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Universitatea Titu Maioresc

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Pancreatic Disease

. Body related
posteriorly to left
crus, left adrenal,
left renal vein, and
splenic vein
Celiac Axis (trunk,
artery) lies
superior to body

Detailed Anatomy continued


. Head of Pancreas

Body & Tail of Pancreas:

Anatomy & Physiology


III
1-2

L alkaline, clear, isoosmolar enzyme rich fluid


Na & K at plasma levels (165mmol/L)
20 enzymes are secreted
Secretion is regulated by: Secretin, CCK, Vagus and l
ow Ph
Proteolytic enzymes (Tryp, Chemotryp, elastase etc
Lipolytic (lipase, colipase, phospholipase..etc)
amyloytic
Endocrine function: insulin, glucagon, somatostatin..e
tc)

Acute Pancreatitis

An inflammation of the pancrease


caused by the activation,
Pancreatic Protective Factors
interstitial liberation and the auto Produced in pro-enzymes
Storeddigestion
of the gland by its own
in lysosomes (zymogen)
Acidic nature & low Ca prevent against activation
enzymes

1.

Acute Hemorrhagic Pancreati


tis

http://www.pathguy.com/~lulo/lulo0028.htm

Pancreatitis
Pathogenesis
1.
2.
3.
4.
5.

Obstruction- Secretion
Common Channel theory
Duodenal reflux
Increased permeability of pancre
atic duct
Enzyme Auto-activation

Pancreatitis
Aetiology I
1.

2.

3.

Gall stone
1.
90% of acute pancreatitis .
2.
Life risk of 3-5%
3.
Age 40s .
4.
F>m
5.
Transient obstruction
Alcohol 75% of chronic pancreatitis
1.
Spasm of the sphinctor of Oddi
2.
Increases the concentration of enzymes
3.
Structural damage caused by the precipitation of calciu
m
4.
Transient reduction of blood flow
Drugs
1.
Steroids, AZT
2.
Sulphonomids, Tetracyclin
3.
Oestrogen

Acute Pancreatitis
Clinical Presentation

Abdominal Pain
Constant, quick onset, variable in severity
Epigastric
Radiating to the back in 50% of patients
Associated with nausea, vomiting & retching
Relieved by lying on to the L side, legs-up
Other precipitating factors
Fever in 70%
Jaundice in 30%
Shock +/_ in 10%
Hematemasis & malena in 5%

Acute Pancreatitis
Clinical Presentation II

Dyspnoea in 10%
Tender Abdomen: Mild to severe
Peritonitis,could be diffuse
BS: hypoactive
Abdominal Mass:
Phlegmon
Pseudocyst,
Abcess Ascitis
Cullens
Gray-turner signs
Erythametous skin lesions

Differential diagnosis
Perforated

DU
Perforated GB
Emphsymatous cholecystitis
Mesenteric infarction
AAA
Others

Acute Pancreatitis
Investigation II

High amylase may be caused by:


1. Perforated DU
2. Cholecystitis
3. Small bowel obstruction
4. Perforated Small bowel
5. Ectopic pregnancy

Acute Pancreatitis
Investigation III

Radiological:
Plain X- rays:

AXR: calcification, sentinle lo


op SB,colonic spasm
CXR: pleural effusion & diffe
rntial
USS: GB stones, pancreatic peripa
ncreatic info
CT: Diagnosis, prognosis, F/U
Endoscopic USS
MRCP
ERCP

Others:

FBC: Hct, WBC, Plat.


U&E, LFT, Ca, glucose.
ABG

Acute Pancreatitis
Complications II

Systemic
Metabolic

I.

Hypokalaemia, Hypochloraemia
& Metabolic alkalosis
Hypocalcaemia
Hypomagnesemia
Hypoxemia

Acute Pancreatitis
Treatment
I.

II.

Conservative
( Admit in ICU VS Common Surgical Ward)
NBM vs Early nutrition
? NGT
Analgesia: narcotic
Adequate fluid replacement ( Initial crystalloid then colloi
d)
Antibiotics (organisms & penetration)
??Anticholinergics, somatostatin have no proven benifit
Minimally invasive
Early ERCP & sphinctorotmy for impacted stones
CT-guided drainage of Psedocusysts

Treatment II
Surgery is contraindicated in uncomplicated
attacks.
1.
2.
3.
4.
5.
6.

The indications for surgical intervention are:


Uncertain diagnosis
Early cholecystectomy
CBD stone extraction
Debridement of necrotic pancreatic tissue
Pancreatic abcess (Infected Necrosis)
Complicated Pseudocysts

Surgical intervention to assist in the diagnosis of pancreatit


is, to establish pancreatic drainage, and to debride a necrot
ic tissue.

Multiple sump tubes are used after pancreatic surgery. Triple-lumen tubes consist
of ports that provide tubing for irrigation, 18
air venting, and drainage.

Summary of treatment
All

patients

Nasogastric suction
NPO
Monitor and maintenance of intravascular volume
Respiratory monitoring and support
Antibiotics(selective)
Early laparotomy only fordiagnosis
Estimate prognosis by early signs

Patients

with severe pancreatitis

Peritoneal lavage
Nutritional support
Suspect and treat pancreatic sepsis
Heparin if hypercoagulable

Pancreatitis

Necrotizing Pancreatitis

Pathophysiology
Disruption in the normal separation of lysosomal

and pancreatic enzymes which leads to the exposur


e of pancreatic proenzymes to lysosomal enzymes l
eading to pancreatic autodigestion

Biliary pancreatitis
obstructing stone at ampulla allows bile to reflu
x into the pancreatic duct
obstructing stone at ampulla produces pancreat
ic duct hypertension

Radiographic studies
Abdominal x-ray
typically nonspecific
may exclude other causes of abdominal pain
may show a sentinel loop or a colon cutoff sign
Ultrasound
typically shows a diffusely enlarged,
hypoechoic pancreas
sensitivity of 67% and near 99% specificity in
the diagnosis of acute pancreatitis
MRCP

CT findings of necrotizing pancreatitis

Conclusions
Necrotizing

pancreatitis continues to hav


e significant morbidity and mortality des
pite advances in medical therapy

Patients

with necrotizing pancreatitis sho


uld all receive antibiotic prophylaxis

Surgery

should be delayed as long as pos


sible and has no proven role in sterile nec

Pancreatitis
Chronic Pancreatitis

Chronic pancreatitis - Sympto


ms
Severe

dull epigastric pain radiating to th

e back
Nausea, Vomiting
Severe weight loss when steatorrhoea is p
resent
Overt diabetes mellitus

Chronic pancreatits- Treatmen


t
Pain

control (slow release opioid patches)


Abstinence from alcohol
Pancreatic enzyme supplements
Endoscopic procedures to remove duct st
ones (extracorporal lithotripsy, stenting)
Surgery (Begers procedure)

TUMOURS OF THE PANCREAS

Pancreatic tumours Types


Benign

exocrine serous cyst ade


noma, mucinous cyst adenoma
Malignant exocrine ductal aden
ocarcinoma, mucinous cyst adenoc
arcinoma
Endocrine Gastrinoma, Insulino
ma, other

Pancreatic Tumors
Pancreatic Cancer

CLINICAL FEATURES:

The diagnosis of pancreatic cancer


varies from the simple and clinically
obvious to the most difficult and al
most impossible the initial symptom
s and signs depend on the site and e
xtent of the pancreatic cancer.

Modes of presentation:

Weight loss

Pain

Jaundice

Steatorrhoea

Diabetes Mellitus

Acute Pancreatitis

Malignant Ascites

Gastric Outlet Obstruction

Approach to Investigations:
(Selective Investigations)

Ultrasound Scan

C.T. Scan

MR Imaging Scan

ERCP

Histology & Cytology

Angiography (Coeliac, Superior - Mese


nteric)
Laparoscopy

Pancreatic Tumors, In head


c. Nausea
d. Weight loss
e. Increased plasma amylase
f. Increased alkaline phosphatase
g. May involve compression of
pancreatic duct, CBD

Pancreatic tumors,
In Body of Pancreas:
a. Gnawing pain radiating to back
b. Pain increases after eating or
lying down
c. Weight loss, anorexia
d. Large tumor may compress IVC,
portal vein

MANAGEMENT OF PANCREATIC CANCER:

A. Surgical Treatment
B. Non Surgical Treatment

SURGICAL TREATMENT:
Pancreatic

Cancer is essentially incur


able since metastasis occurs at such
early stage. Any treatment must be r
egarded as palliative.

Pancreas Tumors

ENDOCRINE TUMORS:

INSULINOMA:
The commonest islet cell tumour and ari
se from the beta cell and situated anywh
ere on the surface or within the substan
ce of the pancreas.

Most tumours are benign adenomas but


15% are low grade carcinomas and secre
te (insulin).

Necrolytic erythema migrans is pathognomic in patients with


glucagonoma INSULINOMA

Bornman, P C et al. BMJ 2001;322:721-723

Copyright 2001 BMJ Publishing Group Ltd.

n
Surgery of the pancreas
includin
g transplantation

Patient with jaundice, bruising, and weight loss due to pancreatic


carcinoma

Bornman, P C et al. BMJ 2001;322:721-723

Copyright 2001 BMJ Publishing Group Ltd.

Liver Transplantation
for
Alcoholic
Liver Disease
Pancreas

Transplantation

Robotic
Step 3 Hepatic Hilum
Pancreaticoduodenectomy

The Robotic Training Lab


Procedures performed at
UIC and offered for training
include:

Splenectomy
Total
gastrectomy
Lung
lobectomy
Colorectal
surgery
Thyroidectomy

Adrenalectomy
Esophagectomy
Major
hepatectomies
CBD Procedures
Whipple

Universitatea Titu Maioresc


u
Bucuresti

GASTROENTEROLOGY

Bowel and colon disease


Prof Univ Dr Ion C. intoiu

Small intestine
Made

up of three parts:
ileum, jejunum, and duodenu

m.
Main

function is absorption

Alteration in elimination bowel


Inflammatory
Small

bowel disease

bowel obstruction

Cancer of

the colon and ostomies.

Diarrhea
It

is a symptom not a p
rimary disorder.

It

is the increase in: flu


id, volume, and fluid c
ontent of the stool.

Causes:
Bacteria toxins
Parasitic infections
Malabsorption syndro

mes
Medication
Systemic disease
Allergies
Psychogenic

Malabsorbtion and Maldigesti


on syndrome

Irritable Bowel Syndrome

Irritable Bowel Syndrome


Functional meteorism
Functional constipation
Functional diarrhea
Irritable bowl syndrome
Undifferentiated functional bowl disorders

Irritable Bowl syndrome


Prevalence
15% of adult population
Etiology not clear
Visceral hypersensitivity
Motility disorder
Neurotransmitter inbalance
Infection
Psychosocial factors

Inflammatory bowel
disease
Nonspecific

ulce
rative colitis (U
C)-RCUH
Crohns disease
(CD)
Crohns disease
Nonspecific ulcerative colitis

Colitis of unknown etiology

Ulcerative colitis

Crohns disease

Localization
of damage
Volume of
damage
Depth of
damage

Ulcerative colitis
(RCUH)

Ulcerative colitis
Affects

the mucous and the submucosa of


the colon and rectum.

Primarily

affects the young (15-30)


More common in whites
Cause

unknown found in families with h


x. of the same, hx crohns, Hx certain art
hritis.

Ulcerative colitis
Chronic diffuse inflammation of large intestine with

edema and superficial ulceration of mucosa


Starts always from damage of rectum, and than the
process involves other parts of large intestine
Symptoms: rectal bleeding, fever, diarrhea, abdominal
pain, moderate anemia.
Complications:
Toxic megacolon (dilation of the gut w
ith thinning of gut wall, high risk
of perforation)
Large intestine carcinoma (const
ant regeneration of epithelium---

Polyps changes that occur in


ulcerative colitis

Ulcerative colitis

Ulcerative Colitis signs and sy


mptoms
Insidious

onset
Attacks last 1-3 months
Occur at intervals of months to years
Diarrhea is the predominant symptoms o
f all types of ulcerative colitis.
Typically

30-40 stools per day, ood a


nd mucus.

Treatment of Ulcerative Colitis


Pharmacological
Dietary

management

Surgical

management

Pharmacological treatment
Sulfasalazine

(Azulfidine) SALAZOPIRI
NA anti-inflamatory
inhibits prostaglandin production in the bo

wel.

Mesalamine

(Rowasa) & Olsalazine (Dipent


um) -Same action as above.

Corticosteroids-anti-inflammatory effects
Use as a treatment during acute attacks.

Crohns disease

Crohns disease
Primarily

affects young people (10-30 yea

rs)
Can

occur anywhere in the GI tract.

Most

frequently affects the terminal ileu


m and right colon.

Crohns disease
Cause
Like

is unknown

ulcerative colitis can have arthritis,


uveitis, thromboembolism, and vascular
disorders. Also the pt can have cystitis, re
nal calculus, and ureteral obstruction.

Pathophysiology of Crohns di
sease
Begins with an aphthoid lesion similar to can

ker sore in the mucosa and submocosa of the


bowel.

Deeper ulcerations, lesions, lumen takes on

a cobblestone appearance.

Fibrotic changes in the bowel cause to thicke

n and lose of flexibility.

Aphtoid lesions of the mucosa

View of the intestine with Cro


hns

Late stages of crohns

Manifestations of Crohns dise


ase
Continuous or episodic diarrhea
Stools are liquid or semiformed and typically

do not contain blood.

Abdominal pain and tenderness are common


A palpable RLQ mass is often present
Fever, malaise, weight loss, fatigue, and anemi

a are common.

Management of Crohns Disea


se
Surgery
Bowel obstruction is the leading cause for surg

ery

With Crohns disease there is increased risk fo

r fistula formation.

With Crohns disease, the surgery does

not cure as it does with ulcerative colitis.

Crohns disease recur 50 to 75% of the time

Neoplastic Disorders:Polyps
and Colorectal Cancer
1

Colorectal Polyps
1

Polyps
Polyps are masses of tissues that arise from t

he bowel wall and protrude into the lumen.


Most polyps are benign but some have the po
tential to become malignant.
Familial polyposis is an uncommon disorder

characterized by hundreds of adenomatous p


olyps throughout the large intestine. The risk
of malignancy is almost 100% by the age 40.

Polyposis

Symptoms of polyps
Most

are asymptomatic

Intermittent
Dark

painless rectal bleeding

or bright blood

Diagnostic for polyps


Barium

enema

Sigmoscopy
Digital

examination

Colonoscopy

Once

identify polyps ne
ed to be remove becaus
e of the risk of maligna
ncy.
They can be remove du
ring colonoscopy using
electrocautery snare or
hot biopsy forceps pass
ed through the scope

Colorectal Cancer

Adenoma to Carcinoma Pathway


Normal

APC
loss

Adenoma

K-ras
mutation

Chrom 18
loss

Cancer

p53
loss

Normal
HyperEarly Intermediate Late
Cancer
Epithelium proliferation Adenoma Adenoma Adenoma

Risk of colorectal cancer


Age

>50 years

Polyps

of the colon and or rectum

Cancer elsewhere in
Family

the body

Hx of colorectal cancer

Ulcerative

Colitis Crohns disease

Symptoms of Colorectal Cancer


Caecum
Anaemia
Obstruction
Mass
Dyspepsia
Appendicitis

Rectum
Bleeding
Altered bowel habi
t
Tenesmus
Pain
Bladder symptoms

Treatment of bowel cancer is


surgery
Treatment

of bowel cancer is surgery

Chemotherapy

djunct)

(adjunct) and radiation (a

Colostomies take the name of the


portion of the colon from which t
hey are found

Total Mesorectal Excision

Laparoscopic Resection

Radiation therapy
While

radiation ther
apy is not effective as
a primary treatment
for colon cancer it is
recommended as adj
unct therapy speciall
y for rectal tumors.

Small

rectal cancer
may be treated with i
ntracavitary, externa
l,or implantation rad
iation.

Radiation

reduce the
recurrences of rectal
and pelvic tumors

Gata????

Universitatea Titu Maioresc


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Titu Maiorescu University


Curs Medicina Interna

NEPHROLOGY- I
Prof univ dr Ion C Tintoiu

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 713 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

-Nephron

struc

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

Functions of the Nephron


Reabsorptio
n
Filtration

Secretion
Excretion

Glomerular Filtration

Figure 26.10a, b

Proximal Tubule (PCT)


Reabsorption
NaCl
Water
Bicarbonate
Glucose
Proteins
Aminoacids
K+, Mg, PO +, uric acid,
4
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 Clreabsorption
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:
cells secrete K+ aldosterone
mediated Na+ reabsorption
Intercalated cells acid base regulation
Principal

Nephron symphony

. Renal

Pathology

Diseases of the kidney


1-Glomeruli
Glomerulonephritis
Primary
Secondary
Chronic
2-Tubulointerstitium
Acute tubular necro
sis
Pyelonephritis
Acute
chronic
3-Vessels
Nephrosclerosis

4-Urinary obstruction
Stones
Hydronephrosis
5- Cystic diseases of the ki
dney
6-Tumors
Benign
Malignan
7-Litiazis

Glomerular diseases

GLOMERULONEPHRITIS
Acute

Glomerulonephritis:
Rapidly Progressive Glomerulonep
hritis
Chronic Glomerulonephritis
Nephrotic Syndrome
Asymptomatic urinary abnormalit
ies

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

Acute Glomerulonephritis

Definition
Acute glomerulonephritis is the inflammatio
n of the glomeruli which causes the kidneys
to malfunction
It is also called Acute Nephritis, Glomerulo
nephritis and Post-Streptococcal Glomerulo
nephritis
Predominantly affects children from ages 2
to 12
Incubation period is 2 to 3 weeks

Acute Glomerulonephritis

General Symptoms
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

Signs and Symptoms


Hematuria:

dark brown or smoky urine


Oliguria: urine output is < 400 ml/day
Edema: starts in the eye lids and face the
n the lower and upper limbs then become
s generalized; may be migratory
Hypertension: usually mild to moderate
Hypoproteinemia, hypercholesterolemi
a),
mixed

Acute Glomerulonephritis

Etiology
Infectious
Streptococcal
Nonstreptococcal postinfectious glomerulo

nephritis
Bacterial
Viral
Parasitic

Noninfectious
Multisystem systemic diseases
Primary glomerular diseases

Acute Glomerulonephritis
INVESTIGATIONS

Base line measurements:

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

Acute Glomerulonephritis
Complications
Hypertensive

encephalopathy,
Heart failure and acute
Pulmonary edema may occur in severe
cases
Acute

renal necrosis due to injury of ca


pillary or capillary thrombosis

Acute Glomerulonephritis P
revention
proper hygiene
prompt

medical assessment for necessa


ry antibiotic therapy should be sought
when infection is suspected
prophylactic immunizations

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 s

pread of infection to close contacts.


Antimicrobial therapy does not appear to prevent the development of GN, ex
cept if given within the first 36 hours.

Loop

diuretic therapy

Loop diuretics may be required in patients who are edematous and hypertens

ive in order to remove excess fluid and to correct hypertension.


Relieves edema and controls volume, thereby helping to control volume-relate
d elevation in BP.

Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxid


e) 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 cir
culatory congestion subside.

Chronic glomerulonephritis

Chronic glomerulonephritis
The condition is characterized
1 - irreversible and progressive glomerular a
nd tubulointerstitial fibrosis
2-ultimately leading to a reduction in the glo
merular filtration rate (GFR) and
3- retention of uremic toxins
.
. The diagnosis of CKD can be made without
knowledge of the specific cause.

Chronic glomerulonephritis

Etiology
Nearly all forms of acute glomerulonephritis have a t
endency to progress to chronic glomerulonephritis.
The progression from acute glomerulonephritis to ch
ronic glomerulonephritis is variable.
Whereas complete recovery of renal function is the r
ule for patients with poststreptococcal glomerulon
ephritis, several other glomerulonephritides,
such as immunoglobulin A (IgA) nephropath
y, often have a relatively benign course and many
do not progress to ESRD.

Chronic glomerulonephritis
Pathogenesis
Reduction in nephron mass from the initial injury re
duces the GFR.
This reduction leads to hypertrophy and hyperfiltrat
ion 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 func
tional consequences of nephron loss.
The changes, however, are ultimately detrimental be
cause they lead to glomerulosclerosis and furt

her nephron loss.

Chronic glomerulonephritis Histo

logic Findings
In early stages, the glomeruli may still sh
ow some evidence of the primary diseas
e.
In advanced stages, the glomeruli are hy
alinized and obsolescent.
The tubules are disrupted and atrophic,
and marked interstitial fibrosis and art
erial and arteriolar sclerosis occur.

Chronic glomerulonephritis Hi
stologic Findings

1-Minimal-Change Disease
2-Focal segmental glomerulos
clerosis
3-Mesangiocapillary GN
4-Membranous nephropathy

Chronic glomerulonephritis
Minimal change Disease

Focal Segmental Glomerulosclerosis


Segmental areas of glomerular sclerosis, hyalinization of
glomerular capillaries

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.

Membranous Nephropathy
thickened BM, IF +ve for IgG & C3 and
subepithelial deposits on EM

Chronic glomerulonephritis Clini

cal Manifestations
Uremia-specific findings
Edemas
Hypertension
Jugular venous distension

(if severe volume

overload is present)
Pulmonary rales (if pulmonary edema is pr
esent)
Pericardial friction rub in pericarditis
Tenderness in the epigastric region or blood
in the stool (possible indicators for uremic g
astritis or enteropathy)

Chronic glomerulonephritis

Lab Studies

Urinalysis
Urinary protein excretion
Serum chemistry
Serum creatinine and urea nitrogen levels a
re elevated.
Impaired excretion of potassium, free water, and a
cid results in hyperkalemia, hyponatremia, and lo
w serum bicarbonate levels, respectively.
Impaired vitamin D-3 production results in hypoc
alcemia, hyperphosphatemia, and high levels of pa
rathyroid hormone.
Low serum albumin levels may be present if uremi
a interferes with nutrition or if the patient is nephr
otic.

Chronic glomerulonephritis Imagi

ng Studies
Renal

ultrasonogram
Obtain a renal ultrasonogram to dete
rmine renal size, to assess for the pre
sence of both kidneys, and to exclude
structural lesions that may be respon
sible for azotemia.
Small kidneys often indicate an irrev
ersible process.
Kidney biopsy

Chronic glomerulonephritis Treat

ment

The target pressure for patients with proteinuria greater


than 1 g/d is less than 125/75 mm Hg; for patients with pr
oteinuria less than 1 g/d, the target pressure is less than 1
30/80 mm Hg.
Angiotensin-converting enzyme inhibitors (ACEIs)
angiotensin II receptor blockers (ARBs)
Diuretics are often required because of decreased freewater clearance, and high doses may be required to co
ntrol edema and hypertension when the GFR falls to l
ess than 25 mL/min.
Beta-blockers, calcium channel blockers, central alph
a-2 agonists (eg, clonidine), alpha-1 antagonists, and
direct vasodilators (eg, minoxidil, nitrates) may be use
d to achieve the target pressure.

Chronic glomerulonephritis Treatm

ent
Minimal change glomerulonephritis
1-Corticosteroids induce remission in >90% of
children and 80% of adults (slower response).
2-immunosuppression: (cyclophosphamide, ci
closporin (=cylosporin)): early/ frequent relapses;
steroid SEs/dependence.
Prognosis: 1% progress to ESRF.

Chronic glomerulonephritis Treat

ment
Focal segmental glomerulosclerosis
Poor response to corticosteroids (1030
%). Cyclophosphamide or ciclosporin (=cyl
osporin) may be used in steroid-resistant cases.
Prognosis: 3050% progress to ESRF.

Chronic glomerulonephritis Treat

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

Chronic glomerulonephritis Treat

ment
Membranous nephropathy
If renal function deteriorates, consider corti
costeroids and chlorambucil. Prognosis: U
ntreated, 15% complete remission, 9% ESR
F at 25yrs and 41% at 15yrs.

. Rapidly Progressive
Glomerulonephritis

Rapidly Progressive Glomerulonephritis

Rapidly progressive glomerulonephr


itis (RPGN) is a disease of the kidn
ey that results in a rapid decrease i
n the glomerular filtration rate of a
t least 50% over a short period, fro
m a few days to 3 months.

Rapidly Progressive Glomerulonephritis Et

iology
The cause of RPGN is unknown. A geneti
c predisposition may exist for the devel
opment of this disease.
Multiple studies have demonstrated that
ANCA- (antineutrophil cytoplasmic an
tibodies) activated neutrophils attack v
ascular endothelial cells.
ANCA-associated vasculitis.
A viral etiology is possible.

Rapidly Progressive Glomerulonephritis

Pathology
Renal biopsshow
A diffuse, proliferative, nec
rotizing glomerulonephri
tis with crescent formatio
n.
The main pathologic findin
g is fibrinoid necrosis (>9
0% of biopsy specimens);
extensive crescent format
ion is present in at least 5
0% of glomeruli.

Rapidly Progressive Glomerulonephritis

Clinic

al Manifestations
Symptoms

and signs of renal failur

e,
pain,
haematuria,
systemic symptoms (fever, malaise,
myalgia, weight loss).

Rapidly Progressive Glomerulonephritis La

b Studies

The most important requirement in the diagnosis of antine


utrophil cytoplasmic antibodies (ANCA) ANCA-associated
disease is a high index of suspicion. Rapid diagnosis is esse
ntial for organ preservation. Laboratory studies include th
e following:
Routine chemistry: The most common abnormality is a
n increased serum creatinine level.
Urinalysis with microscopy:
Antinuclear antibody (ANA) titer:
ANCA
Urine and serum protein electrophoresis: Perform this in a
ny middle-aged or elderly person presenting with RPGN to
exclude the presence of light-chain disease or overt multipl
e myeloma as a cause of the clinical findings.

Rapidly Progressive Glomerulonephritis Tr

eatment
1-High-dose corticosteroids; cyclo
phosphamide plasma exchang
e/ renal
2-Transplantation.
Prognosis:
Poor if initial serum creatinine
>600mol/L.

Nephrotic syndrome

What is Nephrotic syndrome?


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

Generalized
Oedema

The Nephrotic Syndrome


Is

not a disease but a group of signs and s


ymptoms seen in patients with heavy prot
einuria
presents with oedema
proteinuria usually > 3.5g / 24hrs (>0.05g
/ kg / 24hrs in children)
serum

albumin < 30g/l


other features: hyperlipidaemia, and hypercoagu
able state

The Nephrotic Syndrome


Pathophysiology

proteinuria: due to an increase in glomerular permeabi


lity
hypoalbuminuria: occurs when liver synthesis cannot k
eep up with urine losses
oedema mechanism is complex and still in dispute: p
rimary salt and water retention associated with redu
ced 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 antit
hrombin III

Nephrotic syndrome Pathogenesis

DAMAGED

Proteinuria

Nephrotic syndrome
Etiology

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

Nephrotic syndrome Etiol


ogy

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).

Nephrotic syndrome
Clinical Presentation

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

Nephrotic syndrome
Diagnostic

1st Goal: To confirm the clinical diagnosis


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.

2nd Goal: to seek a possible cause


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.

3rd Goal: To assess renal function


BUN, creatinine, creatinin clearnce.Na,
K,bicarbonates,chloride

4th Goal: to identify biochemical disorders


related to the nephrotic state.
CBC , serum albumin, serum proteins, calcium,
Lipid profile, Coagulation tests

Renal biopsy

Nephrotic syndrome
Treatment

ms
o
t
p
sym

Compli
cation
Diseasespesific

162

Management of symptoms
Oedema
Low salt diet
Diuretics
serial measurement of body
weight
Proteinuria
ACE inhibitors or ARBs

Hypoalbuminaemia

High protein diet not indicated


0.81 g/kg/day
Ref: Up to date online 17.3.

Management of complication
Hyperlipidaemia
Regular Lipid profile
Statin if severe long lasting nephrotic
syndrome
Control other CVD risk factorstarget 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
Ref:
Up to date online 17.3.

Management of the nephrotic synd


rome
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

Nu s-a terminat !

Titu Maiorescu University


Curs Medicina Interna

NEPHROLOGY-II
Prof univ dr Ion C Tintoiu

Other Renal Diseases

Other Renal Diseases


1.
2.
3.
4.
5.

1-Interstitial Nephritis
2-Diabetic Nephropathy
3-Microscopic Vasculitis and SLE
4-Gout and the Kidney
5-Myeloma Kidney

1-Interstitial Nephritis

Causes of interstitial nephritis


Drugs
Infection
Autoimmune
Metabolic
Radiation
Neoplastic

infiltration
Mechanical

Drugs and interstitial nephritis


methicillin 17%
other penicillins <1%
cephalosporins <1%
rifampicin 1%
ciprofloxacin 1%
cotrimoxazole
omeprazole ?

fenoprofen <1%
frusemide <1%
bumetanide <1%
cimetidine <1%
allopurinol <1%
5 aminosalicylates
ranitidine (rare)

Bacterial infection
bacterial

infection of the renal parenchyma cau


ses interstitial nephritis
infection without anatomical abnormality seldo
m produces permanent damage
obstruction (stones, prostate etc) in combinatio
n with infection can cause progressive disease
tuberculosis causes extensive destruction from
granulomata, fibrosis and caseation

Autoimmune
systemic

lupus ery
thematosus
transplant rejectio
n

deposition

of :

calcium salts
uric acid

Infiltration in neoplastic and other dis


eases
lymphoma

and leukaemias

myeloma
Bence-Jones protein (light chains from maligna

nt plasma cell clone) causes interstitial nephriti


s, tubular obstruction(cast nephropathy) and am
yloid deposition
called myeloma kidney
sarcoidosis

mechanical causes of interstitial nephr


itis
reflux

nephropathy

calculi
ureteric

fibrosis
prostatic hypertrophy
urethral stenosis
tumours

pathophysiolgical changes in interstiti


al 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 hypersens
itivity reactions
renal biopsy
improvement after withdrawal of drugs and toxins

use

of corticosteroids (prednisone)
water and and electrolyte
treatment of hypertension

2-Diabetic nephropathy

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 hyperkalae
mia

Pathophysiology of Diabetic Nephropathy

renal hypertrophy and hyperfiltration


microalbuminuria (< 100mg/24hrs and negative to prot
ein test strip-albustix)
hypertension
hyperfiltration and microalbuminuria can be improved
by good diabetic control
microalbuminuria is a predictor of diabetic nephropath
y and mortality in diabetics - it probably has no predict
ive value for other renal diseases

. 3- Lupus Nephritis
Vasculitis

ype V : membranous

Type III : focal


proliferative

Type IV : diffuse
proliferative

WHO classification

Lupus Nephritis Type I no pathology

Type II : mesangial

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 pathol
ogy, 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, tiredne

ss, 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 cyclo
phosphamide

Gout, Uric Acid and Renal


.
Disease

Gout, Uric Acid and Renal Disease


uric

acid calculi, parenchymal deposits of


uric acid and tubular obstruction with ur
ate can cause renal damage
an elevated plasma uric acid does not in i
tself seem to cause renal damage
1/4 of patients with gout get uric acid sto
nes
1/4 of patients with uric acid stones will h
ave gout

Acute and Chronic urate nephropathy

acute nephropathy with overproduction of uric acid an


d kidney obstruction with uric acid crystals
can occur with treatment of malignant disease with cyt
otoxics, heat stroke and status epilepticus
treat with fluids and prophylaxis with allopurinol
role of uric acid in chronic renal failure disputed but do
es occur with some familial disorders
association between hyperuricaemia, hypertension vas
cular disease, hyperlipidaemia and diabetes

. Amyloidosis and Myeloma


Kidney

Amyloidosis and Myeloma Kidney


amyloid

represents a family of proteins which p


olymerize to produce the beta pleated sheet of a
myloid and deposit in tissues
AL amyloid (primary amyloid) made from light
chains associated with plasma cell disorders, m
ostly overt myeloma
AA amyloid (secondary amyloid) is made from
A protein and is an acute phase reactant associa
ted with chronic inflammatory diseases like rhe
umatoid arthritis and bronchiectasis

Inca nu s-a terminat !

Titu Maiorescu University


Curs Medicina Interna

NEPHROLOGY-III
Prof univ dr Ion C Tintoiu

Acute and chronic


.
Renal Failure

. Acute Renal Failure

Acute renal failure -ARF


Deterioration

of renal function over a period of hours to days, resulting i

n
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

Causes of acute renal failure

Hilton, R. BMJ 2006;333:786-790

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
Antiglomerular basement membrane (GBM) disease (Goodpasture syndr
ome)
Antineutrophil cytoplasmic antibody-associated glomerulonephritis (AN
CA-associated GN) (Wegener granulomatosis, Churg-Strauss syndrome, m
icroscopic polyangiitis)
Immune complex GN (lupus, postinfectious, cryoglobulinemia, primary m
embranoproliferative glomerulonephritis)

Tubular
Ischemi
Totoxic
Heme pigment (rhabdomyolysis, intravascular hemolysis)
Crystals (tumor lysis syndrome, seizures, ethylene glycol poisoning, m
egadose vitamin C, acyclovir, indinavir, methotrexate)
Drugs (aminoglycosides, lithium, amphotericin B, pentamidine, cisplati
n, 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, ede

ma, 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 volu

me status
Avoidance of further renal insults
Optimization of nutrition
If necessary, institution of renal replace
ment therapy
The function has to be temporarily
replaced by dialysis

Indication for dialysis


Symptoms

of uremia ( encephalopat

hy,)
Uremic pericarditis
Refractory volume over load
Refractory hyperkalemia
Refractory metabolic acidosis

Titu Maiorescu University


Curs Medicina Interna

NEPHROLOGY
Prof univ dr Ion C Tintoiu

. Chronic Renal Failure

Definitions
Chronic Renal Failure
Results

form gradual, progressive loss of renal f

unction
Occasionally results from rapid progression of
acute renal failure
Symptoms occur when 75% of function is lost b
ut considered cohrnic if 90-95% loss of function
Dialysis is necessary D/T accumulation or urem
ic toxins, which produce changes in major orga
ns

Subjective symptoms
Chronic Renal Failure
Subjective

symptoms are relatively same as acu

te
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 = RBCs, WBCs, and casts

Chronic Renal Failure


Objective

symptoms
Cardiovascular

Hypertension
Arrythmias
Pericardial effusion
CHF
Peripheral edema

Neurological

Burning, pain, and itchin


g, parestnesia
Motor nerve dysfunction
Muscle cramping
Shortened memory span
Apathy
Drowsy, confused, seizur
es, coma, EEG changes

Chronic Renal Failure


Objective

symptoms

GI
Stomatitis
Ulcers
Pancreatitis
Uremic fetor
Vomiting
consitpation

Respiratory
^ chance of infecti
on
Pulmonary edema
Pleural friction ru
b and effusion
Dyspnea
Kussmauls respir
ations from acidosi
s

Chronic Renal Failure


Objective

symptoms

Endocrine

Stunted growth in childr


en
Amenorrhea
Male impotence
^ aldosterone secretion
Impaired glucose levels
R/T impaired CHO meta
bolism
Thyroid and parathyroid
abnormalities

Hemopoietic

Anemia
Decrease in RBC surviva
l time
Blood loss from dialysis a
nd GI bleed
Platelet deficits
Bleeding and clotting dis
orders purpura and he
morrhage from body orif
ices , ecchymoses

Chronic Renal Failure


Objective

symptoms

Skeletal

Muscle and bone pain


Bone demineralization
Pathological fractures
Blood vessel calcificati
ons in myocardium, jo
ints, eyes, and brain

Skin

Yellow-bronze skin wit


h pallor
Puritus
Purpura
Uremic frost
Thin, brittle nails
Dry, brittle hair, and
may have color chang
es and alopecia

Chronic Renal Failure


Lab findings
BUN indicator of glomerular filtration rate and is

affected by the breakdown of protein. Normal is 1020mg/dL. When reaches 70 = dialysis


Serum creatinine waste product of skeletal muscle
breakdown and is a better indicator of kidney functi
on. Normal is 0.5-1.5 mg/dL. When reaches 10 x nor
mal, it is time for dialysis
Creatinine clearance is best determent of kidney fun
ction. Must be a 12-24 hour urine collection. Normal
is > 100 ml/min
K+ Hypocalcemia = tetany

Chronic Renal Failure


Other abnormal

findings
Metabolic acidosis
Fluid imbalance
Insulin resistance
Anemia
Immunoligical problems

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

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

Chronic Renal Failure


Peritoneal

dialysis

Semipermeable membran

e
Catheter inserted through
abdominal wall into perito
neal cavity
Cost less
Fewer restrictions
Can be done at home
Risk of peritonitis
3 phases inflow, dwell an
d outflow

Automated peritoneal di
alysis
Done at home at night
Maybe 6-7 times /week

CAPD
Continous ambulatory pe

ritoneal dialysis
Done as outpatient
Usually 4 X/d

Chronic Renal Failure


Transplant
Must find donor
Waiting period long
Good survival rate 1 year 95-97%
Must take immunosuppressants 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
Imuran
Cytoxan
Cellcept
T-cell

inhibit T and B lymphocytes

depressors - Cyclosporin

Tot nu s-a terminat !

Titu Maiorescu University


Curs Medicina Interna

NEPHROLOGY
Prof univ dr Ion C Tintoiu

. RENAL TUMOURS

CYSTIC DISEASES
. OF
THE KIDNEY

CYSTIC DISEASES OF
THE KIDNEY
Fluid

filled spaces within the k

idney
May involve cortex or medulla or
both
May be unilateral or bilateral
May be unilocular or multilocula
r
May be congenital or acquired
May be sporadic or genetically d

CLASSIFICATIONS OF
RENAL CYSTIC DISEASES
Polycystic

kidney diseases:
1. Autosomal recessive (ARPKD)
classic infantile polycy
stic disease
with congenital hepat
ic fibrosis
2. Autosomal dominant (ADPKD)
Simple renal cysts
Acquired renal cystic disease

RENAL CYSTIC DISEASES


Enlarged

but normally shaped pelvi-ca


lyceal system
Normal reniform shape complete with f
etal lobation & normal sized (undilat
ed) ureter
Normal glomeruli and tubules
Normal interstitium and no dysplasia
Congenital hepatic fibrosis is almost
always present
Normal numbers of nephrons, no inters
titial fibrosis and no dysplasia

RENAL CYSTIC DISEASES P


athological Features
Bilaterally

enlarged kidneys (up to 4

000 gms)
Diffuse cystic (1-2% cystic nephrons)
change with uninvolved intervening pa
renchyma
Varying sized, numerous to innumerabl
e generally spherical unilocular cyst
s, distributed in cortex and medulla
obscuring normal reniform shape and c
orticomedullary junction, containing
yellowish to turbid to brown to black
colored fluid
Distorted pelvi-calyceal system

Simple Renal Cysts


Extremely

common as age advances


Incompletely understood pathogen
esis
Commonly associated with scarred
kidneys
Asymptomatic with normal renal f
unction
May be solitary/multiple/unilate
ral/bilateral
Generally unilocular, round to o

Adult polycystic kidney disease

Renal cancer

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 nephrog


enic blastemal cells
can differentiate in to several cell line

s blastemal, epithelial and stromal


many replicate developing kidneys
Common

in young children / uncommon i


n neonates and infants
90% in < 6yrs. old ( mean: 3yrs. in b
oys 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 multicen
tric (7%) or bilateral (5%)
Imaging technique to reveal smaller
lesions
No specific tumor markers identifie
d

NEPHROBLASTOMA
prognosis and treatment
Depends

upon :
stage, age and histology
Surgery with chemotherapy for :
stage I & II with favorable his
tology
surgery with chemotherapy and r
adiotherapy for higher stages a
nd unfavorable histology

RENAL CELL CARCINOMA


Hypernephroma / Grawitz
s tumour

seems

to be arising from matu


re renal tubules

RENAL CELL CARCINOMA


Clinical Features & Diagnosis
classic

triad :
hematuria, flank pain and abdom
inal mass
may be clinically occult, 30% pr
esents with metastatic lesion
Polycythemia due to erythropoiet
in
constitutional symptoms
imaging techniques - useful

RENAL CELL CARCINO


MA
Influenced

prognosis

by multiple factors :
tumour size
infiltrative margins
histological type
tumour stage - most important
Can be expressed in terms of histol
ogical types

Renal cell carcinoma

RENAL CELL ADEN


OMA

Incidental

findings at autopsy

(22%)
Well demarcated, unencapsulated
Pale yellow-gray, discrete cort
ical mass
Up to 2 cms. in maximum dimensi
on

Bladder Carcinoma
Derived
Present

from transitional epithelium

with painless hematuria

Prognosis
Overall

depends on grade and depth of invasion

5y survival = 50%

Nu s-a terminat !

. DIALYSIS

Dialysis
Definition
Artificial process that partially replaces renal f
unction
Removes waste products from blood by diffusi
on (toxin clearance)
Removes excess water by ultrafiltration (maint
enance of fluid balance)
Wastes and water pass into a special liquid di
alysis 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: Dial
yser
The dialyser removes the excess fluid and wast
es from the blood and returns the filtered blood
to the body
Haemodialysis needs to be performed three tim
es 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

D Rx)
Avoid sleeping on fistula arm
Grafts (synthetic) may be used to create an AV fistula

AV Fistula

AV Fistula

Vascular Access Catheter

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 los

s 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, H
IV

Peritoneal Dialysis (PD)


Uses

natural membrane (peritoneum) for dialys

is
Access is by PD catheter, a soft plastic tube
Catheter and dialysis fluid may be hidden unde
r clothing
Suitability
Excludes patients with prior peritoneal scarring e.g.

peritonitis, laparotomy
Excludes patients unable to care for self

Peritoneal Dialysis
.

Principles of Peritoneal Dialysis (PD)


Standard dialysis solution
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
Sodium lactate
Pure HCo3-

contains:

buffer:

HCo3- /Lactate combinations

Lactate

is absorbed and converted to HCo 3- by th

e 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
Check

Need

kidneys remove fluids as urine

for fluid and sodium retention

to restrict fluid intake

VITAMINS
Folic
Iron
Do

acid

supplements

not take OTCs without consulting the do


ctor.

MANAGING DIET
INDICATORS OF GOOD CONTROL:

Weight loss or gain

Blood

pressure

Swelling
Blood

of hands and feet

samples

Plasmapheresis:
plasma exchange and immunoadsorption

An adult donor kidney transplanted to the left iliac


fossa of an adult recipient.

?
.

. Kidney Stones

ETIOLOGY
HYPEREXCRETION OF RELATIVELY INSOLUBLE URINARY
CONSTITUENTS

Oxalate Though oxalate is the major component of 70%


of all renal stones, yet hyperoxaluria as a cause of formation of such
1.

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.

LOCATION OF STONES IN
KIDNEY

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 NEPHROLI
THIASIS

ASYMPTOMATIC CALCULI
TREATMENT
Solitary kidney
Occupation (pilot, business traveler
Simultaneous contralateral treatment
Its 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


.

SHOCK WAVE LITHOTRIPSY


STONE FRAGMENTATION

SHOCK WAVE LITHOTRI


PSY
INDICATIONS
Surgical stone
No obstruction
Reasonable chance
of expeditious removal

SHOCK WAVE LITHOTRI


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

SHOCK WAVE LITHOTRIPSY


CLINICAL SIDE-EFFECTS
Hematuria
Pain
Obstruction
(Steinstrasse)

SHOCK WAVE LITHOTRI


PSY
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 MANAGE


MENT
CURRENT ROLE OF PNL

SURGICAL STONE
MANAGEMENT
STAY OUT OF TROUBLE

Pre-op KUB

Pre-op IVP

URETERAL CALCULI

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

?
.

Gata s-a terminat !

. FINAL

ACUTE AND CHRONIC INTE


RSTITIAL NEPHRITIS
.

Morphology of the interstitium


Fibrosis

develops after infiltration by mono


nuclear cells (lymphocytes) which is accom
panied by deposition of fibronectin, collage
n type I, III, VI and IV.
There is a physiological balance between on
going matrix formation and - degradation.

Morphology of the interstitium


Composed

of a loosely organized matrix co


nsisting of the collagen types I and III, prote
oglycans containing the interstitial cells:
matrix producing fibroblasts
macrophages
dendritic reticulum cells
endothelial cells

Importance of interstitial cells


Interstitial fibroblasts:
Fibrogenesis
Production of erythropoietine (they lose this function durin

g 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 inter
stitial volume (=fibrosis) and inflammation

Interferences with the inters


titium: broad spectrum

Infection:
direct (BK virus, TBC, acute pyelonephritis),
indirect( Streptococci)
Immunologic
Allergic: drug induced
Auto-immune: Sjgren syndrome
Alloimmune: acute cellular allograft rejection
Unknown: IgG4- associated acute interstitial nephritis
Toxic: Pb poisoning, cadmium poisoning, Balkan endemic nephro
pathy
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 glome

rular diseases: 1%
d) idiopathic disease: 4%

Acute interstitial nephritis: dru


gs

Etiology: AB (penicillins and cephalosporins, methicillin),


diuretics, NSAIDs, chinese herbs, lithium
Pathogenesis:
T cell mediated allergic - immune reaction on drug or drug-self pro
tein conjugate (hapten) later followed by accumulation of lympho
cytes, 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 obstructio
n of nephron).

AcuteOedema
drug
induced interstitial
and focal inflammation
nephritis

Granuloma

EOS

Granuloma

Acute drug induced interstitial


nephritis
Normally

are the glomeruli not afflicted.


One exception: use of NSAIDs: can combi
ne ARF with Nephrotic Syndrome (effect o
f cell- mediated lymphokine directed reacti
on) inducing Minimal Lesions (effacement
of foot processes of podocytes)

Acute interstitial nephritis: clin


ics
Acute Renal Failure and
reduced glomerular fil
tration rate:

depends on the severity of infla


mmation
interstitial oedema causes eleva
ted intratubular pressure
intratubular obstruction through
intra luminal cells
tubular backleak
vasoconstriction
tubuloglomerular feedback

Outcome of drug- induced inte


rstitial nephritis
Recovery?
Drug withdrawal: 60-9

0% in 1 to 12 mths
Irreversible with analg
esics, NSAIDs, longter
m use

Adverse

prognostic fe

atures
Marked interstitial infl

ammation
Granuloma (50% irrev
ersible)
Tubular atrophy
Fibrosis

Acute interstitial infectious nep


hritis
Infectious:direct

invasion or remote infections bac


teria ( hemolytic streptococci), parasites (Leishm
ania) and viruses (EBV, measles)
Pathogenesis: immunological hypersensitivity reac
tion to the infectious agent, effect of chemokines p
roduced by the kidney in response
Histology:
Early signs: invasion by lymphocytes, eosinophils around the vein

s
In casu there is tubular destruction: histiocytes accumulate
Tubulitis with disappearance of the brush border in proximal tubul
es

ACUTE INTERSTITIAL INFECTIOUS NEPHRITIS

Acute interstitial nephritis: syst


emic
Association

with: Goodpasture syndrome, l


upus nephritis, mixed cryoglobulinemia, m
embranoproliferative glomerulonephritis

Chronic interstitial nephritis


Etiology:

chronic drug intake (analgesics, lithi


um), urinary obstruction, chronic reflux,
Pathogenesis: persistence of damageing factor:
ischemia, chronic immune reaction
Histology: fibrosis + diffuse infiltration by lym
phos, plasmos, histiocytes (with granuloma). T
ubular changes (atrophy, compensatory hypert
rophy 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

Papillary sclerosis

CIN

Interstitium in transplants
Calcineurin inhibitors:
Heart, liver, pancreas, kidney transplants in diff

erent 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 uncer
tain pathogenesis but is probably vascular.

Toxicity of calcineurin inhibitor


s

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 enz
ymes and toxic molecules, direct contact or penetr
ation of the host cell by the infectious agent and th
e inflammatory response mediated by antibodies,
T cells
Histology:
Tubules are damaged by neutrophils (Congored)

Acute pyelonephritis

Chronic pyelonephritis
Etiology:

reflux
Histology:
- wedge shaped interstitial fibrosis(follows the
traject of the papillae and ascending tubules) acco
mpanied by tubular atrophy, vascular atheromatosi
s, glomerular sclerosis, inflammation
- outside the wedges: normal parenchyma but
with secondary changes in the glomeruli: glomerul
ar hypertrophy, FSGS

Chronic pyelonephritis

Chronic pyelonephritis

Tamm Horsfall protein

Tubular disease
Acute

tubular damage:

Ischemia: vasoconstriction with endothelial activation

will determinate the extent of the tubular cell loss: cellu


lar, geographic, focal
Toxins:

Myoglobinuria
Heavy metal exposure (Pb, Cd)
Oxalate crystal deposits: ethylene glycol toxicity
Calcineurin inhibitors: megamitochondria, isometric vacuolisat
ion

Tubular damage

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

URETERAL CALCULI
PARAMETERS FOR COMPARISON
Effectiveness
Morbidity
Convalescence
Cost

SWL FOR
URETERAL CALCULI
DORNIER HM-3
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%

Lingeman, et al, 1993

DISTAL URETERAL CALCULI


COMPARISON OF
MONOTHERAPY STUDIES
URS is 10 - 18% more effective than SWL (dep
ending 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

DISTAL URETERAL CALCULI


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

DISTAL URETERAL CALCULI


PROSPECTIVE, RANDOMIZED TRIAL
80 patients randomized to receive SWL or URS 40 pa
tients 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 ureteros
copes (basket vs. pneumatic lithotripsy)

Peschel & Bartsch, 1999

DISTAL URETERAL CALCULI


PROSPECTIVE, RANDOMIZED TRIAL
STONES < 5 MM
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 rate0 15%
Peschel & Bartsch, 1999

SWL OF DISTAL
URETERAL CALCULI
ADVERSE EFFECTS TO
FEMALE REPRODUCTIVE TRACT?
Initial animal studies suggest ovarian trauma Imp
aired fertility
Mutagenesis
Subsequent animal investigations demonstrate no im
pact on fertility or offspring
Mice
Rats Rabbits

SWL OF DISTAL
URETERAL CALCULI
ADVERSE EFFECTS TO
FEMALE REPRODUCTIVE TRACT?

Analyzed Rx data and radiation exposur


e in 84 women of reproductive age
7 children born to 6 patients with no malf
ormations or chromosomal anomalies
Miscarriages in 3 patients (but occurred
Viewig & Miller, 1992
at least 1 year after SWL)

URETEROSCOPY

URETERAL CALCULI
FLEXIBLE URETEROSCOPY

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

URETERAL CALCULI
PERCUTANEOUS APPROACH

URETERAL STONE MANAGEMEN


T
IN SITU SWL
Advantages
Minimal anesthesia requirements
Non-invasive procedure
No stenting/less complications
Similar approach for all ureteral c
alculi
Disadvantages
Lower success rate than URS

URETERAL STONE MANAGEMEN


T
URETEROSCOPY
Advantages
Highest success rate
Definitive Rx - No waiting for stone p
assage
Disadvantages
More invasive than SWL
Higher complication rate
Requires greater technical expertise

URETERAL CALCULI: CURRENT


OPTIONS
PROX AND MID URETERAL STONES
Approach Invasive StentS-F Rate *Re-RxRat
e
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

URETERAL CALCULI: CURRENT


OPTIONS
DISTAL URETERAL STONES
Approach Invasive StentS-F Rate *Re-RxRat
e
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

SURGICAL STONE MANAGE


MENT
CHANGING TREATMENT
PHILOSOPHIES
1980s 1990s 2000s 2010s
Shock wave lithotripsy 95% 85% 75% ???
Endoscopic procedures 5% 15% 25% ???
Open stone surgery < 1% < 1% < 1% 0

NEPHROLITHIASIS
NATURAL HISTORY & RISK FACTORS
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%

SHOCK WAVE LITHOTRIPSY


RECURRENT STONE FORMATION
Years
SWL
Stone Free
New stones
10%
Residual Stones
Stone growth
21%

One Year

Two

Post SWL

Post

8%
22%

Lingeman, et al, 1989

SHOCK WAVE LITHOTRIPSY


EFFECT ON STONE RISK FACTOR
S Urine Values
Pre(mg/day)
Calcium
Uric Acid
Citrate
Oxalate

3 Mo PostLithotripsy
Lithotripsy
254
261
552
548
249
257
42
41 Brown, et al, 1989

MEDICAL MANAGEMENT OF NEP


HROLITHIASIS
PROGRESS
Elucidation

Urinary environment conducive to stone


formation
Diagnosis
Detection of underlying physiologic
abnormalities
Medical Therapy
Development of new treatment strategies

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

DIETARY CALCIUM
IMPACT OF LOW CALCIUM DIET
Early recommendations suggest that low calcium diet
will decrease urinary Ca++ excretion, thereby reducing r
isk of stone formation
Potential risk factors involving low calcium diet:
Reduced bone mass
Increased urinary oxalate

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

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

CALCIUM SUPPLEMENTS
RECOMMENDATIONS:
PREMENOPAUSAL WOMEN
Give HCTZ during initial three months to prevent hyp
ercalciuria, then discontinue for one month
If urinary calcium up at 4 months, re-start HCTZ
Alternative: Significantly increase fluid intake for firs
t three months and then check 24-hour urinary calcium

Henoch Schnlein Purupura

Answer 1.
Renin Angiotensin II- ACE- ADH Aldosterone
That is not correct
Please try again

Peritoneal Dialysis

Is performed as an intracorp
oreal (inside the body) therap
y making use of the peritonea
l membrane.
Is the process of cleaning the
blood by using the lining of th
e peritoneal cavity (peritoneu
m) as a filter the peritoneu
m acts as a dialyzing membra
ne, permitting wastes from th
e body to cross it and empty i
nto the instilled dialysate flui
d.
Is a type of dialysis usually do
ne by the patient at home.

What do
the kidneys do??

Hemodialysis
3-4

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

Peritoneal Dialysis
Abdominal
3

lining filters blood

types

Continuous ambulatory
Continuous cyclical
Intermittent

Questions?