Nephrology - DR Abo-ElAsrar - by El Azhar Medical Students 2012

( BETA EDITION)
With
Prof. Dr Mohammed Abo El-Asrar
Edited By
El-Azhar Medical students 2012
Nepgrology Dr. Abo-Asrar

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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Nepgrology Dr. Abo-Asrar

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Nephrology Prof. Dr. Abo El-Asra r

1:27 .... 11
NEPHROLOGY
4
) 1- nephrotic syndrome ( $
) 2- nephritic syndrome ( $
3- renal failure
4- hematuria

glomeruli Boumman's capsule + glomeruli capillary tuft affernent efferent Aff. Eff. pressure glomerulus B. capsule
plasma plasma protein filterate ( 3 layers ): ) ( 1- basement membrane of kidney
) ( 2- endothelium of capillaries
) ( 3- epithelium of B. capsule
filterate endothelium capillaries basement membrane fenastra epithelium B. capsule
layers the basement membrane ( BM ) :
endothelium epithelium
BM BM called anatomical fenestra ) sialo protein (ionaizable ve charge magnetic field anatomical fenastra
magnetic fieldphysiological fenastra
p. protein urine .. glomerulus sheding of mucoprotein that cover cells of tubules
urine < 30 mg / 24 hrs
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glomerulus
:
1- if > anatomical fenestra
anatomical haptoglobine globulin high molecular weight protein
2- if < physiological fenestra
physiological As crystalloids as Na, K, etc .
3- if > physiological but < anatomical :
anatomical physiological 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 ( LMW protein ve charge
As albumin , transferring , IgG , tuftsin , lipoprotein lipase ( which destruct cholesterol ) , protein C ,
protein S & antithrombin iii
LMW protein sialo protein selective proteinuria ) HMW protein ( urine
sialprotein selective
LMW+HMW BM non selective proteinuria
12 11
12
efferent afferent And aff. : eff. = 7:1 WHY ?? To increase the pressure inside the glomerular capillaries
( pressure (
plasma protein glomerular filterate selective proteinuria sialoprotein 1- in the most common type of nephrotic $ minimal change nephrotic
2- also, in congenital nephrotic $
selective proteinuria 2 1 non selective proteinuria BM -
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proteinuria ... urine urine :

24 Protein in urine >= 150 mg/24 hrs urine
30 .. 150 30 ) Called microproteinuria may be treatable or complicated by macroproteinuria ( 150 mg
- Grades of proteinuria
1- if protein in urine 150-500 mg/24 hrs urine mild proteinuria
2- if > 500 & < 2000 moderate as 1 gm /24 hrs
3- if >= 2000 mg ( 2 gm ) heavy or massive
( ) silaprotein destruction of BM nephrons
1- Heavy proteinuria hypoprotenmia
?? what is the effects
- plasma protein in urine plasma protein hypoproteinemia

capillaries arterial side venous side heart

capillary nutrients o2 waste products
.. .. water interstitial space interstitial space ( ) osmotic pressure 25 mmHg plasma protein
hydrostatic pressure 32 mmHg - in arterial side
12 mmHg - venous side
1 mmHg 1 liter of water arterial end = 25 = 25 X 1 * = 32 7 = 25 -32 = interstitial space
7 O2 ( nutrients ) - venous side = 25 = 25 1 * = 12 ( 13 = 12-25 )
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waste products blood 13 ) (

13 7
( venous end 1.5 arterial end interstatium .. 1.5 = 7 / 13
)
interstitial space odema
: hypoproteinemia 2- generalized massive odema :
Due to :
A - osmotic pressure say 15 ( not 25 as normal )
) ( interstitial space
) 17 = 15 -32 ( 17 arterial side ) 3 = 12-15 ( 3 venous side generalized massive odema ) ( 14 interstatium osmotic pressure
odema B - ADH :
) interstatium ( 14 venous side arterial side
atria
volume receptors atria urine to collecting tubules kidney ADH hypothalamus
reabsorption
osmotic .. pressure
urine ADH . osmotic pressure
C - renine aldosterone
COP VR - VR COP renal Bl. Flow
juxtaglomerular apparatus columnar cells afferent 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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liver osmotic pressure synthesis of albumin as a compensation

urine kidney .. albumin over compensation marked hyperactivity liver cells cholesterol lipoproteins
intake
liver NB. ) liver (

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 )
child adult proteinuria grades nephrotic osmotic pressure aldosterone : osmotic pressure osmolarity : - osmolarity
extravascular intravascular
) ( urea Na
body fluids
NB. All called extracellular fliud
- but osmotic pressure depends on plasma protein that only intravascular

as a drainage system odema lymphatic system : odema lymphatic arm .. : :
: : 1- odema of BM
fenastra 3 proliferation of endothelium -2
2 proliferation of epithelium of B. capsule -3
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glomerular filtration 1- so , oliguria

24 urine - if < 400 ml / m2 surface area/24 hrs = oliguria
= m2 surface area
surface area chart columns 3 surface area height surface area
( )) 7 + ( 4 Wt ) / 90 + Wt ( not accurate
surface area 400 - ..... 200
oliguria
- Anuria < 180 ml / mm2 SA / day
- absolute anuria NO urination
2- Hypertension :
.. hypervolemia hypertension intravascular pressure
osmotic pressure hydrostatic .. :- arterial side say 36 * - venous side say 15
..3- Mild odema :
- at the arterial side 36-25 = 11 liter water .
- at the venous side 25-15 = 10 liter water
1 ( 14 ) mild odema that appears only in dependant areas
knee & elbow position - dependant areas as : - puffines of the eyelids
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.. dorsum of the hands & foots odema 4- Hematuria :

capillaries intravascular pressure so, may epistaxis
( capillaries pressure Hematuria ) .. ( bleeding )
5- mild proteinuria :
plasma protein as here there is hematuria that contain not only RBCs but also plasma
mild proteinuria
both H&LMW protein non-selective : non selective selective nephritic $ - that defined as clinical $ characterized by oliguria , hypertension , hematuria , mild odema & mild
proteinuria
) ( 200 1 m2 surface area ) nephritic ( that indicate severe hypertension 160 /
nephritic criteria .. ) oliguria ( 200 ml/day urine capllaires BM 200,000 .. nephrons 2 : ) 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 $ 5 4
- causes & Pathogenesis :
nephritic nephrotic Page |
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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
selective heavy proteinuria sialoprotein Abs : 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
complement .. antigen-antibody and cause nephritc,nephrotic or both kidney c1-c9
investigations ... C3 so, consumed in any complement aggregations classic pathway So, 1- if C3 means immune complex mediated pathology
2- if normal
normal C3 congenital nephrotic $ : normal C3 minimal change nephrotic
immune complexes C3 post.streptococcal GN
slide biopsy immuno fluorescein complement fluorescence slide light microscope
complement fluorescein immune complex fluorescein slide
washing - so, if C3 so, +ve immuno fluorescein test
- so, in congenital -ve
in minimal change -ve
post. Strept. +ve
Fl EM Page |
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- linear on glomeruli or lumbi deposition

1- if linear depositions on tha whole BM
antigenic kidney 2- if lumbi depositions
kidney immune complex end stage RF ) linear ( linear - but if lumbi
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Nephrotic syndrome
Definition
Clinical condition that characterized by 1- heavy protenuria
2- hypoproteinemia
3- massive genarlized odema
4- +/- hypercholetremia
Etiology : 1ry & 2ry
1ry
: ) ( pathology 1ry 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 )
affected kidney lupus 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
) means about 2.5 gm / 24 hrs ( + 4 albumin urine analysis - total protein 3 gm - serum albumin 2 gm ( hypoproteinemia )
nephrotic Q : enumerate causes & discuss how to diagnose one of them ??
dorsum of hand & foot odema puffiness - 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
TB infection measles
1- male > female 2:1
2- most common cause of nephrotic $
3- age of onset 2-7 years
rare rare range - 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 : generalized odema manifestations nephrotic
: by exclusion of other causes of odema renal 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
fibrinogen active factor iiia antithrombin iii Convert fibrinogen to fibrin
- antithrombin III lost in urine
d- loss of protein C & S in urine
coagulation factors
inactivation - 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 ??
BMR odematous 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
fusion foot process BM
epithelium of B. capsule
adhesion Abs sialprotein
.. normal minimal change nephrotic $ fusion of foot process EM
- TTT :
: ttt nephrology complete rest in bed + 3 D
1- complete bed rest
catabolism BMR -
) (flat position ) ( erect position glomerular capillaries pressure RBF -
- so, flat proteinuria so, loss of protein
2- Diet
: Protein fat CHO + minerals + vitamins + water
: a- CHO
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) b- fat due to increased cholesterol ( already increased in this patient

c- protein
pure protein ..
.. ( ) .. .. .. fat .. .. cholesterol .
!!! .. rickets .. vit D vit D
( ) ..
3 .. 100 gm 300 gm
.. .. !!! .. .. .. .. ( ) ..

d- minerals salts
aldosterone odema e- vitamins & water
odema3- diuretics
) ( - lasix loop
K+ loss so, give K +
- aldactone weak
aldosterone
block
lasix ( aldactone ) K
- osmotic diuretics as mannitol IV
.. effect lasix
- salt free albumin :
osmotic pressure
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( albumin 200 ) .. .. interstitial space bl. Volume kidney .. hypervolemia

congestive HF
.. urine LASIX .. odema liver compensation cholesterol & coagulation factors
diuretics step .. -1 diuretics .. autoimmune
-2 odema ( .. 26 20 )
immunosuppressive drugs .. Kg high .. dose odema
-3 ascites .. renal vessels .. renal perfusion
immunosuppressive drugs
response
-4 .. immunosuppressive exclusion to serious infections
urine culture TB : IgG LMW protein globulin
: globulin HMWt
.. .. .. diuretics4- Drugs immunosuppressive drugs
) - cortisone ( prednisone ) 2 mg / kg / day ( max 60 mg / m2 / day
) test of proteinuria ( coagulation
.. albumin free ( )
.. albumin cortisone suprarenal shutdown
% 70
1 month ( albumin ) urine .. renal biopsy renal biopsy
minimal change .. cortisone .. ( )
focal glomerulosclerosis ( frequent relapser .. ) cortisone .. - cytotoxic drug cortisone .. side effects cortsisone
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6 .. ) 2 2 2 ( 6 ( single dose cortisone in the early morning every other day )

.. 3 6 ) as cyclophosphamide endoxan ( cytotoxic drug .. 3
incidence of thrombosis membrano - proliferative GN ) 3 ( cytotoxic . anticoagulant
membranous - & its prognosis :
10 % renal failure
90 % death from complications
14 13
: 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 generalized odema ) age of onset since birth ( sialoprotein 2-7 years minimal change .. neonatal period
has no ttt (bad prognosis( congenital .. selective proteinuria 2- Focal glomerulosclerosis :
cortisone
presentation minimal change ) ( frequent relapsing .. 3- membranous glomerulonephritis
- age of onset not common in pediatrics 10

) BM ( non-selective ) 10% & 90% ( prognosis .. 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 nephrotic nephritic .. Page |
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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 ..
+
.. urine cortisone + diuretics +
( 6 .. ) 4 6 ( 2/3
)
cortisone 6 ( cytotoxic focal G.sclerosis )
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
) criteria 4 ) ( nephrotic (
- enumerate causes & how to diagnose one of them ??
) .. congential nephrotic ( 3 .. 15 A causes of nephrotic $ in 1
st
year of life :
1- 1ry :
1- congenital nephrotic $ ( common )
2- minimal change NS not common ( 2-7 years )
3- membranous GN of idiopathic cause
4- focal g. sclerosis
2- 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
2ry kidney 1ry .. gene factor 4- Nephroblastoma ( embryogenic tumor )
5- Hemolytic uremic $
+ coagulation ) GIT ( verotoxin E-Coli bleeding disorders hemolysis in + nephritic kidney deposition immune complexes
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 :
pericardial effusion pleural effusion ascites genetalia UL & LL puffiness complications nephritic odema .. infection immunosuppressive
( odema loss of IgG & tuftsin ) ..
.. thrombosis ) congenital ( steroids
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 :
rest - 1
protein , CHO , low fat , low salt special milk formula .. diet -2
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diuretics -3
RENAL TRANSPLANTATION curative ttt -4
Post streptococcal GN
clinical
Etiology & pathogenesis
- streptococcal strain ( 12 pharyngitis ) ( 49 skin infection )
immune complexes complement Abs 2 strains proliferation irritation .. filter deposition glomeruli
also, ) irritation ( of endothelium & epithelium of B. capsule
Diffuse proliferatve GN juxta glomerular appartus, mesyngemal cells
between endothelium & BM subendothelium immune complexs antigenic part not in kidney lumbi deposition EM oliguria or even anuria GFR fenestra odema of BM etc
- then hypervolemia hypertension hysdrostatic pressure mild odema
- then some rupture of some capillaries hematuria
... nephritic C / P
1- oliguria & hematuria :
frank or smoky ) RBCs ( .. < 400 ml 2- hypertension :
hypertension headache 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

) hypertension ( hydrostatic pressure
.. -
generalized odema 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 )
.. nephiritis .. glomerular hematuria .. hematuria RBCs
But
bilharziasis separated RBcs

UTI separated RBcs
stone separated RBcs
tumor separated RBcs
.. .. :
.. tubule mucoprotein ) ( tubule RBCs -1

.. biconcave RBCs -2
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
so, cause suppression to lipoprotein lipase enz. urea .. RF
hypercholestremia
c- protein as urea from protein
protein liver impairment .. renal impairment :
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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.. arrhythemia of heart dialysis 7 so the toxic level is very very narrow

1- glucose + insulin
) ( so, give glucose + insulin
2- bronchodilators :
bronchodilators
B2
stimulation smooth ms of bronchus so, give B2 agonist by inhalation smooth ms of bronchus hypokalemia
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 :
electrolyte disturbance ion exchange resin 5- peritonial dialysis & its indications are :
- persistent hyperkalemia
- hypervolemia , urea , creatinine
15 14
:
- DD of poststreptococcal GN
- introduction to renal failure
BM transplant & renal transplant ) ( RF - DD of poststreptococcal GN
. poststreptococcal GN typical oliguria , hypertension , hematuria , mild odema nephritic nephritic $ or acute GN -1
poststreptococcal or acute GN microscopic or macroscopic hematuria -2
as cardiac or hepatic or nutritional
mild odema mild odema -3

hypertension -4
2 .. 1 - other causes of acute GN :

A - alport $ = heridiatry nephritis
gene factor mainly autusomal dominant
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- age of onset 1st
autosomal recessive or X linked

6 months or max. 1st 12 months
: -
1- nephritic $
2- other manifestations as :
- SNHL ..
- Keratoconus
.. ) transplantation ( kidney
B - IgA nephropathy
mucosa IgA serum ) 1
st
protective mechanism ( mucosa IgA ) viral ( infection -
kidney
.. serum IgA .. odema of BM deposition .. ) immune complexes (
so, all manifestations of neohritic $ but severe hematuria proliferation so, recurrent nephritis nephritis infection ..
) hematuria ( IgA with any infection ..
- IgA in serum , normal C3 ( also in alport C3 is normal )
- biopsy deposites IgA
kidney kidney .. kidney transplant 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
anemia RBCs RBCs stem cells of BM .. RF Page |
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2- thrombopiotein
mother cells of platlets megakaryocytes stem cells receptors thrmbocytopenia RF 3- as kidney activate vit D so, if failure Rickets ( if still growing bone )
ultra violet vit D3 .. vit D rays
convert cholestreol to vit D3 ( cholecalcifirol ) wcich is non-functioning vit.
: 2 hydroxylations functioning vit
- in liver at C25 give 25 hydroxy cholecalcifirol
- in kidney hydroxylation at C1 ( parathyroid hormone dependant )
1-25 ( active form parathrmone receptors kidney
) dihydroxycholecalcifirol
liver
) 1 alpha ( 1-hydroxy 1-25 dihydroxy . ). vit D ( 1-25 dihydroxy
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
.. hypertension RF hypo hyper ..
B Excretory functions :
endogenous toxins .. toxins ..
: ..
1- macrotoxins :
& include acute & chronic toxic effect appears so early failure - urea , acetotic materials ( organic acid ) , K+ , phosphorus & uric acid
2- microtoxins :
acute RF failure chronic
- & include urochrome pigment, phenolic materails , aluminium
RF 1- urea = Azot so, uremia = azotemia
( ) main site of excretion kidney ( urea : .. )
1 ) through saliva :
salivation
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urea .. ( ) bad taste of any thing ( .. )

.. destruction .. taste buds .. uremic smell or amonia smell 2 ) through GIT secretions
a- stomach
irritation heart burn gastritis gastric mucosa( .. )
gastritis .. gastric ulcer hematemesis .. .. gastritis vomiting
) black stool ( melena ..b- colon secretions leading to colitis
NB. Colon contain stretch receptors
stool .. colon wall .. spinal reflex .. stimulation soinalcord
segment stool contraction .. stool
rectum & anus
( ) defecation reflex
( irritation ) .. stretch receptors .. motility of colon desire to .. defecate ( .. ) ulcer . dysentry
) ( not amoebic dysentry .. not bacillary ( shigella ) dysentry .. but uremic dysentry
3 ) through sweat :
.. .. irritationitching effect ) receptors of histamine ( to H1
.. .. ..
.. ( called urea frost )
4 ) through Resp. secretions
urea .. secretions of bronchus .. airway chest airway .. ( ) cough
( .. chest free ) chest
.. ( ) - .. ulceration hemoptysis bleeding
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chest .. ) wheezing ( .. bronchospasm ) asthma wheeze ( asthma

manifestations ( kidney )
.. .. 1- suppression to cyclooxygenase Enz. Inside the platlet (
) leading to thrombathenia
.. RF purpura .. thrombocytopenia 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
hypochole. liver F
RF excess fat post. Strept. GN 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 )

coma drousy .. .. manifestations of azotemia
serosal membranes .. - 5
1- pericardium dry pericarditis
2- pleura dry pleursy
3- peritoneum dry peritonitis
1,2 & 3 all leading to stitching pain
2- organic Acid :
kidney PH .. organic acids
) PH alkaline .. acidic (
PH bicarbonate reabsorption .. active process organic acids acidosis
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kidney ...
: acidosis
a- failure of excretion of organic acid
b- loss of bicarb. In urine
acidosis 1- Kussmaul respiration ( air hunger ) : WHY ??
CO2 + H2O .. lung organic acids .. resp. system PH leading to deep respiration respi.center irritate CO2 Kussmaul respiration ( air hunger ) ..
Acidosis .. CO2 so, air hunger is a compensation for acidosis .
2- rickets if still growing bone ( due to melting of bone )
bicarb Ca .. Ca-carbonate bone .. bicarb bone Rickets bone
- 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
motility K+ ) absorption ( diarrhea .. colic motility : 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
.. hypotonia skeletal Ms tone K+
4- Phosphate :
- RF no excretion of Ph WHY ??
parathyroid hormone .. Ca Ph Parathormone leding to excretion of Ph & reabsorption of Ca
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kidney ( receptors parathormone ) .. .. Ca Ph

) ( - so, in urine Ca & Ph
Ca Ph .. .. ..
parathyroid gland parathyroid hormone .. :

a- kidney
b- Bone
osteoblast & osteoclast .. parathormone activity .. osteoclast ( Ph & Ca bone ) osteoblast
- gland
parathyroid .. parathormone Ph
parathormone .. Ca & Ph Ph .. kidney

Ph Ca
kidney .. .. Ca .. Ph Ph
.. parathormone .. ... Viscous circle parathormone
X ray cysts .. Ca & Ph
.. Rickets
) not cyst ( deminerlaized area ostietis fibrosa cystica
Rickets .. RF 3 :2- acidosis leading to melting of bone 3- parathormone
1- Vit D activation
5- Uric acid
arthritis Microtoxins :
1- Phenolic materials :
( ) ..
.. RF irritation AHCs ( fasciculation ) irritation .. phrenic n ( Hiccup spontinous contraction of diaphragm ) ) hiccup occur in 30 % of RF ( RF
2- melanine degradation urochrome pigments
urine .. .. .. pigment ..
.. .. .. .. .. ( clear
) urine
- pigment
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3- Alumonium
( ) ( )
( .. pure ) .. delivery

kidney .. .. RF :1- frontal lobe affection memory disturbance
2- deposites in BM may pancytopenia
thrombocytopenia : RFa- thrombopiotein
b- alumonium toxicity
- causes of purpura in RF :
2- urea thrombathenia
1- causes of thrombocytopenia
15 16
.. endocrine & exocrine functions of the kidney function kidney

C - Power of concentration & dilution :
( specific gravity )
- specific gravity of urine normally = 1015 1030
1025
1030 .. 1015
specific gravity urine or plasma specific gravity .. osmolarity .. Na
- normal specific gravity of plasma = 1010
.. glomerular filtrate plasma ( .. ) plasma protein plasma protein specific gravity
specific gravity glomerular filtrate plasma 1010 Gl. Filtrate proximal convoluted tubule reabsorption .. Na & water .. PCT specific gravity ..
..
So, specific gravity at loop of henle = 1010
loop of henle reabsorption of Na .. reabsorption of water .. filterate specific gravity 1010
distal convoluted tubules .. dependant on aldosterone reabsortion of Na .. specific gravity
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.. collecting tubules ( .. ) gates .. controled by ADH .. interstatial medulla ) reabsorption of water only ( not salt
specific gravity .. specific gravity urine= concentration of urine
.. ADH .. urine output + specific gravity BUT if ADH urine output + specific gravity
- & dilution ( kidney
) power of concentration of urine
.. 12-8 .. ( ) water intake

water intake .. .. .. ADH :
.. specific gravity + ( 1030 )
( 2 ) .. water intake) ADH to basal level urine output + specific gravity ( 1015
specific gravity normal .. 1030 1015 ( .. ) 1015 ( ) 1030
) ( this is called normal power of concentration & dilution
: specific gravity : .. ( )
.. .. ..
.. ( ) ..
..
( )
: kidney reabsorption of water .. during fasting

reabsorption of water over hydration .
.. 1- iterstatial medulla ( due to high osmolarity in it )
2- ADH
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RF ADH .. .. interstitial medulla .. glomerular filterate

with specific gravity 1010 as plasma ( in acute & chronic RF ) (low specific gravity)
specific gravity .. urine volume .. glomerular filterate .. fixed .. 1010
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 :
: renal anomalies .. 5 Ch. RF - Hypogenesis , agenesis ( aplasia of the kidney ) or urinary tract anomalies
chronic acute
- 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
g- chest pain or abdominal pain
f- bronchial secretions
h- CNS affection
4 3 ) .. (
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 :
) 2 ( kidney 180 000 ml / 24 hrs = 180 24 glomerular filterate urine output = 500 1500 ml / m2 / 24 hrs Page |
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polyuria 1500 .. anuria 180 .. oliguria 400

urine ) ( if nephrons < 0.5 milion renal impairment ) .. ( :
2 000 000 nephrons give 180 000 ml
So, 200 nephrons give 18 ml & 100 nephrons give 9 ml
100 000 .. 0.5 chronic RF ..
As 100 9
so , 100 000 give 9000 ml
.. polyuria .. 9 urine volume .. 9

10 000 .. 3- 2 .. .. 10 000 900 ml urine output
..
1000 .. So, 1000 90 ml ( oliguria even anuria according to surface area )
: chronic RF urine volume 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 . iron & folic acid .. ammonia
b- loss :
1- hemolysis of RBCs by urea & other toxins .
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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 ??
bone deformity 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 :
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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+
.. active process excretion
- 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 .. 9 1 gm .. .. fat renal transplant
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c- protein
urea ...
d- minerals
- Na or is there salt loss or retention ??
- K +
- Ca
fat .. ) skimmed milk ( - Ph
.. .. .. .. ..
as Posphate binder .. Ph excretion e- vitamins
- increase fat soluble Vit.
- increase water soluble vit . ( )
.. water soluble vit .. dialysis
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
dialysis .. manifestations .. 4- Renal transplantation
5- social & psychological ttt
6- Drug dosage
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kidney .. 17 16
Acute renal failure

written
Definition
acute renal failure
. waste products kidney stop of filteration :
ARF
chronic .. may be reversible urine output .. filteration chronic .. oliguria .. ARF .. Causes :
: filteration .. filteration filteration
1- glomerular capillary pressure
) plasma protein ( . ) ( efferent .. diameter ) afferent ( Afferent diameter : efferent diameter = 7 : 1
. capillary pressure
2- Bowman's capsule
. pressure filterate 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
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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
etc........................ RBF .. renal arterial pressure
4- post surgery cardiac surgery
.. intestine motility .. paralytic ileus
motility .. IV fluids ..
.. not stool .... ) passing Flatus ( oral intake ) !! (
. motility auscultation .. .. dehydration .. IV fluids creatinie urea renal functions ..
..
renal impairment ..
.. .. motility
5- Nephrotic $ :
vessels .. osmotic pressure .. urine intrerstatium
....... ... blood volume .. severe cases intravascular interstatium there is Hypotnsion pre renal causes B - Bowman's capsule pressure ( called post renal causes )
: .. urine pathway obstruction 1- Acquired :
- as stricture pf urethra or stone .
2- congenital :
- posterior urethral valve
urethra urination fold of mucosa obstruction ureter back pressure .. bladder retention of urine .. obstruction pelvis of kidney
then back pressure to all nephron's parts then to Bowman's capsule
so, hypervolemia & hypertension blood volume .. filteration
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2 back pressure .. ) ( urethra obstruction .. kidneys

kidney .. ) ureter .. ( unilateral obstruction
.. renal impairment ..
single .. unilateral obstruction ARF functioning kidney
C Renal causes as :
1- filter closure ( )
.. nephritic .. acute GN .. odema or proliferation of cells of BM
..
2- nephrons destruction ( )
- as in severe anoxic tubular necrosis
.. ) diarrhea ( dehydration . pre renal cause .. nephrons .. renal ischemia
3- toxins as all nephrotoxic drugs as
- all anesthetic drugs
- aminglycosides
pre aminoglycosides .. dehydrated gastroenteritis renal cause
- carbon tetrachloride
4- infarction as an effect of embolus
5- congenital anomalies :
- agenesis ( ) or hypogenesis
Hypertension .. bl. Volume .. renal pre , post or renal .. ARF : pre renal .. .. do catheterization post or renal renal .. bladder post renal urine ) ( Clinical picture :
macrotoxins .. acute renal failure 1- oliguria or anuria
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.. : magor toxins 2- urea manifestations of azotemia

3- metabolic acidosis manifestations as air hunger
.. loss of bicarb .. retention of organic acid acute RF acidosis ) ( 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
) 24 ( 2 3 cm urine a- volume oliguria ( < 400 ml / m2 / 24 hrs )
b- low fixed specific gravity ( 1010 )
.. specific gravity .. urine specific gravity ARF -1
.. end stage chronic renal failure -2
c- RBCs casts
mucoprotein RBCs d- Na
2- serum analysis :
- urea & creatinine - K & uric acid ( all major toxins increased )
- Na dilutional hyponatremia
dehydration pre post & renal .. .. 200 ml water container .. 130 mEq / L
NB. mEq = milliequivalents
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container .. 2 + 600 ml water .. .. ( .. 300 %

100 % )
.. post renal & renal filteration .. salt & water .. retention Na retained .. salt dilutional
hyponatremia
( .. ) 3- ECG
4- investigation of underlying etiology .
Treatment :
.. acute .. .. chronicRF
:a- history of precipitating factors .
b- oliguric
c- rapid deep respiration
LINES OF ttt
1- measure Bl. Pressure if low :
.. ... low .. pre renal .... glomrular capillary pressure ringer lactate
lactate liver .. bicarbonate acidosis
( 20 ml / Kg dose ) emergency .. ( ) bl. Volume
.. filteration .. .. urine
urine .. osmotic diuresis .. mannitol .
.. lasix .. urine .. .. chronic ( RF anoxic tubular necrosis nephrons )
2- If High Bl. Pressure : so, renal or post renal
.. .. post renal .. renal functions .. obstruction .
3- if renal :
- .. urine renal filteration
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post. Streptococcal GN ( fliud chart K complications ) dialysis

: pre renal .. lasix ..
: lasixUrinary Hues
written
urineA - Dark urine :
:a- retained urine :
.. retained urine urochrome pigment b- bile pigments
obstructive J .. direct bilirubin .B red urine :
red urine1- hematuria
2- hemoglobinuria
3- myoglobin in urine
.. .. ms ( myoglobin ) Hb
4- porphyrin
Hb iron + protoporhyrin5- Iron in chronic hemolytic anemia
chelating agents .. .. .. desferroxasmine iron
urine
6- urates
) 7- Drugs rifampicin ( rimactan
8- Foods as beets
.. .. ( )
C Dark brown or black urine :
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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 .
urine homogentisic acid .. homogentisic acid oxidase .. sclera .. cartilage alkaptonuria
Hematuria
> 5 RBCs / high power field of microscope ( HPF ) urine RBCs .. RBCs urine ..
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
urethra pelvis od the kidney urinary tract 1- Congenital anomalies as :
a- polycystic kidney
hematuria .. cyst b- hemangioma in kidney pelvis leakage hematuria .
2- Infections in urinary tract :
- acute pyelonephritis or cystitis
. UTI / .. infections 3- Tumors as wilms tumor
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) advanced ( very late .. hematuria ) early ( hematuria .. hypernphroma

) hematuria ( medulla .. cortex wilms
medulla hypernephroma
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 :
hematuria .. heavy exercise a- erect position congestion of kidney
exercise
b- during exercise may minir trauma
DD between glomerular & non glomerular causes :
-1
. .. glomerular .. non .. .. relation to micturation .. -2
. .. glomerular : non urinary bladder *
urethra *
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-3 oligurai , odema & hypertension

glomerular nephritic .. non .. :* .. urethra
* .. bladder suprapubic refion
* .. pyelonephritis loin pain
( .. )
* .. .. .. .....
-4 urine analysis
- glomerular casts , protein >= +2
- if non glomerular no casts , proteinuria < +2
.. + ..
: nephrostomy
: ureter .. .. pelvis of the kidney( )
20 17
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Nephrology - DR Abo-ElAsrar - by El Azhar Medical Students 2012

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( BETA EDITION)

Nepgrology Dr. Abo-Asrar

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Nepgrology Dr. Abo-Asrar

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Nephrology Prof. Dr. Abo El-Asra r

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Nephrology Prof. Dr. Abo El-Asra r

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Nephrology Prof. Dr. Abo El-Asra r

proteinuria ... urine urine :

capillaries arterial side venous side heart

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Nephrology Prof. Dr. Abo El-Asra r

waste products blood 13 ) (

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Nephrology Prof. Dr. Abo El-Asra r

liver osmotic pressure synthesis of albumin as a compensation

liver NB. ) liver (

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Nephrology Prof. Dr. Abo El-Asra r

glomerular filtration 1- so , oliguria

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Nephrology Prof. Dr. Abo El-Asra r

.. dorsum of the hands & foots odema 4- Hematuria :

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Nephrology Prof. Dr. Abo El-Asra r

WHAT IS THE ETIOLOGY ?

in minimal change -ve

post. Strept. +ve

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Nephrology Prof. Dr. Abo El-Asra r

- linear on glomeruli or lumbi deposition

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Nephrology Prof. Dr. Abo El-Asra r

4- sickle cell anemia immune complex formation

6- shistsoma mansoni & malaria

7- drugs as gold , penicllin etc

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

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Nephrology Prof. Dr. Abo El-Asra r

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Nephrology Prof. Dr. Abo El-Asra r

" " " : ,, : " "

Nephrology Prof. Dr. Abo El-Asra r

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Nephrology Prof. Dr. Abo El-Asra r

) b- fat due to increased cholesterol ( already increased in this patient

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Nephrology Prof. Dr. Abo El-Asra r

( albumin 200 ) .. .. interstitial space bl. Volume kidney .. hypervolemia

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Nephrology Prof. Dr. Abo El-Asra r

6 .. ) 2 2 2 ( 6 ( single dose cortisone in the early morning every other day )

: D.D. of minimal change

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Nephrology Prof. Dr. Abo El-Asra r

( hypertension , oliguria , hematuria )

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Nephrology Prof. Dr. Abo El-Asra r

- lead poisoning arsenic poisoning

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Nephrology Prof. Dr. Abo El-Asra r