Grading

The severity of changes can be indicated by the grade:^[40]

Grade	Criteria
Grade I	GBM thickening on EM only
Grade II	Mild-to-moderate mesangial expansion only on LM
Grade III	Glomerulus with mesangial nodules (Kimmelstiel–Wilson nodules)
Grade IV	Stage III + global sclerosis in >50% of glomeruli

IF

Negative.
+/-Nonspecific linear IgG.

EM

Severe thickening of GBM.
Mesangial sclerosis.

Lupus nephritis

Abbreviated LN.

General

Main article: Systemic lupus erythematosus

Bread & butter of nephropathology.
The biopsy is done to determine treatment, i.e. how much immunosuppression is needed.

Immunofluorescence

"Full house" = all of 'em light up.

Classification

International Society of Nephrology/Renal Pathology Society (ISN/RPS) classification:^[41]^[42]

Class I - minimal mesangial LN.
Class II - mesangial proliferative LN.
- Mesangial hypercellularity. (???)
Class III - focal lupus nephritis; <50% of glomeruli.
- Mesangial hypercellularity. (???)
Class VI-S - diffuse segmental LN; >50% of glomeruli.
- Mesangial hypercellularity. (???)
Class VI-G - global LN; >50% of glomeruli.
Class V - Membranous lupus nephritis.
- Membranous nephropathy due to SLE.
Class IV - Advanced sclerosing LN; essentially end-stage kidney.

Notes:

Most of the action is in Class III and Class IV.
- Class I is near normal - doesn't get biopsied.
- Class IV is essentially a dead kidney - doesn't get biopsied.

Images

SLE nephritis - schematic. (WC)

Membranous lupus:

Nephrotic syndrome

Main article: Nephrotic syndrome

This classically includes the following:

It also includes:

IgA nephropathy.
Pre-eclampsia - uncommon.^[43]

Mixed nephrotic and nephritic

IgA nephropathy

AKA Berger disease.
- Should not be confused with Buerger disease (thromboangiitis obliterans).

General

More common in Asians.
Associated with an increased incidence of Celiac disease.^[44]
IgA nephropathy, in children, with a skin rash (leukocytoclastic vasculitis) = Henoch–Schönlein purpura.
May present as nephrotic syndrome.^[45]^[46]
May present as isolated hematuria.^[19]

Microscopic

Features:

Variable:
- Mesangial hypercellularity - may be only light microscopy finding.

Note:

Diagnosis based on immunofluorescence (IgA+).

Images

HSP - IgA IHC (WC)

Scoring

IgA nephropathy can be scored using an assessment of mesangial proliferation, endocapillary proliferation, glomerulosclerosis and tubular atrophy and interstitial fibrosis (abbreviated MEST).^[47]

IF

IgA +ve in a branching pattern - diagnostic.

EM

Mesangial deposits.
- These are electron dense, ergo dark on EM images.

Membranoproliferative glomerulonephritis

Abbreviated MPGN.
Old name MPGN type 1.

General

Clinical:

Nephrotic syndrome or nephrotic/nephritic syndrome.

Pathology:

May be primary, i.e. idiopathic, or secondary, i.e. a consequence of another pathologic process.^[33]

Secondary causes

In adults most common cause: hepatitis C.

Other causes:

HIV.^[48]
SLE - usu. has "full house" on IF.^[33]
Cryoglobulinemia.
Hepatitis B.
Portocaval shunt.^[48]

Microscopic

Features:

Endothelial cell proliferation.
Basement membrane double layering (tram-tracking).
Mesangial hypercellularity.

DDx:

Nodular glomerulosclerosis.

Images

MPGN - intermed. mag. (WC/Nephron)
MPGN - very high mag. (WC/Nephron)

MPGN - several images (upmc.edu).

EM

Features:

Subendothelial immune deposits - classic finding.^[49]
Subepithelial immune deposits - historically considered uncommon.^[50]

Dense deposit disease

Abbreviated DDD.
AKA MPGN type 2 (old name).

General

Usually children and young adults.
No longer considered a type of MPGN.^[51]

Microscopic

Features:

Variable - may be like MPGN.
- Four patterns:^[51]
  1. Hypercellularity and lobular (membranoproliferative-like).
  2. Mesangial proliferative.
  3. Crescentic.
  4. Acute proliferative and exudative.

Images:

IF

Linear C3 with mesangial rings (donut-like).
IgG negative.
IgA negative

Images:

DDD - IF (nature.com).

EM

Electron dense transformation of GBM lamina densa - key feature.
- Dense = darker.

Images:

DDD (nature.com).

Nephritic syndrome

Rapidly progressive glomerulonephritis

Abbreviated RPGN.
AKA crescentic glomerulonephritis.

General

Acute renal dysfunction.
Nephritic syndrome.

DDx:

Linear immunofluorescence.
- Antiglomerular basement membrane disease, Goodpasture syndrome.
Granular immunofluorescence
Pauci-immune.
- Wegener granulomatosis.
- Microscopic polyangiitis.

Microscopic

Features:

Glomerular crescents.
Interstitial inflammation.
+/-Vasculitis.

Images

RPGN (WC/KGH)
RPGN (WC/KGH)
RPGN - intermed. mag. (WC/Nephron)
RPGN - high mag. (WC/Nephron)

Post-infectious glomerulonephritis

Abbreviated PIGN.

Main article: Post-infectious glomerulonephritis

Rare diseases

Antiglomerular basement membrane disease

Abbreviated AGBM.

General

Known as Goodpasture disease (AKA Goodpasture syndrome), if renal failure is accompanied by pulmonary hemorrhage.^[52]
Rare - estimated incidence 1/1-2 million.^[53]
Antibody mediated hypersensitivity.
Thought to occur in genetically susceptible individuals.^[53]
- Associated with a specific HLA type (HLA-DRB1*1501) and two gene families.
- Antibodies directed against COL4A3,^[54] which is not mutated.
Oligouria - poor prognosticator.^{[citation needed]}

Tx:

Immune suppression & plasma exchange.^[55]

Clinical DDx:

Wegener granulomatosis.
Azathioprine toxicity.^[56]

Microscopic

Features:

RPGN.
- Crescentic glomerulonephritis.

Images

RPGN - intermed. mag. (WC/Nephron)
RPGN - high mag. (WC/Nephron)

www:

AGBM disease - several images (upmc.edu).

IF

Linear IgG deposits - diagnostic.
Fibrinogen in crescents.

DDx:

Goodpasture syndrome with the pulmonary hemorrhage.

Image:

Linear IgG in AGBM disease (upmc.edu).

Thin glomerular basement membrane disease

General

Collagen IV mutation - the same protein is involved in Alport syndrome.

Clinical:

Hematuria.
FHx.
Nonprogressive.

Microscopic

Normal.

IF

Normal.

EM

GBM thin <200-250 - key feature.

Note:

Normal GBM: 300-350 nm.

Alport syndrome

General

Clinical:

Hearing loss (sensorineural).
Hematuria - usually preceeds hearing loss.^[57]

Can be thought of a pathologic form of thin basement membrane disease.^[58]

Etiology:

Genetic defect - collagen type IV.

Inheritance:^[57]

X-linked - 80%.
Autosomal recessive - 15%.
Autosomal dominant - 5%.

Microscopic

Features:^[59]

Usu. normal.
+/-Foamy appearing renal tubular cells.^[60]

IF

Negative.

EM

Features:^[59]

Abnormal glomerular basement membrane (GBM); thinning or thickening.
- Classically thinning with thick lamellation (splitting/multi-layering).

Idiopathic nodular glomerulosclerosis

General

Not diabetic - key feature.

Associations:^[61]

Smoking - common; thought to be important in the etiology.^[62]
Hypertension.

Microscopic

Features:^[61]

Looks like diabetic nodular glomerulosclerosis.

IF

Nonspecific.

EM

Nonspecific.

Fabry disease

Main article: Fabry disease

Myeloma

See: Haematopathology.

AKA myeloma kidney.

Myeloma cast nephropathy

General

Renal failure.

Microscopic

Features:^[63]

Crap in tubules, eosinophilic.
- Classically angulated.
- Refractile.
Cast with cellular reaction - virtually diagnostic.
- Macrophages (CD68 +ve).

Images

www:

Myeloma cast nephropathy - high mag. (WC/Nephron)
Myeloma cast nephropathy - cropped - very high mag. (WC/Nephron)

Stains

Myeloma casts = PAS -ve.
- Hyaline casts = PAS +ve.

Amyloidosis

Main article: Amyloidosis

Usually associated with lambda clone.

Light chain deposition

Usually associated with kappa clone.

Immunotactoid glomerulopathy

General

Uncommon.
Thought to be a primary glomerulopathy.
- Must exclude lupus nephritis, paraproteinemias, fibrillary glomerulopathy, cryoglobulinemia, renal amyloidosis.
"Not universally" considered distinct from fibrillary glomerulopathy.^[64]

Presentation:

Nephrotic range proteinuria ~ 60% of cases.^[65]
Hypertension.

Microscopic

Features:

Mesangial expansion.

DDx:

Other causes of mesangial expansion.

IHC

Congo red stain -ve.

Fibrillary glomerulonephritis

AKA fibrillary glomerulopathy.

General

Rare ~ 1% native kidney biopsies.^[64]
Presents as nephrotic syndrome.
Prognosis poor; large number progress to ESRD.

Microscopic

Features:

Mesangial matrix expansion.
Thickened capillary walls.

Images:

www:
- FG (asnjournals.org).^[64]
- Fibrillary glomerulopathy (upmc.edu).

IF

IgG predominant.^[64]

Stains

Congo red stain -ve.

EM

Fibrils:^[64]
- Non-branching.
- Randomly arranged.
- Usu. 18-20 nm in diameter -- larger than amyloid (see below).
  - Size range 12-24 nm.

Note:

Amyloid between 8 and 15 nm (diameter), most often 8-12 nm.^[64]

Aristolochic acid nephropathy

Abbreviated AAN.
AKA chinese herb nephropathy.^[66]^[67]

General

Nephropathy due to chinese herbs for slimming.^[68]
Associated with urothelial atypia/urothelial carcinoma.

Clinical:

Chinese herb use.
Low-molecular weight proteinuria.

Microscopic

Features:^[68]

Extensive interstitial fibrosis.
Tubular atrophy - typically greater in outer cortex than inner cortex.
Glomeruli spared.
+/-Nuclear atypia of the urothelium.

DDx:

Balkan endemic nephropathy.

Image:

AAN (uninet.edu).^[67]

Cystic kidney diseases

Main article: Cystic kidney diseases

These are discussed in a separate article and include:

Autosomal dominant polycystic kidney disease (ADPKD).
Adult-onset medullary cystic disease.
Acquired renal cystic disease.
Autosomal recessive polycystic kidney disease (ARPKD).
Medullary sponge kidney.
Nephronophthisis.
Cystic renal cell carcinoma.

Pyelonephritis

Pyelonephritis is a misnomer; it is not an inflammatory process affecting the renal pelvis, as the name suggests. Pyelonephritis actually refers to a nephritis or tubulointerstitial nephritis.^[69]

It can be subdivided into:

Acute pyelonephritis

AKA acute infectious tubulointerstitial nephritis.
AKA diffuse suppurative nephritis.

General

Typically preceeded by a (lower) urinary tract infection (UTI).
Usually diagnosed clinically:
- Urine C&S, urine R&M, +/-CT abdomen.
- Fever, costovertebral tenderness.

Gross

Features:

+/-Necrosis of renal papillae.^[70]

Microscopic

Features:

Neutrophils within the renal tubules and interstitium.^[71]

Images

Acute pyelonephritis - intermed. mag. (WC/Nephron)
Acute pyelonephritis - high mag. (WC/Nephron)
Acute pyelonephritis - very high mag. (WC/Nephron)

Chronic pyelonephritis

Reflux nephropathy is considered synonym in some sources.^[72]

General

Inflammation of the kidney (nephritis) and renal pelvis (pyelo-^[73]).
May be associated with vesicoureteral reflux.
Chronic pyelonephritis may be a reason for nephrectomy.^[74]

Gross

Dilated and distorted renal pelvis.^[75]
+/-Necrosis of renal papillae.^[70]

Microscopic

Features:^[75]

Mononuclear tubulointerstitial infiltrate.
- Usu. more dense at the pelvis.
Interstitial fibrosis.
+/-Renal casts (PAS positive); may result in a thyroid-like apparance.

DDx:

Stains

PAS +ve -- renal tubular casts.

Disease that does not commonly get biopsied

End-stage kidney

Main article: End-stage kidney

Malignant hypertension

See: hyperplastic arteriolosclerosis.

See: thrombotic microangiopathy.

May be seen in scleroderma.

Acute tubular necrosis

Often abbreviated ATN.

General

Diagnosed clinically:

Using urine R&M - hemegranular casts^[76] are diagnostic.
Anuria or low urine output.

Gross

Poorly defined corticomedullary junction - soft finding.
Slightly heavier ~ 180 grams.^[77]

Microscopic

Features:^[77]

Tubular epithelial whorls - present in approx. one third of cases - most important.
- Detached epithelium within the luminal space surrounded by epithelium.
  - Similar to epithelial telescoping seen in endometrial biopsies.
Tubulorrhexis - present in approx. one third of cases.
- Disruption of the tubular basement membrane.
Interstitial edema - sensitive... but not specific.

Notes - not particularily useful findings:

Mitoses.
Casts in tubules.

IHC

Ki-67 - focal nuclear staining of the tubular epithelium.^[77]

Hepatorenal syndrome

General

Acute renal failure secondary to liver failure (e.g. fulminant liver failure, cirrhosis with marginal liver function).

Clinical:

Urine sodium is low,^[78] unlike in ATN (the main DDx).

Pathophysiology:

Renal vasoconstriction.^[79]

Treatment: Medical and surgical:^[80]

Vasoconstrictors (e.g. midodrine, terlipressin (counteracts splanchnic vasodilation), norepinephrine).
Albumin.
TIPS (transjugular intrahepatic portosystemic shunt).
Liver transplantation.

Note:

I suspect a portal vein pump would work... it reduces portal pressure and would likely increase hepatic function.

Microscopic

Features (kidney):

Normal.

Nephrocalcinosis

General

Hypercalcemia.

Microscopic

Features:

Calcification of the renal parenchyma - key feature.

Images:

Nephrocalcinosis (upmc.edu).

Renal transplant pathology

Main article: Renal transplant pathology

Acute rejection.
Chronic rejection.
Polyomavirus.
Transplant glomerulopathy.
Calcineurin-inhibitor toxicity.

References

↑ Mendelssohn DC, Barrett BJ, Brownscombe LM, et al. (August 1999). "Elevated levels of serum creatinine: recommendations for management and referral". CMAJ 161 (4): 413–7. PMC 1230545. PMID 10478168. http://www.cmaj.ca/cgi/content/full/161/4/413.
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↑ URL: http://www.unc.edu/~rowlett/units/scales/clinical_data.html. Accessed on: 8 November 2010.
↑ URL: http://www.kidney.org/professionals/KLS/gfr.cfm. Accessed on: 8 November 2010.
↑ Ruggenenti P, Gaspari F, Perna A, Remuzzi G (February 1998). "Cross sectional longitudinal study of spot morning urine protein:creatinine ratio, 24 hour urine protein excretion rate, glomerular filtration rate, and end stage renal failure in chronic renal disease in patients without diabetes". BMJ 316 (7130): 504–9. PMC 2665663. PMID 9501711. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665663/pdf/9501711.pdf.
↑ URL: http://www.fpnotebook.com/urology/lab/urnprtntcrtnrt.htm. Accessed on: 8 November 2010.
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↑ Guzman, RP.; Zierler, RE.; Isaacson, JA.; Bergelin, RO.; Strandness, DE. (Mar 1994). "Renal atrophy and arterial stenosis. A prospective study with duplex ultrasound.". Hypertension 23 (3): 346-50. PMID 8125561.
↑ URL: http://www.nlm.nih.gov/medlineplus/ency/article/003586.htm. Accessed on: 20 September 2010.
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↑ Berden, AE.; Ferrario, F.; Hagen, EC.; Jayne, DR.; Jennette, JC.; Joh, K.; Neumann, I.; Noël, LH. et al. (Oct 2010). "Histopathologic classification of ANCA-associated glomerulonephritis.". J Am Soc Nephrol 21 (10): 1628-36. doi:10.1681/ASN.2010050477. PMID 20616173. http://jasn.asnjournals.org/content/21/10/1628/T1.expansion.html.
↑ AH. 17 July 2009.
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↑ Smerud, HK.; Fellström, B.; Hällgren, R.; Osagie, S.; Venge, P.; Kristjánsson, G. (Aug 2009). "Gluten sensitivity in patients with IgA nephropathy.". Nephrol Dial Transplant 24 (8): 2476-81. doi:10.1093/ndt/gfp133. PMID 19332868.
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↑ Costa, AF.; Gomes dos Santos, WA.; Filho, MA.; Farias, FT.; Modesto dos Santos, V.. "Nodular glomerulosclerosis in a non-diabetic hypertensive smoker with dyslipidemia.". An Sist Sanit Navar 34 (2): 301-8. PMID 21904413.
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↑ Mills, Stacey E; Carter, Darryl; Greenson, Joel K; Reuter, Victor E; Stoler, Mark H (2009). Sternberg's Diagnostic Surgical Pathology (5th ed.). Lippincott Williams & Wilkins. pp. 1725. ISBN 978-0781779425.
↑ ^70.0 ^70.1 Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 251. ISBN 978-1416002741.
↑ Mills, Stacey E; Carter, Darryl; Greenson, Joel K; Reuter, Victor E; Stoler, Mark H (2009). Sternberg's Diagnostic Surgical Pathology (5th ed.). Lippincott Williams & Wilkins. pp. 1726. ISBN 978-0781779425.
↑ Mills, Stacey E; Carter, Darryl; Greenson, Joel K; Reuter, Victor E; Stoler, Mark H (2009). Sternberg's Diagnostic Surgical Pathology (5th ed.). Lippincott Williams & Wilkins. pp. 1728. ISBN 978-0781779425.
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↑ ^75.0 ^75.1 Mills, Stacey E; Carter, Darryl; Greenson, Joel K; Reuter, Victor E; Stoler, Mark H (2009). Sternberg's Diagnostic Surgical Pathology (5th ed.). Lippincott Williams & Wilkins. pp. 1729. ISBN 978-0781779425.
↑ Kanbay, M.; Kasapoglu, B.; Perazella, MA. (Jun 2010). "Acute tubular necrosis and pre-renal acute kidney injury: utility of urine microscopy in their evaluation- a systematic review.". Int Urol Nephrol 42 (2): 425-33. doi:10.1007/s11255-009-9673-3. PMID 19921458.
↑ ^77.0 ^77.1 ^77.2 Kocovski, L.; Duflou, J. (Mar 2009). "Can renal acute tubular necrosis be differentiated from autolysis at autopsy?". J Forensic Sci 54 (2): 439-42. doi:10.1111/j.1556-4029.2008.00956.x. PMID 19207286.
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↑ Angeli P, Merkel C (2008). "Pathogenesis and management of hepatorenal syndrome in patients with cirrhosis". J. Hepatol. 48 Suppl 1: S93-103. doi:10.1016/j.jhep.2008.01.010. PMID 18304678.
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External links

[pmid-1] Mendelssohn DC, Barrett BJ, Brownscombe LM, et al. (August 1999). "Elevated levels of serum creatinine: recommendations for management and referral". CMAJ 161 (4): 413–7. PMC 1230545. PMID 10478168. http://www.cmaj.ca/cgi/content/full/161/4/413.

[2] URL: http://www.nlm.nih.gov/medlineplus/ency/article/003475.htm. Accessed on: 8 November 2010.

[3] URL: http://www.sydpath.stvincents.com.au/other/Conversions/ConversionMasterF3.htm. Accessed on: 8 November 2010.

[4] URL: http://www.unc.edu/~rowlett/units/scales/clinical_data.html. Accessed on: 8 November 2010.

[5] URL: http://www.kidney.org/professionals/KLS/gfr.cfm. Accessed on: 8 November 2010.

[pmid9501711-6] Ruggenenti P, Gaspari F, Perna A, Remuzzi G (February 1998). "Cross sectional longitudinal study of spot morning urine protein:creatinine ratio, 24 hour urine protein excretion rate, glomerular filtration rate, and end stage renal failure in chronic renal disease in patients without diabetes". BMJ 316 (7130): 504–9. PMC 2665663. PMID 9501711. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665663/pdf/9501711.pdf.

[7] URL: http://www.fpnotebook.com/urology/lab/urnprtntcrtnrt.htm. Accessed on: 8 November 2010.

[pmid4549215-8] Levo Y, Pick AI (1974). "The significance of C3 and C4 complement levels in lupus nephritis". Int Urol Nephrol 6 (3-4): 233–8. PMID 4549215. http://www.springerlink.com/content/l1657797661468g1/fulltext.pdf.

[pmid3892188-9] 9.0 ^9.1 Nusinow SR, Zuraw BL, Curd JG (May 1985). "The hereditary and acquired deficiencies of complement". Med. Clin. North Am. 69 (3): 487–504. PMID 3892188.

[10] URL: beckmancoulter.com. Accessed on: 9 November 2010.

[11] URL: beckmancoulter.com. Accessed on: 9 November 2010.

[pmid21339221-12] Kallenberg, CG. (Mar 2011). "Pathogenesis of ANCA-associated vasculitides.". Ann Rheum Dis 70 Suppl 1: i59-63. doi:10.1136/ard.2010.138024. PMID 21339221.

[pmid8125561-13] Guzman, RP.; Zierler, RE.; Isaacson, JA.; Bergelin, RO.; Strandness, DE. (Mar 1994). "Renal atrophy and arterial stenosis. A prospective study with duplex ultrasound.". Hypertension 23 (3): 346-50. PMID 8125561.

[14] URL: http://www.nlm.nih.gov/medlineplus/ency/article/003586.htm. Accessed on: 20 September 2010.

[15] URL: http://emedicine.medscape.com/article/238158-overview. Accessed on: 9 November 2010.

[16] URL: http://www.nephrologychannel.com/agn/index.shtml. Accessed on: 9 November 2010.

[17] URL: http://books.google.com/books?id=5bmg8xiLxkMC&pg=PA249&lpg=PA249&dq=Nephritic+syndrome+PHAROH#v=onepage&q=Nephritic%20syndrome%20PHAROH&f=false. Accessed on: 9 December 2009.

[18] URL: http://www.emedicine.com/med/topic886.htm and http://www.emedicine.com/ped/topic1564.htm. Accessed on: 8 November 2010.

[pmid19949735-19] 19.0 ^19.1 Kim, BS.; Kim, YK.; Shin, YS.; Kim, YO.; Song, HC.; Kim, YS.; Choi, EJ. (Dec 2009). "Natural history and renal pathology in patients with isolated microscopic hematuria.". Korean J Intern Med 24 (4): 356-61. doi:10.3904/kjim.2009.24.4.356. PMID 19949735.

[20] URL: http://bestpractice.bmj.com/best-practice/monograph/207/basics/classification.html. Accessed on: 17 November 2011.

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@@ Line 1: / Line 1: @@
-This article describes '''medical renal disease''' or the '''medical kidney'''.  Much in medical kidney depends on the clinical information.  Most of the disease seen by pathologists is... glomerular disease.  If in doubt... the answer to most questions is ''[[diabetes mellitus]]'' or ''[[systemic lupus erythematosus]]''.  Medical kidney is niche area in pathology.  It is one of the few areas that routinely requires [[electron microscopy]].
+[[Image:Acute thrombotic microangiopathy - pas - very high mag.jpg|250px|thumb|[[Micrograph]] showing a glomerulus with an [[thrombotic microangiopathy|acute thrombotic microangiopathy]]. [[PAS stain]].]]
+This article describes '''medical renal disease''' or the '''medical kidney'''.  Much in medical kidney depends on the clinical information.  Most of the disease seen by pathologists is... glomerular disease. It is one of the few areas that routinely requires [[electron microscopy]].
+Medical kidney is niche area in pathology. In the context of exams for general pathologists, if in doubt... the answer to most questions is ''[[diabetes mellitus]]'' or ''[[systemic lupus erythematosus]]''.
 Kidney tumours are dealt with in the ''[[kidney tumours]]'' article, and ''[[pediatric kidney tumours]]'' article.
 =Clinical=
@@ Line 9: / Line 12: @@
 Notes:
-*Dinosaurs use the units mg/dL; normal with these units is: 0.8 to 1.4 mg/dL.<ref>URL: [http://www.nlm.nih.gov/medlineplus/ency/article/003475.htm http://www.nlm.nih.gov/medlineplus/ency/article/003475.htm]. Accessed on: 8 November 2010.</ref>
+*In some parts of the world they use the units mg/dL; normal with these units is: 0.8 to 1.4 mg/dL.<ref>URL: [http://www.nlm.nih.gov/medlineplus/ency/article/003475.htm http://www.nlm.nih.gov/medlineplus/ency/article/003475.htm]. Accessed on: 8 November 2010.</ref>
 *Conversion: 1.0 mg/dL = 88.4 umol/L.<ref>URL: [http://www.sydpath.stvincents.com.au/other/Conversions/ConversionMasterF3.htm http://www.sydpath.stvincents.com.au/other/Conversions/ConversionMasterF3.htm]. Accessed on: 8 November 2010.</ref><ref>URL: [http://www.unc.edu/~rowlett/units/scales/clinical_data.html http://www.unc.edu/~rowlett/units/scales/clinical_data.html]. Accessed on: 8 November 2010.
 </ref>
@@ Line 25: / Line 28: @@
 Cut points:<ref>URL: [http://www.fpnotebook.com/urology/lab/urnprtntcrtnrt.htm http://www.fpnotebook.com/urology/lab/urnprtntcrtnrt.htm]. Accessed on: 8 November 2010.</ref>
 *Normal (2 years and older): <0.2 g protein / g Creatinine
-*Nephrotic range: >3.5 g protein / g Creatinine.
+*[[Nephrotic syndrome|Nephrotic]] range: >3.5 g protein / g Creatinine.
 ===Complement===
@@ Line 31: / Line 34: @@
 *Changed:
 **[[Systemic lupus erythematosus]] (SLE); levels decreased = increased disease activity.
-**Post-infectious GN - decreased.
+**[[Post-infectious GN]] - decreased.
-**MPGN - decreased. (???)
+**[[MPGN]] - decreased. (???)
 **Infection.<ref name=pmid3892188>{{cite journal |author=Nusinow SR, Zuraw BL, Curd JG |title=The hereditary and acquired deficiencies of complement |journal=Med. Clin. North Am. |volume=69 |issue=3 |pages=487–504 |year=1985 |month=May |pmid=3892188 |doi= |url=}}</ref><ref>URL: [http://www.google.com/url?sa=t&source=web&cd=3&sqi=2&ved=0CB0QFjAC&url=http%3A%2F%2Fwww.beckmancoulter.com%2Fliterature%2FClinDiag%2FBulletin%25209282C3_C4.pdf&rct=j&q=C3%2C%20C4%20decreased%2C%20l&ei=0evYTPLHHcX9ngfetNDzCQ&usg=AFQjCNFR26FHyAmy4lZ3tm-tLgW-oD73Zg&cad=rja beckmancoulter.com]. Accessed on: 9 November 2010.</ref>
 **Hemolytic [[anemia]].<ref name=pmid3892188>{{cite journal |author=Nusinow SR, Zuraw BL, Curd JG |title=The hereditary and acquired deficiencies of complement |journal=Med. Clin. North Am. |volume=69 |issue=3 |pages=487–504 |year=1985 |month=May |pmid=3892188 |doi= |url=}}</ref><ref>URL: [http://www.google.com/url?sa=t&source=web&cd=3&sqi=2&ved=0CB0QFjAC&url=http%3A%2F%2Fwww.beckmancoulter.com%2Fliterature%2FClinDiag%2FBulletin%25209282C3_C4.pdf&rct=j&q=C3%2C%20C4%20decreased%2C%20l&ei=0evYTPLHHcX9ngfetNDzCQ&usg=AFQjCNFR26FHyAmy4lZ3tm-tLgW-oD73Zg&cad=rja beckmancoulter.com]. Accessed on: 9 November 2010.</ref>
@@ Line 46: / Line 49: @@
 **Previously p-ANCA.
 **Seen in ANCA-[[vasculitides]], esp. [[microscopic polyangiitis]].
-*PR3-ANPA (proteinase 3 antineutrophil cytoplasmic autoantibody).
+*PR3-ANCA (proteinase 3 antineutrophil cytoplasmic autoantibody).
 **Previously c-ANCA.
-**Seen in ANCA-[[vasculitides]], esp. [[Wegener granulomatosis]].
+**Seen in ANCA-[[vasculitides]], esp. [[granulomatosis with polyangiitis]] (Wegener granulomatosis).
 ===C4d===
 *Suggests humoral immunity (antibody-mediated immunity) at play.
 *Important in monitoring of renal transplant recipients.
-*Immunostain also available - see below.
+*[[Immunostain]] also available - see below.
 ===Other blood work===
@@ Line 103: / Line 106: @@
 ====Mixed====
-*Features of nephritic syndrome and nephrotic syndrome.
+*Features of nephritic syndrome and [[nephrotic syndrome]].
 =Clinical DDx=
@@ Line 126: / Line 129: @@
 ===Isolated hematuria===
-*[[IgA nephropathy]].
+*[[IgA nephropathy]].<ref name=pmid19949735>{{Cite journal  | last1 = Kim | first1 = BS. | last2 = Kim | first2 = YK. | last3 = Shin | first3 = YS. | last4 = Kim | first4 = YO. | last5 = Song | first5 = HC. | last6 = Kim | first6 = YS. | last7 = Choi | first7 = EJ. | title = Natural history and renal pathology in patients with isolated microscopic hematuria. | journal = Korean J Intern Med | volume = 24 | issue = 4 | pages = 356-61 | month = Dec | year = 2009 | doi = 10.3904/kjim.2009.24.4.356 | PMID = 19949735 }}</ref>
 *[[Alport syndrome]].
 *[[Thin glomerular basement membrane disease]].
@@ Line 145: / Line 148: @@
 ===Nephritic syndrome===
 Classic:
-*Post-infectious glomerulonephritis.
+*[[Post-infectious glomerulonephritis]].
 **Classically streptococcal.
 *Crescentic glomerulonephritis ([[AKA]] rapidly progressive glomerulonephritis (RPGN)).
@@ Line 177: / Line 180: @@
 *[[Membranoproliferative glomerulonephritis]] (MPGN).
-=Normal=
+=Normal kidney=
 ===Cells of the glomerulus===
 *Podocytes.
@@ Line 194: / Line 197: @@
 **Another autopsy series suggests the mean diameter is: 225 micrometers.<ref>{{Cite journal  | last1 = Nyengaard | first1 = JR. | last2 = Bendtsen | first2 = TF. | title = Glomerular number and size in relation to age, kidney weight, and body surface in normal man. | journal = Anat Rec | volume = 232 | issue = 2 | pages = 194-201 | month = Feb | year = 1992 | doi = 10.1002/ar.1092320205 | PMID = 1546799 }}</ref>
+Note:
+*If the glomerulus fills half the field at 40x on a microscope with 22 mm diameter eye pieces it is ~ 0.275 mm or 275 micrometers.
 ====Glomerular basement membrane====
 The glomerular basement membrane (GBM) should be thinner than the tubular basement membrane.
+===Images===
+<gallery>
+Image: Benign kidney -- very low mag.jpg | Benign kidney - very low mag.
+Image: Benign kidney -- low mag.jpg | Benign kidney - low mag.
+Image: Benign kidney - alt -- low mag.jpg | Benign kidney - low mag.
+Image: Benign kidney -- intermed mag.jpg | Benign kidney - intermed. mag.
+</gallery>
 =Basic approach to renal biopsy=
@@ Line 203: / Line 217: @@
 *Interstitium.
 *Vessels.
+Memory device ''GI TV'': glomeruli, interstitium, tubules, vessels.
 ===Glomeruli===
@@ Line 249: / Line 265: @@
 Consider:
-*Vasculitis? - inflammatory cells in vessel wall.
+*[[Vasculitis]]? - inflammatory cells in vessel wall.
-*Amyloid? - pink.
+*[[Amyloid]]? - pink.
-*Rejection? - PMNs.
+*Rejection? - [[PMN]]s.
-*Cholesterol emboli?
+*[[Cholesterol emboli]]?
 ====Arteriolar hyalinosis====
@@ Line 272: / Line 288: @@
 *'''A'''ging, '''D'''iabetes, '''H'''ypertension, '''D'''rugs.
-Image:
+=====Image=====
-*[http://commons.wikimedia.org/wiki/File:Renal_arterial_hyalinosis_-_he_-_very_high_mag.jpg Arterial hyaline - HE - very high mag. (WC)].
+<gallery>
-*[http://commons.wikimedia.org/wiki/File:Renal_arterial_hyalinosis_-_pas_-_very_high_mag.jpg Arterial hyaline - PAS - very high mag. (WC)].
+Image:Renal_arterial_hyalinosis_-_he_-_very_high_mag.jpg | Arterial hyaline - HE - very high mag. (WC/Nephron)
-*[http://commons.wikimedia.org/wiki/File:Renal_arterial_hyalinosis_-_hps_-_very_high_mag.jpg Arterial hyaline - HPS - very high mag. (WC)].
+Image:Renal_arterial_hyalinosis_-_pas_-_very_high_mag.jpg | Arterial hyaline - PAS - very high mag. (WC/Nephron)
+Image:Renal_arterial_hyalinosis_-_hps_-_very_high_mag.jpg | Arterial hyaline - HPS - very high mag. (WC/Nephron)
+</gallery>
 ====Atherosclerosis====
@@ Line 364: / Line 382: @@
 Can be:
 *Subepithelial - distal to basement membrane (BM), closer to the urinary space.
+**[[Membranous nephropathy]], [[Post-infectious glomerulonephritis]] (hump-like), [[MPGN]].
 *Subendothelial - proximal to BM, closer to the glomerular capillary.
+**[[MPGN]] - classic location.
 ==Pathologic differential diagnosis==
@@ Line 442: / Line 461: @@
 |Normal light microscopy
 | Normal histology
-| none
+| none ''or'' few glomeruli in a biopsy of an under sampled FSGS
-| [[membranous nephropathy]], FSGS
+| [[membranous nephropathy]], [[focal segmental glomerulosclerosis]] (FSGS)
 | normal kidney, [[minimal change disease]], [[thin glomerular basement membrane disease]], [[Alport syndrome]], early [[membranous nephropathy]]
-| Image?
+| [[Image:Benign kidney -- intermed mag.jpg|thumb|center|150px|Benign kidney (WC)]]
 |-
 |Nodular mesangial expansion
@@ Line 452: / Line 471: @@
 | diffuse proliferative GN, membranous nephropathy
 | [[diabetic nephropathy]], [[idiopathic nodular glomerulosclerosis]], [[renal amyloidosis]], light chain deposition disease, [[fibrillary glomerulopathy]], [[immunotactoid glomerulopathy]]
-| [http://commons.wikimedia.org/wiki/File:Nodular_glomerulosclerosis.jpeg (WC)]
+| [[Image:Nodular_glomerulosclerosis.jpeg|thumb|center|150px|Nodular GS (WC)]]
 |-
 |[[Membranous nephropathy]] (MN)
@@ Line 459: / Line 478: @@
 | normal light microscopy, light chain deposition disease
 | [[hepatitis B]], [[hepatitis C]], carcinoma, NSAID toxicity, SLE, idiopathic (MN); light chain deposition disease ([[plasma cell neoplasm]])
-| [http://commons.wikimedia.org/wiki/File:Membranous_nephropathy_-_mpas_-_very_high_mag.jpg (WC)]
+| [[Image:Membranous_nephropathy_-_mpas_-_very_high_mag.jpg|thumb|center|150px|MN (WC)]]
 |-
 |[[Focal segmental glomerulosclerosis]]
@@ Line 465: / Line 484: @@
 | +/-glomerular enlargement, +/- tuft-capsule adhesions
 | [[rapidly progressive glomerulonephritis]], nodular mesangial expansion
-| primary FSGS, secondary FSGS ([[HIV]], [[IVDU]], obesity, [[parvovirus B19]], [[Alport syndrome]]
+| primary FSGS, secondary FSGS ([[HIV]], [[IVDU]], [[obesity]], [[parvovirus B19]], [[Alport syndrome]]
-| [http://commons.wikimedia.org/wiki/File:Focal_segmental_glomerulosclerosis_-_high_mag.jpg (WC)]
+| [[Image:Focal_segmental_glomerulosclerosis_-_high_mag.jpg|thumb|center|150px|FSGS (WC)]]
 |-
 |Diffuse proliferative glomerulonephritis
@@ Line 473: / Line 492: @@
 | nodular glomerulosclerosis
 | [[post-infectious glomerulonephritis]], [[MPGN]], [[dense deposit disease]], diffuse proliferative [[lupus nephritis]] (class IV), cryoglobulinemic GN
-| [http://commons.wikimedia.org/wiki/File:Membranoproliferative_glomerulonephritis_-_very_high_mag.jpg (WC)]
+| [[Image:Membranoproliferative_glomerulonephritis_-_very_high_mag.jpg|thumb|center|150px|MPGN (WC)]]
 |-
 |[[Rapidly progressive glomerulonephritis]]
@@ Line 480: / Line 499: @@
 | [[FSGS]], diffuse proliferative glomerulonephritis
 | [[AGBM]], [[post-infectious glomerulonephritis]], pauci-immune GN, immune complex diseases ([[lupus nephritis]], [[IgA nephropathy]], others)
-| [http://en.wikipedia.org/wiki/File:Crescentic_glomerulonephritis_%282%29.jpg (WC)]
+| [[Image:Crescentic_glomerulonephritis_%282%29.jpg|thumb|center|150px|Crescentic GN (WC)]]
 |-
 |Tubular injury
@@ Line 487: / Line 506: @@
 | normal light microscopy
 | [[acute tubular necrosis]], [[chronic allograft nephropathy]]
-| [http://commons.wikimedia.org/wiki/File:Chronic_allograft_nephropathy_-_intermed_mag.jpg (WC)]
+| [[Image:Chronic_allograft_nephropathy_-_intermed_mag.jpg|thumb|center|150px|CAN (WC)]]
 |-
 |Small vessel pathology
@@ Line 494: / Line 513: @@
 | none
 | [[thrombotic microangiopathy]] (malignant hypertension, [[scleroderma]] renal crisis, DIC, HUS, TTP,
-| [http://commons.wikimedia.org/wiki/File:Renal_arterial_hyalinosis_-_pas_-_very_high_mag.jpg hyalinosis (WC)], [http://commons.wikimedia.org/wiki/File:Thrombotic_microangiopathy_-_very_high_mag.jpg TMA (WC)]
+| [[Image:Renal_arterial_hyalinosis_-_pas_-_very_high_mag.jpg |thumb|center|150px| Hyalinosis (WC)]] [[Image:Thrombotic_microangiopathy_-_very_high_mag.jpg|thumb|center|150px| TMA (WC)]]
 |-
 |Large vessel pathology
@@ Line 501: / Line 520: @@
 | none
 | [[atherosclerosis]], [[cholesterol embolism]], other types of embolism, [[thrombosis]]
-| [http://commons.wikimedia.org/wiki/File:Cholesterol_embolus_-_intermed_mag.jpg (WC)]
+| [[Image:Cholesterol_embolus_-_intermed_mag.jpg |thumb|center|150px| Cholesterol embolus (WC)]]
 |- <!--
 | Pattern
@@ Line 526: / Line 545: @@
 | GBM thickening, both afferent and efferent arteriole hyalinized
 | EM?
-| nephrotic (???)
+| proteinuria - typical presentation, nephrotic syndrome{{fact}}
 | [[diabetes mellitus]] (DM)
 | [[amyloidosis]], [[idiopathic nodular glomerulosclerosis]] (nodular GS without DM)
-| [http://commons.wikimedia.org/wiki/File:Nodular_glomerulosclerosis.jpeg (WC)]
+| [[Image:Nodular_glomerulosclerosis.jpeg|thumb|center|150px|Nodular GS (WC)]]
 |-
 |[[Focal segmental glomerulosclerosis]] (FSGS)
@@ Line 538: / Line 557: @@
 | primary FSGS, secondary FSGS ([[HIV]], [[IVDU]], obesity, [[parvovirus B19]], [[Alport syndrome]]); unresponsive to steroids, worse prognosis than MCD
 | [[minimal change disease]]
-| [http://commons.wikimedia.org/wiki/File:Focal_segmental_glomerulosclerosis_-_high_mag.jpg (WC)]
+| [[Image:Focal_segmental_glomerulosclerosis_-_high_mag.jpg|thumb|center|150px|FSGS (WC)]]
 |-
 |[[Membranous nephropathy]]<br>(AKA membranous GN)
@@ Line 547: / Line 566: @@
 | [[hepatitis B]], [[hepatitis C]], carcinoma, NSAID toxicity, SLE, idiopathic
 | Nodular glomerulosclerosis (?)
-| [http://www.flickr.com/photos/jian-hua_qiao_md/3989875091/in/set-72157622411941607 silver stain (flickr.com)]
+| [[Image:Membranous_nephropathy_-_mpas_-_very_high_mag.jpg|thumb|center|150px|MN (WC)]]
 |-
 |[[Minimal change disease]] (MCD)
@@ Line 565: / Line 584: @@
 | primary vs. secondary (Henoch-Schoenlein purpura)
 | [[RPGN]]
-| [http://commons.wikimedia.org/wiki/File:Henoch-Sch%C3%B6nlein_nephritis_IgA_immunostaining.jpg (WC)]
+| [[Image:Henoch-Sch%C3%B6nlein_nephritis_IgA_immunostaining.jpg|thumb|center|150px|HSN - IgA IHC (WC)]]
 |-
 |[[Membranoproliferative glomerulonephritis]] (MPGN)
@@ Line 572: / Line 591: @@
 | subepithelial deposits
 | mixed nephrotic/nephritic
-| [[SLE]], cryoglobulinemia, [[hepatitis B]], [[hepatitis C]]
+| [[SLE]], [[cryoglobulinemia]], [[hepatitis B]], [[hepatitis C]]
 | Pathol. DDx?
-| [http://commons.wikimedia.org/wiki/File:Membranoproliferative_glomerulonephritis_-_very_high_mag.jpg (WC)]
+| [[Image:Membranoproliferative_glomerulonephritis_-_very_high_mag.jpg|thumb|center|MPGN (WC)]]
 |-
 |[[Focal proliferative glomerosclerosis|Focal proliferative<br> glomerosclerosis]] (FPGS)
@@ Line 615: / Line 634: @@
 ===Diffuse proliferative glomerulonephritis===
 {| class="wikitable sortable" style="margin-left:auto;margin-right:auto"
-| '''Pattern'''
+! Pattern
-| '''Key feature'''
+! Key feature
-| '''Clinical'''
+! Clinical
 |-
 | [[Post-infectious glomerulonephritis]]
@@ Line 624: / Line 643: @@
 |-
 | [[Membranoproliferative glomerulonephritis]] (MPGN)
-|
+| mesangial proliferation with thickening of the glomerular capillary loops<ref name=pmid11682680>{{Cite journal  | last1 = Smet | first1 = AD. | last2 = Kuypers | first2 = D. | last3 = Evenepoel | first3 = P. | last4 = Maes | first4 = B. | last5 = Messiaen | first5 = T. | last6 = Van Damme | first6 = B. | last7 = Vanrenterghem | first7 = Y. | title = 'Full house' positive immunohistochemical membranoproliferative glomerulonephritis in a patient with portosystemic shunt. | journal = Nephrol Dial Transplant | volume = 16 | issue = 11 | pages = 2258-62 | month = Nov | year = 2001 | doi =  | PMID = 11682680 | URL = http://ndt.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=11682680 }}</ref>
 | low C3, normal C4; primary vs. secondary (often hepatitis C)
 |-
@@ Line 650: / Line 670: @@
 *Due to [[diabetes mellitus]] - '''key feature'''.
 **If there is no history of diabetes... it is ''[[idiopathic nodular glomerulosclerosis]]''.
-*Most common cause of end stage renal disease (ESRD).
+*Most common cause of [[end-stage renal disease]] (ESRD).
 *Biopsied only if the (clinical) features are atypical.
@@ Line 660: / Line 680: @@
 Others:
-*Armanni-Ebstein change = cytoplasmic vacuolization of tubular cells (usu. loop of Henle) -- innermost cortex, outer medulla;<ref name=pmid13478656>{{cite journal |author=RITCHIE S, WAUGH D |title=The pathology of Armanni-Ebstein diabetic nephropathy |journal=Am. J. Pathol. |volume=33 |issue=6 |pages=1035–57 |year=1957 |pmid=13478656 |pmc=1934668 |doi= |url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934668/?page=1}}</ref> not specific to diabetes mellitus.<ref name=pmid20875709>{{cite journal |author=Zhou C, Byard RW |title=Armanni-Ebstein phenomenon and hypothermia |journal=Forensic Sci Int |volume= |issue= |pages= |year=2010 |month=September |pmid=20875709 |doi=10.1016/j.forsciint.2010.08.018 |url=}}</ref>
+*Armanni-Ebstein change = cytoplasmic vacuolization of tubular cells (usu. loop of Henle) -- innermost cortex, outer medulla;<ref name=pmid13478656>{{cite journal |author=Ritchie S, Waugh D |title=The pathology of Armanni-Ebstein diabetic nephropathy |journal=Am. J. Pathol. |volume=33 |issue=6 |pages=1035–57 |year=1957 |pmid=13478656 |pmc=1934668 |doi= |url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934668/?page=1}}</ref> not specific to diabetes mellitus.<ref name=pmid20875709>{{cite journal |author=Zhou C, Byard RW |title=Armanni-Ebstein phenomenon and hypothermia |journal=Forensic Sci Int |volume= |issue= |pages= |year=2010 |month=September |pmid=20875709 |doi=10.1016/j.forsciint.2010.08.018 |url=}}</ref>
 *Capsular drop = hyaline material deposited in the Bowman's capsule.<ref name=ndt-edu>URL: [http://www.ndt-educational.org/ferrariodiabete.asp http://www.ndt-educational.org/ferrariodiabete.asp]. Accessed on: 29 April 2012.</ref>
 *Fibrin cap = subendothelial deposition of hyaline material.<ref name=ndt-edu/>
@@ Line 668: / Line 688: @@
 Memory device:
-*GBM = ''thick '''G'''BM'', '''''b'''oth afferent & efferent artiole thickened'', '''''m'''esangial matrix expansion''.
+*GBM = ''thick '''G'''BM'', '''''b'''oth afferent & efferent arterioles thickened'', '''''m'''esangial matrix expansion''.
-Images:
+====Images====
-*[http://commons.wikimedia.org/wiki/File:Nodular_glomerulosclerosis.jpeg Nodular glomerulosclerosis (WC)].
+<gallery>
+Image:Diabetic_glomerulosclerosis_%281%29_HE.jpg | Diabetic glomerulosclerosis. (WC/KGH)
+Image:Diabetic_glomerulosclerosis_(2)_HE.jpg | Diabetic glomerulosclerosis. (WC/KGH)
+Image:Diabetic_glomerulosclerosis_%283%29_HE.jpg | Diabetic glomerulosclerosis. (WC/KGH)
+Image:Nodular_glomerulosclerosis.jpeg | Nodular glomerulosclerosis. (WC)
+</gallery>
+www:
 *[http://library.med.utah.edu/WebPath/jpeg1/RENAL027.jpg Nodular GS (med.utah.edu)].
 *[http://www.markwickmd.com/images/pages/armani_ebstein_lesion.jpg Armanni-Ebstein lesion (markwickmd.com)].
@@ Line 734: / Line 760: @@
 **Class IV is essentially a dead kidney - doesn't get biopsied.
-Images:
+====Images====
-*[http://commons.wikimedia.org/wiki/File:SLE_Nephritis_Pathology_Diagram.svg SLE nephritis - schematic (WC)].
+<gallery>
+Image:SLE_Nephritis_Pathology_Diagram.svg| SLE nephritis - schematic. (WC)
+</gallery>
 *Membranous lupus:
 **[http://www.flickr.com/photos/jian-hua_qiao_md/3989875425/in/set-72157622411941607 H&E (flickr.com)].
@@ Line 743: / Line 771: @@
 =Nephrotic syndrome=
 {{Main|Nephrotic syndrome}}
-This includes the following:
+This classically includes the following:
 *[[Minimal change disease]].
 *[[Focal segmental glomerulosclerosis]].
 *[[Membranous nephropathy]].
+It also includes:
+*[[IgA nephropathy]].
+*Pre-eclampsia - uncommon.<ref name=pmid20033418>{{Cite journal  | last1 = Wei | first1 = Q. | last2 = Zhang | first2 = L. | last3 = Liu | first3 = X. | title = Outcome of severe preeclampsia manifested as nephrotic syndrome. | journal = Arch Gynecol Obstet | volume = 283 | issue = 2 | pages = 201-4 | month = Feb | year = 2011 | doi = 10.1007/s00404-009-1338-z | PMID = 20033418 }}</ref>
 =Mixed nephrotic and nephritic=
@@ Line 756: / Line 788: @@
 *Associated with an increased incidence of [[Celiac disease]].<ref name=pmid19332868>{{Cite journal  | last1 = Smerud | first1 = HK. | last2 = Fellström | first2 = B. | last3 = Hällgren | first3 = R. | last4 = Osagie | first4 = S. | last5 = Venge | first5 = P. | last6 = Kristjánsson | first6 = G. | title = Gluten sensitivity in patients with IgA nephropathy. | journal = Nephrol Dial Transplant | volume = 24 | issue = 8 | pages = 2476-81 | month = Aug | year = 2009 | doi = 10.1093/ndt/gfp133 | PMID = 19332868 }}</ref>
 *''IgA nephropathy'', in children, with a skin rash ([[leukocytoclastic vasculitis]]) = [[Henoch–Schönlein purpura]].
+*May present as [[nephrotic syndrome]].<ref name=pmid7849391>{{Cite journal  | last1 = Komatsuda | first1 = A. | last2 = Wakui | first2 = H. | last3 = Yasuda | first3 = T. | last4 = Imai | first4 = H. | last5 = Miura | first5 = AB. | last6 = Tsuda | first6 = A. | last7 = Nakamoto | first7 = Y. | title = Successful delivery in a pregnant women with crescentic IgA nephropathy. | journal = Intern Med | volume = 33 | issue = 11 | pages = 723-6 | month = Nov | year = 1994 | doi =  | PMID = 7849391 }}</ref><ref name=pmid22322610>{{Cite journal  | last1 = Kim | first1 = JK. | last2 = Kim | first2 = JH. | last3 = Lee | first3 = SC. | last4 = Kang | first4 = EW. | last5 = Chang | first5 = TI. | last6 = Moon | first6 = SJ. | last7 = Yoon | first7 = SY. | last8 = Yoo | first8 = TH. | last9 = Kang | first9 = SW. | title = Clinical features and outcomes of IgA nephropathy with nephrotic syndrome. | journal = Clin J Am Soc Nephrol | volume = 7 | issue = 3 | pages = 427-36 | month = Mar | year = 2012 | doi = 10.2215/CJN.04820511 | PMID = 22322610 }}</ref>
+*May present as isolated hematuria.<ref name=pmid19949735>{{Cite journal  | last1 = Kim | first1 = BS. | last2 = Kim | first2 = YK. | last3 = Shin | first3 = YS. | last4 = Kim | first4 = YO. | last5 = Song | first5 = HC. | last6 = Kim | first6 = YS. | last7 = Choi | first7 = EJ. | title = Natural history and renal pathology in patients with isolated microscopic hematuria. | journal = Korean J Intern Med | volume = 24 | issue = 4 | pages = 356-61 | month = Dec | year = 2009 | doi = 10.3904/kjim.2009.24.4.356 | PMID = 19949735 }}</ref>
 ===Microscopic===
@@ Line 765: / Line 799: @@
 *Diagnosis based on immunofluorescence (IgA+).
-Images:
+====Images====
 *[http://library.med.utah.edu/WebPath/jpeg2/RENAL096.jpg IgA nephropathy (med.utah.edu)].
 *[http://path.upmc.edu/cases/case96.html HSP (upmc.edu)].
+<gallery>
+Image:Henoch-Sch%C3%B6nlein_nephritis_IgA_immunostaining.jpg | HSP - IgA IHC (WC)
+</gallery>
 ====Scoring====
 IgA nephropathy can be scored using an assessment of '''m'''esangial proliferation, '''e'''ndocapillary proliferation, glomerulo'''s'''clerosis and '''t'''ubular atrophy and interstitial fibrosis (abbreviated ''MEST'').<ref>{{Cite journal  | last1 = Coppo | first1 = R. | last2 = Cattran | first2 = D. | last3 = Roberts Ian | first3 = SD. | last4 = Troyanov | first4 = S. | last5 = Camilla | first5 = R. | last6 = Cook | first6 = T. | last7 = Feehally | first7 = J. | title = The new Oxford Clinico-Pathological Classification of IgA nephropathy. | journal = Prilozi | volume = 31 | issue = 1 | pages = 241-8 | month = Jul | year = 2010 | doi =  | PMID = 20693944 }}</ref>
@@ Line 808: / Line 844: @@
 *[[Nodular glomerulosclerosis]].
-Images:
+====Images====
-*[http://commons.wikimedia.org/wiki/File:Membranoproliferative_glomerulonephritis_-_intermed_mag.jpg MPGN - intermed. mag. (WC)].
+<gallery>
-*[http://commons.wikimedia.org/wiki/File:Membranoproliferative_glomerulonephritis_-_very_high_mag.jpg MPGN - very high mag. (WC)].
+Image:Membranoproliferative_glomerulonephritis_-_intermed_mag.jpg | MPGN - intermed. mag. (WC/Nephron)
+Image:Membranoproliferative_glomerulonephritis_-_very_high_mag.jpg | MPGN - very high mag. (WC/Nephron)
+</gallery>
 *[http://path.upmc.edu/cases/case593.html MPGN - several images (upmc.edu)].
+===EM===
+Features:
+*Subendothelial immune deposits - classic finding.<ref name=pmid21839367>{{Cite journal  | last1 = Sethi | first1 = S. | last2 = Fervenza | first2 = FC. | title = Membranoproliferative glomerulonephritis: pathogenetic heterogeneity and proposal for a new classification. | journal = Semin Nephrol | volume = 31 | issue = 4 | pages = 341-8 | month = Jul | year = 2011 | doi = 10.1016/j.semnephrol.2011.06.005 | PMID = 21839367 }}</ref>
+*Subepithelial immune deposits - historically considered uncommon.<ref name=pmid2263028>{{Cite journal  | last1 = Sato | first1 = H. | title = [Ultrastructural study on membranoproliferative glomerulonephritis with special reference to subepithelial deposits]. | journal = Nihon Jinzo Gakkai Shi | volume = 32 | issue = 9 | pages = 973-83 | month = Sep | year = 1990 | doi =  | PMID = 2263028 }}</ref>
 ==Dense deposit disease==
@@ Line 873: / Line 916: @@
 *+/-[[Vasculitis]].
-Images:
+====Images====
-*WC - KGH:
+<gallery>
-**[http://commons.wikimedia.org/wiki/File:Crescentic_glomerulonephritis_%282%29.jpg RPGN (WC)].
+Image:Crescentic_glomerulonephritis_%282%29.jpg | RPGN (WC/KGH)
-**[http://commons.wikimedia.org/wiki/File:Crescentic_glomerulonephritis_%281%29.jpg RPGN (WC)].
+Image:Crescentic_glomerulonephritis_%281%29.jpg | RPGN (WC/KGH)
-*WC:
+Image:Crescentic_glomerulonephritis_-_intermed_mag.jpg | RPGN - intermed. mag. (WC/Nephron)
-**[http://commons.wikimedia.org/wiki/File:Crescentic_glomerulonephritis_-_intermed_mag.jpg RPGN - intermed. mag. (WC)].
+Image:Crescentic_glomerulonephritis_-_high_mag.jpg | RPGN - high mag. (WC/Nephron)
-**[http://commons.wikimedia.org/wiki/File:Crescentic_glomerulonephritis_-_high_mag.jpg RPGN - high mag. (WC)].
+</gallery>
 ==Post-infectious glomerulonephritis==
 *Abbreviated ''PIGN''.
-===General===
+{{Main|Post-infectious glomerulonephritis}}
-*Classically post-streptococcal infection.
-**Lab test: Antistreptolysin O titer (ASOT) +ve.
-===Microscopic===
-Features:
-*+/-Neutrophils - in glomerulus.
-*[[Glomerular crescents]].
-Images:
-*[[WC]]:
-**[http://commons.wikimedia.org/wiki/File:Post-infectious_glomerulonephritis_-_high_mag.jpg Post-infectious GN - high mag. (WC)].
-**[http://commons.wikimedia.org/wiki/File:Post-infectious_glomerulonephritis_-_very_high_mag.jpg Post-infectious GN - very high mag. (WC)].
-**[http://commons.wikimedia.org/wiki/File:Acute_Glomerulonephritis_Pathology_Diagram.svg Post-infectious GN - schematic (WC)].
-*www:
-**[http://path.upmc.edu/cases/case671.html Post-infectious glomerulonephritis - several images (upmc.edu)].
-===IF===
-*Granular immune deposits.
-===EM===
-*Subepithelial deposits - hump-like.
-**Larger when measured perpendicular to the basement membrane, if compared to [[membranous nephropathy]].
-**Typically focal.
 =Rare diseases=
@@ Line 918: / Line 937: @@
 **Associated with a specific HLA type (HLA-DRB1*1501) and two gene families.
 **Antibodies directed against COL4A3,<ref>{{OMIM|120070}}</ref> which is ''not'' mutated.
+*Oligouria - poor prognosticator.{{fact}}
 Tx:
@@ Line 931: / Line 951: @@
 **Crescentic glomerulonephritis.
-Images:
+====Images====
-*[[WC]]:
+<gallery>
-**[http://commons.wikimedia.org/wiki/File:Crescentic_glomerulonephritis_-_intermed_mag.jpg RPGN - intermed. mag. (WC)].
+Image:Crescentic_glomerulonephritis_-_intermed_mag.jpg | RPGN - intermed. mag. (WC/Nephron)
-**[http://commons.wikimedia.org/wiki/File:Crescentic_glomerulonephritis_-_high_mag.jpg RPGN - high mag. (WC)].
+Image:Crescentic_glomerulonephritis_-_high_mag.jpg | RPGN - high mag. (WC/Nephron)
-*www:
+</gallery>
-**[http://path.upmc.edu/cases/case541.html AGBM disease - several images (upmc.edu)].
+www:
+*[http://path.upmc.edu/cases/case541.html AGBM disease - several images (upmc.edu)].
 ===IF===
 *Linear IgG deposits - '''diagnostic'''.
+*Fibrinogen in crescents.
 DDx:
@@ Line 987: / Line 1,009: @@
 ===Microscopic===
 Features:<ref name=pmid9727383/>
-*Normal.
+*Usu. normal.
+*+/-Foamy appearing renal tubular cells.<ref name=Ref_Klatt246>{{Ref Klatt|246}}</ref>
 ===IF===
@@ Line 1,016: / Line 1,039: @@
 ==Fabry disease==
-===General===
+{{Main|Fabry disease}}
-*Rare X-linked genetic disease.
-**Caused by defect in ''alpha-galactosidase A gene'' (''GLA gene'').<ref name=omim301500>{{OMIM|301500}}</ref>
-**Women partially affected
-*[[Lysosomal storage disorder]] - 2nd in prevalence only to [[Gaucher disease]].
-*Multisystem disease affecting small vessels and [[kidney]].
-====Presentation====
-*Women: usually proteinuria.
-*Men: [[angiokeratoma]]s, proteinuria.
-====Tx====
-*Symptomatic treatment.
-*Enzyme replacement - ''agalsidase alpha'' (Replagal) or ''agalsidase beta'' (Fabrazyme).
-===Microscopic===
-Features:<ref name=pmid16799480>{{cite journal |author=Fischer EG, Moore MJ, Lager DJ |title=Fabry disease: a morphologic study of 11 cases |journal=Mod. Pathol. |volume=19 |issue=10 |pages=1295-301 |year=2006 |month=October |pmid=16799480 |doi=10.1038/modpathol.3800634 |url=http://www.nature.com/modpathol/journal/v19/n10/abs/3800634a.html}}</ref>
-*Foamy podocyte inclusions, best visualized with ''[[toluidine blue]]''.
-*Mild mesangial hypercellularity.
-Images:
-*[http://path.upmc.edu/cases/case137/micro.html Fabry disease (upmc.edu)].
-*[http://path.upmc.edu/cases/case610.html Fabry disease - several images (upmc.edu)].
-===EM===
-Features:<ref name=pmid16799480/>
-*Myelin-like inclusions.
-**Concentric bodies with an onion-skin-like appearance.
-*Zebra bodies.
-**Ovoid inclusions with striped pattern.
-Note:
-*Myelin-like inclusion are not [http://en.wikipedia.org/wiki/Pathognomonic pathognomonic] for Fabry disease; they may result from drug use:<ref name=pmid16799480/>
-**Amiodarone.
-**Aminoglycosides.
-**Chloroquine.
 ==Myeloma==
@@ Line 1,069: / Line 1,057: @@
 **Macrophages (CD68 +ve).
-Images:
+=====Images=====
-*www:
+www:
-**[http://www.kidneypathology.com/Imagenes/Amiloidosis%20y/MM.3.w.jpg Cast nephropathy in myeloma (kidneypathology.com)].
+*[http://www.kidneypathology.com/Imagenes/Amiloidosis%20y/MM.3.w.jpg Cast nephropathy in myeloma (kidneypathology.com)].
-**[http://www.kidneypathology.com/Imagenes/Amiloidosis%20y/MM.5.w.jpg Cast nephropathy in myeloma - refractile crap (kidneypathology.com)].
+*[http://www.kidneypathology.com/Imagenes/Amiloidosis%20y/MM.5.w.jpg Cast nephropathy in myeloma - refractile crap (kidneypathology.com)].
-*[[WC]]:
+<gallery>
-**[http://commons.wikimedia.org/wiki/File:Cast_nephropathy_-_high_mag.jpg Myeloma cast nephropathy - high mag. (WC)].
+Image:Cast_nephropathy_-_high_mag.jpg | Myeloma cast nephropathy - high mag. (WC/Nephron)
-**[http://commons.wikimedia.org/wiki/File:Cast_nephropathy_-_2_cropped_-_very_high_mag.jpg Myeloma cast nephropathy - cropped - very high mag. (WC)].
+Image:Cast_nephropathy_-_2_cropped_-_very_high_mag.jpg | Myeloma cast nephropathy - cropped - very high mag. (WC/Nephron)
+</gallery>
 ====Stains====
 *Myeloma casts = PAS -ve.
@@ Line 1,096: / Line 1,084: @@
 Presentation:
-*Nephrotic range proteinuria ~ 60% of cases.<ref>{{Cite journal  | last1 = Korbet | first1 = SM. | last2 = Schwartz | first2 = MM. | last3 = Lewis | first3 = EJ. | title = Immunotactoid glomerulopathy. | journal = Am J Kidney Dis | volume = 17 | issue = 3 | pages = 247-57 | month = Mar | year = 1991 | doi =  | PMID = 1996564 }}</ref>
+*Nephrotic range proteinuria ~ 60% of cases.<ref name=pmid1996564>{{Cite journal  | last1 = Korbet | first1 = SM. | last2 = Schwartz | first2 = MM. | last3 = Lewis | first3 = EJ. | title = Immunotactoid glomerulopathy. | journal = Am J Kidney Dis | volume = 17 | issue = 3 | pages = 247-57 | month = Mar | year = 1991 | doi =  | PMID = 1996564 }}</ref>
 *[[Hypertension]].
@@ Line 1,112: / Line 1,100: @@
 *[[AKA]] ''fibrillary glomerulopathy''.
 ===General===
-*Rare ~ 1% native kidney biopsies.<ref name=pmid18045849>{{Cite journal  | last1 = Alpers | first1 = CE. | last2 = Kowalewska | first2 = J. | title = Fibrillary glomerulonephritis and immunotactoid glomerulopathy. | journal = J Am Soc Nephrol | volume = 19 | issue = 1 | pages = 34-7 | month = Jan | year = 2008 | doi = 10.1681/ASN.2007070757 | PMID = 18045849 | URL = http://jasn.asnjournals.org/content/19/1/34.long }}</ref>
+*Rare ~ 1% native kidney biopsies.<ref name=pmid18045849>{{Cite journal  | last1 = Alpers | first1 = CE. | last2 = Kowalewska | first2 = J. | title = Fibrillary glomerulonephritis and immunotactoid glomerulopathy. | journal = J Am Soc Nephrol | volume = 19 | issue = 1 | pages = 34-7 | month = Jan | year = 2008 | doi = 10.1681/ASN.2007070757 | PMID = 18045849 | URL = http://jasn.asnjournals.org/content/19/1/34.full }}</ref>
 *Presents as [[nephrotic syndrome]].
 *Prognosis poor; large number progress to ESRD.
@@ Line 1,140: / Line 1,128: @@
 Note:
-*[[Amyloid]] between 8 and 15 nm (diameter), most often 8-12 nm.<ref name=pmid18045849>{{Cite journal  | last1 = Alpers | first1 = CE. | last2 = Kowalewska | first2 = J. | title = Fibrillary glomerulonephritis and immunotactoid glomerulopathy. | journal = J Am Soc Nephrol | volume = 19 | issue = 1 | pages = 34-7 | month = Jan | year = 2008 | doi = 10.1681/ASN.2007070757 | PMID = 18045849 | URL = http://jasn.asnjournals.org/content/19/1/34.long }}</ref>
+*[[Amyloid]] between 8 and 15 nm (diameter), most often 8-12 nm.<ref name=pmid18045849>{{Cite journal  | last1 = Alpers | first1 = CE. | last2 = Kowalewska | first2 = J. | title = Fibrillary glomerulonephritis and immunotactoid glomerulopathy. | journal = J Am Soc Nephrol | volume = 19 | issue = 1 | pages = 34-7 | month = Jan | year = 2008 | doi = 10.1681/ASN.2007070757 | PMID = 18045849 | URL = http://jasn.asnjournals.org/content/19/1/34.full }}</ref>
 ==Aristolochic acid nephropathy==
@@ Line 1,170: / Line 1,158: @@
 {{Main|Cystic kidney diseases}}
 These are discussed in a separate article and include:
-*Autosomal dominant polycystic kidney disease (ADPKD).
+*[[Autosomal dominant polycystic kidney disease]] (ADPKD).
 *Adult-onset medullary cystic disease.
-*Acquired renal cystic disease.
+*[[Acquired renal cystic disease]].
-*Autosomal recessive polycystic kidney disease (ARPKD).
+*[[Autosomal recessive polycystic kidney disease]] (ARPKD).
 *Medullary sponge kidney.
 *Nephronophthisis.
@@ Line 1,190: / Line 1,178: @@
 *[[AKA]] ''diffuse suppurative nephritis''.
 ===General===
-*Typically preceeded by a (lower) urinary tract infection (UTI).
+*Typically preceeded by a (lower) [[urinary tract infection]] (UTI).
 *Usually diagnosed clinically:
 **Urine C&S, urine R&M, +/-CT abdomen.
@@ Line 1,201: / Line 1,189: @@
 ===Microscopic===
 Features:
-*Neutrophils within the renal tubules and interstitum.<ref name=Ref_Sternberg5_1726>{{Ref Sternberg5|1726}}</ref>
+*[[Neutrophil]]s within the renal tubules and interstitium.<ref name=Ref_Sternberg5_1726>{{Ref Sternberg5|1726}}</ref>
+====Images====
+<gallery>
+Image:Acute_pyelonephritis_-_intermed_mag.jpg | Acute pyelonephritis - intermed. mag. (WC/Nephron)
+Image:Acute_pyelonephritis_-_2_-_high_mag.jpg | Acute pyelonephritis - high mag. (WC/Nephron)
+Image:Acute_pyelonephritis_-_2_-_very_high_mag.jpg | Acute pyelonephritis - very high mag. (WC/Nephron)
+</gallery>
 ==Chronic pyelonephritis==
 *''Reflux nephropathy'' is considered synonym in some sources.<ref name=Ref_Sternberg5_1728>{{Ref Sternberg5|1728}}</ref>
 ===General===
+*Inflammation of the kidney (''nephritis'') and renal pelvis (''pyelo-''<ref>URL: [http://medical-dictionary.thefreedictionary.com/pyelo- http://medical-dictionary.thefreedictionary.com/pyelo-]. Accessed on: 5 June 2015.</ref>).
 *May be associated with vesicoureteral reflux.
-*Chronic pyelonephritis may be a reason for nephrectomy.<ref>URL: [https://secure.health.utas.edu.au/intranet/cds/pathprac/Files/Cases/Renal/Case44/Case44.htm https://secure.health.utas.edu.au/intranet/cds/pathprac/Files/Cases/Renal/Case44/Case44.htm]. Accessed on: 26 July 2011.</ref>
+*Chronic [[pyelonephritis]] may be a reason for nephrectomy.<ref>URL: [https://secure.health.utas.edu.au/intranet/cds/pathprac/Files/Cases/Renal/Case44/Case44.htm https://secure.health.utas.edu.au/intranet/cds/pathprac/Files/Cases/Renal/Case44/Case44.htm]. Accessed on: 26 July 2011.</ref>
 ===Gross===
@@ Line 1,219: / Line 1,214: @@
 *Interstitial fibrosis.
 *+/-Renal casts (PAS positive); may result in a thyroid-like apparance.
+DDx:
+*[[End-stage kidney]].
+*[[Myeloma cast nephropathy]].
 ===Stains===
@@ Line 1,225: / Line 1,224: @@
 =Disease that does not commonly get biopsied=
 ==End-stage kidney==
-===General===
+{{Main|End-stage kidney}}
-*Many end-stage renal disease (ESRD) kidneys have a similar appearance.
-**Notable exception: polycystic kidney diseases have distinctive appearance, e.g. [[ADPKD]].
-===Gross===
-*Small kidneys.
-*Thinned renal cortex.
-*+/-Dilated renal calyces.
-*+/-Cysts.
-Note:
-*Normal kidneys are ~11 cm from pole-to-pole.<ref name=pmid20030823>{{Cite journal  | last1 = Glodny | first1 = B. | last2 = Unterholzner | first2 = V. | last3 = Taferner | first3 = B. | last4 = Hofmann | first4 = KJ. | last5 = Rehder | first5 = P. | last6 = Strasak | first6 = A. | last7 = Petersen | first7 = J. | title = Normal kidney size and its influencing factors - a 64-slice MDCT study of 1.040 asymptomatic patients. | journal = BMC Urol | volume = 9 | issue =  | pages = 19 | month =  | year = 2009 | doi = 10.1186/1471-2490-9-19 | PMID = 20030823 | URL = http://www.biomedcentral.com/1471-2490/9/19 }}</ref>
-===Microscopic===
-Features:
-*Global sclerosis of the glomeruli.
-*Interstitial fibrosis.
-*+/-Thyroidization - colloid-like hyaline cast formation that impart an appearance that mimics the [[thyroid gland]]:<ref name=pmid19594588>{{Cite journal  | last1 = Ito | first1 = S. | last2 = Kobayashi | first2 = A. | last3 = Tsuchiya | first3 = T. | last4 = Moriyama | first4 = Y. | last5 = Kikuchi | first5 = M. | last6 = Deguchi | first6 = T. | last7 = Yamaguchi | first7 = Y. | title = Thyroidization in renal allografts. | journal = Clin Transplant | volume = 23 Suppl 20 | issue =  | pages = 6-9 | month = Aug | year = 2009 | doi = 10.1111/j.1399-0012.2009.01001.x | PMID = 19594588 }}</ref>
-**Typical of [[chronic pyelonephritis]] and obstructive nephropathy.
-Image:
-*[http://library.med.utah.edu/WebPath/RENAHTML/RENAL108.html Thyroidization of the kidney (utah.edu)].
 ==Malignant hypertension==
@@ Line 1,256: / Line 1,234: @@
 *Often abbreviated ''ATN''.
 ===General===
-*Best diagnosed clinically (using urine R&M) - hemegranular casts are diagnostic.
+Diagnosed clinically:
+*Using urine R&M - hemegranular casts<ref name=pmid19921458>{{Cite journal  | last1 = Kanbay | first1 = M. | last2 = Kasapoglu | first2 = B. | last3 = Perazella | first3 = MA. | title = Acute tubular necrosis and pre-renal acute kidney injury: utility of urine microscopy in their evaluation- a systematic review. | journal = Int Urol Nephrol | volume = 42 | issue = 2 | pages = 425-33 | month = Jun | year = 2010 | doi = 10.1007/s11255-009-9673-3 | PMID = 19921458 }}</ref> are diagnostic.
+*Anuria or low urine output.
+===Gross===
+*Poorly defined corticomedullary junction - soft finding.
+*Slightly heavier ~ 180 grams.<ref name=pmid19207286/>
 ===Microscopic===
-Features:<ref>PS. April 2009.</ref>
+Features:<ref name=pmid19207286>{{Cite journal  | last1 = Kocovski | first1 = L. | last2 = Duflou | first2 = J. | title = Can renal acute tubular necrosis be differentiated from autolysis at autopsy? | journal = J Forensic Sci | volume = 54 | issue = 2 | pages = 439-42 | month = Mar | year = 2009 | doi = 10.1111/j.1556-4029.2008.00956.x | PMID = 19207286 }}</ref>
-*Hemegranular casts in the lumen.
+*Tubular epithelial whorls - present in approx. one third of cases - '''most important'''.
-*Regenerative activity.
+**Detached epithelium within the luminal space surrounded by epithelium.
-**Mitoses - '''diagnositic''' but uncommon.
+***Similar to ''epithelial telescoping'' seen in endometrial biopsies.
+*Tubulorrhexis - present in approx. one third of cases.
+**Disruption of the tubular basement membrane.
+*Interstitial edema - sensitive... but not specific.
+Notes - not particularily useful findings:
+*Mitoses.
+*Casts in tubules.
 ===IHC===
-*Ki-67 - focal nuclear staining of the tubular epithelium.
+*Ki-67 - focal nuclear staining of the tubular epithelium.<ref name=pmid19207286/>
 ==Hepatorenal syndrome==
@@ Line 1,324: / Line 1,315: @@
 *[http://www.fondazionedamico.org/biopsiarenale_atlas/seco/crio/crio.htm Cryoglobulinemic nephritis (fondazionedamico.org)].
-[[Category: Genitourinary pathology]]
+[[Category: Medical kidney pathology]]

Difference between revisions of "Medical kidney diseases"

Latest revision as of 03:21, 22 February 2017

Clinical

Creatinine

Glomerular filtration rate

Urine protein to creatinine ratio

Complement

ANCA

C4d

Other blood work

Renal ultrasound

Urine dip

Urine crystals

Clinical presentations

Nephrotic syndrome

Nephritic syndrome

Mixed

Clinical DDx

Renal failure 101

Renal causes

Isolated hematuria

Proteinuria

Nephritic syndrome

Rapidly progressive glomerulonephritis

Nephrotic syndrome

Mixed presentation

Normal kidney

Cells of the glomerulus

Epithelium

Glomerulus

Glomerular basement membrane

Images

Basic approach to renal biopsy

Basic components

Glomeruli

Components of the glomeruli (anatomical)

Obsolete glomeruli

Glomerular disease terms

Vessels

Arteriolar hyalinosis

Image

Atherosclerosis

Tubules

Interstitium

Important terms/process related

Staining

Immunofluorescence

Negative immunofluorescence

Positive immunofluorescence

Immune complex-related disease

Pathologic differential diagnosis

Tram-tracking of BM

Mesangial hypercellularity

Mesangial expansion

Glomerular crescents

General

Microscopic

Bland necrotic crescents

Primary light microscopy patterns

Diagnoses - Table

Diffuse proliferative glomerulonephritis

Common diseases

Diabetic nephropathy

General

Microscopic

Images

Grading

IF

EM

Lupus nephritis

General

Immunofluorescence

Classification

Images

Nephrotic syndrome

Mixed nephrotic and nephritic

IgA nephropathy

General

Microscopic

Images