1 curs nefrologie-de prezentat-ii- 23 februariei-2016

Characteristics of Renal Structure and
Function
I. Physiological Anatomy of the Kidney

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

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

-Nephron struc
and
Functions
Glomerulus
Proximal Tubule (PCT)
Loop of Henle
Distal tubule
Collecting tubule

Functions of the Nephron
Filtration
Reabsorption Secretion
Excretion

Glomerular Filtration
Figure 26.10a, b

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

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

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

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

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

GLOMERULONEPHRITIS
 Acute Glomerulonephritis:
 Rapidly Progressive
Glomerulonephritis
 Chronic Glomerulonephritis
 Nephrotic Syndrome
 Asymptomatic urinary
abnormalities

Glomerular disease
– Primary Glomerulonephritis
 Minimal change GN
 Membranous GN
 Focal segmental GS
 Membranoproliferative GN
 Diffuse proliferative GN
 Crescentic GN

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

Glomerular diseases:
Primary Glomerulonephritis

 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

 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
General Symptoms

 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
Signs and Symptoms

Etiology
 Infectious
– Streptococcal
– Nonstreptococcal postinfectious
glomerulonephritis
 Bacterial
 Viral
 Parasitic
 Noninfectious
– Multisystem systemic diseases
– Primary glomerular diseases

INVESTIGATIONSBase line measurements:
- ↑ Urea
- ↑ Creatinine
- Urinalysis (MSU):
a) Urine microscopy (red cell cast)
b) proteinuria

 Hypertensive encephalopathy,
 Heart failure and acute
 Pulmonary edema may occur in severe
cases
 Acute renal necrosis due to injury of
capillary or capillary thrombosis
Complications

 proper hygiene
 prompt medical assessment for
necessary antibiotic therapy should be
sought when infection is suspected
 prophylactic immunizations
Prevention

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.

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.

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.

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.

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.

Histologic Findings
1-Minimal-Change Disease
2-Focal segmental
glomerulosclerosis
3-Mesangiocapillary GN
4-Membranous nephropathy
„
 .

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.

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)

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.

 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
Imaging Studies

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.

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.

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.

Treatment
Mesangial proliferative GN
1-Antibiotics,
2-Diuretics, and
3-Antihypertensives as necessary.
4-Dialysis is rarely required.
Prognosis: Good.

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.

.Rapidly Progressive
Glomerulonephritis

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.

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.
Etiology

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.

Clinical Manifestations
Symptoms and signs of renal
failure,
pain,
haematuria,
systemic symptoms (fever, malaise,
myalgia, weight loss).

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.

Treatment
1-High-dose corticosteroids;
cyclophosphamide ± plasma
exchange/ renal
2-Transplantation.
Prognosis:
Poor if initial serum creatinine
>600µmol/L.

Proteinurea
≥3.5 g/day
(protein: creatinine
ratio >3-3.5)
Generalized
Oedema
Hypoalbuminaeia
<3g/L

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
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

Primary (idiopathic):
 Minimal change disease
Most common cause in children
 Membranous Nephropathy
Most common cause in Adults
 Focal Segmental Glomerulosclerosis
 MembranoProliferative
Glomerulonephritis

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).

•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

•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.

BUN, creatinine, creatinin clearnce.Na,
K,bicarbonates,chloride
CBC , serum albumin, serum proteins, calcium,
Lipid profile, Coagulation tests
Renal biopsy

67
Disease-
spesific
Compli
cation
symptoms

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.

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.

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

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

ACUTE AND CHRONIC
INTERSTITIAL NEPHRITIS
.

Causes of interstitial nephritis
 Drugs
 Infection
 Autoimmune
 Metabolic
 Radiation
 Neoplastic infiltration
 Mechanical

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.

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

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

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

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%

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).

Acute drug induced interstitial
nephritis
Granuloma
Oedema and focal inflammation
EOS

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)

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

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

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

ACUTE INTERSTITIAL INFECTIOUS NEPHRITIS

systemic
 Association with: Goodpasture syndrome,
lupus nephritis, mixed cryoglobulinemia,
membranoproliferative glomerulonephritis

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

Chronic interstitial nephritis

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

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

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)

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

Autoimmune
 systemic lupus
erythematosus
 transplant
rejection
 deposition of :
– calcium salts
– uric acid

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

mechanical causes of interstitial
nephritis
 reflux nephropathy
 calculi
 ureteric fibrosis
 prostatic hypertrophy
 urethral stenosis
 tumours

pathophysiolgical changes in
interstitial nephritis
 hypertension (50%)
 proteinuria (~1-2 g/24hrs)
 reduced urinary concentrating ability
 salt wasting
 renal tubular acidosis

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

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

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

.3- Lupus Nephritis
Vasculitis

WHO classification
Lupus Nephritis Type I no pathology
ypeV:membranous
Type II : mesangial
TypeIII:focal
proliferative
TypeIV:diffuse
proliferative

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

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

.
Gout, Uric Acid and Renal
Disease

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

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

.Amyloidosis and Myeloma
Kidney

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

.
Acute and chronic
Renal Failure

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

Hilton, R. BMJ 2006;333:786-790
Causes of acute renal failure

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
– 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)

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)

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

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
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

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
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
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

Indication for dialysis
 Symptoms of uremia (
encephalopathy,…)
 Uremic pericarditis
 Refractory volume over load
 Refractory hyperkalemia
 Refractory metabolic acidosis

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

Subjective symptoms
 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

– 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

– 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

– 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

– 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

 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

 Other abnormal findings
– Metabolic acidosis
– Fluid imbalance
– Insulin resistance
– Anemia
– Immunoligical problems

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

 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

 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

 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

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

.
CYSTIC DISEASES OF
THE KIDNEY

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

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

 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

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

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

Adult polycystic kidney disease

Renal cancer
In infants and children :
–Nephroblastoma ( Wilms’
tumour )
In adults :
–Renal cell carcinoma
–Renal cell adenoma
–Renal oncocytoma

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 )

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

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

RENAL CELL CARCINOMA
Hypernephroma / Grawitz’s
tumour
 seems to be arising from mature
renal tubules

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

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

RENAL CELL
ADENOMA
 Incidental findings at autopsy (22%)
 Well demarcated, unencapsulated
 Pale yellow-gray, discrete cortical mass
 Up to 2 cms. in maximum dimension

Bladder Carcinoma
 Derived from transitional epithelium
 Present with painless hematuria
 Prognosis depends on grade and depth of invasion
 Overall 5y survival = 50%

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

Types
 Haemodialysis (HD)
 Peritoneal Dialysis (PD)
 They work on similar principles: Movement
of solute or water across a semipermeable
membrane (dialysis membrane)

Diffusion
 Movement of solute
 Across semipermeable membrane
 From region of high concentration to one of
low concentration

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

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

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

Hemodialysis
 3-4 times a week
 Takes 2-4 hours
 Machine filters
blood and
returns it to
body

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

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

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%

Types
 Continuous Ambulatory Peritoneal Dialysis
(CAPD)
 Automated peritoneal Dialysis (APD)
– Continuous cyclical
– Intermittent

Continuous Ambulatory Peritoneal Dialysis
(CAPD)

CONTROLLING DIET
Foods to control are those containing:
 Protein
 Potassium
 Sodium
 Phosphorous
 Fluid

FLUIDS
 Healthy kidneys remove fluids as urine
 Check for fluid and sodium retention
 Need to restrict fluid intake

VITAMINS
 Folic acid
 Iron supplements
 Do not take OTC‟s without consulting the
doctor.

MANAGING DIET
INDICATORS OF GOOD CONTROL:
 Weight loss or gain
 Blood pressure
 Swelling of hands and feet
 Blood samples

Plasmapheresis:
plasma exchange and immunoadsorption

An adult donor kidney transplanted to the left iliac
fossa of an adult recipient.

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

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.

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

.
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.

(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.

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

MANAGEMENT OF
NEPHROLITHIASIS
.

ASYMPTOMATIC CALCULI
TREATMENT
Solitary kidney
Occupation (pilot, business traveler
Simultaneous contralateral treatment
It‟s difficult to make an asymptomatic patient
feel any better !

STONE MANAGEMENT
OPTIONS
Open surgery
Percutaneous
nephrolithotomy
Ureteroscopy
Shock wave lithotripsy
Medical therapy

STONE MANAGEMENT
OPEN surgery NEPHROLITHOTOMY

SHOCK WAVE LITHOTRIPSY
STONE FRAGMENTATION

SHOCK WAVE
LITHOTRIPSY
INDICATIONS
Surgical stone
No obstruction
Reasonable chance
of expeditious removal

SHOCK WAVE
LITHOTRIPSY
RELATIVE CONTAINDICATIONS
Large stones
Calcium oxalate > 20 mm
Struvite > 30
mm
Cystine stones
Distal obstruction
Poorly informed patients

CLINICAL SIDE-EFFECTS
Hematuria
Pain
Obstruction
(Steinstrasse)

SHOCK WAVE
LITHOTRIPSY
IDEAL CANDIDATES
Small stone (< 1.5 cm)
Mid or upper pole location
Normal renal anatomy
No distal obstruction

SHOCK WAVE
LITHOTRIPSY
LIMITATIONS
Completeness of stone fragmentation
Completeness of fragment elimination

STONE MANAGEMENT
PERCUTANEOUS NEPHROLITHOTOMY

SURGICAL STONE
MANAGEMENT
CURRENT ROLE OF PNL

SURGICAL STONE
MANAGEMENT
STAY OUT OF TROUBLE
Pre-op KUB Pre-op IVP

URETERAL CALCULI
TREATMENT OPTIONS
Observation
Shock wave lithotripsy
Ureteroscopy
Blind basket extraction
Percutaneous approach
Open surgery

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

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.

Toxicity of calcineurin
inhibitors

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++

Cellular rejection
Tubulitis
CD3

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)

URETERAL CALCULI
Stone-free is not everything !!
PARAMETERS FOR COMPARISON

URETERAL CALCULI
Effectiveness
Morbidity
Convalescence
Cost
PARAMETERS FOR COMPARISON

SWL FOR
URETERAL CALCULI
Upper Middle Lowe
r
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%
DORNIER HM-3
Lingeman, et al, 1993

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

SWL URS
Effectiveness Slightly better
Morbidity Less
Hospitalization Less
Cost Slightly less
OVERVIEW OF HISTORICAL
CONTROL STUDIES

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

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 1
5%
PROSPECTIVE, RANDOMIZED TRIAL
STONES < 5 MM
Peschel & Bartsch, 1999
*
*
*
*
*

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?

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

URETERAL CALCULI
FLEXIBLE URETEROSCOPY

ANTEGRADE MANIPULATION OF
URETERAL CALCULI
Large stone burden
Body habitus
Urinary diversion
Transplant kidney
INDICATIONS

URETERAL CALCULI
PERCUTANEOUS APPROACH

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

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

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%
*
Defined as complete stone removal with single procedure

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%
*
Defined as complete stone removal with single procedure

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

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

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

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

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

STONE FORMATION
Concentration / solubility of stone-forming
salts
Promoters of crystallization and aggregation
Inhibitors of crystallization and aggregation
MAJOR FORCES

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

DIETARY CALCIUM
Moderate calcium restriction in patients with
AH
Limit dietary intake of oxalate
Spinach, tea, chocolate, nuts
Limit dietary sodium intake
RECOMMENDATIONS

CALCIUM SUPPLEMENTS
Calciuric response to calcium supplementation
Depends on duration of treatment and patient
population
PHYSIOLOGICAL EVIDENCE

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

Answer 1.
Renin – Angiotensin II- ACE- ADH – Aldosterone
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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.

Peritoneal Dialysis
 Abdominal lining filters blood
 3 types
– Continuous ambulatory
– Continuous cyclical
– Intermittent

1 curs nefrologie-de prezentat-ii- 23 februariei-2016

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