Download 1: Minimal change nephropathy.

Forth stage
‫عماد البدراني‬.‫د‬
Medicine
Lec-8
2/11/2015
Classification of glomerulonephritis
It is confusing the original classification nephrotic and nephritic has given way to
histological classification:
1: Minimal change nephropathy.
It is the most cause of N.S in childhood and in one fourth of adult patients. Nephrotic
syndrome in those patients usually does not progress to renal impairment.
2: focal segmental glomerulosclerosis
Presented with idiopathic N.S shows poor response to corticosteroid and often progress to
renal impairment and usually recur after renal transplantation.
3: Membranous nephropathy:
It is regarded as most common cause of N.S in adulthood a proportion of cases associated
with known causes as :
A( persons with certain HLA and DR
B) Certain drugs and heavy metals
C) H.B .V
D) Certain malignancy as lymphoma. but most cases are idiopathic.
Membranous glomerulonephritis showed the following course
1. Third of the cases remit spontaneously
2. Third of the cases remain in nephrotic state
3. Third of the cases progress to renal failure.
They found that short term with high dose of corticosteroid and alkylating agents may
improve nephrotic state and long term prognosis.
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4: IgA nephropathy:
Is the most recognized type of glomerulonephritis and can be present in many ways;
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Hematuria is almost universal
Proteinuria is usual and may be severe proteinuria
Hypertension is very common
The disease is a common cause of E.S.R.D
One type of IgA nephropathy is Henoch-shoenlion purpura;
Her systemic vasculitis occur in response to upper respiratory tract infection .mostly
occur in children and rare in adult.
 There is characteristic petechial rash, cutaneous vasculitis, abdominal pain, with
gastro-intestinal vasculitis with mild G.N presented as hematuria.
5. Acute post-infective glomerulonephritis;
 Mostly seen after streptococcus infection but can occur after other infection
 Mostly in children occur after 10 days of infection which indicate immune mechanism
certain strains are accused
 Clinical features:
Acute nephritis with varying severity occur
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Na and water retention with edema.
Hypertension
Decrease of G.F.R
Proteinuria but rarely exceed 2g/24 hours
Hematuria
Decrease in urine volume (oliguria) and the urine become red or smoky
Low serum C 3, C 4
Evidence of streptococcus infection like increase A.S.O titer or culture of
throat swab renal function begin to improve spontaneously After 10 -14 days
 Treatment:
 antibiotic
 restriction of Na and fluid
 use of diuretic and hypotensive drugs
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 renal lesion is almost in all children and most adult resolve completely
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6. Glomerulonephritis associated with chronic diseases like :
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G.N with malaria
HB virus
Visceral leishmaniasis
in those conditions of G.N the most histological pattern are membranous
nephropathy and membrano-proliferative
 Focal –segmental glomerulosclerosis with HIV infection is highly prevalent.
Cystic diseases of the kidney
Polycystic kidney disease :
Type I: Infantile polycystic kidney disease
It is:
1. Rare
2. Autosomal recessive
3. Associated with hepatic fibrosis.
4. fatal in first year of life.
Type II : Adult poly cystic kidney disease
It is:
1. Common
2. Incidence 80 / 100,000
3. Autosomal dominant
There are two types of APKD according to gene affected
1. Type one gene affected on chromosome 16 and this type is common
2. Type two gene affected on chromosome 4 and this type is rare.
Pathology; small cysts appear in proximal tubular epithelium
Which are numerous in number and variable sizes
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Clinical features;
1. May be asymptomatic till twenty year of age
2. Hypertension usually after 20 year
3. Patients may complain of vague abdominal discomfort
4. Acute loin pain or renal colic
5. Hematuria
6. Urinary tract infection
7. May present with renal failure.
Associated features with APKD
1.30% of cases have hepatic cysts but there is no disturbance in liver functions
2. Berry aneurysm of cerebral vessels and 10% of cases may suffer from subarachnoid
hemorrhage
3. Mitral and aortic regurgitation is frequent
4. Colonic diveriticulation may occur
5. We may see abdominal hernia.
Investigations and diagnosis;
1. Family history.
2. Clinical examination
3. Ultrasound study of abdomen.
4. Genetic defect detection
Management;
1. Good control of blood pressure
2. Treatment of urinary tract infection
3. If chronic renal failure developed we start treatment of it
Screening and genetic counseling
Interstitial Nephritis
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Acute interstitial nephritis
Refers to acute inflammation within the tubule-interstitium
Aetiology:
1. Drugs; penicillin’s, non-steroidal anti-inflammatory drugs, Allopurinol, Furosemide.
2. Systemic diseases like sarcoidosis, Sjogren disease
3. Infections; like
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leptospirosis
tuberculosis
pyelonephritis
cytomegalovirus
Diagnosis:
1-30% of pt. with drug induced AIN have generalize drug hypersensitivity like fever; rash;
and eosinophilia
2-70%shows eosinophilia in urine
3-history and examination and specific test may point to Dx.
4-renal Biopsy has definitive Dx.
Management:1-if ARF due to Rx is usually conservative and dialysis needed only in sever case.
2-in drug induced AIN withdrawal of drug is sufficient
3- Corticosteroid are frequently used but there effect is doubtful.
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