Nephrology - Dr Abo-ElAsrar - By El Azhar Medical Students 2012 ( للطباعة )

( BETA EDITION)

With

Prof. Dr Mohammed Abo El-Asrar

Edited By El-Azhar Medical students 2012

Nepgrology Dr. Abo-Asrar

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Nephrology INDEX

Total pages = 47

Total time = about 9.5 hours

Lecture number Pages

1- lecture 11 4 - 5

Introduction ( page 4 )

inheritance 6 ( Autosomal inheritance 6 )

2- lecture 12 5 - 12

cont. Introduction ( page 5 )

3- lecture 13 12 19

Nephrotic $ ( page 12 )

4- lecture 14 19 - 25

cont. minimal change ( page 19 )

congenital nephrotic ( page 21 )

5- lecture 15 25 - 32

cont. post str. GN ( page 25 )

introduction to RF ( page 26 ) ..

6- lecture 16 32 - 38

cont. introdiction to RF ( page 32 )

chronic RF ( page 34 )

7- lecture 17 39 - 47

acute RF ( page 39 )

Urinary Hues ( page 44 )

Hematuria ( page 45 )

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Nephrology Prof. Dr. Abo El -Asrar

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glomerulus

:

1- if > anatomical fenestra

- anatomical

high molecular weight protein globulin haptoglobine

2- if < physiological fenestra

- physiological

. As crystalloids as Na, K, etc

3- if > physiological but < anatomical :

- physiological anatomical

So, should pass through the magnetic field

A - So, if +ve charged

- Hb intravascular hemolysis Hb

And leading to acute tubular necrosis

B but if ve :

- ve charge LMW protein ( ve )

As albumin , transferring , IgG , tuftsin , lipoprotein lipase ( which destruct cholesterol ) , protein C ,

protein S & antithrombin iii

- sialo protein LMW protein

urine ( HMW protein ) selective proteinuria

selective sialprotein

- BM LMW+HMW

non selective proteinuria

11 12

12

- afferent efferent

And aff. : eff. = 7:1 WHY ?? To increase the pressure inside the glomerular capillaries

( pressure (

-

- glomerular filterate plasma protein

- sialoprotein selective proteinuria

1- in the most common type of nephrotic $ minimal change nephrotic

2- also, in congenital nephrotic $

- 1 2 selective proteinuria

- BM non selective proteinuria


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( ) 13 blood waste products

7 13

13 / 7 = 1.5 .. interstatium arterial end 1.5 venous end (

)

- interstitial space

odema

- hypoproteinemia :

2- generalized massive odema :

Due to :

A - osmotic pressure say 15 ( not 25 as normal )

- arterial side 17 ( 32 -15 = 17 ) interstitial space ( )

- venous side 3 ( 15-12 = 3 )

- interstatium 14 ( ) massive odema generalized

osmotic pressure

- odema

B - ADH :

- arterial side venous side 14 ( interstatium )

- atria volume receptors atria

hypothalamus ADH kidney to collecting tubules urine

reabsorption

- .. osmotic

pressure

- ADH urine

osmotic pressure .

C - renine aldosterone

- VR COP

- VR COP renal Bl. Flow

- afferent columnar cells juxtaglomerular apparatus

if RBF secrete renine hormone convert angiotensongen to angiotensen I then to ii to suprarenal

that secrete aldosterone to distal tubules reabsorption of Na then Na take water to

intravascular

- osmotic pressure

odema

-

3- hyperlipedemia or hypercholestremia :


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- osmotic pressure liver

synthesis of albumin as a compensation

- kidney urine

- liver cells marked hyperactivity over compensation albumin ..

lipoproteins cholesterol

- intake

- liver

( liver) NB.

- liver

need lipoprotein lipase which is one of LMW protein that lost in urine

- ( ) so, hyperlipedemia or hypercholestremia

- nephrotic $ :

clinical $ that characterized by heavy proteinuria , hypoprotenmia , massive generalized odema with or

without hypercholetremeia ) heavy proteinuria = >= 2 gm/24 hrs )

-

- grades proteinuria adult child

- nephrotic

-: aldosterone osmotic pressure

-: osmolarity osmotic pressure

- osmolarity

Na urea ( ) intravascular extravascular

body fluids

NB. All called extracellular fliud

- but osmotic pressure depends on plasma protein that only intravascular

-: lymphatic system odema as a drainage system

-: .. arm lymphatic odema

:

- :

- :

1- odema of BM

- fenastra

2 - proliferation of endothelium 3

3 - proliferation of epithelium of B. capsule 2

-


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- ..

- odema dorsum of the hands & foots

-

4- Hematuria :

- intravascular pressure capillaries

so, may epistaxis

- capillaries pressure (

) bleeding ( .. ) Hematuria

5- mild proteinuria :

- plasma protein

as here there is hematuria that contain not only RBCs but also plasma

mild proteinuria

- selective non selective : non-selective both H&LMW protein

- nephritic $

- that defined as clinical $ characterized by oliguria , hypertension , hematuria , mild odema & mild

proteinuria

- ( )

- ( nephritic ) surface area 1 m2 200

/ 160 that indicate severe hypertension

- urine 200 ml/day ( oliguria .. ) criteria nephritic

- 2 nephrons .. 200,000 BM capllaires

( 10% of nephrons ) :

- hematuria become frank + protein heavy proteinuria ( > 2 gm / day )

+ urine output 350 ml ( still oliguric )

+ Bl. Pressure become 160/120 but still hypertensive

+ osmotic pressure so, massive odema ( due to heave proteinuria )

- :

1- still oliguria

2- still hypertension

3- hematuria

4- odema

5- preoteinuria

- called nephritic nephrotic $ 4 5

- causes & Pathogenesis :

- nephrotic nephritic


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WHAT IS THE ETIOLOGY ?

1- congenital congenital nephrotic $

sialoprotein

- so, heavy selective proteinuria hypoproteinemia massive generalized odema

& if healthy liver hypercholetremia but if diseased liver no hypercholestremia

2- immunemediated

A- direct antigen antibody reaction part of the kidney is antigenic reaction

- : Abs sialoprotein selective heavy proteinuria

one of nephrotic called minimal change nephrotic $

B- destruction of the basement membrane ( BM )

non selective proteinuria and other manifestations of nephrotic

- as in membranous glomerulonephritis ( GN ) or rapidly progressive GN

C- also, antigen antibody reaction proliferation in the kidney

- so, proliferation of endothelium or epithelium of B. capsule or odema of BM

Nephritic $ or may complicated by nephrotic

D- Immune complexes

- antigen-antibody .. complement

c1-c9 kidney and cause nephritc,nephrotic or both

-

- investigations

- C3...

- classic pathway so, consumed in any complement aggregations

So, 1- if C3 means immune complex mediated pathology

2- if normal

- : congenital nephrotic $ C3 normal

minimal change nephrotic C3 normal

post.streptococcal GN C3 immune complexes

- complement immuno fluorescein biopsy slide

light microscope slide fluorescence

- fluorescein complement

- washing slide fluorescein immune complex

- so, if C3 so, +ve immuno fluorescein test

- so, in congenital -ve * in minimal change -ve * post. Strept. +ve

- EM Fl


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- linear on glomeruli or lumbi deposition

1- if linear depositions on tha whole BM

- kidney antigenic

2- if lumbi depositions

- immune complex kidney

-

- ( linear ) end stage RF

- linear

- but if lumbi

100

12 13

Nephrotic syndrome

Definition

Clinical condition that characterized by 1- heavy protenuria

2- hypoproteinemia

3- massive genarlized odema

4- +/- hypercholetremia

Etiology : 1ry & 2ry

1ry

- 1ry pathology ( : )

1- congenital Nephrotic $

2- minimal change nephrotic $

3- membranous GN.

4- focal GN.

5- membrano-proliferative GN.

6- rapidliy progressive GN.

2ry causes : due to systemic diseases

1- collagen diseases as SLE ( multi systems affection )

- lupus kidney affected

2- Endocrine diabetic nephropathy 5

3- allergic vasculitis blood

- as Henoch shoneline purpura


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4- sickle cell anemia immune complex formation

5- lymphoma 6- shistsoma mansoni & malaria

7- drugs as gold , penicllin etc

-

- congenital & minimal change pure nephrotic only & the rest either nephritic , nephrotic or both

-

- ascities , scrotal odema , puffiness of the eyelid

generalized odema

- urine analysis albumin + 4 ( means about 2.5 gm / 24 hrs )

- total protein 3 gm - serum albumin 2 gm ( hypoproteinemia )

- nephrotic

Q : enumerate causes & discuss how to diagnose one of them ??

- puffiness odema dorsum of hand & foot

- urine analysis RBCs in urine

- urine output < 400 ml / m2 + headache

- nephritic

- 1- congenital 2- minimal change

NB . most common cause of nephrotic minimal change = 70 % of all pediatric nephrotic

- ..

-

- minimal change nephrotic

Minimal change nephrotic

- Cause autoimmune

- antibodies against sialoprotein selective heavy proteinuria

- improves by measles infection due to suppression of T-cells all autoimmune process

measles infection TB

1- male > female 2:1

2- most common cause of nephrotic $

3- age of onset 2-7 years

- range rare rare

- Clinically

-

( !!! .. ) ( ) :

1 - ONLY massive generalized odema


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- eyelid .. ..

- puffiness of eyelid then extremites ( dorsum of hand & foot )

- then genetalia ( scrotal in male labial in female ) + L.L odema

- abdominal & chest wall + ascites , pleural effusion & pericardial effusion

- causes of this odema

1- osmotic pressure due to plasma protein

2- ADH odema

3- aldosterone Na & water retention more & more odema

2- important ve data :

- No oliguria No hematuria No hypertension

- nephritic

- :

nephrotic manifestations generalized odema

- odema renal by exclusion of other causes of odema :

1- cardiac L.L then ascites then allover the body

2- liver disease ascites then L.L then allover the body

3- nutritional odema with loss of Wt

+ no history of cardiac or liver diseases

-

Either nephrotic or nephritic-nephrotic

- nephrotic

- :

..

NB hypertension may occurs in 10-20% of minimal change N

complications

- may present with complication of nephrotic $

- 2 complications

A - incidence of infections

1- odema precipitating factor for infection

- .. " "

organism ..

2- loss of 2 important immuno components in urine


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- loss of IgG & tuftsin ( opsonin ) that help in phagocytosis of capsulated organisms

3- use of immuno suppressive drugs in the ttt as cortisone

B - risk of thrombosis 3

a- blood viscosity

- .. thrombosis

b- coagulation factors

- liver

c- coagulation factors

- antithrombin iii active factor iiia fibrinogen

Convert fibrinogen to fibrin

- antithrombin III lost in urine

d- loss of protein C & S in urine

- inactivation coagulation factors

- WHY blood viscosity ??

1- odema

interstitum

2- in ttt diuretics used shift water from intravascular to urine

3- cholesterol viscosity

4- polycyathemia due to using os steroids for long term & polycyathemia is one of

the most importrant side effect of steroid

- laboratory diagnosis ( investigations ) :

- odema

- heavy proteinuria

1- urine analysis 24

For measurement of total amount of proteins + type of proteins in urine by elsectrophoresis of urine

- :

- protein > 2 gm / 24 hrs ( heavy proteinuria )

- protein electrophoresis low molecular Wt protein so, selective ( albumin , trasnsferrin , & IgG ) ( no

globulin , no etc all HMW protein (

2- for hypoproteinemia total protein & serum albumin

- normal serum level protein = 6-8 gm %

- normal abumin = 4.5 5 gm % ( here < 2.5 gm / dl ) WHY ??

a- loss of protein in urine


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b- gut wall odema gut secretions which is mucous which is protein in nature

- stool

c- catabolism of protein WHY ??

- odematous BMR

consumption

3- serum cholesterol > 300 mg / dl ( normal level = 150-250 mg % ) WHY ??

a- synthesis by the liver

b- metabolism due to lipoprotein lipase enz.

4- C3 Normal ( not immune complex )

5- renal functions normal

6- U/S for detection of ascites chest X ray for detection of pleural effusion

7- renal biopsy ( not a routein investigation )

- steroid

- light microscope every thing is normal

- fluorescein -ve

- EM fusion of foot processes

- epithelium of B. capsule BM foot process fusion

sialprotein Abs adhesion

- minimal change nephrotic $ normal ..

EM fusion of foot process

- TTT :

- nephrology ttt :

complete rest in bed + 3 D

1- complete bed rest

- BMR catabolism

- RBF glomerular capillaries pressure erect position ( ) flat position( )

- so, flat proteinuria so, loss of protein

2- Diet

- :

Protein fat CHO + minerals + vitamins + water

- :

a- CHO


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- 6 ( 2 2 2 ) .. 6

single dose cortisone in the early morning every other day ) (

- cytotoxic drug (as cyclophosphamide endoxan ) 6 3 ..

3 ..

- membrano - proliferative GN incidence of thrombosis

- . cytotoxic ( 3 )

anticoagulant

- membranous

- & its prognosis :

10 % renal failure

90 % death from complications

13 14

- :

D.D. of minimal change

nephrotic syndrome in 1st year if life

post streptococcal GN

D.D. of minimal change NS

1- congenital nephrotic $

- autosomal recessive gene ( )

- sialoprotein ( age of onset since birth ) generalized odema

neonatal period .. minimal change 2-7 years

- selective proteinuria .. congenital (has no ttt (bad prognosis

2- Focal glomerulosclerosis :

- minimal change presentation cortisone

- .. frequent relapsing ( )

3- membranous glomerulonephritis

- age of onset not common in pediatrics 10

- non-selective ( BM )

- .. prognosis ( 10% & 90% )

4- membrano-proliferative GN :

- immune complex .. immune complex :

C3 + +ve immunoflourscentstydy + EM finding

- BM

proliferation of endothelium of capillary tuft & epithelium of B. capsule

- .. nephritic nephritic nephrotic


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( hypertension , oliguria , hematuria )

- bad prognosis age of onset mainly > 10 years ( )

5- 2ry to systemic diseases :

- .. other criteria of systemic disease

-: ( cortisone

heavy proteinuria , selective ..)

- +

+ diuretics + cortisone urine ..

2/3 ( 6 4 ) .. 6 (

)

- 6 cortisone

- focal G.sclerosis cytotoxic (

)

- 3

presented with puffy eyelid & generalized odema , protein in urine 3 gm / 24 hrs

, serum albumin 1.5 gh / dl serum choletreol 400 mg / dl

( nephrotic ( ) 4 criteria )

- enumerate causes & how to diagnose one of them ??

- .. 3 ( congential nephrotic .. )

- 15

A causes of nephrotic $ in 1st year of life :

a- 1ry :

1- congenital nephrotic $ ( common )

2- minimal change NS not common ( 2-7 years )

3- membranous GN of idiopathic cause

4- focal g. sclerosis

b- 2ry :

1- 2ry to infection

a- congenital toxoplasmosis

- 2ry to infection

b- syphilis membranous GN 2ry type

- .. idiopathic

2- 2ry to teratogens :


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- lead poisoning arsenic poisoning

- kidney

3- 2ry to genetic disease as :

- Nail-Patella $ charectrized by nephrotic + nail atrophy + absent patella

- gene factor .. 1ry kidney 2ry

4- Nephroblastoma ( embryogenic tumor )

5- Hemolytic uremic $

- bleeding disorders E-Coli verotoxin ( GIT ) coagulation +

immune complexes deposition kidney nephritic + hemolysis in

RBCs

- ....

B Discuss diagnosis of one of them :

- congenital nephrotic $ ( ) :

congenital nephrotic $

1- Etiology :

autosomal recessive gene abscent of sialoprotein

2- C/P :

- massive generalized odema :

- puffiness UL & LL genetalia ascites pleural effusion pericardial effusion

- odema nephritic complications

- infection ..

immunosuppressive

( odema loss of IgG & tuftsin ) ..

- thrombosis ..

steroids ( congenital)

3- Investigations :

1- urine analysis : heavy proteinuria > 3 gm / 24 hrs

2- total serum protein & serum albumin

- choletrerol

3- normal renal function

4- renal biopsy ( diagnostic )

4- TTT :

1 - rest

2 - diet .. special milk formula protein , CHO , low fat , low salt


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3 - diuretics

4 - curative ttt RENAL TRANSPLANTATION

Post streptococcal GN

clinical

Etiology & pathogenesis

- streptococcal strain ( 12 pharyngitis ) ( 49 skin infection )

- 2 strains Abs complement immune complexes

glomeruli deposition filter .. irritation proliferation

of endothelium & epithelium of B. capsule ( irritation ) also,

juxta glomerular appartus, mesyngemal cells Diffuse proliferatve GN

- immune complexs subendothelium between endothelium & BM

- EM lumbi deposition not in kidney antigenic part

- odema of BM fenestra GFR oliguria or even anuria

etc

- then hypervolemia hypertension hysdrostatic pressure mild odema

- then some rupture of some capillaries hematuria

- nephritic ...

C / P

1- oliguria & hematuria :

- < 400 ml .. ( RBCs ) frank or smoky

2- hypertension :

- headache hypertension

a- due to GFR

b- also due to proliferation of juxtaglomerular appartus

renine aldosterone salt & water retention volume of the blood hypertension

c- peripheral vasculitis :

immune complexes deposition on endothelium of peripheral vessles irritation & proliferation lumen

peripheral resistance hypertension ( called peripheral vasculitis )

3- mild odema :

- mild odema ..

odema of dorsum of the hand & foot

- .. hydrostatic pressure ( hypertension )

- odema generalized

1- if complicated with nephrotic


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2- may associated with HF.

3- acute RF without restriction of fliud

- complications :

1- HF

a- hypertension ( congestive HF )

b- toxic myocarditis immune complexes

c- volume overload

2- hypertensive encephalopathy

a- brain odema ICT headache not relived by usual analgesic .. only

relived by morhine.

b- projectile vomiting not precided by nausea

c- convulsion may occur

3- acute RF

- Investigations :

1- Nephritic or not ?? ( glomerular bleeding or not ?? ) so, do urine analysis

a- volume < 400 ml 24

b- specific gravity

- .. specific gravity ..

c- proteinuria mild

d- RBCs casts ( diagnostic )

- hematuria .. glomerular hematuria .. nephiritis ..

RBCs

But bilharziasis separated RBcs

UTI separated RBcs

stone separated RBcs

tumor separated RBcs

- .. ..

:

1 - RBCs tubule ( ) mucoprotein tubule ..

2 - RBCs biconcave ..

2- poststreptococcal or not ?? markers

- in winter antistreptolysin O titre ( ASOT) due to throat infections


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- in summer antihyalouridinase due to skin infections

- immune complexes in blood

- C3 level

3- Renal biopsy :

- LM proliferation ( as it is diffuse proliferative GN )

- immunoflourscen + ve

- EM subendothelial depositions ( lumpi form )

NB complications or not ?? clinically ( ) as hypertensive encephalitis or not ( clinically )

4- Reanl failure or not ?? do renal function tests

- ttt :

- streptococci

1- eradication of streptococcal infection give penicillin for 10 days ( )

2- Diet ( )

a- CHO b- fat

RF .. urea suppression to lipoprotein lipase enz. so, cause

hypercholestremia

c- protein as urea from protein

: renal impairment .. liver impairment protein

d- Na e- K+

f- water so, fluid restriction

- fluid chart ( ) .. :

- volume of urine / 24 hrs ( ) + 400 ml / m2 ( for extrarenal water loss through

respiration , sweat etc (

-

( )

3- ttt of hypertension ( antihypertensive drugs )

..

4- for hyperkalemia

-

( k K

)

- K- citrate ..

- normal serum K 3.5-5 mEq / L


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- 7 dialysis arrhythemia of heart ..

so the toxic level is very very narrow

-

1- glucose + insulin

- ( )

so, give glucose + insulin

2- bronchodilators :

- smooth ms of bronchus stimulation B2 bronchodilators

hypokalemia smooth ms of bronchus so, give B2 agonist by inhalation

3- Ca gluconate

- Ca gluconate :

- Ca brasyarrythemia ( cardioprotective against tachyarryrhemia of K + )

- gluconate give K-gluconate wcich is fat slouble to liver excreted in bile

4- ion exchange resin :

- ion exchange resin electrolyte disturbance

5- peritonial dialysis & its indications are :

- persistent hyperkalemia

- hypervolemia , urea , creatinine

14 15

:

- DD of poststreptococcal GN

- introduction to renal failure

- BM transplant & renal transplant

- RF ( )

- DD of poststreptococcal GN

- typical poststreptococcal GN.

- nephritic oliguria , hypertension , hematuria , mild odema

1 - nephritic $ or acute GN

2 - hematuria microscopic or macroscopic poststreptococcal or acute GN

3 - mild odema mild odema as cardiac or hepatic or nutritional

4 - hypertension

- 1 .. 2

- other causes of acute GN :

A - alport $ = heridiatry nephritis

gene factor mainly autusomal dominant


P a g e | 26

" " : ,, : " " " 2012

autosomal recessive or X linked

- age of onset 1st 6 months or max. 1st 12 months

- :

1- nephritic $

2- other manifestations as :

- SNHL ..

- Keratoconus

- ..

kidney ( transplantation)

B - IgA nephropathy

- IgA mucosa

- infection ( viral ) IgA mucosa ( 1st protective mechanism ) serum

- IgA serum .. kidney

( immune complexes .. ) deposition odema of BM ..

- proliferation so, all manifestations of neohritic $ but severe hematuria

- infection nephritis so, recurrent nephritis

..

.. IgA with any infection ( hematuria )

-

- IgA in serum , normal C3 ( also in alport C3 is normal )

- biopsy deposites IgA

- kidney transplant .. kidney kidney

IgA deposites

avoid infections

C - hemolytic uremic $

D - rapidly progressive GN

Renal failure

INTRODUCTION

- organ failure

- so, we must 1stly know functions of the kidney 3

A Endocrinal functions :

1- erythropiotein

- RF .. stem cells of BM RBCs RBCs anemia


P a g e | 27

" " : ,, : " " " 2012

2- thrombopiotein

- receptors stem cells megakaryocytes mother cells of platlets

- RF thrmbocytopenia

3- as kidney activate vit D so, if failure Rickets ( if still growing bone )

- vit D .. vit D3 ultra violet

rays

convert cholestreol to vit D3 ( cholecalcifirol ) wcich is non-functioning vit.

functioning vit 2 hydroxylations:

- in liver at C25 give 25 hydroxy cholecalcifirol

- in kidney hydroxylation at C1 ( parathyroid hormone dependant )

kidney receptors parathrmone active form ( 1-25

dihydroxycholecalcifirol)

- 1-25 dihydroxy . 1-hydroxy ( 1 alpha ) liver

1-25 dihydroxy ( vit D . )

4- kidney secrets renine from juxtaglomerular appartus ( )

from columnar cells at the end of afferent arterioles just befors glomerular capllaries

- if irrtative pathology renine hypertension

- if destructive pathology renine hypotension

- RF hypertension ..

.. hyper hypo

B Excretory functions :

- .. toxins .. endogenous toxins

.. :

1- macrotoxins :

- failure toxic effect appears so early acute & chronic & include

- urea , acetotic materials ( organic acid ) , K+ , phosphorus & uric acid

2- microtoxins :

- failure acute RF

chronic

- & include urochrome pigment, phenolic materails , aluminium

- RF

1- urea = Azot so, uremia = azotemia

- urea ( kidney main site of excretion ) (

.. ) :

1 ) through saliva :

salivation


82 | e g a P

2102 " " " : ,, : " "

gniht yna fo etsat dab ) ( .. aeru -

) .. (

.. .. sdub etsat noitcurtsed .. -

llems ainoma ro llems cimeru -

snoiterces TIG hguorht ) 2

hcamots -a

nrub traeh sitirtsag asocum cirtsag noitatirri -

) .. (

sisemetameh .. .. reclu cirtsag sitirtsag -

gnitimov .. sitirtsag

)loots kcalb ( anelem .. -

sitiloc ot gnidael snoiterces noloc -b

srotpecer hcterts niatnoc noloC .BN

lanios .. xelfer lanips .. noitalumits .. llaw noloc loots -

droc

loots .. noitcartnoc loots tnemges

suna & mutcer

)xelfer noitacefed (

ot erised .. noloc fo ytilitom .. srotpecer hcterts ) ( noitatirri -

. yrtnesyd ) .. reclu ( .. etacefed

) yrtnesyd cimeru tub .. yrtnesyd ) allegihs ( yrallicab ton .. yrtnesyd cibeoma ton (

: taews hguorht ) 3

noitatirri .. .. -

tceffe gnihcti )enimatsih fo srotpecer ( 1H ot

.. .. -

..

.. -

) ( tsorf aeru dellac

snoiterces .pseR hguorht ) 4

.. yawria .. suhcnorb fo snoiterces aeru -

)hguoc ( .. yawria tsehc

)tsehc .. eerf tsehc (

) ( .. -

sisytpomeh gnideelb .. noitareclu -


P a g e | 29

" " : ,, : " " " 2012

- bronchospasm .. ( wheezing .. ) chest

asthma ( wheeze asthma )

- kidney ( manifestations

)

- .. ..

1- suppression to cyclooxygenase Enz. Inside the platlet ( ) leading to thrombathenia

- RF thrombocytopenia .. purpura RF ..

.

2- deposition on cell membrane of RBCs rupture hemolysis ( due to deformity of cell membrane )

3- suppression to lipase enz. cholesterol hypercholestremia in RF

liver F hypochole.

- post. Strept. GN excess fat RF

4- if urea reach brain leading to

a- irritation of vomiting center ( chemoreceptor triger zone )

- RF :

A local cause gastritis B central cause irritation of vomiting center

b- to arousal center ( reticular formation )

- drousy coma

- manifestations of azotemia .. ..

5 - .. serosal membranes

1- pericardium dry pericarditis

2- pleura dry pleursy

3- peritoneum dry peritonitis

1,2 & 3 all leading to stitching pain

2- organic Acid :

- kidney

organic acids .. PH

( acidic .. alkaline PH )

- organic acids active process .. reabsorption bicarbonate PH

acidosis

... kidney


P a g e | 30

" " : ,, : " " " 2012

acidosis :

a- failure of excretion of organic acid

b- loss of bicarb. In urine

- acidosis

1- Kussmaul respiration ( air hunger ) : WHY ??

- PH resp. system .. organic acids lung .. CO2 + H2O

- CO2 irritate respi.center leading to deep respiration

.. Kussmaul respiration ( air hunger )

- CO2 .. Acidosis

so, air hunger is a compensation for acidosis .

2- rickets if still growing bone ( due to melting of bone )

- bicarb

- bone bicarb .. bone Ca-carbonate .. Ca

bone Rickets

- so, Rickets has 2 causes in RF :

a- failure of activation of vit D

b- Ca from as a compensation to bicarb level ( )

3- K+ in RF K+ level

- normal level 3.5 5

- manifestations of K+ level :

a- irritation of SA node SA node tachycardia .

b- motility of GIT

- K+ motility

- motility colic .. diarrhea ( absorption )

- :

a- urea colitis dysentry

b- K+ motility of GIT

NB . effect of K+ on skeletal Ms is the opposite of of its effect on smooth Ms

K+ tone skeletal Ms hypotonia ..

4- Phosphate :

- RF no excretion of Ph WHY ??

- Ph Ca .. parathyroid hormone

Parathormone leding to excretion of Ph & reabsorption of Ca


13 | e g a P

2102 " " " : ,, : " "

aC .. ) .. enomrohtarap srotpecer ( yendik -

hP

) ( hP & aC eniru ni ,os -

.. .. .. hP aC dnalg dioryhtarap -

: .. enomroh dioryhtarap

yendik -a

enoB -b

tsalcoetso & tsalboetso .. -

( aC & hP enob .. tsalcoetso ytivitca enomrohtarap -

tsalboetso )

hP .. enomrohtarap dioryhtarap dnalg -

yendik .. hP .. hP & aC enomrohtarap

aC hP

hP .. hP aC .. .. yendik -

enomrohtarap ... elcric suocsiV .. enomrohtarap ..

.. hP & aC stsyc yar X .. stekciR

acitsyc asorbif siteitso ) tsyc ton ( aera dezialrenimed

: 3 .. FR stekciR -

enomrohtarap -3 enob fo gnitlem ot gnidael sisodica -2 noitavitca D tiV -1

dica cirU -5

sitirhtra -

: snixotorciM

: slairetam cilonehP -1

) .. ( -

) ( noitalucicsaf sCHA noitatirri .. FR -

) ( pucciH mgarhpaid fo noitcartnoc suonitnops .. n cinerhp noitatirri -

) FR fo % 03 ni rucco puccih ( FR

stnemgip emorhcoru noitadarged eninalem -2

eniru -

.. tnemgip .. .. .. -

.. .. .. -

raelc ( .. ..

)eniru

tnemgip -


23 | e g a P

2102 " " " : ,, : " "

muinomulA -3

) ( ) ( -

.. yreviled ) erup .. (

.. yendik -

: .. FR -

ecnabrutsid yromem noitceffa ebol latnorf -1

ainepotycnap yam MB ni setisoped -2

:FR ainepotycobmorht -

yticixot muinomula -b nietoipobmorht -a

: FR ni aruprup fo sesuac -

ainehtabmorht aeru -2 ainepotycobmorht fo sesuac -1

61 51

.. yendik eht fo snoitcnuf enircoxe & enircodne -

yendik noitcnuf

: noitulid & noitartnecnoc fo rewoP - C

) ( ytivarg cificeps -

0301 5101 = yllamron eniru fo ytivarg cificeps -

5201

.. 5101 0301

amsalp ro eniru ytivarg cificeps -

.. .. ytiralomso ytivarg cificeps -

aN

0101 = amsalp fo ytivarg cificeps lamron -

( amsalp etartlif raluremolg .. -

ytivarg cificeps nietorp amsalp ) .. nietorp amsalp

0101 amsalp etartlif raluremolg ytivarg cificeps -

.. retaw & aN noitprosbaer elubut detulovnoc lamixorp etartliF .lG -

.. ytivarg cificeps .. TCP

..

0101 = elneh fo pool ta ytivarg cificeps ,oS

retaw fo noitprosbaer .. aN fo noitprosbaer elneh fo pool -

0101 ytivarg cificeps etaretlif ..

aN fo noitrosbaer .. enoretsodla no tnadneped selubut detulovnoc latsid -

ytivarg cificeps ..


33 | e g a P

2102 " " " : ,, : " "

laitatsretni .. .. HDA yb delortnoc ) .. setag ( .. selubut gnitcelloc -

) tlas ton ( ylno retaw fo noitprosbaer alludem

eniru ytivarg cificeps .. ytivarg cificeps -

eniru fo noitartnecnoc =

.. .. HDA -

ytivarg cificeps + tuptuo eniru HDA fi TUB ytivarg cificeps + tuptuo eniru

) eniru fo noitartnecnoc fo rewop noitulid & ( yendik -

.. 21-8 .. -

) ekatni retaw (

.. HDA .. .. ekatni retaw -

:

) ( 0301 .. ytivarg cificeps +

ekatni retaw ) .. 2 ( -

) 5101 ( ytivarg cificeps + tuptuo eniru level lasab ot HDA

( .. 5101 0301 lamron ytivarg cificeps -

) 0301 ( ) .. 5101

) ( noitulid & noitartnecnoc fo rewop lamron dellac si siht

ytivarg cificeps : -

.. :-

) (

.. .. .. -

.. -

) .. ( ..

) (

: -

.. gnitsaf gnirud retaw fo noitprosbaer yendik

. noitardyh revo retaw fo noitprosbaer

.. -

) ti ni ytiralomso hgih ot eud ( alludem laitatsreti -1

HDA -2


P a g e | 34

" " : ,, : " " " 2012

- RF

- interstitial medulla .. .. ADH

glomerular filterate ..

with specific gravity 1010 as plasma ( in acute & chronic RF ) (low specific gravity)

- .. glomerular filterate .. urine volume .. specific gravity

1010 .. fixed

so, in RF urine has Low fixed specific gravity

Chronic RF

- Definition :

- inability of the kidney to maintain body homeostatsis ( )

- Causes :

1- in child < 5 years :

- Ch. RF 5 .. renal anomalies :

- Hypogenesis , agenesis ( aplasia of the kidney ) or urinary tract anomalies

acute chronic

- or any obstructive uropathy ( )

2- If child > 5 years

- may congenital as polycystic kidney & alport's $

- may acquired as GN or hemolytic iremic $

- clinical manifestations :

1- manifestations of azotemia( urea )

a- saliva as bad taste ..etc

b- bad odour of mouth

c- stomach d- colon e- sweat f- bronchial secretions

g- chest pain or abdominal pain h- CNS affection

- 3 4

( .. )

2- Air hunger ( rapid deep resp. ) due to acidosis ( metabolic ) due to :

a- loss of HCO3 in urine b- failure to excrete acidic materials

3- urine volume :

- kidney ( 2 )

- glomerular filterate 24 180 = 180 000 ml / 24 hrs

- urine output = 500 1500 ml / m2 / 24 hrs


P a g e | 35

" " : ,, : " " " 2012

400 oliguria .. 180 anuria .. 1500 polyuria

- urine

- renal impairment if nephrons < 0.5 milion ( )

: ( .. )

2 000 000 nephrons give 180 000 ml

So, 200 nephrons give 18 ml & 100 nephrons give 9 ml

- chronic RF 0.5 .. 100 000

..

As 100 9 so , 100 000 give 9000 ml

9 .. urine volume 9 .. polyuria ..

- .. .. 2- 3 .. 10 000

10 000 900 ml urine output

..

- .. 1000

So, 1000 90 ml ( oliguria even anuria according to surface area )

- urine volume chronic RF :

Polyuria normal oliguria or anuria or even absolute anuria

- complications : ( )

1- Racketic manifestations = renal osteodystrophy ..

a- no hydroxylation of vit. D in kidney

b- acidosis melting of bone Ca

c- Ph parathotmone osteitits fibrosa cystica

2- pallor or manifestations of anemia : WHY ??

a- production of RBCs due to :

1- erythropiotein

2- BM suppression by alumonium toxicity

3- iron & folic acid as a requirements ( )

- iron & folic acid ..

ammonia .. iron & folic acid.

b- loss :

1 ) hemolysis of RBCs by urea & other toxins .


P a g e | 36

" " : ,, : " " " 2012

2 ) He due to bleeding tendancy

3 ) bleeding tendancy :

a- thrombocytopenia

b- thrombathenia

c- Coagulopathies as urea prevent activation of coagulation factors

4- Growth failure ( dwarfism short stature )

a- renal osteodystrophy HOW ??

- deformity bone

b- restriction of protein in diet .

c- anemia ( chronic )

d- uremia suppress GH receptors leading to end organ resistance to GH .

5- CVS complications :

A- Hypertension WHY ??

1- renin ( if irritative pathology ) Na & water retention .

2- End stage renal failure volume overload ( )

3- cholesterol ( hyperlipedemia )

B Pericarditis

C HF WHY ??

1- hypertension

2- end stage RF hypervolemia

3- anemic HF

4- toxic mycarditis ( due to uremia or other toxins )

6- Neuropsychatric disorders : due to :

a- urea

b- hypertensive encephalopathy

c- trace elements & vitamins

d- Aluminium toxicity

7- recurrent infections due to suppression of immune system by uremic toxins .

- Investigations :


P a g e | 37

" " : ,, : " " " 2012

1- urine analysis :

- Low fixed specific gravity ( 1010 )

- volume

2- urea & creatinine elevated .

3- CBC

normocytic normochromic

or microcytic hypochromic ( iron )

or macrocytic normochromic ( folic acid )

4- Bl. Gases metabolic acidosis

5- Electrolytes :

- Na if renin ( irritative pathology ) & Na if renin ( destructive pathology )

- K+

excretion active process ..

- Ca ++ decreased - Ph increased

- alkaline phosphatase as he has RICKETS .

6- ECHO

7- assessment of nutritional state

Level of serum albumin , transferring , zinc , iron , folic acid , lipid ..etc

8- assess tone

9- investigations to detect etiology

.. ..

( heridatry )

- ttt :

1- Diet ( )

chronic RF

a- CHO

- .. ..

b- Fat give digested fat

- medium chain triglycerides

- fat .. .. 1 gm 9 ..

renal transplant


P a g e | 38

" " : ,, : " " " 2012

c- protein

... urea

d- minerals

- Na or is there salt loss or retention ??

- K +

- Ca

- ( skimmed milk .. ) fat

- Ph

- .. ..

- .. .. ..

- Ph excretion .. as Posphate binder

e- vitamins

- increase fat soluble Vit.

- increase water soluble vit . ( )

dialysis .. water soluble vit ..

f- water :

- if oligurai or anuria give urine volume + 400 ml / m2 / day ( fliud chart )

2- ttt of complications :

- hypertension

- anemia by dialysis ( aluminium ) + give iron & folic acid + erythropiotein

- Rickets :

give active vit D

correct acidosis

if resistant cases parathyroidectomy

3- dialysis : ??

- if GFR = 10 ml / minute

- or severe manifestations of azotemia

- or K+ reach 7 tachyarrythmia

- .. manifestations .. dialysis

4- Renal transplantation

5- social & psychological ttt

6- Drug dosage


P a g e | 39

" " : ,, : " " " 2012

- .. kidney

16 17

Acute renal failure

written

Definition

acute renal failure

: stop of filteration kidney waste products .

ARF

- may be reversible .. chronic

- filteration .. urine output

- .. oliguria .. chronic

- .. ARF

Causes :

- :

- filteration .. filteration

filteration

1- glomerular capillary pressure

- ( plasma protein )

- ( afferent ) diameter .. efferent ( ) .

Afferent diameter : efferent diameter = 7 : 1

capillary pressure .

2- Bowman's capsule

- filterate pressure .

3- basement membrane & the whole nephron :

( )

- ARF .. ARF

A - glomerular capillary pressure : ( called prerenal causes )

1- Dehydration ( Blood volume )

- dehydration :

a- loss of fliud ( as in diarrhea , vomiting , polyuria , excessive sweating )

b- intake of fluid as in fasting

dehydration

Dehydration Blood volume renal blood flow ( RBF ) glomerular capillary pressure

filteration that may leading to ARF according to severity of dehydration


P a g e | 40

" " : ,, : " " " 2012

2- loss of blood as Hge same mechanism as dehydration .

3- shock as

- hypovolemic shock or other tyoes of shock that leading to VD of peripheral bl vessels

renal arterial pressure .. RBF........................ etc

4- post surgery cardiac surgery

- .. motility intestine ..

paralytic ileus

- IV fluids .. motility

..

- oral intake ( passing Flatus .... ) not stool ..

( !!)

- .. .. auscultation motility .

- IV fluids .. dehydration

.. .. renal functions urea creatinie

.. renal impairment

- .. ..

motility

5- Nephrotic $ :

- urine .. osmotic pressure .. vessels

intrerstatium

- severe cases .. blood volume ... .......

- interstatium intravascular

- pre renal causes there is Hypotnsion

B - Bowman's capsule pressure ( called post renal causes )

- obstruction pathway urine .. :

1- Acquired :

- as stricture pf urethra or stone .

2- congenital :

- posterior urethral valve

- fold of mucosa urination urethra

- obstruction

- obstruction .. retention of urine bladder .. back pressure ureter

pelvis of kidney

then back pressure to all nephron's parts then to Bowman's capsule

filteration .. blood volume so, hypervolemia & hypertension


P a g e | 41

" " : ,, : " " " 2012

- .. obstruction urethra ( .. ) back pressure 2

kidneys

unilateral obstruction ( .. ureter .. ) kidney

.. renal impairment ..

- ARF unilateral obstruction .. single

functioning kidney

C Renal causes as :

1- filter closure ( )

- acute GN .. nephritic ..

odema or proliferation of cells of BM ..

..

2- nephrons destruction ( )

- as in severe anoxic tubular necrosis

- dehydration ( diarrhea ) ..

renal ischemia .. nephrons .. pre renal cause .

3- toxins as all nephrotoxic drugs as

- all anesthetic drugs

- aminglycosides

- gastroenteritis dehydrated .. aminoglycosides pre

renal cause

- carbon tetrachloride

4- infarction as an effect of embolus

5- congenital anomalies :

- agenesis ( ) or hypogenesis

- renal .. bl. Volume .. Hypertension

-: ARF .. pre , post or renal

- pre renal

- post or renal do catheterization .. ..

- bladder .. renal

- ( ) urine post renal

Clinical picture :

- acute renal failure .. macrotoxins

1- oliguria or anuria


P a g e | 42

" " : ,, : " " " 2012

- ..

- magor toxins :

2- urea manifestations of azotemia

3- metabolic acidosis manifestations as air hunger

- acidosis acute RF retention of organic acid .. loss of bicarb ..

filteration ( )

- chronic .

4- manifestations of hyperkalemia as :

- tachycardia due to stimulation os SA node .

- abdominal colic & diarrhea ( motility of intestine )

- generalized ms. Weakness & hypotonia

NB. NO manifestations of hyperphosphatemia or hyperuricemia

chronic

Investigations :

1- urine analysis

- 2 3 cm urine ( 24 )

a- volume oliguria ( < 400 ml / m2 / 24 hrs )

b- low fixed specific gravity ( 1010 )

- urine .. specific gravity ..

1 - ARF specific gravity

2 - end stage chronic renal failure ..

c- RBCs casts

- RBCs mucoprotein

d- Na

2- serum analysis :

- urea & creatinine - K & uric acid ( all major toxins increased )

- Na dilutional hyponatremia

- post & renal pre dehydration

- .. container 200 ml water .. ..

130 mEq / L

NB. mEq = milliequivalents


34 | e g a P

2102 " " " : ,, : " "

.. 2 + retaw lm 006 .. reniatnoc -

.. % 003 ( ..

) % 001

retaw & tlas .. noitaretlif .. laner & laner tsop -

lanoitulid .. tlas deniater aN .. noitneter

aimertanopyh

) .. ( GCE -3

. ygoloite gniylrednu fo noitagitsevni -4

: tnemtaerT

cinorhc .. .. .. etuca -

FR

: -

. srotcaf gnitatipicerp fo yrotsih -a

cirugilo -b

noitaripser peed dipar -c

ttt FO SENIL

: wol fi erusserP .lB erusaem -1

.. laner erp wol ... .. -

etatcal regnir .... erusserp yrallipac ralurmolg

sisodica .. etanobracib revil etatcal

.. )ycnegreme ( gK / lm 02 esod -

) emuloV .lb (

.. eniru .. noitaretlif ..

.. lotinnam .. siseruid citomso eniru -

.

.. xisal -

cinorhc .. .. .. eniru -

) sisorcen ralubut cixona snorhpen ( FR

laner tsop ro laner ,os : erusserP .lB hgiH fI -2

.. .. laner tsop .. -

. noitcurtsbo .. snoitcnuf laner

: laner fi -3

noitaretlif laner .. eniru -


44 | e g a P

2102 " " " : ,, : " "

K trahc duilf ( NG laccocotpertS .tsop -

) sisylaid snoitacilpmoc

.. xisal .. laner erp :

xisal : -

seuH yranirU

nettirw

eniru -

: eniru kraD - A

: -

: eniru deniater -a

tnemgip emorhcoru .. eniru deniater -

stnemgip elib -b

. .. niburilib tcerid J evitcurtsbo -

: eniru der B

eniru der -

airutameh -1

airunibolgomeh -2

eniru ni nibolgoym -3

sm .. .. -

) bH ( nibolgoym

niryhprop -4

niryhropotorp + nori bH -

aimena citylomeh cinorhc ni norI -5

.. stnega gnitalehc -

nori enimsaxorrefsed .. ..

eniru

setaru -6

) natcamir ( nicipmafir sgurD -7

steeb sa sdooF -8

.. .. -

) (

: eniru kcalb ro nworb kraD C


P a g e | 45

" " : ,, : " " " 2012

1- melanine deposites as in melanoma

2- homogentisic acid

- tyrosine :

- Tyrosin give para hydroxy phenyl pyruvate by tyrocinase .

- then para hydroxy phenyl pyruvate give homogentisic acid by para hydroxy phenyl pyruvate oxidase .

- then homogentisic acid give succinic acid by homogentisic acid oxidase .

- then succinic acid excreted in urine .

- homogentisic acid oxidase .. homogentisic acid urine

- cartilage .. sclera ..

alkaptonuria

Hematuria

- RBCs urine > 5 RBCs / high power field of microscope ( HPF )

.. urine RBCs ..

Types

2 types

1- Microscopic ..

2- Macroscopic

Causes

A Glomerular causes :

ALL CAUSES OF NEPHRITIC $

-:

- Alport's , IgA nephropathy , SLE , anaphylactoid purpura , Post streptococcal GN , proliferative GN ,

progressive GN etc

B Non glomerular causes

- urinary tract pelvis od the kidney urethra

1- Congenital anomalies as :

a- polycystic kidney

- cyst .. hematuria

b- hemangioma in kidney pelvis leakage hematuria .

2- Infections in urinary tract :

- acute pyelonephritis or cystitis

- infections .. / UTI .

3- Tumors as wilms tumor


P a g e | 46

" " : ,, : " " " 2012

- hematuria .. very late ( advanced)

- hypernphroma .. hematuria ( early)

wilms cortex .. medulla ( hematuria )

hypernephroma medulla

4- Drugs : as cyclophsphamide that cause Hemorrhagic cystitis .

5- Vascular cause :

as renal infarction , renal vein thrombosis , leading to congestion of the kidney

hematuria

6- trauma :

- extrenal trauma

- internal trauma as stones

: ( ) C I N D V T ( .. )

- C

- I

- N

- D

- V

- T

7- exercise induced hematuria :

- heavy exercise .. hematuria

a- erect position congestion of kidney

exercise

b- during exercise may minir trauma

DD between glomerular & non glomerular causes :

1 -

- glomerular .. .

- non ..

2 - .. relation to micturation .. ..

- glomerular .. .

- non :

* urinary bladder

* urethra


74 | e g a P

2102 " " " : ,, : " "

noisnetrepyh & amedo , iarugilo - 3

citirhpen .. raluremolg -

: .. non -

.. arhteru *

noifer cibuparpus .. reddalb *

niap niol .. sitirhpenoleyp *

) .. (

..... .. .. .. *

sisylana eniru - 4

2+ => nietorp , stsac raluremolg -

2+ < airunietorp , stsac on raluremolg non fi -

.. + ..

ymotsorhpen :

yendik eht fo sivlep .. .. reteru :-

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71 02

Date post:	10-Oct-2015
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Nephrology - Dr Abo-ElAsrar - By El Azhar Medical Students 2012 ( للطباعة )

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