The document provides a comprehensive overview of glomerulonephritis (GN), detailing its structure, types, etiology, clinical features, diagnosis, and treatment options. GN is primarily an inflammatory condition affecting the glomeruli, leading to various symptoms such as hematuria, hypertension, and proteinuria. The text also discusses the complications and preventive measures associated with GN, emphasizing the importance of early diagnosis and appropriate treatment to prevent progression to chronic kidney disease.

1.  
MUNKHTULGA G.

2.  Structure and functions of glomeruli
 Introduction of Glomerulonephritis /GN/
 Prevalence
 Etiology and risk factor
 Classification and types
 Pathogenesis and pathologic changes
 Clinical features and symptoms
 Diagnosis
 Treatment
 Differential diagnosis
 Complications
 Screening
 Prevention
 Reference

5. Range
Pressure
/mmHg/
Hydrostatic 60-90
Oncotic 25-30
Glomerular
10-20
capsules

6. Lacis cells –
Гурмагтиг

9.  GN is group disease of glomerulus, an inflammatory
process that involves glomerular structures, caused by
immune disruption, is the leading cause of renal
interstitial tissue damage.

10.  2-7% of internal patients have GN.

11. Exogenic Endogenic
- Infectious - HLA - A2, BW 35, B7, B8, B15
- Bacterial /β-streptococcal-1, 4, - Cancer, tuberculosis …
12, 18, 25, 55, 60; - Disturbance of T/B lymphocyte ratio
staphylacoccal, pneumococcal/ - Congenital deficiency of T
- Viral lymphocyte
- Non-infectious /sulfanylamid, - Deficiency of complement
penicillin, iodine, mercury, brome, synthesize
aspirin . . ./ - Auto-antigen
“Бөөр судлал” Гэлэгжамц.Х нар

12. By clinical and disease progress
 Acute GN
o Nephrotic Acute GN /minimal GN/
o Nephritic AGN
o Classical type
 Rapidly progressive GN /Crescentic GN/
 Chronic GN
o Latent Chronic GN
o With Hematuria
o Nephrotic CGN
o Hypertensive CGN
“Бөөр судлал” Гэлэгжамц.Х нар

14. Source: Robbins & Cotran Pathologic Basis of Disease

15.  Auto-Antibody/autoimmune/ - In situ
 Immune complex

17. Granular, IC deposition Linear, IC deposition

20. 

21. Nephrotic syndrome Nephritic syndrome
Proteinuria >3,5 g/l Hematuria
Lipiduria, hyperlipidemia Cylinderuria
Hypoproteinemia, Leucocyturia, Glucosuria,
Hypoalbuminemia Ketonuria,
Edema Hypo-Hyperstenuria …

22.  By far the most common cause of nephrotic syndrome in adolescent
 Declining to about 25% of cases of nephrotic syndrome in older
adults
 Lesion of podocytes constitution
 GBMs charge changed
 No depositions in GBM
 Present with nephrotic syndrome
 No RBC and WBC in urine

23.  Most common glomerular disease worldwide, is IgA nephropathy
(Berger’s disease)
 Mesangial widened
 Mesangial cells proliferation
 Mesangial matrix concentration
 Hematuria, some times flank pain,
 Hypertension is common
 Nephrotic syndrome is uncommon
 30%  progressive renal failure

24.  IC accumulated in
mesangiocyte &
endothelium 
mesangium thickened
 IgG, IgA, C3
 Berger’s disease
 Etiology is unknown

25.  Sub-epithelial immune deposits, thickened GBM
 Most common cause of nephrotic syndrome in adults
 Prognosis:
 25%  End stage renal disease over 25 years
 25%  spontaneous remission

26.  Second most common cause of nephrotic syndrome in
adults
 Prognosis: Up to 75%  develop progressive renal
failure over 20 years.

27. Prognosis: 50%  End stage kidney failure over 20 years
There is no effective therapy

29. Type 1 Type 2

30. 1. Acute GN
2. Membranous GN
3. Membrano-
proliferative GN
4. Mesangial GN or
IgA GN

31.  Glomerulonephritis is an inflammatory process
affecting primarily the glomerulus, with infiltration
and proliferation of acute inflammatory cells.
 These are principally mononuclear cells and
neutrophils in post-infectious glomerulonephritis.

32.  The inflammation is immunologically mediated with
immune deposits in the glomerulus. Onset of symptoms
is usually acute.
 Usually Acute GN occurs after upper respiratory tracts
infection, 10-21 days.
 Children and guys

33. * Post streptococcal GN
1. Bacterial: endocarditis,
pneumococcal pneumonia,
* Non- meningococcecemia
1 Infectious
streptococcal 2. Viral: B, C hepatitis, салхин
GN цэцэг, Коксаки
3. Parasite: mosquito, malaria,
toxoplasmosis
2 Systemically disease: SLE, RA, Schonlein-Henoch vasculitis
Primary renal disease: Mesangial capillary GN, Berger’s disease,
3
Mesangial proliferative GN
4 Холимог: serum disease, Гийен-Баррын хам шинж
A groups, 4, 19, 25, 49 β hemolytic streptococcal angina
“Бөөр судлал” Гэлэгжамц.Х нар

34.  Acute Nephritic syndrome
o Hypertension /Hypervolemia, hyperhydration/
o Hematuria
o Swelling, urine volume ↓
 Facies nephritica
 Dry skin /lose nutrient/
 Striae distansae
 Fragile nail and hair
 Swelling  weakness, anasarca
 Edema  Face, back around, abdomen, genital organ

35.  Tachypnea,
 Palpitation,
 Loss of appetite
 Tympanitis
 Thirst
 Oligo-anuria
 Weakness

36.  Presented with nephritic syndrome
 Classical type of AGN
 Presented with nephrotic syndrome

37.  Slowly beginning
 Puffiness around the eyes and face
 Flank pain
 Usually no urine color changes
 Symptoms are Latent  chronic nephritis
 Mild hypertension /70-80%/
 Proteinuria less than 1 gr/l
 RBC, cylinder is seen in the urine
 Macrohematuria occurs in few cases

38.  Acute Nephritic syndrome is clear
 GFR ↓
 Sodium reabsorption in tubule ↑ Nephritic
edema
 Imbalance of water-salt exchange
 Nephritic edema level < Nephrotic edema level
 Arterial Hypertension 140/100 – 170/110 ↑
 Palpitation, tachypnea, left ventricle failure
 Proteinuria 1-3 gr/l
 Urine volume ↓
Heavy condition: pre-eclampsia, eclampsia, acute kidney and heart failure

39.  Proteinuria >3gr/l per day
 Decreased protein in blood  serum oncotic pressure ↓
  Edema
 Anasarca
 Foam in urine (slowly removed)
 Hyperlipidemia
 No hematuria
 Arterial hypertension is rare

40.  Acute Heart failure
 Eclampsia
 Nephrotic crisis
 Acute renal failure

41.  After 14-21 days of angina and other infections, young
people could have acute nephritic syndrome and
backache.
 Important things:
o Never had renal disease
o Never had changes in the urinalysis
 In urinalysis:
o Proteinuria 1-3 gr/l [in heavy case: 3-20gr/l]
o Detected erythrocytes, few leucocytes/lymphocytes/ and
cylinders
o Specific gravity is normal [during excess proteinuria  SG ↑]

42.  CBCC /Complete Blood Cell Count/
o Decreased hemoglobin /water accumulated in body then it leads
dissolved blood/
o Lightly increased WBC, УЭТХ ↓
 Blood Function Test
o During nephrotic syndrome, Serum protein and albumin ↓
o γ-globulin↑, disproteinemia
o Lipid and cholesterol ↑
o C3 ↓, after 6-8 weeks becomes normal
o GFR slightly ↓
o During heavy acute nephritis, serum creatinine, urea, leftover
nitrogen ↑

43.  Scan tests:
 Fundus photography:
o Arterial hypertension  arterioles constricted, bulbous n. opticus
swollen and stroke
 Ultrasound:
o Renal size is normal or little enlarged.

44.  Urinalysis, identify: protein in daily urine
 CBCC: Hgb
 Хоолойн арчдас авч, нян ургуулах
 BFT: total protein, protein group, total
lipid, cholesterol, leftover nitrogen, creatinine, K+ Na+ C-
reactive protein
 Coagulogram: protrombin, fibrinogen
 Immunology: ЦИК, IgA, M, G, complement, T, B
lymphocytes
 Renal ultrasound: Size, cortex thick
 Renal biopsy
 Fundus photography, chest x-ray, ECG

45.  Chronic GN
o Whether patient had renal disease or urine changes
o After grater influenced, GNs symptoms and edema increased within
short term
o During Chronic GN, urine changes keeps for long term
o Arterial hypertension increased, constantly
o GFR ↓ - constantly, irreversible
o Ultrasound: Parenchymal dense ↑, kidney size normal or small
 Pyelonephritis
o Dysuria, чинэрч өвдөнө, шээлэйн дагуу дамжиж өвдөнө
o Fever, loss of appetite, weakness
o Palpate or push to Angle cost-vertebral/Symptom Pasternatski/:
Clear
o Urinalysis: Protein 0,5-1,0 gr/l, leucocyte and bacterium +

46.  Administrate to hospital for 30 days
 Keep treatment for 3 months to 1 year
 In not heavy case: symptomatic therapy for 14 days
o Anti-infection treatment: if it caused by infection
o Immunosupressant: if immune activation is high or heavy nephrotic
syndrome
 General principle of treatment
o Regimen
o Diet
o Drug
o Sanatorium care

47.  Bed rest or decubitus for 14-21 days
Diet:
 First 1-2 days restraint food, only given apple, fruit juice
& rice glop
 Next 5-7 days, limited animal protein 0,5 gr/kg, only use
non-animal protein
 After 10 days, protein 1gr/kg
 Kcal – 2300-2800 kcal
 No salt /2-3 week/

48.  Post-streptococcal:
o Хагас нийлэг penicillin oxicillin, amoxicillin – 1-2 mill U/day
o Penicillin G 1-2 mill U/day by injection
o Vitamin C oral or inject
 Keep symptomatic treatment for 2-6 months
 Immunosuppressant/if there is no result >2 months/:
o During nephrotic syndrome, prednisone 0,8-1,2 mg/day, slowly
decrease dosage by clinical and laboratory changes
o Keep treatment for 6 months to 1 year
o If patient can’t use glucocorticoid, We can use cytostatic drugs

49.  Improve renal blood supply:
o Heparin 15000-20000 ED/day
o Anti-aggregant: Curantil 200-300 mg/day for 2-4 months by
slowly decrease dosage
o Nicotine acid 1%
 Anti-hypertensive and diuretics
o Anti-hypertensive drugs /6 groups/
o Diuretics: Thiazides – furosemide 20-80 mg/day 2-3 times

50.  Under doctors control for 2 years
 Avoid manual labor about 1 year
 Second prevention!!!
 Urinalysis - every 3 months
 Blood function test – every 3months
 Zimnitskii, Reberg’s test and isotopic renogram - every
1 year
 If there was no deterioration or were no changes in
analysis in 2 years we will suggest that the patient is
recovered

51.  Rapidly progressive glomerulonephritis (RPGN) is a
syndrome associated with severe glomerular injury and
does not denote a specific etiologic form of
glomerulonephritis. It is characterized clinically by rapid
and progressive loss of renal function associated with
severe oliguria and signs of nephritic syndrome; if
untreated, death from renal failure occurs within weeks
to months.[7]
 The U.S – 7:1,000,000
 The U.K – 2:100,000
 Male : Female – 1:1
 2-92 age

52. Rapidly Progressive
Glomerulonephritides
TYPE I (ANTI-GBM ANTIBODY)
Renal limited
Goodpasture syndrome
TYPE II (IMMUNE COMPLEX)
Idiopathic
Post-infectious glomerulonephritis
Lupus nephritis
Henoch-Schönlein purpura (IgA nephropathy)
Others
TYPE III (PAUCI - IMMUNE)
ANCA-associated
Idiopathic
Wegener granulomatosis
Microscopic polyangiitis Source: Robbins & Cotran Pathologic Basis of Disease

54.  Hematuria
 Edema acute
 Arterial hypertension
 After 2-3 months:
o Azotemia
o Anemia
 RENAL BIOPSY

55.  4 complexes treatment:
o Hormone
o Cytostatic
o Plasmophoresis
o Hemosorbtive
 2nd  combination treatment

56.  Nearly all forms of acute glomerulonephritis have a
tendency to progress to chronic glomerulonephritis. The
condition is characterized by irreversible and progressive
glomerular and tubulo-interstitial fibrosis, ultimately
leading to a reduction in the glomerular filtration rate
(GFR) and retention of uremic toxins. If disease
progression is not halted with therapy, the net results
are chronic kidney disease(CKD), end-stage renal
disease (ESRD), and cardiovascular disease.[10]

58.  Exogenic
 Endogenic
 Immunogenic
 Non-Immunogenic
o Renal function
o Circulatory
o Coagulation
o Metabolism

60. By Clinical
 Latent CGN
o CGN with Proteinuria Nephritic syndrome
o CGN with Hematuria
 Nephrotic CGN
 CGN with arterial hypertension
 CGN холимог хэлбэр

61.  Only Urine changes
 No complains,
 No urine color & volume changes
 In few case: swelling
 Urinalysis:
o Protein less than 3 gr/l
o Erythrocytes and cylinder is seen
 Renal functions measurements keep normal range foe
20-30 year

62.  Usually occurs children, young people
 Hematuria
 Decreased blood in urine within few days
 Protein in urine: 1-2 gr/L
 Old erythrocytes and cylinder in urine
 No renal pain, no edema, no hypertension
 Disease progress: 30-40 years

63.  Dry skin
 Urine has foam
 Daily urine volume ↓
 First, puffiness around the eyes and face,
 Then, anasarca
 Sometimes, fluid accumulated in organ that has cavity
 Loss of appetite
 Sensitive to cold
 Proteinuria: 3,5-20 gr/l
 Anemia

64.  Complication of infection /immune weakness/
 Fluid accumulation in thorax leads wound(pus)
 Pneumonia
 Urinary tract infection
 Venous thrombosis
 Tingle around kidney
 Blood pressure ↓
 Acute Renal failure
 Nephrotic crisis  fever, nausea, vomiting, tingle around
abdomen, detected symptom of peritonitis

65.  High blood pressure
 Nephritic syndrome
 Initial phase – normal blood pressure
 Deterioration period – high blood pressure
 Headache, dizziness, worsen eyesight, pain around the
heart.
 2nd sound loudly around the aorta and systolic clamor
 Left ventricle hypertrophy, arhythmia/heavy case/
 Urinalysis: 1-3 gr/l protein, few erythrocyte & cylinder
 BFT: Lipid↑, cholesterol↑

66.  Hypertension + Nephrotic syndrome
 Swelling, hypertension
 Complication: After 3-5 years  Renal failure

67.  Decreased production of erythropoietin, thus resulting in
anemia
 Decreased production of vitamin D, resulting in
hypocalcemia, secondary
hyperparathyroidism, hyperphosphatemia, and renal
osteodystrophy
 Reduction in acid, potassium, salt, and water
excretion, resulting in
acidosis, hyperkalemia, hypertension, and edema
 Platelet dysfunction, leading to increased bleeding
tendencies

68.  After deteriorate, suddenly swelling
 During deterioration: Urine changes ↑, long term
 Ultrasound: shallow parenchyma, kidney size ↓
 Necessary test:
o CBCC, Urinalysis
o Identify protein in daily urine
o Ничепоренко, Аддис-Каковскийн сорил
o Зимницкийн сорил
o Blood function test: Total protein, proteins group, lipid,
cholesterol, creatinine, BUN, leftover nitrogen, K, Na, Ca, P

69.  Cystitis
 Renal tuberculosis
 Hereditary nephritis
 Chronic Pyelonephritis:
o Urine color and odor changes, smoky urine
o Neutrophilic leucocyturia and microbe in urine
o Fever, pain around kidney
o Scan test: Detected calyx and pelvis changes
 Acute GN ???
 Interstitial tissue and tubular nephritis/toxicosis/

70.  During deterioration, administrate to hospital for 14-30 days
 Regimen and nutrient therapy
 Pathophysiological treatment
o Glucocorticoid – Prednisone 1mg/kg for 2-9 weeks
o Cytostatic – Имуран/азатиоприн/ 100-150 мг, циклофосфамид
2-3 мг/кг/өдөр
o Anti-coagulant – Heparin 10,000-40,000 U/day
o Anti-aggregant – Дипиридамол/курантил/ 225-400 мг/өдөр
o Anti-hypertensive
o Symptomatic
 Specific therapy for each types of CGN

71.  Bed rest or decubitus for 2-3 weeks
 Nephrotic, Hypertensive GN:
o Protein 0,5 gr/kg, after 3rd week 1 gr/kg
o Hyperproteinuria, hypoalbuminemia : add egg, fish, chicken
o 2800-3000 kcal/day
o Apple, banana, cream, honey, jam – allow
o Parching, grilled, preserved products, spicy… - Not-allowed
o Salt decrease about 2-3 gr  hypertension

72. Stage GFR The action plan
mL/min
1 ≥90 Diagnosis and treatment,
Treatment of comorbid conditions,
Slowing of the progressing of kidney disease
Reduction of cardiovascular disease risks
2 60-90 Estimation of the progression of kidney
disease
3 30-59 Evaluation and treatment of complications
4 15-29 Preparation for renal replacement therapy
5 - Kidney failure, Kidney replacement if the
patient is uremic
www.emedicine.medscape.com

73.  Urinalysis – every 3 months
 BFT – every 6 months
 On time treatment:
o Respiratory tract infection
o Every deterioration of CGN

74. 1. Бөөр судлал, Гэлэгжамц.Х, Ариунаа.Т нар, 2010 он
2. Color atlas of pathophysiology, Silbernagl et al. 2000
3. Color atlas of physiology, 5th edition Agamemnon
Despopoulos et al. 2003
4. Clinical nephrology, Woo Keng Thye, 1998
5. Fox: Human physiology, 8th edition, 2003
6. Harrison's Principles of Internal Medicine, 17th edition
7. Pathologic Basis of Disease, Robbins & Cotran, 8th edition,
2009
8. Pathophysiology: Concepts of Altered Health States, Carol
Mattson Porth, 7th edition, 2004
9. Textbook of medical physiology, 11th edition Guyton & Hall,
2006
10. www.emedicine.medscape.com