Kursk State Medical University

Internal Diseases
Propedeutics Department
Professor T.A. Dronova
Lecture
GLOMERULONEPHRITIS

GLOMERULONEPHRITIS
3rd most common cause (after diabetes &

hypertension) of end-stage renal disease

in Europe & USA
Group of diseases with affection of
glomerulus (often inflammatory in nature)
Immunologically mediated injury to
glomeruli
Both kidney involvement (symmetrical)

GLOMERULONEPHRITIS
Nomenclature
Inflammation with leukocyte infiltration,
antibody deposition, &/or compliment
activation
Primary - when major problem starts in
the glomeruli
Secondary - when involvement is part of
systemic disease (SLE, diabetes mellitus,
amyloidosis)

GLOMERULONEPHRITIS
Nomenclature
Glomerular injury
Acute over days or weeks
Subacute or rapidly progressive - over weeks
or few months
Chronic - over many months or years
Glomeruli involvement
Focal minority (< 50%)
Diffuse majority (> 50%)
Segmental - part
Global almost all

GLOMERULONEPHRITIS
Nomenclature
Proliferative increase in glomerular cell
number (due to infiltration by leukocytes or
resident glomerular cells proliferation)
Proliferation of resident glomerular cells:
Intracapillary / endocapillary endothelial or
mesangial cells
Extracapillary Bowmans space (most
proximal portion of renal tubule)

GLOMERULONEPHRITIS
Nomenclature
Crescent half-moon-shaped collection of cells

in Bowmans space
Crescentic glomerulonephritis associated
with rapid progression of renal failure (weeksmonths) = rapidly progressive glomerulonephritis
Membranous expansion of glomerular
basement membrane by immune deposits

GLOMERULONEPHRITIS
Essentials of diagnosis
Hematuria, dysmorphic red cells, red

cell casts & mild proteinuria

Dependent edema & hypertension
Acute renal insufficiency
Renal biopsy gold standard

GLOMERULONEPHRITIS
Primary
Minimal change glomerular disease
Membranous glomerulonephritis
Membranoproliferative glomerulonephritis
Ig A nephropathy (Bergers disease)
Crescentic rapidly progressive

glomerulonephritis (Goodpastures syndrome)

Focal segmental glomerulonephritis

GLOMERULONEPHRITIS
Secondary
Common
SLE
Polyarteritis nodosa
Diabetes mellitus
Amyloidosis
Schonlein-Henoch disease
Malarial nephropathy

GLOMERULONEPHRITIS
Secondary
Uncommon
Pre-eclampsia & eclampsia
Malignancy associated paraproteinemia
Cryoglobulinemia
Rheumatoid artritis
Scleroderma
Hemolitic uremic syndrome
Wegeners granulomatosis
Cytomegalovirus nephropathy
AIDS nephropathy

GLOMERULONEPHRITIS
Pathogenesis (2 main processes )
Circulating immune complex deposition

most common

Circulating antigen-antibody complexes

deposited in the kidney or complexes formed

locally (circulating free antigen has become
trapped in the glomerulus - produce injury by
binding of complement system)
Anti-GBM

antibody disease (<5%)

Antibodies reacts with an antigen in the

glomerular basement membrane & produce

glomerulonephritis Goodpastures syndrome

GLOMERULONEPHRITIS
Secondary mechanisms
Circulating immune complex deposition &

anti-GBM antibody disease - secondary

mechanisms activation with glomerular
damage: complement activation, fibrin
deposition, platelet aggregation,
inflammation with inflammatory cytokines
& free radical induced damage

GLOMERULONEPHRITIS
Pathogenesis
Antigens
Exogenous:
Bacteria
Viruses
Parasites
Drugs
Endogenous:
Host antigens

Immune complex-mediated
glomerulonephritis - causes
Bacteria:
Beta-hemolitic streptococcus group A
Streptococcus viridans (in endocarditis)
Streptococcus pneumoniae
Staphylococcus
Treponema pallidum (syphilis)
Gonococcus
Salmonella
Meningococcus

Immune complex-mediated
glomerulonephritis - causes
Viruses:
Hepatitis B & C
Epstein-Barr virus
Coxsackie virus
Varicella
HIV
Mumps
Measles

Immune complex-mediated
glomerulonephritis - causes
Parasites:
Plasmodium malariae
Schistosomatosis
Filariasis
Toxoplasmosis
Drugs:
Penicillamine
Host antigens:
DNA in SLE
Malignant tumors

GLOMERULONEPHRITIS
Macroscopic appearances
Kidneys in acute glomerulonephritis:
Size - normal or enlarged & edematous
Surface punctate haemorrhages

Kidneys in chronic glomerulonephritis:

Size - normal or small with finely granular

cortical scarring

GLOMERULONEPHRITIS
Histological types & clinical features correlation
Histological types

Clinical features

Subtypes of proliferative
glomerulonephritis:
Diffuse

Acute nephritic

Focal segmental

syndrome
Haematuria,
proteinuria

There is not a complete correlation

between histological types & clinical features

GLOMERULONEPHRITIS
Histological types & clinical features correlation
Histological types
Subtypes of proliferative
glomerulonephritis:
With crescent formation
(rapidly progressive
glomerulonephritis)
Mesangiocapillary
(membranoproliferative)

Clinical features

Progressive renal

failure
Haematuria,

proteinuria, acute
nephritic or nephrotic
syndrome

GLOMERULONEPHRITIS
Histological types & clinical features correlation
Histological types

Clinical features

Membranous

Nephrotic syndrome

glomerulonephritis
Minimal-change
nephropathy
Ig A nephropathy

in adults
Nephrotic syndrome
especially in children
Asymptomatic
haematuria
Focal glomerulonephritis Proteinuria or
nephrotic syndrome
There is not complete correlation between histological types & clinical features

GLOMERULONEPHRITIS
Clinical picture
1 of 5 clinical presentations:
Asymptomatic proteinuria &/or

microscopic hematuria
Acute nephritic syndrome
Nephrotic syndrome
Rapidly progressive glomerulonephritis
Chronic glomerulonephritis

ACUTE NEPHRITIC SYNDROME

Acute glomerular inflammation most dramatic
Sudden onset (days-weeks) of acute renal

failure & oliguria (< 400 ml/day)

Glomerular capillary lumen obstruction
impaired glomerular filtration rate - tubular salt
& water reabsorption
Glomerular capillary wall injury red blood cell
casts in urine, dysmorphic red blood cells,
leukocytes, subnephrotic proteinuria (<3,5g/24h
nephritic urinary sediment)

ACUTE NEPHRITIC SYNDROME

Acute nephritic syndrome = proliferative

glomerulonephritis
Poststreptococcal glomerulonephritis
leading cause of acute nephritic
syndrome

GLOMERULAR DISEASES WITH

NEPHRITIC PRESENTATION
Post-streptococcal glomerulonephritis

(most common)
Ig A nephropathy
Schonlein-Henoch purpura
Wegeners granulomatosis
Goodpastures syndrome
Polyarteritis nodosa
Acute interstitial nephritis
Essential mixed cryoglobulinemia

Poststreptococcal glomerulonephritis
After pharyngeal or cutaneous infection with

nephritogenic strains of beta-hemolytic

streptococci group A identification by
serotyping of M-protein (cell wall antigen)
Acute glomerulonephritis following cutaneous

streptococcal infection (impetigo) commonly

associated with poor personal hygiene,
overcrowding, concomitant cutaneus diseases
(scabies)

Poststreptococcal glomerulonephritis
Latent period b/w earliest infection

manifestations & onset of signs & symptoms of

nephritis:
pharyngeal infections 6-10 days
cutaneous infections about 2 weeks

Poststreptococcal glomerulonephritis
Diagnosis at least 2 of 3 features:
Group A beta-hemolytic streptococcus (nephritic

strains: M types 1, 2, 4, 12, 18, 25, 49, 55, 57 &

60) in throat or skin lesion
Immune response to 1 or > streptococcal
exoenzymes (anti-streptolysin O, antistreptokinase, anti-deoxyribonuclease B, or antihyaluronidase)
Transient decline of serum concentration of C3
component of complement system with return to
normal within 6-8 weeks after first sign of renal
disease

Poststreptococcal glomerulonephritis
Diagnosis:

1-3 weeks interval b/w infection &

development of sign & symptoms of

renal involvement - immune complex
formation & deposition of glomerular
injury

Poststreptococcal glomerulonephritis
ESR usually elevated
C reactive protein normal
Rheumatoid factor normal or

undetectable

Post-streptococcal glomerulonephritis
ACUTE NEPHRITIC SYNDROME
Age: common in childhood (2-6 years of age)
Sex: > males
Nature of disease: post-streptococcal

glomerulonephritis (streptococcal infection 13 week before)

Group A beta- hemolytic streptococcus
infection of nephritogenic type

ACUTE NEPHRITIC SYNDROME

CLINICAL PICTURE
Acute nephritic syndrome consists of the

abrupt onset of hematuria & proteinuria,

often accompanied by azotemia, renal salt &
water retention:
Hematuria (red or smoky urine)
Proteinuria
Hypertension
Edema
Oliguria
Uraemia

ACUTE NEPHRITIC SYNDROME

CLINICAL PICTURE
Headache
Generalized symptoms:
Anorexia
Nausea
Vomiting
Malaise
Dull pain in flank or back (renal capsule

swelling)
Decreased diuresis sometimes anuria
(may be frequent tenesmus)

ACUTE NEPHRITIC SYNDROME

CLINICAL PICTURE
Hypervolemia
Edema: on the face, under the eyes (facies

nephritica) extend onto entire body &

extremitis usually leg or sacral (disordered
capillary permeability & aldosterone
hypersecretion), may be plueral effusion
Deranged vision (retinal vessels spasm,
hemorrhage into retina)
Hypertension

ACUTE NEPHRITIC SYNDROME

CLINICAL PICTURE
Pallid skin
Edematous face (swollen eyelids)
Trunk edema & extremitis
Semireclining or sitting position

(pronounced dyspnea sometimes with

attacks of asphyxia)
Renal eclampsia may develop (convulsive
attack - onset by increased BP & severe
headache)

Facies nephritica
Brights face
Edematous face

swelling around the

eyes (slit-like eyes)
in the morning

ACUTE NEPHRITIC SYNDROME

CLINICAL PICTURE
In generalized edema fluid in the pleural

cavity & congestion in lung root region: chest

percussion dulled tympany
Harsh respiraton, in pronounced congestion
dry & moist rales
Tense & slow pulse
Apex beat shifted to the left & increased
(myocardial hypertrophy due to hypertension)
Bradycardia, S1 decreased at the apex,
may be gallop rhythm,
S2 accentuated over aorta
Increased BP

ACUTE NEPHRITIC SYNDROME

INVESTIGATION
Urine: reduced volume (oliguria), dark colour

(reddish-brown - looks like meat wastes or

cola-colored urine), proteinuria, red cell & cell
cast (mainly hyaline casts), renal epithelium
cells
Blood urea & serum creatinine rised
Creatinine clearance reduced
Immunological shifts: increased content of
alpha-2 & gamma globulins in blood

ACUTE NEPHRITIC SYNDROME

INVESTIGATION
Throat swab culture - positive
Anti-streptolysin-O titre elevated
Transient hypergammaglobulinemia, anti-

deoxyribonuclease B, antistreptokinase, antinicotinyl adenine dinucleotidase,

antihyaluronidase
Serum complements: low C3 & C4 level
(return to normal at 6-12 weeks)

ACUTE NEPHRITIC SYNDROME

INVESTIGATION
Sphygmomanometry BP increase (200-220

mm Hg systolic / 100-160 mm Hg - diastolic)

X-ray of the chest (pleural effusion, lung roots
congestion & left ventricular hypertrophy)
ECG: left ventricular hypertrophy & overload,
decreased ECG waves amplitude in
pronounced trunk edema
Renal biopsy (not required in children, usually
in adults with acute nephritic syndrome):
glomerulonephritis

ACUTE NEPHRITIC SYNDROME

Investigations (etiology search)
Special tests (history & preliminary evaluations):
Complement level
Antinuclear antibodies (ANA)
Antinuclear cytoplasmic antibodies (ANCA)
Cryoglobulines
Hepatitis panel
Serum Ig A
Anti-GBM antibodies
ASO titers
C3 nephritic factor

ACUTE NEPHRITIC SYNDROME

MANAGEMENT

Bed rest
Salt free diet
Protein restriction in ureamia
Daily record of fluid intake & excretion
Daily weighing (body fluid status change)
Regular measurement of blood pressure
Diuretics (reduce hypertension & edema)
Anti-hypertensive drugs
Antibiotics (in poststreptococcal
glomerulonephritis positive culture)

ACUTE NEPHRITIC SYNDROME

COMPLICATIONS
Acute renal failure
Acute heart failure with pulmonary

edema (salt & water retention)

Urinary tract infection
Hypertensive encephalopathy

NEPHROTIC SYNDROME
Features
Heavy proteinuria (> 3g/24 hours)
Hypoalbuminemia (serum albumin

<30g/l)
Edema
Hyperlipidemia (due to increased
hepatic lipoprotein synthesis)
Hypercoagulability

NEPHROTIC SYNDROME
PATHOGENESIS
Proteinuria: capillary wall injury of glomeruli

- increase permeability to plasma protein,

allowing protein to escape from plasma into
glomerular filtrate (proteinuria)
Hypoalbuminaemia: proteinuria (3-5g/day)
- decrease serum albumin

NEPHROTIC SYNDROME
PATHOGENESIS
Generalized edema:
Salt & water retention
Hypoalbuminemia - decrease colloid

osmotic pressure which allows fluid to

escape from vessels (generalized edema)
Hyperlipidemia: hypoalbuminemia
triggers increase synthesis of all forms
of plasma protein including lipoprotein
resulting in hyperlipidemia

NEPHROTIC SYNDROME
PATHOGENESIS
Hypercoagulability:
Increased urinary antithrombin III loss
Altered levels &/or activity of protein C &

protein S
Hyperfibrinogenemia increased hepatic
synthesis
Impaired fibrinolysis
Increased tendency of platelet
aggregation

NEPHROTIC SYNDROME

1.
2.
3.
4.
5.
6.

6 entities account > 90% of causes

of nephrotic syndrome in adult:
Minimal change disease
Focal & segmental glomerulosclerosis
Membranous glomerulopathy
Membranoproliferative glomerulonephritis
Diabetic nephropathy
Amyloidosis

NEPHROTIC SYNDROME
CLINICAL FEATURES
Edema:
Peripheral oedema involving upper &
lower limb
Intense edema of scrotum or vulva
may occur
May be bilateral hydrothorax

NEPHROTIC SYNDROME
Clinical Features
Edema of intestine causes anorexia,

diarrhea & vomiting

Malnutrition: due to proteinurea, frequent
infection & muscle wasting
Features of underlining causes: (butterfly
rash in SLE & neuropathy or retinopathy in
diabetes mellitus

NEPHROTIC SYNDROME
Clinical Features
Hypercoagulability: peripheral arterial

or venous thrombosis, renal vein

thrombosis & pulmonary embolism
Infections: increased susceptibility to
infection due to urinary loss of Ig G
antibodies

NEPHROTIC SYNDROME
INVESTIGATIONS
Urine - proteinuria
24 hours urinary proteins: usually > 3 g/day
Serum albumin: < 3g/day (total serum protein <6

mg/dl)
Low density lipoprotein - elevated,
high density lipoprotein - normal
Raised ESR due to increased serum fibrinogen
Urine red cells & red cell cast
Blood sugar for diabetes & antinuclear factor for
SLE
Hepatitis B serology, serum complements

NEPHROTIC SYNDROME
INVESTIGATIONS
Renal biopsy: confirms diagnosis
Renal biopsy contraindicated:
Children under 10 years
Known diabetes mellitus
Patient on drug (penicillamine)

NEPHROTIC SYNDROME
COMPLICATIONS
Protein malnutrition
Hypercoagulability - due to rise in

many clotting factors

Impaired resistance to infection (due to
low body-immunoglobulins as a result
of hypoproteinaemia
Sepsis, blood loss & acute
hypovolemia may lead to acute
oliguric renal failure

NEPHROTIC SYNDROME
MANAGEMENT
Diet: low salt diet, moderate

protein restriction (0,5-0,6 g/kg/d)

- increased protein intake
adverse effect on renal function in
some diseases
Diuretics
Hypercholesterolemia
treatment (statins)

NEPHROTIC SYNDROME
COMPLICATION MANAGEMENT
A. Venous thrombosis due to

hypercoaguloability
Prolonged bed rest should be avoided
In renal vein thrombosis - anticoagulants
B. Sepsis
Aggressive treatment of infection with
antibiotics
C. Oliguric renal failure
Maintain blood pressure & fluid volume
Albumin infusion, mannitol may initiate
diuresis

NEPHROTIC SYNDROME
MANAGEMENT
Specific therapy:
Minimal change disease (most common cause of
nephrotic syndrome in children, 20% in adult) prednisolone
Membraneous gloumerolunephritis (most
common cause of nephrotic syndrome in adult
after 30 age [5th-6th decade], high incidence of
renal vein thrombosis, in 50% - occult neoplasm
of lung, stomach & colon) - prednisolone &
azathioprine, chlorambucil or cyclophosphamide
Other causes - SLE: prednisolone & azathioprine

Preeclampsia-eclampsia
Toxemia syndrome

(usually 3rd trimester of primigravidas):

Hypertension
Proteinuria
Edema
Consumptive coagulopathy
Sodium retention
Hyperreflexia (preeclampsia) & convulsions
(eclampsia)
Preeclampsia-related hypertension:
4- or 6-houres period measurements BP > 140/85
mm Hg

Eclampsia (Gk ek lampein to flash)

Pathogenesis
In acute diffuse glomerulonephritis, aggravated

chronic glomerulonephritis, nephropathy of

pregnancy:
Increased intracranial pressure
Cerebral tissue edema
Cerebral angiospasm

Eclampsia in pronounced edema & increased

BP

Preeclampsia
Clinical picture
Rapid BP rise (preeclampsia-related

hypertension: 4- or 6-h period measurements

BP > 140/85 mm Hg)
Unusual somnolence & flacidity
Severe headache
Vomiting
Temporary blindness (amaurosis)
Aphasia
Transient paralysis
Mental confusion (then stupor, sopor, coma)

Eclampsia
Clinical picture
After cry or noisy deep inhalation convulsions (tonic

& clonic)
Cyanotic face
Swollen neck veins
Firm eyeballs (aside or up) with dilated pupils (without
light reaction)
Bitten tongue
Foam from mouth
PS tense, slow
Temperature may be rised
Involuntary defecation & urination

CHRONIC
GLOMERULONEPHRITIS
Persistent proteinuria &/or hematuria & renal
insufficiency with slow progression over years
Diagnosis:
upon routine urinanalysis
routine blood tests with unexplained anemia
elevated blood urea nitrogen & creatinine
discovery of bilateral small kidneys on abdominal
imaging
5. during evaluation for secondary causes of
hypertension
6. during clinical exacerbation of glomerulonephritis
triggered by pharyngitis or other infections
1.
2.
3.
4.

CHRONIC
GLOMERULONEPHRITIS
Manifestation of virtually all of major

glomerulonephritis
Renal biopsy typically reveals a variable
combination of proliferative, membranous,
sclerotic changes, depending on the causative
glomerulopathy

CHRONIC
GLOMERULONEPHRITIS
Arteriosclerosis, induced by secondary

hypertension, - common finding in renal

vasculature
Tubulointerstitial inflammation & scarring frequent additional finding (poor prognosis)
Glomerular hypertension & hyperinfiltration
through remnant functioning nephrons can
hasten progression to end-stage renal disease

CHRONIC
GLOMERULONEPHRITIS
2 periods:
I. Renal compensation stage (nitrogen

secretory function insignificantly impaired)

II. Renal decompensation stage (nitrogen
secretory function substantially impaired)

CHRONIC
GLOMERULONEPHRITIS
I. Renal compensation stage (signs &

symptoms same as in acute

gloumerolunephritis):
Weakness
Persistent headache
Vertigo
Edema
Often asymptomatic (in early stage of disease
patient may be asymptomatic - renal insufficiency
revealed by proteinuria, anaemia, hypertension or
raised blood urea during routine examination)

CHRONIC
GLOMERULONEPHRITIS
I. Renal compensation stage:
Increased BP
Left ventricular hypertrophy
Urinalysis: proteinuria, cylindruria (waxy casts)
Leached erythrocytes (usually - small qauntity)
Increased serum cholesterol
Hypoproteinemia due to permanent proteinuria

CHRONIC
GLOMERULONEPHRITIS
II. Renal decompensation stage (nitrogen

secretory function substantially impaired)

CHRONIC RENAL FAILURE - irreversible
deterioration in renal function which
results from a diminished mass of
effective functional renal, resulting in
impairment of the excretory, metabolic &
endocrine function of the kidney which
leads to the development of the clinical
syndrome of uraemia

CHRONIC RENAL FAILURE

Clinical features
1.Anorexia, nausea, vomiting
Most common symptoms due to ammonia

formation in upper GIT from urea

2. Anaemia
Normocytic normochromic anaemia - clinical
features: dyspnoea on excertion, fatigue

CHRONIC RENAL FAILURE

Clinical features
3. Renal osteodystrophy:
Osteomalacia
Osteoporosis
Secondary hyperparathyroid bone

disease
Osteosclerosis

CHRONIC RENAL FAILURE

Renal osteodystrophy
Osteomalacia: kidney failure to convert

cholecalciferol (vit D) to active metabolite1,25

dihydroxycholecalciferol - deficiency leads to
diminished intestinal absorption of calcium,
hypocalcemia & reduction in calcification of
osteoids

CHRONIC RENAL FAILURE

Renal osteodystrophy
Hyperparathyroid bone disease: secondary

hyperparathyroidism - parathyroid glands

stimulation by low plasma calcium
Osteoporosis: due to malnutrition
Osteosclerosis: unknown cause & mainly in
sacrum, base of skull & vertebrae

CHRONIC RENAL FAILURE

Clinical features
4. Endocrine abnormalities

Amenorrhea in females
Loss of libido in both sexes
5. CVS Disorders
Hypertension
Atherosclerosis
Pericarditis

CHRONIC RENAL FAILURE

Clinical features
6. Acidosis
Decline renal function associated with

metabolic acidosis - acid base imbalance in

kidney
7. Infections
Cellular & humoral immunity impaired increased susceptibility to infection

CHRONIC RENAL FAILURE

Clinical features

8. Skin abnormalities
Yellow brown pigmentation due to accumulation
of urinary pigment in skin especially urochromes
9. Neuromuscular disturbances
a. Neuropathy

sensory neuropathy

motor neuropathy

autonomic neuropathy
b. Myopathy

CHRONIC RENAL FAILURE

INVESTIGATION
1. Blood urea & serum creatinine raised
2. Blood test normocytic, normochromic

anemia
3. Ultrasound examination describes renal
size & defines or excludes obstructions
4. IVP size, shape & position of kidney &
calculi

CHRONIC RENAL FAILURE

MANAGEMENT
1. Diet
Protein restriction to 40g daily
Carbohydrate & fat - adequate to provide
body energy
2. Fluid
Fluid intake 3 liter per day (because of
impaired concentration power in large
volume of urine, about 2.5 liter daily
needed to excrete waste products)
Fluid restriction - in cardiac failure
or glomerular functional rate < 5ml/min

CHRONIC RENAL FAILURE

Management
3.Electrolytes

Na - in absence of edema, cardiac failure

or hypertension
Na restriction contraindicated
K when creatinine clearance has fallen
below 10ml/min
K restriction is required & achieved by
avoiding high K food (banana, coffee,
tomato)

CHRONIC RENAL FAILURE

Management
4. Blood pressure control
Hypertension treatment (diuretics, beta-

blockers or vasodilators effective; angiotensin

converting enzymes inhibitors most effective)
Salt intake reduced
Patient with chronic pyelonephritis maybe
unable to conserve salt & water - hypertension
& hypovolemia may develop (salt & water
intake improves the condition)

CHRONIC RENAL FAILURE

Management
5.Treatment for anemia
Control of severe anemia may reduce

hemolysis & marrow depression

Blood transfusion
Human recombinant erythropoietin increase
Hb in chronic renal failure

CHRONIC RENAL FAILURE

Management
6.Treatment for renal osteodystrophy
7.Replacement of renal function
The excretory function of kidney partially

replaced by dialysis
The endocrine & metabolic functions renal transplantation

CHRONIC RENAL FAILURE

Management

Low protein diet

High fluid intake
Normal Na and low K diet
Blood pressure control
Treatment of anemia by blood
transfusion
Alpha calciferol & aluminum hydroxide
for renal osteodystrophy
Dialysis
Renal transplantation

Pyelonephritis
kidney infection
Possible causes of kidney infection:
infections in the bladder
use of a catheter to drain urine from the bladder
use of a cystoscope to examine the bladder and

urethra
surgery on the urinary tract
conditions such as prostate enlargement and
kidney stones that prevent the efficient flow of
urine from the bladder
defects or abnormalities in the urinary tract that
block the flow of urine

Symptoms
of pyelonephritis
back, side, and groin pain
urgent, frequent urination
pain or burning during urination
fever
nausea and vomiting
pus and blood in the urine

Complications
of pyelonephritis
Severe or recurrent infections may cause

permanent kidney damage and lead to

chronic kidney disease
Infection in the kidney may spread to the
bloodstream sepsis (rare)
Acute renal failure
Chronic renal failure

Diagnosis
of pyelonephritis
Urine test to identify bacteria and

formations of white blood cells (casts)

If an infection cannot be easily cured, x rays
might be done to look for abnormalities in
the kidneys, ureters, and bladder

Chronic pyelonephritis
Renal injury induced by recurrent or persistent renal

infection
It occurs almost exclusively in patients with major
anatomic anomalies, including urinary tract
obstruction, struvite calculi, renal dysplasia, or, most
commonly, vesicoureteral reflux in young children.
Radiologic evidence
Vesicoureteral reflux - congenital defect that results in
incompetence of the ureterovesical valve due to a
short intramural segment (present in 30-40% of young
children with symptomatic urinary tract infection and
in almost all children with renal scars.
Vesicoureteral reflux may also be acquired by patients
with a flaccid bladder due to spinal cord injury

Chronic pyelonephritis
pathophysiology
associated with progressive renal scarring can lead to end-

stage renal disease (Intrarenal reflux of infected urine is

suggested to induce renal injury, which heals with scar formation.
In some cases, scars may form in utero in patients with renal
dysplasia with perfusion defects. Infection without reflux is less
likely to produce injury. Dysplasia may also be acquired from
obstruction. Scars of high-pressure reflux can occur in persons
of any age. In some cases, normal growth may lead to
spontaneous cessation of reflux by age 6 years.
Factors that may affect the pathogenesis of chronic
pyelonephritis are as follows: (1) the sex of the patient and his or
her sexual activity; (2) pregnancy, which may lead to progression
of renal injury with loss of renal function; (3) genetic factors; (4)
bacterial virulence factors; and (5) neurogenic bladder
dysfunction. In cases with obstruction, the kidney may become
filled with abscess cavities (see Pyonephrosis).

URINARY TRACT INFECTIONS

Urinary tract infection associated with

multiplication of organisms in urinary

tract (> 100 000 organisms per ml in
midstream sample of urine)

Urinary tract infection

Microorganisms
Organism

Approximate
frequency

E.coli & coli forms

68%

Proteus mirabilis

12 %

Klebsiela
aerogens

4%

Urinary tract infection

Microorganisms
Organism

Approximate
frequency

Streptococcus
faecalis

6%

Staphylococcus
saprophyticus
or epidermidis

10%

Urinary tract infection

Pathogenesis
Routes of spread:

Ascending transurethral route

Blood stream
Lymphatics
Direct extension

Urinary tract infection

Microorganisms
Organism

Approximate
frequency

E.coli & coli forms

68%

Proteus mirabilis

12 %

Klebsiela
aerogens

4%