NEPHRITIS

PRESENTED BY:- PAVAN J. SORATHIYA

BAMS 4TH YEAR
R. K. UNIVERSITY AYURVEDIC COLLEGE AND HOSPITA
BRIEF INTRODUCTION OF NEPHRON:-

• Nephron is defined as the structural and functional unit of Kidney.

• Each kidney consists of 1 to 1.3 million nephrons.

• The number of Nephrons starts decreasing after about 45 to 50 years of age at the rate
of 0.8 to 1% every year.

• Nephron is formed by two parts-

1. A blind end – renal corpuscle or malpighian corpuscle

2. A tubular portion - renal tubule
PARTS OF NEPHRON:-
 NEPHRITIS:-
 DEFINITION:-
• Nephritis is a condition in which the nephrons,
the structural and functional units of the kidney
become inflamed or it is condition in which
tissues of the kidney become inflamed and having
problems in filtering waste from the blood.

• There are several types of nephritis including:-

1. Glomerulonephritis
2. Lupus nephritis
3. Hereditary nephritis (Alport nephritis)
4. IgA neuropathy
5. Interstitial nephritis
  GLOMERULONEPHRITIS:-

 DEFINITION:-

• Glomerulonephritis is an inflammation either at the glomeruli or the small blood

vessels in the kidney.
 ETIOLOGY AND RISK FACTORS:-

• Streptococcal infection of the throat or skin

• Hereditary diseases

• Immune diseases

• Diabetes

• High blood pressure

• Vasculitis (Inflammation of the blood vessels)

• Viruses : HIV, Hepatitis – A, Hepatitis – C virus

• Infections of the valves of the heart (Endocarditis)

 TYPES:-

GLOMERULONEPHRI
TIS

ACUTE CHRONIC

- Begins suddenly - Develops gradually

- It occurs after 5-21 over several years
days of - It occurs after acute
streptococcal phase
infection
 1. ACUTE GLOMERULAR NEPHRITIS:-

• It is the inflammation of the glomeruli of kidneys caused by antigen –

antibody reaction with respect to streptococci.

• It is characterized pathologically by diffuse inflammatory changes in the

glomeruli and clinically by abrupt onset of hematuria, proteinuria, oedema,
hypertension, impaired kidney function with or without oliguria.

• Not all features may be present at same time.

• It produces damage to the glomeruli by decreasing GFR, accumulation of

organic salts and other wastes into the body.
 CAUSES:-

• Initially URTI (Upper respiratory tract infection) or Skin infection., usually 1-3 weeks
before the onset of symptoms.

• Most commonest and frequent causative organism is Group A Beta haemolytic

streptococci.
 PATHOPHYSIOLOGY:-

The streptococcal infection from throat or elsewhere from body

It attacks the immune system, the immune system produces antibodies

against streptococcal antigen

Antigen – antibody reaction takes place with complex formation

It gets trapped in the basement membrane of glomerulas

 The complexes combines with leucosomal enzyme (complement)

Destruction of cell occurs

Inflammatory changes occurs in glomerulas

Decreased in the GFR & increased permeability of glomerular walls

Edema, proteinuria and microscopic hematuria

Acute Glomerulonephritis
 CLINICAL FEATURES:-
• Fever and chills

• Weakness, pallor

• Generalised oedema

• Bodyache

• Weight gain

• Headache, convulsions
 G.I. disturbances:-  Renal disturbances:-

o Nausea, vomiting o Proteinuria

o Anorexia o Oligouria
o Ascites o HTN
o Abdominal pain o Decreased PH of urine

 Cardiac disturbances:-  Ophthalmic disturbances:-

o Pulmonary oedema o Visual acuity is reduced

o CCF (Congestive cardiac
failure)
 SIGNS:-

1. OEDEMA:-
• May come on suddenly or gradually
• Puffiness of face and whitish pallor, known as nephritic facies
• Swelling of face usually in morning

2. HYPERTENSION:-
• Occurs in majority of cases, diastolic BP usually 90 to 120 mm Hg
• In 5 to 10% cases encephalopathy develops

3. IMPAIRED RENAL FUNCTION:- Oligouria, in some cases acute renal failure

 INVESTIGATIONS:-

1. Urine Analysis:- 2. Blood test:-

• Urine volume reduced • ESR elevated

• Dark in colour or smoky when fresh
• Tea coloured after haemolysis
• Proteinuria variable
• RBC, RBC casts, WBC, WBC casts and
granular casts present
• Blood levels of urea creatinine
elevated
• Serum Potassium and sodium is
elevated if oligouria continuous

 Throat swab culture which may show hemolytic streptococci organism

 Renal Biopsy
 Serum complement level is decreased
 COMPLICATIONS:-
• Chronic glomerular nephritis

• Left ventricular failure

• Pulmonary oedema

• Acute renal failure

• Hypertensive encephalopathy

• UTI if oligouria prolonged

• Urinary tract pain

 MANAGEMENT:-
1. Bed rest

2. Restriction of fluid

3. Antibiotics:-
• Benzathine penicillin G to destroy any residual hemolytic streptococci
• Erythromycin 250mg if Penicillin is not tolerated.

4. Diet:-
• Low protein diet
• Diet contain very little sodium

5. Dialysis

6. Diuretics
7. Management of complications:-

• Convulsions:- Diazepam IV 10 mg slowly

• Hypertension:- Antihypertensive, ACE inhibitors, angiotensin II receptor antagonist
 2. CHRONIC GLOMERULO NEPHRITIS

• It is an advanced irreversible impairment of renal function with or without

symptoms.

• It may develop as a primary glomerular disease or may occur secondary in SLE

(Systemic lupus erythematosus – Lupus nephritis), drug iduced nephropathy.
 ETIOLOGICAL FACTORS:-

• Repeated attacks of streptococci

• SLE

• Drug induced nephropathy

• Thickening of basement membrane

• Glomerulo-sclerosis

• Polyarteritis
 SYMPTOMS:-

• Hypertension

• Conjunctivitis

• Kidney disease – Oliguria, Proteinuria

• CNS – Mononeuritis multiplex

• Discoloration of nails
 CLINICAL MANIFESTATION:-

• The condition remains a symptomatic and may be diagnosed during accidental

urine examination.

• The presenting features includes:-

- Oedema
- Severe HTN
- Hematuria, anemia
- bone pain
- Failure to thrive
 DIAGNOSIS:-
1. Urine Analysis:-

• It shows 1+ to 2+ protein
• Thre are RBC, WBC cast which indicated inflammation of glomeruli

2. Blood Analysis:-

• ESR elevated
• Normocytic anemia present due to haemodilution
• The blood levels of urea creatinine elevated
• Serum potassium and sodium is elevated if oliguria continues

3. Renal Biopsy
4. Serum complement level is decreased

5. Throt swab culture which may show hemolytic streptococci organism

6. Increased antistreptolysin titre

 MANAGEMENT:-

• No specific treatment

• Steroid and other immune suppressive drugs are helpful

• Antibiotics

• Antihypertensive

• Symptomatic and supportive treatment

 LUPUS NEPHRITIS

• Lupus is an autoimmune disease, which means that the immune system mistakenely
attacks healthy tissues in the body.

• Over half of the individuals with a lupus diagnosis eventually develop lupus
nephritis. This occurs when the immune system attacks the kidneys.

• The symptoms of lupus nephritis include:-

- Foamy urine
- High BP
- Swelling of the legs, ankles and feet
• People may also notice symptoms in other parts of the body.

• These symptoms may include joint problems, fever and rashes.

• The severity of lupus can vary between patients. Although the disease sometimes
goes into remission, the condition can become serious.

• It is vital for anyone experiencing symptoms of lupus nephritis to seek prompt

medical attention ot limit further kidney damage.
 ALPORT SYNDROME OR HEREDITARY NEPHRITIS

• This disease can lead to kidney failure, as well as vision and hearing problems.

• Alport syndrome is passed on in the genes, and it is usually more severe in men..
  IGA NEPHROPATHY

• This is one of the most common form of nephritis. It develops when IgA antibody
deposits build up in the kidneys and causes inflammation.

• The immune system develops antibodies to combat harmful substances and

organisms that enter the body.

• People with IgA nephropathy have defective IgA antibodies.

• Doctors do not often find IgA nephropathy in young people, as the early symptoms
are easy to miss.

• People can treat this condition with blood pressure medications.

  INTERSTITIAL NEPHRITIS

• Often developing very rapidly, this form of nephritis usually occurs due to
infection or a particular medication.

• It affects the part of the kidney called the interstitium, which is fluid filled space.

• If a doctor takes affected individual off the problametic medication quickly a full
recovery is possible in a few weeks.

• Damage can sometime accumulate to the point of kidney failure.