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Titu Maiorescu University
Curs Medicina Interna
NEPHROLOGY- I
Prof univ dr Ion C Tintoiu
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Characteristics of Renal Structure andFunction
I. Physiological Anatomy of the Kidney
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Renal cortex
Cortical lobules - whichform caps over the
bases of the pyramids Renal columns - which
dip in between thepyramids
Renal medulla
has 10 conical massescalled renal pyramids,their apices form renalpapillae
Renal sinus
Space that extends into kidney from hilus
Contains branches of renal artery and renal vein
Renal pelvis divides into 2-3 major calices and these in turn divide into 7-13 minor calices, each minor calyx (cup of flower) ends in an expansion
which is indented by 1-3 renal papillae
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Histologically, each kidney is composed 1-3 millionuriniferous tubules.Each consists of
Secretory part - which forms urine is callednephron, functional unit of kidney Nephrons open in to collecting tubules. Many such tubules
unite to form the ducts of Bellini which open into minorcalices
Arterial Supply
One renal artery on each side arising from abdominalaorta
At or near hilus, renal artery divides into anterior andposterior branches giving rise to segmental arteries
Lymphatics
Lateral aortic nodes
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Major Functions of the Kidneys
1. Regulation of:
-body fluid osmolarity and volume-electrolyte balance
-acid-base balance
-blood pressure
2. Excretion of
. metabolic products,drugs
.foreign substances (pesticides, chemicals etc.)
.excess substance (water, etc)
3. Secretion of
-erythropoitin
-1,25-dihydroxy vitamin D3(vitamin D activation)
- renin- rosta landin
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-Nephron struc
and
Functions
Glomerulus
Proximal Tubule (PCT)
Loop of Henle
Distal tubule
Collecting tubule
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Functions of the Nephron
Filtration
Reabsorption Secretion
Excretion
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Glomerular Filtration
Figure 26.10a, b
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Proximal Tubule (PCT)Reabsorption
NaCl
Water
Bicarbonate
Glucose Proteins
Aminoacids
K+, Mg, PO4+, uric acid,
ureaSecretion
Organic anions
Organic cations
Ammonia products
Reabsorption of solutes in PCT
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Loop of Henle 25-30% ultrafiltrate reaches loop of Henle
15-20% filtered Na+load reabsorbed Solute and water reabsorption is passive and follows
concentration and osmotic gradients (except thick
ascending loop) Sodium reabsorption is coupled to both K+and Cl-
reabsorption Cl-in tubular fluid is rate limiting factor
Calcium and magnesium reabsorption Parathyroid hormone calcium reabsorption at this
site Loop diuretics inhibit Na and Cl reabsorption in TAL
compete with Cl- for its binding site on carrier protein
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Distal tubule
Very tight junctions between tubular cellsrelatively impermeable to water and Na+
5% of filtered Na+load reabsorbed
Parathyroid hormone and vit D mediatedcalcium reabsorption
The late distal segment (collecting segment) Hormone mediated Ca+reabsorptionAldosterone mediated Na+reabsorption
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Collecting tubule
5-7% of filtered Na+load is reabsorbed
Cortical collecting tubule
two types ofcells:Principal cellssecrete K+aldosterone
mediated Na
+
reabsorptionIntercalated cellsacid base regulation
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A Summary of Renal Function
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Nephron symphony
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.Renal Pathology
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Diseases of the kidney
1-Glomeruli
Glomerulonephritis
Primary
Secondary
Chronic
2-Tubulointerstitium
Acute tubularnecrosis
Pyelonephritis
Acute
chronic
3-Vessels
Nephrosclerosis
4-Urinary obstruction
Stones
Hydronephrosis
5- Cystic diseases of thekidney
6-Tumors
BenignMalignan
7-Litiazis
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.Glomerular diseases
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GLOMERULONEPHRITIS
Acute Glomerulonephritis:
Rapidly Progressive
Glomerulonephritis Chronic Glomerulonephritis
Nephrotic Syndrome
Asymptomatic urinary
abnormalities
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Glomerular disease
Primary Glomerulonephritis
Minimal change GN
Membranous GN
Focal segmental GS
Membranoproliferative GN
Diffuse proliferative GN
Crescentic GN Seconday
SLE, DM, Amyloidosis, Goodpasture, vasculitis
Hereditary
Albort syndrome
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Glomerular diseases:
Primary Glomerulonephritis
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.AcuteGlomerulonephritis
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Acute glomerulonephritis is theinflammation of the glomeruliwhich causesthe kidneys to malfunction
It is also called Acute Nephritis,Glomerulonephritis and Post-StreptococcalGlomerulonephritis
Predominantly affects children from ages 2to 12
Incubation period is 2 to 3 weeks
Acute GlomerulonephritisDefinition
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Fever
Headache
Malaise
Anorexia
Nausea and vomiting
High blood pressure
Pallor due to edema and/or anemia Confusion
Lethargy
Loss of muscle tissue
Enlargement of the liver
Acute GlomerulonephritisGeneral Symptoms
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Hematuria:dark brown or smoky urine
Oliguria: urine output is < 400 ml/day
Edema: starts in the eye lids and facethen the lower and upper limbs then
becomes generalized; may be migratory
Hypertension: usually mild to moderateHypoproteinemia,
hypercholesterolemia),
mixed
Acute Glomerulonephritis
Signs and Symptoms
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Acute GlomerulonephritisEtiology
Infectious
Streptococcal
Nonstreptococcal postinfectious
glomerulonephritis
Bacterial
Viral
Parasitic
Noninfectious
Multisystem systemic diseases
Primary glomerular diseases
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Acute Glomerulonephritis
INVESTIGATIONSBase line measurements:- Urea
- reatinine-Urinalysis MSU):a) Urine microscopy red cell cast)
b) proteinuria
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Hypertensive encephalopathy,
Heart failure and acute
Pulmonary edema may occur in severecases
Acute renal necrosis due to injury of
capillary or capillary thrombosis
Acute Glomerulonephritis
Complications
A t Gl l h iti
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proper hygiene
prompt medical assessment fornecessary antibiotic therapy should be
sought when infection is suspected
prophylactic immunizations
Acute Glomerulonephritis
Prevention
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.Chronic glomerulonephritis
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Chronic glomerulonephritis
The condition is characterized
1 - irreversible and progressive glomerularand tubulointerstitial fibrosis
2-ultimately leading to a reduction in theglomerular filtration rate (GFR) and
3- retention of uremic toxins
.. The diagnosis of CKD can be made withoutknowledge of the specific cause.
Chronic glomerulonephritis
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Chronic glomerulonephritis
Etiology
Nearly all forms of acute glomerulonephritishave atendency to progress to chronicglomerulonephritis.
The progression from acute glomerulonephritis to
chronic glomerulonephritis is variable.
Whereas complete recovery of renal function is therule for patients with poststreptococcal
glomerulonephritis, several otherglomerulonephritides, such asimmunoglobulin A (IgA) nephropathy, oftenhave a relatively benign course and many do notprogress to ESRD.
Ch i l l h iti
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Chronic glomerulonephritis
Pathogenesis
Reduction in nephron mass from the initial injuryreduces the GFR.
This reduction leads to hypertrophy andhyperfiltration of the remaining nephrons and to
the initiation of intraglomerular hypertension.These changes occur in order to increase the GFR of
the remaining nephrons, thus minimizing thefunctional consequences of nephron loss.
The changes, however, are ultimately detrimentalbecause they lead to glomerulosclerosis andfurther nephron loss.
Chronic glomerulonephritis
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Chronic glomerulonephritis
Histo log ic Findings
In early stages, the glomeruli may still
show some evidence of the primary
disease.
In advanced stages, the glomeruli are
hyalinized and obsolescent.
The tubules are disrupted and atrophic,and marked interstitial fibrosis and
arterial and arteriolar sclerosis occur.
Chronic glomerulonephritis
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Chronic glomerulonephritis
Histo log ic Find ings
1-Min imal-Change Disease
2-Focal segmentalg lomerulosc leros is
3-Mesang iocap i l lary GN
4-Membranous neph ropathy
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Mesangial proli ferativeMPGN
1-Hypercellularity,
2-Mesangial proliferation,3-Inflammatory cell infiltrate,
4-Positive IF for IgG and C3 and
5-Subepithelial deposits on EM.
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Chronic g lomerulonephr i t is
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Chronic g lomerulonephr i t is
Clinical Manifestations
Uremia-specific findings Edemas
Hypertension
Jugular venous distension (if severe volumeoverload is present)
Pulmonary rales (if pulmonary edema ispresent)
Pericardial friction rub in pericarditis Tenderness in the epigastric region or blood
in the stool (possible indicators for uremicgastritis or enteropathy)
Chronic g lomerulonephr i t is
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Chronic g lomerulonephr i t is
Lab Stud ies
Urinalysis
Urinary protein excretion
Serum chemistry
Serum creatinine and urea nitrogen levelsare elevated.
Impaired excretion of potassium, free water, andacid results in hyperkalemia, hyponatremia, andlow serum bicarbonate levels, respectively.
Impaired vitamin D-3 production results inhypocalcemia, hyperphosphatemia, and high levelsof parathyroid hormone.
Low serum albumin levels may be present ifuremia interferes with nutrition or if the patient isnephrotic.
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Chron ic glomeruloneph r i tis
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g p
Treatment
Minimal change glomerulonephritis
1-Corticosteroidsinduce remission in >90% of
children and 80% of adults (slower response).
2-immunosuppression:(cyclophosphamide,
ciclosporin (=cylosporin)): early/ frequent
relapses; steroid SEs/dependence.Prognosis: 1% progress to ESRF.
Chronic g lomerulonephr i t is
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Chronic g lomerulonephr i t is
Treatment
Focal segmental glomerulosclerosis
Poor response to corticosteroids(10
30%). Cyclophosphamide or ciclosporin
(=cylosporin) may be used in steroid-resistant
cases.
Prognosis: 3050% progress to ESRF.
Chronic g lomerulonephr i t is
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Chronic g lomerulonephr i t is
Treatment
Mesangial proliferative GN
1-Antibiotics,
2-Diuretics, and3-Antihypertensives as necessary.
4-Dialysis is rarely required.
Prognosis: Good.
Chronic g lomerulonephr i t is
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Chronic g lomerulonephr i t is
Treatment
Membranous nephropathy
If renal function deteriorates, consider
corticosteroids and chlorambucil.
Prognosis:Untreated, 15% complete
remission, 9% ESRF at 25yrs and 41% at
15yrs.
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.Rapidly ProgressiveGlomerulonephritis
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Rapidly Progressive Glomerulonephritis
Rapidly progressive
glomerulonephritis (RPGN) is a
disease of the kidney that results ina rapid decrease in the glomerular
filtration rate of at least 50% over
a short period, from a few days to 3months.
Rapidly Progressive Glomerulonephritis
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The cause of RPGN is unknown. Agenetic predisposition may exist for thedevelopment of this disease.
Multiple studies have demonstrated thatANCA-(antineutrophil cytoplasmicantibodies) activated neutrophils
attack vascular endothelial cells.ANCA-associated vasculitis.
A viral etiology is possible.
Rapidly Progressive Glomerulonephritis
Etiology
R idl P i Gl l h iti
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Rapidly Progressive Glomerulonephritis
Pathology
Renal biopsshowA diffuse, proliferative,
necrotizingglomerulonephritis withcrescent formation.
The main pathologicfinding is fibrinoid
necrosis(>90% of biopsyspecimens); extensivecrescent formation ispresent in at least 50% ofglomeruli.
Rapidly Progressive Glomerulonephritis
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p y g p
Clinical Manifestations
Symptoms and signs of renal
failure,
pain,haematuria,
systemic symptoms (fever, malaise,myalgia, weight loss).
R idl P i Gl l h iti
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Rapidly Progressive Glomerulonephritis
Lab Studies
The most important requirement in the diagnosis ofantineutrophil cytoplasmic antibodies (ANCA) ANCA-associated disease is a high index of suspicion. Rapiddiagnosis is essential for organ preservation. Laboratorystudies include the following:
Routine chemistry: The most common abnormality isan increased serum creatinine level.
Urinalysis with microscopy:
Antinuclear antibody (ANA) titer:
ANCA
Urine and serum protein electrophoresis: Perform this inany middle-aged or elderly person presenting with RPGNto exclude the presence of light-chain disease or overtmultiple myeloma as a cause of the clinical findings.
Rapidly Progressive Glomerulonephritis
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Rapidly Progressive Glomerulonephritis
Treatment
1-High-dose corticosteroids;
cyclophosphamide plasma
exchange/ renal2-Transplantation.
Prognosis:Poor if initial serum creatinine
>600mol/L.
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Proteinurea
3.5 g/day
(protein: creatinine
ratio >3-3.5)
Generalized
Oedema
Hypoalbuminaeia
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The Nephrotic Syndrome
Is not a disease but a group of signs and
symptoms seen in patients with heavy
proteinuria
presents with oedema
proteinuria usually > 3.5g / 24hrs (>0.05g
/ kg / 24hrs in children)
serum albumin < 30g/l
other features: hyperlipidaemia, and
hypercoaguable state
The Nephrotic Syndrome
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p y
Pathophysiology
proteinuria: due to an increase in glomerular
permeability
hypoalbuminuria: occurs when liver synthesis cannot
keep up with urine losses
oedema mechanism is complex and still in dispute:
primary salt and water retention associated withreduced renal function as well as reduced plasma
oncotic pressure are primary factors (overfill and
underfill)
minimal change disease fits the underfill theory best hyperlipidaemia: increased liver synthesis
hypercoagulation: increased fibrinogen and loss of
antithrombin III
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D M GED Proteinuria
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Primary (idiopathic):
Minimal change disease
Most common cause in children
Membranous Nephropathy
Most common cause in Adults
Focal Segmental Glomerulosclerosis
MembranoProliferative
Glomerulonephritis
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Secondary to:DM(the leading cause of secondary nephrotic syndrome)
SLE
AmyloidosisInfections:Hepatitis B and C, HIV,syphilis, post-streptococcal
Malignancy:
multiple myloma , Hodgkin lymphoma, solid tumorDrugs(NSAIDs, gold, penicillamine ,heavy metals etc).
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Generalized Odema
-The predominant feature
-The face, particularly the
periorbital area, is swollen
in the morning& lower extremitiesand genital area later in the day
-In advanced disease: the whole body
(anasarca) shortness of breathFrothy urine and urine dipstick
proteinuria value of 3+
Symptoms & signs for secondary cause if present
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24-hour urine collection>3,5 g/day (nephrotic-range proteinuria)
Alternative : calculating the total protein-to-creatinine ratio (mg/mg)on a random urine specimen.
The history and physical examination
Systemic diseaseSerologic studies (ANA), complement, hepatitis B and hepatitis Cserologies and the measurement of cryoglobulins ,serum or urine protein
electrophoresis.
Renal biopsyrequired to establish the diagnosis in most of times.
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BUN, creatinine, creatinin clearnce.Na,
K,bicarbonates,chloride
CBC , serum albumin, serum proteins, calcium,
Lipid profile, Coagulation tests
Renal biopsy
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69
Disease-
spesific
Complication
symptoms
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OedemaLow salt diet
Diuretics
serial measurement of body weight
ProteinuriaACE inhibitors or ARBs
HypoalbuminaemiaHigh protein diet not indicated0.81 g/kg/day
Ref: Up to date online 17.3.
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HyperlipidaemiaRegular Lipid profileStatin if severe long lasting nephrotic syndrome
Control other CVD risk factorstarget blood pressure
125/75
Thromboembolic riskRoutin Prophylactic anticoagulationnot recommend
High index of suspicion for thromboemboli
InfectionsHigh index of suspicion
Antipneumococcal and influenza vaccinations
Ref: Up to date online 17.3.
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Titu Maiorescu University
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y
Curs Medicina Interna
NEPHROLOGY-II
Prof univ dr Ion C Tintoiu
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.Other Renal Diseases
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Other Renal Diseases
1. 1-Interstitial Nephritis
2. 2-Diabetic Nephropathy
3. 3-Microscopic Vasculitis and SLE
4. 4-Gout and the Kidney
5. 5-Myeloma Kidney
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.1-Interstitial Nephritis
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Causes of interstitial nephritis
Drugs
Infection
Autoimmune
Metabolic
Radiation Neoplastic infiltration
Mechanical
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Drugs and interstitial nephritis
methicillin 17%other penicillins
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Bacterial infection
bacterial infection of the renal parenchyma
causes interstitial nephritis
infection without anatomical abnormalityseldom produces permanent damage
obstruction (stones, prostate etc) in
combination with infection can cause
progressive disease tuberculosis causes extensive destruction from
granulomata, fibrosis and caseation
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Autoimmune
systemic lupus
erythematosus
transplantrejection
deposition of :
calcium salts
uric acid
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Infiltration in neoplastic and other
diseases
lymphoma and leukaemias
myeloma
Bence-Jones protein (light chains frommalignant plasma cell clone) causes interstitial
nephritis, tubular obstruction(cast nephropathy)
and amyloid deposition
called myeloma kidney
sarcoidosis
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mechanical causes of interstitial
nephritis
reflux nephropathy
calculi
ureteric fibrosis
prostatic hypertrophy
urethral stenosis
tumours
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pathophysiolgical changes in
interstitial nephritis
hypertension (50%)
proteinuria (~1-2 g/24hrs)
reduced urinary concentrating ability
salt wasting
renal tubular acidosis
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Diagnosis and Treatment
renal impairment
inactive urine sediment common (cf nephritis)
eosinophils in urine and interstitium in acute
hypersensitivity reactions
renal biopsy
improvement after withdrawal of drugs and toxins
use of corticosteroids (prednisone)
water and and electrolyte
treatment of hypertension
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.2-Diabetic nephropathy
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Diabetic Nephropathy
Pathological lesions:
diffuse glomerular sclerosis
nodular sclerosis (Kimmelstiel -Wilson lesion)
arteriolar hyalinisation
Associated lesions:
Papillary necrosis
Pyelonephritis Bladder dysfunction
Radio contrast renal failure
hyporeninaemic hypoaldosteronism with
hyperkalaemia
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Pathophysiology of Diabetic Nephropathy
renal hypertrophy and hyperfiltration
microalbuminuria (< 100mg/24hrs and negative to
protein test strip-albustix)
hypertension
hyperfiltration and microalbuminuria can be improved
by good diabetic control
microalbuminuria is a predictor of diabetic
nephropathy and mortality in diabetics - it probably
has no predictive value for other renal diseases
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WHO classificationLupus Nephritis Type I no pathology
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Lupus Nephritis Type I no pathology
yp
eV:membranous
Type II : mesangial
TypeIII:fo
cal
proliferative
Ty
peIV:diffu
se
proliferative
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Lupus nephritis
Hematuria and proteinuria
HTN common
Active urine sediment: rbc casts
Decreased C3 and C4
anti-double stranded DNA antibody specific foractive nephritis
Prognosis varies greatly based on initialpathology, usually guarded
Type IV greatest risk of progressing to CKD stage 5
Treatment with steroids, cytoxan
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Systemic Lupus Erythematosus
Diagnosis:
clinical presentation - rash, arthralgia, fever,
tiredness, anaemia etc
hypocomplementaemia - (low C3 and C4)
antinuclear antibodies and anti DNA antibodies
Treatment:
depends on histological severity (WHO class I - V) nearly all get corticosteroids
WHO Class IV usually get corticosteroids and
cyclophosphamide
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.Gout, Uric Acid and Renal
Disease
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Gout, Uric Acid and Renal Disease
uric acid calculi, parenchymal deposits of
uric acid and tubular obstruction with
urate can cause renal damage an elevated plasma uric acid does not in
itself seem to cause renal damage
1/4 of patients with gout get uric acidstones
1/4 of patients with uric acid stones will
have gout
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Acute and Chronic urate nephropathy
acute nephropathy with overproduction of uric acid
and kidney obstruction with uric acid crystals
can occur with treatment of malignant disease with
cytotoxics, heat stroke and status epilepticus
treat with fluids and prophylaxis with allopurinol
role of uric acid in chronic renal failure disputed but
does occur with some familial disorders
association between hyperuricaemia, hypertensionvascular disease, hyperlipidaemia and diabetes
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.Amyloidosis and MyelomaKidney
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Amyloidosis and Myeloma Kidney
amyloid represents a family of proteins which
polymerize to produce the beta pleated sheet of
amyloid and deposit in tissues
AL amyloid (primary amyloid) made from
light chains associated with plasma cell
disorders, mostly overt myeloma
AA amyloid (secondary amyloid) is made fromA protein and is an acute phase reactant
associated with chronic inflammatory diseases
like rheumatoid arthritis and bronchiectasis
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Titu Maiorescu University
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Curs Medicina Interna
NEPHROLOGY-III
Prof univ dr Ion C Tintoiu
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.Acute Renal Failure
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Acute renal failure -ARF
Deterioration of renalfunction over a period of hours to days,resulting in
the failureof the kidney to excrete nitrogenouswaste products and
to maintainfluid and electrolyte homeostasis ARF Rapid deterioration of renal function
(increase of creatinine of >0.5 mg/dl in
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Hilton, R. BMJ 2006;333:786-790
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Pre-renal
Volume depletion Renal losses (diuretics, polyuria)
GI losses (vomiting, diarrhea)
Cutaneous losses (burns, Stevens-Johnson syndrome)
Hemorrhage Pancreatitis
Decreased cardiac output Heart failure
Pulmonary embolus
Acute myocardial infarction Severe valvular heart disease
Abdominal compartment syndrome (tense ascites)
Renal
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Glomerular Antiglomerular basement membrane (GBM) disease (Goodpasture
syndrome)
Antineutrophil cytoplasmic antibody-associatedglomerulonephritis (ANCA-associated GN) (Wegenergranulomatosis, Churg-Strauss syndrome, microscopic polyangiitis)
Immune complex GN (lupus, postinfectious, cryoglobulinemia,
primary membranoproliferative glomerulonephritis) Tubular
Ischemi
Totoxic
Heme pigment (rhabdomyolysis, intravascular hemolysis)
Crystals (tumor lysis syndrome, seizures, ethylene glycolpoisoning, megadose vitamin C, acyclovir, indinavir,methotrexate)
Drugs (aminoglycosides, lithium, amphotericin B,pentamidine, cisplatin, ifosfamide, radiocontrast agents)
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Post-renal
Ureteric obstruction
Stone disease,
Tumor,
Fibrosis,
Ligation during pelvic surgery
Bladder neck obstruction
Benign prostatic hypertrophy [BPH]
Cancer of the prostate
Neurogenic bladder
Drugs(Tricyclic antidepressants, ganglion blockers, Bladder tumor,
Stone disease, hemorrhage/clot)
Urethral obstruction (strictures, tumor)
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Clinical feature-1
Signs and symptoms resulting from loss of
kidney function:
decreased or no urine output, flank pain,edema, hypertension, or discolored urine
Asymptomatic
elevations in the plasma creatinine
abnormalities on urinalysis
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Clinical feature-2
Symptoms and/or signs of renal failure: weakness and
easy fatiguability (from anemia),
anorexia, vomiting, mental status changes or
Seizures
edema
Systemic symptoms and findings: fever
arthralgias,
pulmonary lesions
Acute Renal Failure
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Acute Renal Failure
Diagnosis Blood urea nitrogen and serum creatinine
CBC, peripheral smear, and serology
Urinalysis Urine electrolytes
U/S kidneys
Serology:ANA,ANCA, Anti DNA, HBV, HCV, AntiGBM, cryoglobulin, CK, urinary Myoglobulin
Acute Renal Failure
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Acute Renal Failure
Diagnosis Urinalysis
Unremarkable in pre and post renal causes
Differentiates ATN vs. AIN. vs. AGN Muddy brown casts in ATN
WBC casts in AIN
RBC casts in AGN
Hansel stain for Eosinophils
Acute Renal Failure
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Acute Renal Failure
Diagnosis Laboratory Evaluation:
Scr, More reliable marker of GFR
Falsely elevated with Septra, Cimetidine small change reflects large change in GFR
BUN,generally follows Scr increase
Elevation may be independent of GFR
Steroids, GIB, Catabolic state, hypovolemia
BUN/Cr helpful in classifying cause of ARF
ratio> 20:1 suggests prerenal cause
Treatment of
l f il
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acute renal failure
Optimization of hemodynamic and
volume status
Avoidance of further renal insults Optimization of nutrition
If necessary, institution of renal
replacement therapy The function has to be temporarilyreplaced by dialysis
Indication for dialysis
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Symptoms of uremia (
encephalopathy,)
Uremic pericarditis Refractory volume over load
Refractory hyperkalemia
Refractory metabolic acidosis
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.Chronic Renal Failure
Definitions
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Definitions
Chronic Renal Failure Results form gradual, progressive loss of renalfunction
Occasionally results from rapid progression of
acute renal failure Symptoms occur when 75% of function is lost
but considered cohrnic if 90-95% loss offunction
Dialysis is necessary D/T accumulation oruremic toxins, which produce changes in majororgans
S bj ti t
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Subjective symptoms
Chronic Renal Failure Subjective symptoms are relatively same as
acute
Objective symptoms
Renal Hyponaturmia
Dry mouth
Poor skin turgor
Confusion, salt overload, accumulation of K withmuscle weakness
Fluid overload and metabolic acidosis
Proteinuria, glycosuria
Urine = RBCs, WBCs, and casts
Ch i R l F il
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Chronic Renal Failure
Objective symptoms
Cardiovascular Hypertension
Arrythmias
Pericardial effusion
CHF
Peripheral edema
Neurological Burning, pain, and
itching, parestnesia Motor nerve dysfunction
Muscle cramping
Shortened memory span
Apathy
Drowsy, confused,seizures, coma, EEG
changes
Ch i R l F il
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Chronic Renal Failure
Objective symptoms
GI
Stomatitis
Ulcers
Pancreatitis
Uremic fetor
Vomiting consitpation
Respiratory
^ chance of
infection
Pulmonary edema
Pleural friction
rub and effusion
Dyspnea
Kussmauls
respirations from
acidosis
Ch i R l F il
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Chronic Renal Failure
Objective symptoms
Endocrine
Stunted growth in
children Amenorrhea
Male impotence
^ aldosterone secretion
Impaired glucose levels
R/T impaired CHOmetabolism
Thyroid and parathyroid
abnormalities
Hemopoietic
Anemia
Decrease in RBCsurvival time
Blood loss from dialysis
and GI bleed
Platelet deficits
Bleeding and clotting
disorderspurpura and
hemorrhage from body
orifices , ecchymoses
Ch i R l F il
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Chronic Renal Failure
Objective symptoms
Skeletal
Muscle and bone pain
Bone demineralization
Pathological fractures
Blood vessel
calcifications in
myocardium, joints,
eyes, and brain
Skin
Yellow-bronze skin
with pallor Puritus
Purpura
Uremic frost
Thin, brittle nails
Dry, brittle hair, and
may have color
changes and alopecia
Chronic Renal Failure
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Lab findings
BUNindicator of glomerular filtration rate and isaffected by the breakdown of protein. Normal is 10-20mg/dL. When reaches 70 = dialysis
Serum creatininewaste product of skeletal musclebreakdown and is a better indicator of kidneyfunction. Normal is 0.5-1.5 mg/dL. When reaches 10x normal, it is time for dialysis
Creatinine clearance is best determent of kidneyfunction. Must be a 12-24 hour urine collection.
Normal is > 100 ml/min K+ -
Hypocalcemia = tetany
Ch i R l F il
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Chronic Renal Failure
Other abnormal findings
Metabolic acidosis
Fluid imbalanceInsulin resistance
Anemia
Immunoligical problems
Chronic Renal FailureM di l t t t
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Medical treatment
IV glucose and insulin
Na bicarb, Ca, Vit D, phosphate binders
Fluid restriction, diuretics Iron supplements, blood, erythropoietin
High carbs, low protein
Dialysis - After all other methods have failed
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Chronic Renal Failure
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Chronic Renal Failure
Peritoneal dialysis Semipermeable
membrane
Catheter inserted through
abdominal wall intoperitoneal cavity
Cost less
Fewer restrictions
Can be done at home
Risk of peritonitis 3 phasesinflow, dwell
and outflow
Automated peritoneal
dialysis
Done at home at night
Maybe 6-7 times /week CAPD
Continous ambulatory
peritoneal dialysis
Done as outpatient
Usually 4 X/d
Chronic Renal Failure
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Chronic Renal Failure
Transplant
Must find donor
Waiting period long Good survival rate1 year 95-97%
Must take immunosuppressants for life
Rejection
Watch for fever, elevated B/P, and pain over site
of new kidney
Transplant Meds
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Transplant Meds
Patients have decreased resistance to infection
Corticosteroidsanti-inflammarory
Deltosone
Medrol Solu-Medrol
Cytotoxicinhibit T and B lymphocytes
Imuran
Cytoxan
Cellcept
T-cell depressors - Cyclosporin
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Titu Maiorescu University
C M di i I t
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Curs Medicina Interna
NEPHROLOGY-IV
Prof univ dr Ion C Tintoiu
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.RENAL TUMOURS
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.
YSTIC DISE SES OFTHE KIDNEY
CYSTIC DISE SES OF
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THE KIDNEY Fluid filled spaces within the kidney
May involve cortex or medulla or both
May be unilateral or bilateral May be unilocular or multilocular
May be congenital or acquired
May be sporadic or geneticallydetermined
Clinical significance may be trivial or
CLASSIFICATIONS OF
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RENAL CYSTIC DISEASES
Polycystic kidney diseases:
1. Autosomal recessive (ARPKD)
classic infantile polycystic diseasewith congenital hepatic fibrosis
2. Autosomal dominant (ADPKD)
Simple renal cysts
Acquired renal cystic disease
RENAL CYSTIC DISEASES
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Enlarged but normally shaped pelvi-calyceal
system Normal reniform shape complete with fetal
lobation & normal sized (undilated) ureter
Normal glomeruli and tubules
Normal interstitium and no dysplasia
Congenital hepatic fibrosis is almost always
present
Normal numbers of nephrons, no interstitialfibrosis and no dysplasia
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RENAL CYSTIC DISEASESP th l i l F t
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Pathological Features
Bilaterally enlarged kidneys (up to 4000 gms) Diffuse cystic (1-2% cystic nephrons) change
with uninvolved intervening parenchyma
Varying sized, numerous to innumerable
generally spherical unilocular cysts, distributedin cortex and medulla obscuring normalreniform shape and corticomedullary junction,containing yellowish to turbid to brown to black
colored fluid Distorted pelvi-calyceal system
Cysts arising from any part of nephron orcollecting duct
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Simple Renal Cysts
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Extremely common as age advances Incompletely understood pathogenesis
Commonly associated with scarred
kidneysAsymptomatic with normal renal function
May be
solitary/multiple/unilateral/bilateral
Generally unilocular, round to oval of
varying sizes
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Adult polycystic kidney disease
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Renal cancer
.
Renal cancer
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In infants and children :Nephroblastoma ( Wilms
tumour )In adults :
Renal cell carcinoma
Renal cell adenoma
Renal oncocytoma
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NEPHROBLASTOMA
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prognosis and treatment
Depends upon :
stage, age and histology
Surgery with chemotherapy for :stage I & II with favorable histology
surgery with chemotherapy and
radiotherapy for higher stages andunfavorable histology
RENAL CELL CARCINOMA
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Hypernephroma / Grawitzstumour
seems to be arising from maturerenal tubules
RENAL CELL CARCINOMACli i l F t & Di i
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Clinical Features & Diagnosis
classic triad :
hematuria, flank pain and abdominal
mass may be clinically occult, 30% presents
with metastatic lesion
Polycythemia due to erythropoietin constitutional symptoms
imaging techniques - useful
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RENAL CELL
CARCINOMA
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CARCINOMA
prognosis Influenced by multiple factors :tumour size
infiltrative marginshistological type
tumour stage - most important
Can be expressed in terms of histologicaltypes
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Renal cell carcinoma
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Bladder Carcinoma
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Derived from transitional epithelium
Present with painless hematuria
Prognosis depends on grade and depth of invasion
Overall 5y survival = 50%
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.DIALYSIS
Dialysis
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Definition Artificial process that partially replaces renal
function
Removes waste products from blood bydiffusion (toxin clearance)
Removes excess water by ultrafiltration
(maintenance of fluid balance) Wastes and water pass into a special liquid
dialysis fluid or dialysate
Types
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yp
Haemodialysis (HD)
Peritoneal Dialysis (PD)
They work on similar principles: Movementof solute or water across a semipermeable
membrane (dialysis membrane)
Diffusion
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Movement of solute
Across semipermeable membrane
From region of high concentration to one oflow concentration
Ultrafiltration
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Made possible by osmosis
Movement of water
Across semipermeable membrane From low osmolality to high osmolality
Osmolalitynumber of osmotically active
particles in a unit (litre) of solvent
Haemodialysis
Dialysis process occurs outside the body in a
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Dialysis process occurs outside the body in a
machine The dialysis membrane is an artificial one:
Dialyser
The dialyser removes the excess fluid andwastes from the blood and returns the filteredblood to the body
Haemodialysis needs to be performed threetimes a week
Each session lasts 3-6 hrs
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AV Fistula Access
Matures in about 6 weeks
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Ensure good working order Avoid tight clothing or wrist watch on fistula arm
Assess fistula daily; notify immediately if not working
Avoid BP cuff on fistula arm Avoid blood sampling on fistula arm (except daily
HD Rx)
Avoid sleeping on fistula arm
Grafts (synthetic) may be used to create an AV fistula
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AV Fistula
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AV Fistula
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Vascular Access Catheter
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Hemodialysis
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3-4 times a week
Takes 2-4 hours
Machine filtersblood and
returns it to
body
Problems with HD Rapid changes in BP fainting, vomiting, cramps, chest pain, irritability, fatigue, temporary loss
of vision
Fl id l d
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Fluid overload
esp in between sessions Fluid restrictions
more stringent with HD than PD
Hyperkalaemia
esp in between sessions
Problems with access poor quality, blockage etc. Infection (vascular access catheters)
Bleeding
from the fistula during or after dialysis Infections
during sessions; exit site infections; blood-borne viruses e.g. Hepatitis,HIV
Peritoneal Dialysis (PD)
U l b ( i ) f
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Uses natural membrane (peritoneum) for
dialysis
Access is by PD catheter, a soft plastic tube
Catheter and dialysis fluid may be hidden
under clothing
Suitability
Excludes patients with prior peritoneal scarring e.g.
peritonitis, laparotomy
Excludes patients unable to care for self
Peritoneal Dialysis
.
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Principles of Peritoneal Dialysis(PD)Standard dialysis solution contains:
Na+ 132 mEq/l
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Na+ 132 mEq/l
Cl- 96 -102 mEq/l
Ca2+ 2.53.5 mEq/l
Mg2+ 0.5 -1.5 mEq/l
Dialysis solution buffer: Sodium lactate
Pure HCo3-
HCo3- /Lactate combinations
Lactate is absorbed and converted to HCo3-by
the liver
Dextrose solution strengths: 1.5%, 2.5%, 4.25%
Types
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Continuous Ambulatory Peritoneal Dialysis
(CAPD)
Automated peritoneal Dialysis (APD) Continuous cyclical
Intermittent
Continuous Ambulatory Peritoneal Dialysis
(CAPD)
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CONTROLLING YOURDIET
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Foods to control are those containing: Protein
Potassium
Sodium
Phosphorous
Fluid
FLUIDS
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Healthy kidneys remove fluids as urine
Check for fluid and sodium retention
Need to restrict fluid intake
VITAMINS
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Folic acid
Iron supplements
Do not take OTCs without consulting thedoctor.
MANAGING YOUR DIET
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INDICATORS OF GOOD CONTROL:
Weight loss or gain
Blood pressure
Swelling of hands and feet
Blood samples
Plasmapheresis:
plasma exchange and immunoadsorption
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An adult donor kidney transplanted to the left iliac
fossa of an adult recipient
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.
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.Kidney Stones
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4. CystineCystinuria is an herditary disease which is more common
in infants and children. Only a small percentage of patients with
Cystinuria form stones.
5. Drug induced stones
In rare cases, the long term use of magnesium trisilicate in
the treatment of peptic ulcer has produced radio opaque silicon
stones.
LOC TION OF STONES IN KIDNEY
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.
CLINIC L FE TURESSymptoms- Symptom wise cases can be divided into 4 groups :-
1. Quiescent calculus A few stones, particularly the phosphate
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Q , p y p p
stones, may lie dormant for quite a long period.These stone are also discovered due to symptoms of Urinary
Infection
2. Pain- Plain is the leading symptom of renal calculus in majority of
cases (80%). Three types of pain .
a) Fixed renal pain
b) Ureteric colic
c)Referred pain
3. Hydronephrosis
4. Occasionally haematuriais the leading and only symptom.
(iii) Swelling- When there isHydronephrosis orpyonephrosisassociated with renal calculus, a swelling may be felt
in the flank.
The characteristic of a renal swelling are :-
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g
(a) Oval or reniform in shape
(b) Swelling is almost fixed and cannot be moved.
(c) A kidney lump is ballot able.
3.Radiography
A) STRAIGHT X-RAY-Before taking straight X-ray for KUB region (both
kidneys, ureters and bladder), the bowels must be made empty by giving laxative.
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B) Excretory Urogram
4 Ultrasonography
Helpful to distinguish between opaque and non-opaque stones. It is also of
value in locating the stones for treatment with extra corporeal shock wave therapy.
5 Computed topography
Particularly helpful in the diagnosis of non-opaque stones.
6 Renal Scan
7 I nstrumental examination:- Cystoscopy
8 Examination of the stone
MANAGEMENT OF
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NEPHROLITHIASIS
.
ASYMPTOMATIC CALCULI
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TREATMENT
Solitary kidneyOccupation (pilot, business traveler
Simultaneous contralateral treatment
Its difficult to make an asymptomatic patientfeel any better !
STONE MANAGEMENT
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OPTIONS
Open surgery
Percutaneous
nephrolithotomy
Ureteroscopy
Shock wave lithotripsy
Medical therapy
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SHOCK WAVE LITHOTRIPSY.
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SHOCK WAVE LITHOTRIPSYSTONE FRAGMENTATION
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SHOCK WAVELITHOTRIPSY
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INDICATIONS
Surgical stone
No obstruction
Reasonable chanceof expeditious removal
SHOCK WAVELITHOTRIPSY
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RELATIVE CONTAINDICATIONS
Large stones
Calcium oxalate > 20 mmStruvite > 30
mm
Cystine stones
Distal obstruction
Poorly informed patients
SHOCK WAVE LITHOTRIPSY
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CLINICAL SIDE-EFFECTS
Hematuria
Pain
Obstruction
(Steinstrasse)
SHOCK WAVELITHOTRIPSY
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IDEAL CANDIDATES
Small stone (< 1.5 cm)
Mid or upper pole location
Normal renal anatomy
No distal obstruction
SHOCK WAVE
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LITHOTRIPSY
LIMITATIONS
Completeness of stone fragmentation
Completeness of fragment elimination
STONE MANAGEMENTPERCUTANEOUS NEPHROLITHOTOMY
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SURGICAL STONEMANAGEMENT
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CURRENT ROLE OF PNL
SURGICAL STONEMANAGEMENT
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STAY OUT OF TROUBLE
Pre-op KUB Pre-op IVP
URETERAL CALCULI
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URETERAL CALCULI
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TREATMENT OPTIONS
Observation
Shock wave lithotripsyUreteroscopy
Blind basket extraction
Percutaneous approach
Open surgery
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.
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.FINAL
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ACUTE AND CHRONIC
INTERSTITIAL NEPHRITIS
.
Morphology of the interstitium
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Fibrosis develops after infiltration by
mononuclear cells (lymphocytes) which is
accompanied by deposition of fibronectin,
collagen type I, III, VI and IV.
There is a physiological balance between
ongoing matrix formation and - degradation.
Morphology of the interstitium
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Composed of a loosely organized matrix
consisting of the collagen types I and III,
proteoglycans containing the interstitial
cells:
matrix producing fibroblasts
macrophages
dendritic reticulum cells
endothelial cells
Importance of interstitial cells
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Interstitial fibroblasts:
Fibrogenesis
Production of erythropoietine (they lose this functionduring the process of fibrogenesis)
Can transform into myofibroblasts (expression of SMA)
Changes in the interstitial area play an important negativepredictive value on the long term follow up of the primarykidney disease. Important and determining factors are
interstitial volume (=fibrosis) and inflammation
Interferences with theinterstitium: broad
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spectrum Infection: direct (BK virus, TBC, acute pyelonephritis),
indirect( Streptococci)
Immunologic
Allergic: druginduced
Auto-immune: Sjgren syndrome
Alloimmune: acute cellular allograft rejection
Unknown: IgG4- associated acute interstitial nephritis
Toxic: Pb poisoning, cadmium poisoning, Balkan endemicnephropathy
Metabolic: oxalosis secondary to malabsorbtion , gout
Obstruction: ureteral- pelvic junction stenosis:
Radiation: radiation interstitial nephritis
Idiopathic: sarcoidosis
Different entities of interstitial disease
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Acute interstitial nephritis
Chronic interstitial nephritis
Acute pyelonephritis
Chronic pyelonephritis (reflux related)
Xanthogranulomatous pyelonephritis
Malakoplakie
Myeloma kidney
IgG4 interstitial nephritis
Lead induced interstitial nephritis
Urate nephropathy
TX related Polyoma induced interstitial nephritis
Balkan interstitial nephritis
Acute interstitial nephritis
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Most common etiologies are:
a) those related to the use of medications: 85%
b) those related to infectious agents: 10%
c) those associated to systemic disease or
glomerular diseases: 1%
d) idiopathic disease: 4%
Acute interstitial nephritis:
drugs
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Etiology: AB (penicillins and cephalosporins, methicillin),diuretics, NSAIDs, chinese herbs, lithium
Pathogenesis:
T cell mediated allergic - immune reaction on drug or drug-self
protein conjugate (hapten) later followed by accumulation oflymphocytes, plasmocytes and histiocytes
Histology: Early signs: oedema, lymphocytes focally
Later: eosinophils, lymphocytes, plasmocytes and histiocytes with
granuloma formation(with giant cells) in 30 %, especially after AB Tubulitis (distal tubules): with breaks of TBM, necrosis of tubular
cells and atrophy and loss of tubules.
Tamm Horsfall may find its way to the interstitium (DDobstruction of nephron).
Acute drug induced interstitial
nephritis
Oedema and focal inflammation
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Granuloma
EOS
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Granuloma
Acute drug induced interstitial
nephritis
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Normally are the glomeruli not afflicted.
One exception: use of NSAIDs: can
combine ARF with Nephrotic Syndrome
(effect of cell- mediated lymphokine
directed reaction) inducing Minimal
Lesions (effacement of foot processes of
podocytes)
Acute interstitial nephritis:
clinics
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Acute Renal Failure andreduced glomerularfiltration rate:
- depends on the severity of
inflammation- interstitial oedema causes
elevated intratubular pressure
- intratubular obstruction throughintra luminal cells
- tubular backleak- vasoconstriction
- tubuloglomerular feedback
Outcome of drug- induced
interstitial nephritis
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Recovery?
Drug withdrawal: 60-
90% in 1 to 12 mths Irreversible with
analgesics, NSAIDs,
longterm use
Adverse prognostic
features
Marked interstitial
inflammation Granuloma (50%
irreversible)
Tubular atrophy
Fibrosis
Acute interstitial infectious
nephritis
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Infectious:direct invasion or remote infectionsbacteria ( hemolytic streptococci), parasites(Leishmania) and viruses (EBV, measles)
Pathogenesis: immunological hypersensitivityreaction to the infectious agent, effect ofchemokines produced by the kidney in response
Histology: Early signs: invasion by lymphocytes, eosinophils around the veins
In casu there is tubular destruction: histiocytes accumulate
Tubulitis with disappearance of the brush border in proximaltubules
ACUTE INTERSTITIAL INFECTIOUS NEPHRITIS
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Chronic interstitial nephritis
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Papillary sclerosis
CIN
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Interstitium in transplants
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Calcineurin inhibitors:
Heart, liver, pancreas, kidney transplants indifferent doses
Different levels of interstitial damage Most structural nephrotoxic effects in arterioles
and glomeruli are manifestations of ThromboticMicroAngiopathy(TMA) with different patterns
of severity. The interstitial fibrosis has anuncertain pathogenesis but is probably vascular.
Toxicity of calcineurin
inhibitors
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Cellular rejection in kidney Tx
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Histology:
Very early: eosinophils
Followed by T lymphocytes
Later: Plasmocytes IgG+ if IgM+ : be aware of
polyoma infection
In peritubular capillaries (PTC):
lymphocytes++
Cellular rejection
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Tubulitis
CD3
Acute pyelonephritis
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Etiology: ascending infection from the pyelon
Pathogenesis: microbial release of degradative
enzymes and toxic molecules, direct contact or
penetration of the host cell by the infectious agentand the inflammatory response mediated by
antibodies, T cells
Histology:
Tubules are damaged by neutrophils (Congored)
Acute pyelonephritis
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Chronic pyelonephritis
E i l fl
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Etiology: reflux
Histology:
- wedge shaped interstitial fibrosis(follows the
traject of the papillae and ascending tubules)accompanied by tubular atrophy, vascularatheromatosis, glomerular sclerosis, inflammation
- outside the wedges: normal parenchyma but
with secondary changes in the glomeruli:glomerular hypertrophy, FSGS
Chronic pyelonephritis
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Chronic pyelonephritis
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Tubular disease
A t t b l d
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Acute tubular damage:
Ischemia: vasoconstriction with endothelial activation
will determinate the extent of the tubular cell loss:
cellular, geographic, focal
Toxins:
Myoglobinuria
Heavy metal exposure (Pb, Cd)
Oxalate crystal deposits: ethylene glycol toxicity
Calcineurin inhibitors: megamitochondria, isometricvacuolisation
Tubular damage
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URETERAL CALCULI
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Stone-free is not everything !!
PARAMETERS FOR COMPARISON
URETERAL CALCULI
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Effectiveness
Morbidity
Convalescence
Cost
PARAMETERS FOR COMPARISON
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DISTAL URETERAL CALCULI
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URS is 10 - 18% more effective than SWL(depending on type of SWL unit)
Morbidity / convalescence reduced with SWL
Need for stents 40-60% less with SWL
Cost issues not addressed in monotherapy studies
COMPARISON OFMONOTHERAPY STUDIES
DISTAL URETERAL CALCULI
OVERVIEW OF HISTORICAL
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SWL URSEffectiveness Slightly better
Morbidity Less
Hospitalization LessCost Slightly less
OVERVIEW OF HISTORICALCONTROL STUDIES
DISTAL URETERAL CALCULI
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80 patients randomized to receive SWL or URS 40patients had stones > 5 mm40 patients had stones < 5 mm
SWL performed on Dornier MFL 5000
URS performed with 6.5F or 9.5F semi-rigidureteroscopes (basket vs. pneumatic lithotripsy)
PROSPECTIVE, RANDOMIZED TRIAL
Peschel & Bartsch, 1999
DISTAL URETERAL CALCULI
PROSPECTIVE RANDOMIZED TRIAL
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URS SWL
OR time (min) 19 63Fluoro time (min) 0.8 5.1
Stone-free (days) 0.2 10.8
Stent (days) 7.2 0Re-treatmentrate 0 15%
PROSPECTIVE, RANDOMIZED TRIALSTONES < 5 MM
Peschel & Bartsch, 1999
***
**
SWL OF DISTALURETERAL CALCULI
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Initial animal studies suggest ovarian traumaImpaired fertilityMutagenesis
Subsequent animal investigations demonstrate no
impact on fertility or offspringMice Rats Rabbits
ADVERSE EFFECTS TOFEMALE REPRODUCTIVE TRACT?
SWL OF DISTALURETERAL CALCULI
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Analyzed Rx data and radiation exposurein 84 women of reproductive age
7 children born to 6 patients with no
malformations or chromosomalanomalies
Miscarriages in 3 patients (but occurredat least 1 year after SWL)
ADVERSE EFFECTS TOFEMALE REPRODUCTIVE TRACT?
Viewig & Miller, 199
URETEROSCOPY
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URETERAL CALCULI
FLEXIBLE URETEROSCOPY
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FLEXIBLE URETEROSCOPY
ANTEGRADE MANIPULATION OFURETERAL CALCULI
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Large stone burden
Body habitus
Urinary diversionTransplant kidney
INDICATIONS
URETERAL CALCULI
PERCUTANEOUS APPROACH
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PERCUTANEOUS APPROACH
URETERAL STONEMANAGEMENT
IN SITU SWL
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AdvantagesMinimal anesthesia requirements
Non-invasive procedureNo stenting/less complicationsSimilar approach for all ureteralcalculi
DisadvantagesLower success rate than URSHigher re-treatment rate
IN SITU SWL
URETERAL STONEMANAGEMENT
URETEROSCOPY
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URETEROSCOPYAdvantages
Highest success rate
Definitive Rx - No waiting for stonepassage
Disadvantages
More invasive than SWLHigher complication rateRequires greater technical expertise
URETERAL CALCULI: CURRENTOPTIONS
PROX AND MID URETERAL STONES
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PROX AND MID URETERAL STONES
Approach Invasive Stent S-F Rate Re-
RxRate
URS +++ 100% 75-90% 10-15%
Push/Smash ++ Rarely 92% 9%
SWL + Stent + 100% 75-80% 20-25%
*
Defined as complete stone removal with single procedure
URETERAL CALCULI: CURRENTOPTIONS
DISTAL URETERAL STONES
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DISTAL URETERAL STONES
Approach Invasive Stent S-F Rate Re-
RxRate
URS +++ 100% 98-100% 0-2%
Push/Smash ++ Rarely 92% 9%
SWL + Stent + 100% 75-80% 20-25%
*
Defined as complete stone removal with single procedure
SURGICAL STONEMANAGEMENT
CHANGING TREATMENT
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CHANGING TREATMENTPHILOSOPHIES
1980s 1990s 2000s20
10s
Shock wave lithotripsy 95% 85% 75% ???
Endoscopic procedures 5% 15% 25% ???
Open stone surgery < 1% < 1% < 1% 0
NEPHROLITHIASIS
NATURAL HISTORY & RISK FACTORS
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Peak incidence age 30 - 60
Gender (Male : Female) 3 : 1
Family history 3 - fold risk
Body size risk with weight
Recurrence after first stone:Year 1 10 - 15%Year 5 50 - 60%Year 10 70 - 80%
NATURAL HISTORY & RISK FACTORS
SHOCK WAVE LITHOTRIPSY
RECURRENT STONE
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RECURRENT STONEFORMATION One Year Two Years
Post SWL Post SWL
Stone FreeNew stones 8% 10%
Residual StonesStone growth 22% 21%
Lingeman, et al, 1989
SHOCK WAVE LITHOTRIPSY
EFFECT ON STONE RISK
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EFFECT ON STONE RISKFACTORS
Urine Values Pre- 3 Mo Post-(mg/day) Lithotripsy Lithotripsy
Calcium 254 261Uric Acid 552 548
Citrate 249 257
Oxalate 42 41
Brown, et al, 1989
MEDICAL MANAGEMENT OFNEPHROLITHIASIS
PROGRESS
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PROGRESSElucidation
Urinary environment conducive to stone formation
DiagnosisDetection of underlying physiologic abnormalities
Medical TherapyDevelopment of new treatment strategies
STONE FORMATION
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Concentration / solubility of stone-forming
salts
Promoters of crystallization and aggregation
Inhibitors of crystallization and aggregation
MAJOR FORCES
DIETARY CALCIUM
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Early recommendations suggest that low calcium diet
will decrease urinary Ca++excretion, thereby reducingrisk of stone formation
Potential risk factors involving low calcium diet:
Reduced bone mass
Increased urinary oxalate
IMPACT OF LOW CALCIUM DIET
DIETARY CALCIUM
RECOMMENDATIONS
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Moderate calcium restriction in patients with
AH
Limit dietary intake of oxalate
Spinach, tea, chocolate, nutsLimit dietary sodium intake
RECOMMENDATIONS
CALCIUM SUPPLEMENTS
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Calciuric response to calcium supplementation
Depends on duration of treatment and patient
population
PHYSIOLOGICAL EVIDENCE
CALCIUM SUPPLEMENTS
RECOMMENDATIONS:
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Give HCTZ during initial three months to preventhypercalciuria, then discontinue for one month
If urinary calcium up at 4 months, re-start HCTZ
Alternative: Significantly increase fluid intake for
first three months and then check 24-hour urinarycalcium
RECOMMENDATIONS:PREMENOPAUSAL WOMEN
Henoch Schnlein Purupura
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Answer 1.
ReninAngiotensin II- ACE- ADHAldosterone
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That is not correct
Please try again
Peritoneal Dialysis
Is performed as an
intracorporeal (inside thebody) therapy making use of
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p (body) therapy making use ofthe peritoneal membrane.
Is the process of cleaning theblood by using the lining of
the peritoneal cavity(peritoneum) as a filtertheperitoneum acts as adialyzing membrane,permitting wastes from the
body to cross it and emptyinto the instilled dialysatefluid .
Is a type of dialysis usuallydone by the patient at home.
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Hemodialysis
3-4 times a week
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Takes 2-4 hours
Machine filters
blood and
returns it to
body
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