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Glomerulonephritis /HSUM/
 

Glomerulonephritis /HSUM/

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Pathologic changes

Pathologic changes
Pathogenesis
Acute GN
Subacute GN
Chronic GN
Treatment
Diagnosis
Prognosis
Prevention
Screening

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    Glomerulonephritis /HSUM/ Glomerulonephritis /HSUM/ Presentation Transcript

    •  MUNKHTULGA G.
    •  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
    • RangePressure /mmHg/Hydrostatic 60-90 Oncotic 25-30Glomerular 10-20 capsules
    • Lacis cells –Гурмагтиг
    •  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.
    •  2-7% of internal patients have GN.
    • 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
    • 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
    • Source: Robbins & Cotran Pathologic Basis of Disease
    •  Auto-Antibody/autoimmune/ - In situ Immune complex
    • Granular, IC deposition Linear, IC deposition
    • Nephrotic syndrome Nephritic syndromeProteinuria >3,5 g/l HematuriaLipiduria, hyperlipidemia CylinderuriaHypoproteinemia, Leucocyturia, Glucosuria,Hypoalbuminemia Ketonuria,Edema Hypo-Hyperstenuria …
    •  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
    •  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
    •  IC accumulated in mesangiocyte & endothelium  mesangium thickened IgG, IgA, C3 Berger’s disease Etiology is unknown
    •  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
    •  Second most common cause of nephrotic syndrome in adults Prognosis: Up to 75%  develop progressive renal failure over 20 years.
    • Prognosis: 50%  End stage kidney failure over 20 years There is no effective therapy
    • Type 1 Type 2
    • 1. Acute GN2. Membranous GN3. Membrano- proliferative GN4. Mesangial GN or IgA GN
    •  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.
    •  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
    • * Post streptococcal GN 1. Bacterial: endocarditis, pneumococcal pneumonia, * Non- meningococcecemia1 Infectious streptococcal 2. Viral: B, C hepatitis, салхин GN цэцэг, Коксаки 3. Parasite: mosquito, malaria, toxoplasmosis2 Systemically disease: SLE, RA, Schonlein-Henoch vasculitis Primary renal disease: Mesangial capillary GN, Berger’s disease,3 Mesangial proliferative GN4 Холимог: serum disease, Гийен-Баррын хам шинжA groups, 4, 19, 25, 49 β hemolytic streptococcal angina “Бөөр судлал” Гэлэгжамц.Х нар
    •  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
    •  Tachypnea, Palpitation, Loss of appetite Tympanitis Thirst Oligo-anuria Weakness
    •  Presented with nephritic syndrome Classical type of AGN Presented with nephrotic syndrome
    •  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
    •  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
    •  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
    •  Acute Heart failure Eclampsia Nephrotic crisis Acute renal failure
    •  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 ↑]
    •  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 ↑
    •  Scan tests: Fundus photography: o Arterial hypertension  arterioles constricted, bulbous n. opticus swollen and stroke Ultrasound: o Renal size is normal or little enlarged.
    •  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
    •  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 +
    •  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
    •  Bed rest or decubitus for 14-21 daysDiet: 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/
    •  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
    •  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
    •  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
    •  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
    • Rapidly ProgressiveGlomerulonephritides TYPE I (ANTI-GBM ANTIBODY)Renal limitedGoodpasture syndrome TYPE II (IMMUNE COMPLEX)IdiopathicPost-infectious glomerulonephritisLupus nephritisHenoch-Schönlein purpura (IgA nephropathy)Others TYPE III (PAUCI - IMMUNE)ANCA-associatedIdiopathicWegener granulomatosisMicroscopic polyangiitis Source: Robbins & Cotran Pathologic Basis of Disease
    •  Hematuria Edema acute Arterial hypertension After 2-3 months: o Azotemia o Anemia RENAL BIOPSY
    •  4 complexes treatment: o Hormone o Cytostatic o Plasmophoresis o Hemosorbtive 2nd  combination treatment
    •  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]
    •  Exogenic Endogenic Immunogenic Non-Immunogenic o Renal function o Circulatory o Coagulation o Metabolism
    • By Clinical Latent CGN o CGN with Proteinuria Nephritic syndrome o CGN with Hematuria Nephrotic CGN CGN with arterial hypertension CGN холимог хэлбэр
    •  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
    •  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
    •  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
    •  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
    •  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↑
    •  Hypertension + Nephrotic syndrome Swelling, hypertension Complication: After 3-5 years  Renal failure
    •  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
    •  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
    •  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/
    •  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
    •  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
    • 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
    •  Urinalysis – every 3 months BFT – every 6 months On time treatment: o Respiratory tract infection o Every deterioration of CGN
    • 1. Бөөр судлал, Гэлэгжамц.Х, Ариунаа.Т нар, 2010 он2. Color atlas of pathophysiology, Silbernagl et al. 20003. Color atlas of physiology, 5th edition Agamemnon Despopoulos et al. 20034. Clinical nephrology, Woo Keng Thye, 19985. Fox: Human physiology, 8th edition, 20036. Harrisons Principles of Internal Medicine, 17th edition7. Pathologic Basis of Disease, Robbins & Cotran, 8th edition, 20098. Pathophysiology: Concepts of Altered Health States, Carol Mattson Porth, 7th edition, 20049. Textbook of medical physiology, 11th edition Guyton & Hall, 200610. www.emedicine.medscape.com