1 curs nefrologie-de prezentat-ii- 23 februariei-2016
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Transcript of 1 curs nefrologie-de prezentat-ii- 23 februariei-2016
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Universitatea Titu
Maiorescu
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Characteristics of Renal Structure and
Function
I. Physiological Anatomy of the Kidney
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Renal cortex
Cortical lobules - which form caps over the bases of the pyramids
Renal columns - which dip in between the pyramids
Renal medulla
has 10 conical masses called renal pyramids, their apices form renal papillae
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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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
-prostaglandin
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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,
urea
Secretion
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 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 cells
relatively impermeable to water and Na+
5% of filtered Na+ load reabsorbed
Parathyroid hormone and vit D mediated
calcium reabsorption
The late distal segment (collecting segment) Hormone mediated Ca+ reabsorption
Aldosterone mediated Na+ reabsorption
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Collecting tubule
5-7% of filtered Na+ load is reabsorbed
Cortical collecting tubule – two types of
cells: Principal cells secrete K+ aldosterone
mediated Na+ reabsorption
Intercalated cells acid base regulation
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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 tubular necrosis
Pyelonephritis
Acute
chronic
3-Vessels
Nephrosclerosis
4-Urinary obstruction
– Stones
– Hydronephrosis
5- Cystic diseases of the
kidney
6-Tumors
Benign
Malignan
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
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Secondary Glomerulonephritis
Diabetes most common cause
– most common cause of renal failure
– glycoproteins deposit in basement membrane
Vascular disease
– atherosclerosis
– HTN
Vascultitis
SLE, DM, Amyloidosis, Goodpasture
– Hereditary Albort syndrome
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Glomerular diseases:
Primary Glomerulonephritis
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. Acute Glomerulonephritis
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Acute glomerulonephritis is the inflammation of the glomeruli which causes the kidneys to malfunction
It is also called Acute Nephritis, Glomerulonephritis and Post-Streptococcal Glomerulonephritis
Predominantly affects children from ages 2 to 12
Incubation period is 2 to 3 weeks
Acute Glomerulonephritis
Definition
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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 Glomerulonephritis
General 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 face
then the lower and upper limbs then
becomes generalized; may be migratory
Hypertension: usually mild to moderate
Hypoproteinemia,
hypercholesterolemia),
mixed
Acute Glomerulonephritis
Signs and Symptoms
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Acute Glomerulonephritis
Etiology
Infectious
– Streptococcal
– Nonstreptococcal postinfectious
glomerulonephritis
Bacterial
Viral
Parasitic
Noninfectious
– Multisystem systemic diseases
– Primary glomerular diseases
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Acute Glomerulonephritis
INVESTIGATIONS Base line measurements:
- ↑ Urea - ↑ Creatinine - 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 severe
cases
Acute renal necrosis due to injury of
capillary or capillary thrombosis
Acute Glomerulonephritis
Complications
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proper hygiene
prompt medical assessment for necessary antibiotic therapy should be sought when infection is suspected
prophylactic immunizations
Acute Glomerulonephritis
Prevention
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Treatment
Treat the underlying infections when acute GN is associated with chronic infections.
Antimicrobial therapy – Antibiotics (eg, penicillin) are used to control local symptoms and to prevent
spread of infection to close contacts.
– Antimicrobial therapy does not appear to prevent the development of GN, except if given within the first 36 hours.
Loop diuretic therapy – Loop diuretics may be required in patients who are edematous and
hypertensive in order to remove excess fluid and to correct hypertension.
– Relieves edema and controls volume, thereby helping to control volume-related elevation in BP.
Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxide) may be used if severe hypertension or encephalopathy is present
Diet: – Sodium and fluid restriction
– Protein restriction for azotemic patients
Activity: Recommend bed rest until signs of glomerular inflammation and circulatory congestion subside.
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. Chronic glomerulonephritis
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Chronic glomerulonephritis
The condition is characterized
1 - irreversible and progressive glomerular and tubulointerstitial fibrosis
2-ultimately leading to a reduction in the glomerular filtration rate (GFR) and
3- retention of uremic toxins
.
. The diagnosis of CKD can be made without knowledge of the specific cause.
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Chronic glomerulonephritis
Etiology
Nearly all forms of acute glomerulonephritis have a tendency to progress to chronic glomerulonephritis.
The progression from acute glomerulonephritis to chronic glomerulonephritis is variable.
Whereas complete recovery of renal function is the rule for patients with poststreptococcal
glomerulonephritis, several other glomerulonephritides, such as
immunoglobulin A (IgA) nephropathy, often have a relatively benign course and many do not progress to ESRD.
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Chronic glomerulonephritis
Pathogenesis
Reduction in nephron mass from the initial injury reduces the GFR.
This reduction leads to hypertrophy and hyperfiltration 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 the functional consequences of nephron loss.
The changes, however, are ultimately detrimental because they lead to glomerulosclerosis and further nephron loss.
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Chronic glomerulonephritis
Histologic 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.
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Chronic glomerulonephritis
Histologic Findings
1-Minimal-Change Disease
2-Focal segmental
glomerulosclerosis
3-Mesangiocapillary GN
4-Membranous nephropathy
„
.
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Mesangial proliferative –MPGN
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 glomerulonephritis
Clinical Manifestations
Uremia-specific findings
Edemas
Hypertension
Jugular venous distension (if severe volume overload is present)
Pulmonary rales (if pulmonary edema is present)
Pericardial friction rub in pericarditis
Tenderness in the epigastric region or blood in the stool (possible indicators for uremic gastritis or enteropathy)
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Chronic glomerulonephritis
Lab Studies
Urinalysis
Urinary protein excretion
Serum chemistry
– Serum creatinine and urea nitrogen levels are elevated.
– Impaired excretion of potassium, free water, and acid results in hyperkalemia, hyponatremia, and low serum bicarbonate levels, respectively.
– Impaired vitamin D-3 production results in hypocalcemia, hyperphosphatemia, and high levels of parathyroid hormone.
– Low serum albumin levels may be present if uremia interferes with nutrition or if the patient is nephrotic.
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Renal ultrasonogram
– Obtain a renal ultrasonogram to determine renal size, to assess for the presence of both kidneys, and to exclude structural lesions that may be responsible for azotemia.
– Small kidneys often indicate an irreversible process.
Kidney biopsy
Chronic glomerulonephritis
Imaging Studies
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Chronic glomerulonephritis
Treatment
The target pressure for patients with proteinuria greater than 1 g/d is less than 125/75 mm Hg; for patients with proteinuria less than 1 g/d, the target pressure is less than 130/80 mm Hg.
– Angiotensin-converting enzyme inhibitors (ACEIs)
– angiotensin II receptor blockers (ARBs)
– Diuretics are often required because of decreased free-water clearance, and high doses may be required to control edema and hypertension when the GFR falls to less than 25 mL/min.
– Beta-blockers, calcium channel blockers, central alpha-2 agonists (eg, clonidine), alpha-1 antagonists, and
– direct vasodilators (eg, minoxidil, nitrates) may be used to achieve the target pressure.
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Chronic glomerulonephritis
Treatment
Minimal change glomerulonephritis
1-Corticosteroids induce 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.
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Chronic glomerulonephritis
Treatment
Focal segmental glomerulosclerosis
Poor response to corticosteroids (10–
30%). Cyclophosphamide or ciclosporin
(=cylosporin) may be used in steroid-resistant
cases.
Prognosis: 30–50% progress to ESRF.
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Chronic glomerulonephritis
Treatment
Mesangial proliferative GN
1-Antibiotics,
2-Diuretics, and
3-Antihypertensives as necessary.
4-Dialysis is rarely required.
Prognosis: Good.
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Chronic glomerulonephritis
Treatment
Membranous nephropathy
If renal function deteriorates, consider
corticosteroids and chlorambucil.
Prognosis: Untreated, 15% complete
remission, 9% ESRF at 2–5yrs and 41% at
15yrs.
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. Rapidly Progressive Glomerulonephritis
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Rapidly Progressive Glomerulonephritis
Rapidly progressive
glomerulonephritis (RPGN) is a
disease of the kidney that results in
a rapid decrease in the glomerular
filtration rate of at least 50% over
a short period, from a few days to 3
months.
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The cause of RPGN is unknown. A genetic predisposition may exist for the development of this disease.
Multiple studies have demonstrated that ANCA- (antineutrophil cytoplasmic antibodies) activated neutrophils attack vascular endothelial cells.
ANCA-associated vasculitis.
A viral etiology is possible.
Rapidly Progressive Glomerulonephritis
Etiology
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Rapidly Progressive Glomerulonephritis
Pathology
Renal biopsshow
A diffuse, proliferative, necrotizing glomerulonephritis with crescent formation.
The main pathologic finding is fibrinoid necrosis (>90% of biopsy specimens); extensive crescent formation is present in at least 50% of glomeruli.
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Rapidly Progressive Glomerulonephritis
Clinical Manifestations
Symptoms and signs of renal
failure,
pain,
haematuria,
systemic symptoms (fever, malaise,
myalgia, weight loss).
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Rapidly Progressive Glomerulonephritis
Lab Studies The most important requirement in the diagnosis of
antineutrophil cytoplasmic antibodies (ANCA) ANCA-associated disease is a high index of suspicion. Rapid diagnosis is essential for organ preservation. Laboratory studies include the following:
– Routine chemistry: The most common abnormality is an increased serum creatinine level.
– Urinalysis with microscopy:
– Antinuclear antibody (ANA) titer:
– ANCA
Urine and serum protein electrophoresis: Perform this in any middle-aged or elderly person presenting with RPGN to exclude the presence of light-chain disease or overt multiple myeloma as a cause of the clinical findings.
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Rapidly Progressive Glomerulonephritis
Treatment
1-High-dose corticosteroids;
cyclophosphamide ± plasma
exchange/ renal
2-Transplantation.
Prognosis:
Poor if initial serum creatinine
>600µmol/L.
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Proteinurea
≥3.5 g/day
(protein: creatinine ratio >3-3.5)
Generalized
Oedema
Hypoalbuminaeia
<3g/L
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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
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The Nephrotic Syndrome
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 with
reduced 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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DAMAGED 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
•Amyloidosis
•Infections: Hepatitis B and C, HIV,syphilis, post-streptococcal
•Malignancy: multiple myloma , Hodgkin lymphoma, solid tumor
•Drugs (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 extremities and genital area later in the day -In advanced disease: the whole body (anasarca) shortness of breath •Frothy 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 disease
•Serologic studies (ANA), complement, hepatitis B and hepatitis C
serologies and the measurement of cryoglobulins ,serum or urine protein
electrophoresis.
•Renal biopsy required 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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67
Disease-
spesific
Complication
symptoms
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Oedema •Low salt diet •Diuretics •serial measurement of body weight Proteinuria •ACE inhibitors or ARBs
• Hypoalbuminaemia •High protein diet not indicated •0.8–1 g/kg/day
Ref: Up to date online 17.3.
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Hyperlipidaemia •Regular Lipid profile •Statin if severe long lasting nephrotic syndrome •Control other CVD risk factors…target blood pressure 125/75
Thromboembolic risk •Routin Prophylactic anticoagulation not recommend •High index of suspicion for thromboemboli
Infections •High index of suspicion •Antipneumococcal and influenza vaccinations
Ref: Up to date online 17.3.
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Management of the nephrotic
syndrome Na+< 60 mmol/24 hrs
water restriction
diuretics (if not volume depleted)
reduced protein diet (controversial)
treat infections
prophylaxis for thrombosis
specific therapy
corticosteroids
Immunosuppression
Diabetic Nephropathy
aggressive glucose control and aggressive BP control
with ACE
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Inca nu s-a
terminat !!
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Universitatea Titu
Maiorescu
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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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ACUTE AND CHRONIC
INTERSTITIAL NEPHRITIS
.
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Causes of interstitial nephritis
Drugs
Infection
Autoimmune
Metabolic
Radiation
Neoplastic infiltration
Mechanical
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Morphology of the interstitium
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.
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Morphology of the interstitium
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
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Interferences with the
interstitium: broad
spectrum Infection:
– direct (BK virus, TBC, acute pyelonephritis),
– indirect( βStreptococci)
Immunologic
– Allergic: drug – induced
– Auto-immune: Sjögren syndrome
– Alloimmune: acute cellular allograft rejection
– Unknown: IgG4- associated acute interstitial nephritis
Toxic: Pb poisoning, cadmium poisoning, Balkan endemic nephropathy
Metabolic: oxalosis secondary to malabsorbtion , gout
Obstruction: ureteral- pelvic junction stenosis:
Radiation: radiation interstitial nephritis
Idiopathic: sarcoidosis
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Different entities of interstitial disease
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
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Acute interstitial nephritis
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%
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Acute interstitial nephritis:
drugs Etiology: AB (penicillins and cephalosporins, methicillin),
diuretics, NSAID‟s, chinese herbs, lithium
Pathogenesis:
T cell mediated allergic - immune reaction on drug or drug-self protein conjugate (hapten) later followed by accumulation of lymphocytes, 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 (DD obstruction of nephron).
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Acute drug induced interstitial
nephritis
Granuloma
Oedema and focal inflammation
EOS
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Granuloma
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Acute drug induced interstitial
nephritis
Normally are the glomeruli not afflicted.
One exception: use of NSAID‟s: can
combine ARF with Nephrotic Syndrome
(effect of cell- mediated lymphokine
directed reaction) inducing Minimal
Lesions (effacement of foot processes of
podocytes)
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Acute interstitial nephritis:
clinics Acute Renal Failure and
reduced glomerular filtration rate:
- depends on the severity of inflammation
- interstitial oedema causes elevated intratubular pressure
- intratubular obstruction through intra luminal cells
- tubular backleak
- vasoconstriction
- tubuloglomerular feedback
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Outcome of drug- induced
interstitial nephritis 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
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Acute interstitial infectious
nephritis Infectious:direct invasion or remote infections
bacteria (ß hemolytic streptococci), parasites (Leishmania) and viruses (EBV, measles)
Pathogenesis: immunological hypersensitivity reaction to the infectious agent, effect of chemokines 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 proximal tubules
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ACUTE INTERSTITIAL INFECTIOUS NEPHRITIS
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Acute interstitial nephritis:
systemic
Association with: Goodpasture syndrome,
lupus nephritis, mixed cryoglobulinemia,
membranoproliferative glomerulonephritis
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Chronic interstitial nephritis
Etiology: chronic drug intake (analgesics, lithium), urinary obstruction, chronic reflux,
Pathogenesis: persistence of damageing factor: ischemia, chronic immune reaction
Histology: fibrosis + diffuse infiltration by lympho’s, plasmo’s, histiocytes (with granuloma). Tubular changes (atrophy, compensatory hypertrophy with microcystic changes)
Beware of: – Papillary necrosis, - sclerosis and- calcification: due to sclerosis
of the capillaries under the urothelial epithelium
– Tumor development: papillary tumors, multifocal
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Chronic interstitial nephritis
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Papillary sclerosis
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CIN
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Chronic pyelonephritis
Etiology: reflux
Histology:
- wedge shaped interstitial fibrosis(follows the traject of the papillae and ascending tubules) accompanied by tubular atrophy, vascular atheromatosis, glomerular sclerosis, inflammation
- outside the wedges: normal parenchyma but with secondary changes in the glomeruli: glomerular hypertrophy, FSGS
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Chronic pyelonephritis
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Chronic pyelonephritis
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Tamm Horsfall protein
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Tubular disease
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, isometric
vacuolisation
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Tubular damage
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Drugs and interstitial nephritis
methicillin 17%other penicillins <1%cephalosporins <1%rifampicin 1%ciprofloxacin 1%cotrimoxazole
fenoprofen <1%frusemide <1%bumetanide <1%cimetidine <1%allopurinol <1%5 aminosalicylates
omeprazole ? ranitidine (rare)
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Bacterial infection
bacterial infection of the renal parenchyma
causes interstitial nephritis
infection without anatomical abnormality
seldom 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
transplant
rejection
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 from
malignant 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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. 3- Lupus Nephritis Vasculitis
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WHO classification
Lupus Nephritis Type I no pathology
Typ
e V
: m
emb
ran
ou
s
Type II : mesangial
Typ
e II
I :
foca
l
pro
life
rati
ve
Typ
e IV
: d
iffu
se
pro
life
rati
ve
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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 for active nephritis
Prognosis varies greatly based on initial pathology, 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 acid
stones
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, hypertension
vascular disease, hyperlipidaemia and diabetes
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. Amyloidosis and Myeloma Kidney
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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 from
A protein and is an acute phase reactant
associated with chronic inflammatory diseases
like rheumatoid arthritis and bronchiectasis
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Inca nu s-a
terminat !!
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Universitatea Titu
Maiorescu
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. Acute and chronic
Renal Failure
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. Acute Renal Failure
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Acute renal failure -ARF
Deterioration of renal function over a period of hours to days, resulting in
• the failure of the kidney to excrete nitrogenous waste products and
• to maintain fluid and electrolyte homeostasis
ARF Rapid deterioration of renal function
– (increase of creatinine of >0.5 mg/dl in <72hrs.)
– “azotemia” (accumulation of nitrogenous wastes)
– elevated BUN and Creatinine levels
– decreased urine output (usually but not always)
Oliguria: <400 ml urine output in 24 hours
Anuria: <100 ml urine output in 24 hours
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Hilton, R. BMJ 2006;333:786-790
Causes of acute renal failure
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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)
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Renal
– Glomerular
Anti–glomerular basement membrane (GBM) disease (Goodpasture syndrome)
Anti–neutrophil cytoplasmic antibody-associated glomerulonephritis (ANCA-associated GN) (Wegener granulomatosis, 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 glycol poisoning, 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
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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, Anti
GBM, cryoglobulin, CK, urinary Myoglobulin
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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
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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
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Treatment of
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 temporarily replaced by dialysis
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Indication for dialysis
Symptoms of uremia (
encephalopathy,…)
Uremic pericarditis
Refractory volume over load
Refractory hyperkalemia
Refractory metabolic acidosis
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. Chronic Renal Failure
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Definitions
Chronic Renal Failure Results form gradual, progressive loss of renal
function
Occasionally results from rapid progression of acute renal failure
Symptoms occur when 75% of function is lost but considered cohrnic if 90-95% loss of function
Dialysis is necessary D/T accumulation or uremic toxins, which produce changes in major organs
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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 with muscle weakness
Fluid overload and metabolic acidosis
Proteinuria, glycosuria
Urine = RBC’s, WBC’s, and casts
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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
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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
Kussmaul’s
respirations from
acidosis
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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 CHO
metabolism
Thyroid and parathyroid
abnormalities
– Hemopoietic
Anemia
Decrease in RBC
survival time
Blood loss from dialysis
and GI bleed
Platelet deficits
Bleeding and clotting
disorders – purpura and
hemorrhage from body
orifices , ecchymoses
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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
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Chronic Renal Failure Lab findings
– BUN – indicator of glomerular filtration rate and is affected by the breakdown of protein. Normal is 10-20mg/dL. When reaches 70 = dialysis
– Serum creatinine – waste product of skeletal muscle breakdown and is a better indicator of kidney function. Normal is 0.5-1.5 mg/dL. When reaches 10 x normal, it is time for dialysis
– Creatinine clearance is best determent of kidney function. Must be a 12-24 hour urine collection. Normal is > 100 ml/min
– K+ -
– Hypocalcemia = tetany
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Chronic Renal Failure
Other abnormal findings
– Metabolic acidosis
– Fluid imbalance
– Insulin resistance
– Anemia
– Immunoligical problems
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Chronic Renal Failure 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
Hemodialysis
– Vascular access
Temporary – subclavian or femoral
Permanent – shunt, in arm
–Care post insertion
– Can be done rapidly
– Takes about 4 hours
– Done 3 x a week
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Chronic Renal Failure
Peritoneal dialysis – Semipermeable
membrane
– Catheter inserted through abdominal wall into peritoneal cavity
– Cost less
– Fewer restrictions
– Can be done at home
– Risk of peritonitis
– 3 phases – inflow, 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
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Chronic Renal Failure
Transplant
– Must find donor
– Waiting period long
– Good survival rate – 1 year 95-97%
– Must take immunosuppressant’s for life
– Rejection
Watch for fever, elevated B/P, and pain over site
of new kidney
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Transplant Meds
Patients have decreased resistance to infection
Corticosteroids – anti-inflammarory
– Deltosone
– Medrol
– Solu-Medrol
Cytotoxic – inhibit T and B lymphocytes
– Imuran
– Cytoxan
– Cellcept
T-cell depressors - Cyclosporin
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Universitatea Titu
Maiorescu
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. RENAL TUMOURS
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. CYSTIC DISEASES OF
THE KIDNEY
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CYSTIC DISEASES OF
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 genetically
determined
Clinical significance may be trivial or
grave
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CLASSIFICATIONS OF
RENAL CYSTIC DISEASES
Polycystic kidney diseases:
1. Autosomal recessive (ARPKD)
classic infantile polycystic disease
with congenital hepatic fibrosis
2. Autosomal dominant (ADPKD)
Simple renal cysts
Acquired renal cystic disease
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RENAL CYSTIC DISEASES
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 interstitial
fibrosis and no dysplasia
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RENAL CYSTIC DISEASES 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, distributed in cortex and medulla obscuring normal reniform 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 or collecting duct
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Simple Renal Cysts
Extremely common as age advances
Incompletely understood pathogenesis
Commonly associated with scarred
kidneys
Asymptomatic 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
.
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Renal cancer
In infants and children :
–Nephroblastoma ( Wilms’
tumour )
In adults :
–Renal cell carcinoma
–Renal cell adenoma
–Renal oncocytoma
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NEPHROBLASTOMA ( Wilms’
tumour )
Embryonal tumour arising from nephrogenic
blastemal cells
– can differentiate in to several cell lines - blastemal,
epithelial and stromal
– many replicate developing kidneys
Common in young children / uncommon in
neonates and infants
90% in < 6yrs. old ( mean: 3yrs. in boys and
3.5yrs. in girls )
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NEPHROBLASTOMA Clinical Features
Most common genitourinary cancer
Age: 1-3yrs., 98% in <10yrs
Abdominal mass, pain, & hematuria
Usually unicentric, may be multicentric (7%)
or bilateral (5%)
Imaging technique to reveal smaller lesions
No specific tumor markers identified
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NEPHROBLASTOMA 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 and
unfavorable histology
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RENAL CELL CARCINOMA
Hypernephroma / Grawitz’s tumour
seems to be arising from mature renal tubules
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RENAL CELL CARCINOMA
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
prognosis Influenced by multiple factors :
– tumour size
– infiltrative margins
– histological type
– tumour stage - most important
Can be expressed in terms of histological
types
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Renal cell carcinoma
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RENAL CELL
ADENOMA Incidental findings at autopsy (22%)
Well demarcated, unencapsulated
Pale yellow-gray, discrete cortical mass
Up to 2 cms. in maximum dimension
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Bladder Carcinoma
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
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Dialysis
Definition
Artificial process that partially replaces renal
function
Removes waste products from blood by
diffusion (toxin clearance)
Removes excess water by ultrafiltration
(maintenance of fluid balance)
Wastes and water pass into a special liquid –
dialysis fluid or dialysate
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Types
Haemodialysis (HD)
Peritoneal Dialysis (PD)
They work on similar principles: Movement
of solute or water across a semipermeable
membrane (dialysis membrane)
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Diffusion
Movement of solute
Across semipermeable membrane
From region of high concentration to one of
low concentration
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Ultrafiltration
Made possible by osmosis
Movement of water
Across semipermeable membrane
From low osmolality to high osmolality
Osmolality – number of osmotically active
particles in a unit (litre) of solvent
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Haemodialysis
Dialysis process occurs outside the body in a machine
The dialysis membrane is an artificial one: Dialyser
The dialyser removes the excess fluid and wastes from the blood and returns the filtered blood to the body
Haemodialysis needs to be performed three times a week
Each session lasts 3-6 hrs
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AV Fistula Access
Matures in about 6 weeks
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
3-4 times a week
Takes 2-4 hours
Machine filters
blood and
returns it to
body
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Problems with HD Rapid changes in BP
– fainting, vomiting, cramps, chest pain, irritability, fatigue, temporary loss of vision
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
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Peritoneal Dialysis (PD)
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
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Peritoneal Dialysis
.
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Principles of Peritoneal Dialysis (PD)
Standard dialysis solution contains: Na+ – 132 mEq/l
Cl- – 96 -102 mEq/l
Ca2+ – 2.5 – 3.5 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%
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Types
Continuous Ambulatory Peritoneal Dialysis
(CAPD)
Automated peritoneal Dialysis (APD)
– Continuous cyclical
– Intermittent
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Continuous Ambulatory Peritoneal Dialysis
(CAPD)
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CONTROLLING DIET Foods to control are those containing:
Protein
Potassium
Sodium
Phosphorous
Fluid
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FLUIDS
Healthy kidneys remove fluids as urine
Check for fluid and sodium retention
Need to restrict fluid intake
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VITAMINS
Folic acid
Iron supplements
Do not take OTC‟s without consulting the
doctor.
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MANAGING DIET
INDICATORS OF GOOD CONTROL:
Weight loss or gain
Blood pressure
Swelling of hands and feet
Blood samples
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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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ETIOLOGY HYPEREXCRETION OF RELATIVELY INSOLUBLE URINARY
CONSTITUENTS –
1. Oxalate – Though oxalate is the major component of 70%
of all renal stones, yet hyperoxaluria as a cause of formation of such
stone is relatively rare. Cabbage, rhubarb, spinach, tomatoes, black tea and cocoa
contain large amount of oxalate. Ingestion of excessive amounts of ascorbic acid
and orange juice also increase urinary oxalate excretion.
2. Calcium - On regular diets normal urinary excretion of calcium ranges
between 200 mg to 300 mg per day. The major calcium in foods are in milk and
cheese. Milk and dietary protein also cause increased absorption of calcium from
the gut.
3. Uric acid - Many patients with gout form uric acid calculi particularly when under treatment. If the urine is made alkaline and dilute while treating this disease chance of uric acid stone formation is less
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4. Cystine –
Cystinuria 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.
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LOCATION OF STONES IN KIDNEY
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EFFECTS OF STONE The size and position of the stone usually govern the development
of secondary pathologic changes in the urinary trace.
A. SAME KIDNEY –
1. Obstruction 2. Infection B OPPOSITE KIDNEY 1. Compensatory hypertrophy
2. Stone formation may be bilateral
3. Infection
4. Calculus anuria
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.
CLINICAL FEATURES Symptoms - Symptom wise cases can be divided into 4 groups :-
1. Quiescent calculus – A few stones, particularly the phosphate
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 haematuria is the leading and only symptom.
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(iii) Swelling - When there is Hydronephrosis or
pyonephrosis associated with renal calculus, a swelling may be felt
in the flank.
The characteristic of a renal swelling are :-
(a) Oval or reniform in shape
(b) Swelling is almost fixed and cannot be moved.
(c) A kidney lump is ballot able.
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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.
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 Instrumental examination :- Cystoscopy
8 Examination of the stone
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MANAGEMENT OF NEPHROLITHIASIS
.
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ASYMPTOMATIC CALCULI
TREATMENT
Solitary kidney
Occupation (pilot, business traveler
Simultaneous contralateral treatment
It‟s difficult to make an asymptomatic patient feel any better !
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STONE MANAGEMENT
OPTIONS
Open surgery
Percutaneous
nephrolithotomy
Ureteroscopy
Shock wave lithotripsy
Medical therapy
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STONE MANAGEMENT
OPEN surgery NEPHROLITHOTOMY
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SHOCK WAVE LITHOTRIPSY .
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SHOCK WAVE LITHOTRIPSY STONE FRAGMENTATION
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SHOCK WAVE LITHOTRIPSY
INDICATIONS
Surgical stone
No obstruction
Reasonable chance
of expeditious removal
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SHOCK WAVE LITHOTRIPSY
RELATIVE CONTAINDICATIONS
Large stones Calcium oxalate > 20 mm Struvite > 30 mm
Cystine stones
Distal obstruction
Poorly informed patients
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SHOCK WAVE LITHOTRIPSY
CLINICAL SIDE-EFFECTS
Hematuria
Pain
Obstruction
(Steinstrasse)
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SHOCK WAVE LITHOTRIPSY
IDEAL CANDIDATES
Small stone (< 1.5 cm)
Mid or upper pole location
Normal renal anatomy
No distal obstruction
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SHOCK WAVE LITHOTRIPSY
LIMITATIONS
Completeness of stone fragmentation
Completeness of fragment elimination
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STONE MANAGEMENT PERCUTANEOUS NEPHROLITHOTOMY
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SURGICAL STONE MANAGEMENT
CURRENT ROLE OF PNL
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SURGICAL STONE MANAGEMENT STAY OUT OF TROUBLE
Pre-op KUB Pre-op IVP
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URETERAL CALCULI
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URETERAL CALCULI
TREATMENT OPTIONS
Observation
Shock wave lithotripsy
Ureteroscopy
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
.
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Morphology of the interstitium
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.
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Morphology of the interstitium
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
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Importance of interstitial cells
Interstitial fibroblasts:
– Fibrogenesis
– Production of erythropoietine (they lose this function during the process of fibrogenesis)
– Can transform into myofibroblasts (expression of SMA)
– Changes in the interstitial area play an important negative predictive value on the long term follow up of the primary kidney disease. Important and determining factors are interstitial volume (=fibrosis) and inflammation
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Interferences with the
interstitium: broad
spectrum Infection:
– direct (BK virus, TBC, acute pyelonephritis),
– indirect( βStreptococci)
Immunologic
– Allergic: drug – induced
– Auto-immune: Sjögren syndrome
– Alloimmune: acute cellular allograft rejection
– Unknown: IgG4- associated acute interstitial nephritis
Toxic: Pb poisoning, cadmium poisoning, Balkan endemic nephropathy
Metabolic: oxalosis secondary to malabsorbtion , gout
Obstruction: ureteral- pelvic junction stenosis:
Radiation: radiation interstitial nephritis
Idiopathic: sarcoidosis
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Different entities of interstitial disease
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
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Acute interstitial nephritis
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%
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Acute interstitial nephritis:
drugs Etiology: AB (penicillins and cephalosporins, methicillin),
diuretics, NSAID‟s, chinese herbs, lithium
Pathogenesis:
T cell mediated allergic - immune reaction on drug or drug-self protein conjugate (hapten) later followed by accumulation of lymphocytes, 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 (DD obstruction of nephron).
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Acute drug induced interstitial
nephritis
Granuloma
Oedema and focal inflammation
EOS
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Granuloma
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Acute drug induced interstitial
nephritis
Normally are the glomeruli not afflicted.
One exception: use of NSAID‟s: can
combine ARF with Nephrotic Syndrome
(effect of cell- mediated lymphokine
directed reaction) inducing Minimal
Lesions (effacement of foot processes of
podocytes)
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Acute interstitial nephritis:
clinics Acute Renal Failure and
reduced glomerular filtration rate:
- depends on the severity of inflammation
- interstitial oedema causes elevated intratubular pressure
- intratubular obstruction through intra luminal cells
- tubular backleak
- vasoconstriction
- tubuloglomerular feedback
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Outcome of drug- induced
interstitial nephritis 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
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Acute interstitial infectious
nephritis Infectious:direct invasion or remote infections
bacteria (ß hemolytic streptococci), parasites (Leishmania) and viruses (EBV, measles)
Pathogenesis: immunological hypersensitivity reaction to the infectious agent, effect of chemokines 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 proximal tubules
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ACUTE INTERSTITIAL INFECTIOUS NEPHRITIS
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Acute interstitial nephritis:
systemic
Association with: Goodpasture syndrome,
lupus nephritis, mixed cryoglobulinemia,
membranoproliferative glomerulonephritis
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Chronic interstitial nephritis
Etiology: chronic drug intake (analgesics, lithium), urinary obstruction, chronic reflux,
Pathogenesis: persistence of damageing factor: ischemia, chronic immune reaction
Histology: fibrosis + diffuse infiltration by lympho’s, plasmo’s, histiocytes (with granuloma). Tubular changes (atrophy, compensatory hypertrophy with microcystic changes)
Beware of: – Papillary necrosis, - sclerosis and- calcification: due to sclerosis
of the capillaries under the urothelial epithelium
– Tumor development: papillary tumors, multifocal
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Chronic interstitial nephritis
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Papillary sclerosis
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CIN
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Interstitium in transplants
Calcineurin inhibitors:
– Heart, liver, pancreas, kidney transplants in different doses
– Different levels of interstitial damage
– Most structural nephrotoxic effects in arterioles and glomeruli are manifestations of Thrombotic MicroAngiopathy(TMA) with different patterns of severity. The interstitial fibrosis has an uncertain pathogenesis but is probably vascular.
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Toxicity of calcineurin
inhibitors
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Cellular rejection in kidney Tx
Histology:
– Very early: eosinophils
– Followed by T lymphocytes
– Later: Plasmocytes IgG+ if IgM+ : be aware of
polyoma infection
– In peritubular capillaries (PTC):
lymphocytes++
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Cellular rejection
Tubulitis
CD3
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Acute pyelonephritis
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 agent
and the inflammatory response mediated by
antibodies, T cells
Histology:
– Tubules are damaged by neutrophils (Congored)
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Acute pyelonephritis
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Chronic pyelonephritis
Etiology: reflux
Histology:
- wedge shaped interstitial fibrosis(follows the traject of the papillae and ascending tubules) accompanied by tubular atrophy, vascular atheromatosis, glomerular sclerosis, inflammation
- outside the wedges: normal parenchyma but with secondary changes in the glomeruli: glomerular hypertrophy, FSGS
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Chronic pyelonephritis
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Chronic pyelonephritis
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Tamm Horsfall protein
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Tubular disease
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, isometric
vacuolisation
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Tubular damage
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URETERAL CALCULI
Stone-free is not everything !!
PARAMETERS FOR COMPARISON
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URETERAL CALCULI
Effectiveness
Morbidity
Convalescence
Cost
PARAMETERS FOR COMPARISON
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SWL FOR URETERAL CALCULI
Upper Middle Lower N= 33 N=248 N=381
Success of 94.8% 85.9% 98.2% 1O procedure
Re-tx rate 6.8% 15.7% 1.8%
Complications 10% 15.3% 8.4%
DORNIER HM-3
Lingeman, et al, 1993
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DISTAL URETERAL CALCULI
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 OF MONOTHERAPY STUDIES
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DISTAL URETERAL CALCULI
SWL URS
Effectiveness Slightly better
Morbidity Less
Hospitalization Less
Cost Slightly less
OVERVIEW OF HISTORICAL CONTROL STUDIES
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DISTAL URETERAL CALCULI
80 patients randomized to receive SWL or URS 40 patients had stones > 5 mm 40 patients had stones < 5 mm
SWL performed on Dornier MFL 5000
URS performed with 6.5F or 9.5F semi-rigid ureteroscopes (basket vs. pneumatic lithotripsy)
PROSPECTIVE, RANDOMIZED TRIAL
Peschel & Bartsch, 1999
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DISTAL URETERAL CALCULI
URS SWL
OR time (min) 19 63
Fluoro time (min) 0.8 5.1
Stone-free (days) 0.2 10.8
Stent (days) 7.2 0
Re-treatment rate 0 15%
PROSPECTIVE, RANDOMIZED TRIAL STONES < 5 MM
Peschel & Bartsch, 1999
* * *
* *
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SWL OF DISTAL URETERAL CALCULI
Initial animal studies suggest ovarian trauma Impaired fertility Mutagenesis
Subsequent animal investigations demonstrate no impact on fertility or offspring
Mice Rats Rabbits
ADVERSE EFFECTS TO FEMALE REPRODUCTIVE TRACT?
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SWL OF DISTAL URETERAL CALCULI
Analyzed Rx data and radiation exposure in 84 women of reproductive age
7 children born to 6 patients with no malformations or chromosomal anomalies
Miscarriages in 3 patients (but occurred at least 1 year after SWL)
ADVERSE EFFECTS TO FEMALE REPRODUCTIVE TRACT?
Viewig & Miller, 1992
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URETEROSCOPY
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URETERAL CALCULI
FLEXIBLE URETEROSCOPY
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ANTEGRADE MANIPULATION OF URETERAL CALCULI
Large stone burden
Body habitus
Urinary diversion
Transplant kidney
INDICATIONS
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URETERAL CALCULI
PERCUTANEOUS APPROACH
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URETERAL STONE MANAGEMENT
Advantages Minimal anesthesia requirements Non-invasive procedure No stenting/less complications Similar approach for all ureteral calculi
Disadvantages Lower success rate than URS Higher re-treatment rate
IN SITU SWL
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URETERAL STONE MANAGEMENT
URETEROSCOPY
Advantages Highest success rate Definitive Rx - No waiting for stone passage
Disadvantages More invasive than SWL Higher complication rate Requires greater technical expertise
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URETERAL CALCULI: CURRENT OPTIONS
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%
In situ SWL 0 No 75-80% 20-25%
*
Defined as complete stone removal with single procedure
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URETERAL CALCULI: CURRENT OPTIONS
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%
In situ SWL 0 No 75-80% 20-25%
*
Defined as complete stone removal with single procedure
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SURGICAL STONE MANAGEMENT
CHANGING TREATMENT PHILOSOPHIES
1980‟s 1990‟s 2000‟s 20
10‟s
Shock wave lithotripsy 95% 85% 75% ???
Endoscopic procedures 5% 15% 25% ???
Open stone surgery < 1% < 1% < 1% 0
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NEPHROLITHIASIS
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
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SHOCK WAVE LITHOTRIPSY
RECURRENT STONE FORMATION One Year Two Years
Post SWL Post SWL
Stone Free New stones 8% 10%
Residual Stones Stone growth 22% 21%
Lingeman, et al, 1989
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SHOCK WAVE LITHOTRIPSY
EFFECT ON STONE RISK FACTORS
Urine Values Pre- 3 Mo Post- (mg/day) Lithotripsy Lithotripsy
Calcium 254 261
Uric Acid 552 548
Citrate 249 257
Oxalate 42 41
Brown, et al, 1989
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MEDICAL MANAGEMENT OF NEPHROLITHIASIS
PROGRESS Elucidation
Urinary environment conducive to stone formation
Diagnosis Detection of underlying physiologic abnormalities
Medical Therapy Development of new treatment strategies
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STONE FORMATION
Concentration / solubility of stone-forming
salts
Promoters of crystallization and aggregation
Inhibitors of crystallization and aggregation
MAJOR FORCES
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DIETARY CALCIUM
Early recommendations suggest that low calcium diet will decrease urinary Ca++ excretion, thereby reducing risk of stone formation
Potential risk factors involving low calcium diet:
Reduced bone mass
Increased urinary oxalate
IMPACT OF LOW CALCIUM DIET
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DIETARY CALCIUM
Moderate calcium restriction in patients with
AH
Limit dietary intake of oxalate
Spinach, tea, chocolate, nuts
Limit dietary sodium intake
RECOMMENDATIONS
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CALCIUM SUPPLEMENTS
Calciuric response to calcium supplementation
Depends on duration of treatment and patient
population
PHYSIOLOGICAL EVIDENCE
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CALCIUM SUPPLEMENTS
Give HCTZ during initial three months to prevent hypercalciuria, 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 urinary calcium
RECOMMENDATIONS: PREMENOPAUSAL WOMEN
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Henoch Schönlein Purupura
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Answer 1.
Renin – Angiotensin II- ACE- ADH – Aldosterone
That is not correct
Please try again
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Peritoneal Dialysis
Is performed as an intracorporeal (inside the body) therapy making use of the peritoneal membrane.
Is the process of cleaning the blood by using the lining of the peritoneal cavity (peritoneum) as a filter – the peritoneum acts as a dialyzing membrane, permitting wastes from the body to cross it and empty into the instilled dialysate fluid .
Is a type of dialysis usually done by the patient at home.
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Hemodialysis
3-4 times a week
Takes 2-4 hours
Machine filters
blood and
returns it to
body
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Peritoneal Dialysis
Abdominal lining filters blood
3 types
– Continuous ambulatory
– Continuous cyclical
– Intermittent
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