Download - Glomerulus in health & diseases
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Anannya ghoshRitasman BaisyaShinjan Patra
Chirantan Mandal
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Medical College &Hospital Bengal88 college street,
KolkataWest Bengal
India
Anannya ghoshRitasman BaisyaShinjan Patra
Chirantan Mandal
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Glomerular anatomy Glomerular physiology Glomerular pathology
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Anannya ghosh
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About 70-80% of renal diseases are of glomerular origin.
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Stuctural & functional unit of kidney. Parts—1.renal corpuscle 2.renal tubule
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Bowman’s capsule Glomerulus The average diameter of the glomerulus
is approximately 200 mm in the human kidney
The average glomerular volume has been reported to be 3 to 7 million mm3 in humans
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composed of a capillary network lined by a thin layer of endothelial cells
a central region of mesangial cells with surrounding mesangial matrix material;
the visceral epithelial cells and the associated basement membrane;
and the parietal layer of Bowman's capsule with its basement membrane.
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Between the two epithelial layers
is a narrow cavity called
Bowman's space,
or the urinary space.
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The glomerulus is responsible for the production of an ultrafiltrate of plasma.
protein free filtrate.
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a fenestrated endothelium, the peripheral glomerular basement
membrane (GBM), the slit pores between the foot processes
of the visceral epithelial cells.
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The mean area of filtration surface per glomerulus has been reported to be 0.203 mm2 in the human kidney.
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Structure of the Glomerular Microcirculation
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The glomerular capillaries are lined by a thin fenestrated endothelium ,
pores or fenestrae, in the human kidney range from 70 nm to 100 nm in diameter .
The endothelial cell nucleus usually lies adjacent to the mesangium, away from the urinary space.
Nonfenestrated, ridge-like structures termed cytofolds are found near the cell borders.
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Afferent arterioles lose their internal elastic layer and smooth muscle cell layer prior to entering the glomerular tuft.Efferent arterioles may acquire a smooth muscle cell layer .Smooth muscle cells are replaced by granular cells that are in close contact with the extraglomerular mesangiumThe efferent arteriole is also in close contact with the glomerular mesangium as it forms inside the tuft and with the extraglomerular mesangium as it exits the tuft.
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Negetively charged
the presence of a surface coat or glycocalyx rich in polyanionic glycosaminoglycans and glycoproteins synthesized by the endothelial cells
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Synthesis of NO endothelium-derived relaxing factor,
Presence of eNOS
endothelin-1, a vasoconstrictor
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Synthesis ---glomerular visceral epithelial cells
an important regulator of microvascular permeability.
endothelial cell survival repair in glomerular dis-eases due to
endothelial cell damage
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Slit diaphragm
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The visceral epithelial cells, also called podocytes, are the largest cells in the glomerulus . long cytoplasmic processes or trabeculae, that extend from the main cell body and divide into individual foot processes, or pedicels.
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SLIT DIAPHARGM In the normal
glomerulus, the distance between adjacent foot processes near the GBM varies from 25 nm to 60 nm
. (SLIT PORE)
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Slit diaphragm Zo-1& podocin
protein stitches the slit diaphragm to the foot processes.
Actin & actinin stabilises the diaphargm in the pore.
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Slit diaphargm main protein ---
nephrin other proteins
(CD2AP)P cadherinNEPH-1
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The mesangial cells and their surrounding matrix material constitute the mesangium, separated from the capillary lumen by the endothelium .
Mesangial cells possess an extensive array of microfilaments ( actin, α-actinin, and myosin)
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A glomerular basement membrane (GBM) with a thick electron-dense central layer, the lamina densa, and thinner electron-lucent peripheral layers, the lamina rara interna and lamina rara externa.
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functions as a sieve or filter that allows the passage of small molecules but almost completely restricts the passage of molecules the size of albumin or larger
Ultrastructural tracer studies have provided evidence that the GBM constitutes both a size-selective and a charge-selective barrier
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◦ The parietal epithelium, which forms the outer wall of Bowman's capsule, is continuous with the visceral epithe-lium at the vascular pole
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Glomerular Physiology
RITASMAN BAISYA
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The First Step in Urine Formation
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GLOMERULAR FILTRATION
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Filtration of large amount of fluid through the glomerular capillaries into Bowman’s Capsule which is essentially protein free and devoid of cellular elements including red blood cells.
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In normal adults the GFR ranges from 90 to 140 mL/min in males and 80 to 125 mL/min in females.
Thus in 24 hours as much as 180 L of plasma is filtered by the glomeruli.
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The glomerular filtration barriers determines the composition of plasma ultrafiltrate.
Despite of having three layers, this filtration barrier filtes several hundred times as much water an d solutes as the usual capillary membrane.
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Fenestration(70 to 90 nm)
Slit pore 25 nm
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Effect of Size and Electric charge on GFR
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Filterability of Solute is inversely related to their size.Substance MW Filterability
Water 18 1
Sodium 23 1
Glucose 180 1
Albumin 69000 0.005
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the filtration barrier is freely permeable to water and crystalloids, MW £ 30,000
however, is virtually impermeable to colloids
small quantities, mainly of albumin escape at the rate 50 mg/L
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The negatively charged large molecules are filtered less easily than positively charged molecules of equal molecular size.
In minimum change nephropathy the negative charges on basement membrane are lost even before noticeable changes in kidney, histology resulting in albuminuria.
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Effect of Net Filtration Pressure -
The Starling Forces
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Ultrafiltration occurs because the Starling Forces drive fluid across the filtration barriers.
Algebraic sum of hydrostatic and colloidal osmotic forces across glomerular membrane gives the Net Filtration Pressure.
This is the principle of Starling’s Forces.
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GFR = Kf [(PGC – PB) – (πGC – πB)]
Under Normal condition the πB is considered to be zero.
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PB
NFP
PB -
NFP
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GFR is also dependent on hydraulic H2O permeability and surface area (SA)
GFR = hydraulic permeability x SA x NFP the first two combined to give the
filtration coefficient (Kf) GFR = Kf x NFP
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Kf = GFR/NFP = 125/10 or 12.5 ml/min/mm Hg
In chronic uncontrolled hypertension and diabetes mellitus Kf is decreased by -
i.Decreased no. of glomerular cappillaries leading to decreased surface area.ii.Increased thickness of glomerular capillary membrane leading to decreased permeability.
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Kf can be altered by the Messengial Cells. With contraction of these cells producing decreasing Kf, i.e., largely due to reduction of surface area of filtration.
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Agents influcing Messengial cells:
1.Contraction : Endothelins, Angiotensin-II, Vasopressin, Norepinephrine. PAF, PDGF, etc.2.Relaxation : ANP, Dopamine, PGE2, cAMP, etc.
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FILTRATION FRACTIONThe fraction of renal plasma flow that is filtered. FF = GFR/ Renal Plasma Flow.
The value of FF averages about 0.2.
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Increase PB , decrease GFR.
Precipitation of Calcium or Uric acid (stones) in urinary tract leads to increased PB.
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Increase πGC , decrease GFR.
Two factors determine πGC :
Arterial plasma colloidal OP The Filtration Fraction,
higher the FF higher the πGC, less the GFR.
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Increase PGC, increase GFR.
Factors determining PGC
i.Arterial Pressure ii.Increase afferent arterial resistance, decrease GFR, vice versa.iii.Efferent Arterial resistance.
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Constriction of efferent arteriole.
PGC increase
If within normal limit.
FF increase
If severe.
RPF decrease
GFR decrease.
πGC increaseGFR slightly increase.
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Angiotensin II constricts Efferent arteriole leading to increase PGC which maintains GFR.
Due to Efferent arteriole constriction by Angiotensin II, renal blood flow is decreased, so flow through peritubular capillaries is decreased leading to sodium and water reabsorption.
NO causes renal vasodilatation, GFR is increased.
Postaglandins, Bradykinin cause increase GFR.
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Strong activationof the renal sympathetic nerves can constrict the renal arterioles and decrease renal blood flow.
The renal sympathetic nerves seem to be most important in reducing GFR during severe, acute disturbances lasting for a few minutes to a few hours,such as those elicited by the defense reaction, brain ischemia, or severe hemorrhage.
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Membrane size , pores, charge Particle size, shape, electrostatic charge Filtering forces Amount of blood flow Autoregulation Mesangial cells Sympathetic nerves.
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Glomerulonephritis
shinjan patra
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Primary GlomerulonephropathiesAcute diffuse proliferative glomerulonephritis Poststreptococcal Non-poststreptococcalRapidly progressive (crescentic) glomerulonephritisChronic glomerulonephritis
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Membranous glomerulopathyMinimal change disease
Focal segmental glomerulosclerosis Membranoproliferative
glomerulonephritis IgA nephropathy
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Systemic lupus erythematosusDiabetes mellitus
Amyloidosis Goodpasture syndrome Microscopic polyarteritis/polyangiitis Wegener granulomatosis Henoch-Schönlein purpura Bacterial endocarditis
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◦ Hereditary Disorders◦ Alport syndrome◦ Thin basement membrane disease◦ Fabry disease
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In situ immune complex deposition
Antibodies against fixed intrinsic tissue antigens.
Antibody against planted antigens Circulating Immune Complex
Deposition
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HypercellularityBasement Membrane Thickening.
Hyalinization and Sclerosis.
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Nephritic syndrome ( HEMATURIA)
Morphology. ---1. enlarged, hypercellular glomeruli
2. interstitial edema and inflammation
3.hump appearance
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It is called rapid because of early clinical signs.
glomeruli may show focal necrosis, diffuse or focal endothelial proliferation, and mesangial proliferation
crescents Fibrin strands are prominent between
the cellular layers in the crescents
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The principal lesion is in the visceral epithelial cells, which show a uniform and diffuse effacement of foot processes
The cells of the proximal tubules are often laden with lipid and protein, reflecting tubular reabsorption of lipoproteins passing through diseased glomeruli (thus, the historical term lipoid nephrosis
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Massive proteinuria>3.5 g daily
Hypoalbuminemia
Edema
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END STAGE OF ALL GLOMERULAR DISEASES.
thinned cortex Obliteration of glomeruli Atrophy of tubules
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Glomerular changes Capillary Basement Membrane
Thickening Diffuse Mesangial Sclerosis Nodular Glomerulosclerosis
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Chirantan Mandal
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Focal Segmental Glomerulosclerosis
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HIV also affects glomerular and tubular cells
Resembles that of the collapsing variant of FSGS
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diffuse thickening of the glomerular capillary wall due to the accumulation of Ig deposits
along the subepithelial side of the GBM
thickened GBM producing “duplication”,as if formation of a new basement Membrame
above the existing 1
Membranous Nephropathy
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proliferation of mesangium, capillary loops & glomerular cells (mesangiocapillary
glomerulonephritis)
two major types: Type 1 Type 2 (dense deposits)
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Renal Amyloidosis
Lupus Nephritis
Diabetic Nephropathy
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Renal amyloidosis Deposits thickenings of the mesangial
matrix and along the basement membranes cause capillary narrowing and distortion of the glomerular vascular tuft.
obliterate the glomerulus and capillary lumens completely
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immune complex deposition in the glomeruli, peritubular capillary basement membranes due to
antibodies
Lupus Nephritis
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ClassClass Features Features
Class IClass I Normal looking glomeruliNormal looking glomeruli
Class IIClass II Mesangial expansionMesangial expansion
Class IIIClass III Focal proliferative <50%Focal proliferative <50%
Class IVClass IV Diffuse Prolif. >50%Diffuse Prolif. >50%
Class VClass V MembranousMembranous
Class VIClass VI Adv. sclerosing lesionsAdv. sclerosing lesions
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IgA Nephropathy (Berger Disease)
Alport Syndrome
GoodPasture Syndrome
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presence of prominent IgA1 immune complexes deposited in the mesangiumactivate the complement pathway and
initiate glomerular injury
the most common type & most frequent cause of recurrent gross
glomerulonephritis worldwide
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Alport Syndrome X-linked hereditary disorder of basement
membrane collagen Abnormal mutation of type IV collagen
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1)subepithelial humps, as in acute glomerulonephritis
2) epimembranous deposits, as in MGN
3) subendothelial deposits, as in SLE nephritis & MPGN
4) mesangial deposits, as in IgA nephropathy
5) basement membrane. EN = endotheliumEP = epitheliumLD = lamina densaLRE = lamina rara externaLRI = lamina rara internaMC = mesangial cellMM = mesangial matrix
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