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Introduction to nephrology Acute and chronic glomerulonephritis
Internal medicine department №2 Assist. Kvasnitska O.S.
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The mechanism of urine formation
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Acute glomerulonephritis
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Etiology Infectious Noninfectious Streptococcal
Nonstreptococcal postinfectious glomerulonephritis Bacterial Viral Parasitic Noninfectious Multisystem systemic diseases Primary glomerular diseases
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Glomerulonephritis
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Clinical syndromes urinary (proteinuria ≤1 g/l/24 h, haematuria, leucocyturia), nephritic (hypertension, gross haematuria, proteinuria 1-3 g/l/24 h, edemas), nephrotic (proteinuria ≥3,5 g/l/24 h, hypoproteinemia, hypoalbuminemia, hypercholesterolemia, hypercoagulation, edemas), mixed.
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Glomerulonephritis – Diagnostic Tests
CBC (possible anemia, leucocytosis, formula shift to the left, increasing ESR) Biochemical blood analysis (characterizes the kidney function by the parameters of urea, creatinine, total protein, albumin, serum electrolytes, cholesterol; functional state of the liver (on indicators of ALT, AST, bilirubin) Examination of the urine (red cells, red-cell casts, nephrotic or sub-nephrotic range proteinuria) ASO titer (anti streptolysine O) Kidney scan or biopsy
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1= Light yellow, normal colour of urine
2=Light-brown, urine with presence of low proteinuria and microhaematuria 3=Dark-brown, urine with medium presence of proteinuria and microhaematuria 4=Blood-brown, urine with visible haematuria and high level of proteinuria Source: The Internet Journal of Tropical Medicine ISSN:
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Glomerulonephritis –Treatment
Dietary protein is restricted when renal insufficiency (elevated BUN) develop. Sodium is restricted when the patient has hypertension, edema, and heart failure. Loop diuretic and antihypertensive medications may be prescribed to control hypertension. Bed rest during acute phase.
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Treatment Treat the underlying infections when acute GN is associated with chronic infections. Antimicrobial therapy Antibiotics (eg, penicillin) are used to control local symptoms and to prevent spread of infection to close contacts. Antimicrobial therapy does not appear to prevent the development of GN, except if given within the first 36 hours. Loop diuretic therapy Loop diuretics may be required in patients who are edematous and hypertensive in order to remove excess fluid and to correct hypertension. Relieves edema and controls volume, thereby helping to control volume-related elevation in BP Using ACE-ingibitors, AIIRA (angiotensin II receptor antagonists), statins for treatment high BP and lipid abnormalities Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxide) may be used if severe hypertension or encephalopathy is present
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Rapidly progressive glomerulonephritis (RPGN)
Characterized clinically by A rapid decrease in the GFR of at least 50% over a short period, from a few days to 3 months The term RPGN was first used to describe a Group of patients who had an unusually fulminant poststreptococcal glomerulonephritis and a poor clinical outcome Several years later, The anti-GBM antibody was discovered to produce a crescentic glomerulonephritis in sheep, and, following this discovery, The role of anti-GBM antibody in Goodpasture syndrome was elucidated Anti –GBM: antiglomerular basement membrane
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RPGN: Pathology The main pathologic finding is
Extensive glomerular crescent formation Focal rupture of glomerular capillary walls that can be seen by light microscopy and electron microscopy
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RPGN: Classification Immunological classification: based on the + or - of ANCAs The disorders are also classified based on their clinical presentation
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RPGN: Classification Anti-GBM antibody (Approx. 3% of cases)
Goodpasture syndrome (lung and kidney involvement) Anti-GBM disease (only kidney involvement) Note: 10-40% of patients may be ANCA positive
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RPGN: Classification Immune complex
Postinfectious (staphylococci/streptococci) Collagen-vascular disease Lupus nephritis Henoch-Schönlein purpura (immunoglobulin A and systemic vasculitis) Immunoglobulin A nephropathy (no vasculitis) Mixed cryoglobulinemia Primary renal disease Membranoproliferative glomerulonephritis Fibrillary glomerulonephritis Idiopathic Note: Of all patients with crescentic immune complex glomerulonephritis, 25% are ANCA+; < 5% of patients with noncrescentic immune complex glomerulonephritis are ANCA+
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RPGN: Classification Pauci-immune Wegener granulomatosis (WG)
Microscopic polyangiitis (MPA) Renal-limited necrotizing crescentic glomerulonephritis (NCGN) Churg-Strauss syndrome Note: 80-90% of patients are ANCA+
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RPGN: Symptoms *Edema (swelling) of the face, eyes, ankles, feet, legs, or abdomen *Blood in the urine *Dark or smoke-colored urine *Decreased urine volume *Abdominal pain *Cough & Diarrhea *General ill feeling & Fever *Joint aches & Muscle aches *Loss of appetite & Shortness of breath
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RPGN: Treatment Depends on the underlying cause
Corticosteroids may relieve symptoms in some cases Medications that suppress the immune system may also be prescribed, depending on the cause Plasmapheresis may relieve the symptoms in some cases Persons should be closely watched for signs of progression to kidney failure Dialysis or a kidney transplant may ultimately be necessary
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Chronic glomerulonephritis
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Chronic glomerulonephritis represents the end-stage of all glomerulonephritis with unfavorable evolution. This general (glomerular, vascular and interstitial) affection constitutes the so-called "end stage kidney". In most cases, it is associated with systemic hypertension. (Source:
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Minimal-Change Disease
Nil disease or lipoid nephrosis - normal or very mild abnormalities of the glomeruli Changes can only be seen through electron microscopy. 90 percent of cases of nephrotic syndrome in children under the age of 10 More than 50 percent of cases in older children In adults: use of nonsteroidal antiinflammatory drugs (NSAIDs) Malignancy: Hodgkin lymphoma Source: Source:
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Membranous Nephropathy
Second most common cause of primary nephrotic syndrome in adults Associated with hepatitis B infection Autoimmune diseases, thyroid disease, use of certain drugs Underlying cancer – solid tumor Source:
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Focal segmental glomerulosclerosis
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Mesangiocapillary glomerulonephritis
The glomeruli are enlarged, markedly lobulated and ‘rich’ in cells due to proliferation of mesangial cells (more than 2 cells in a plane section) and accumulation of basement membrane-like material. The capillary walls are thick , their lumens – narrow due to the penetration of mesangium in between the endothelium and basement membrane (so called ‘mesangial interposition’). With silver stain, this phenomenon is seen as a duplication of basement membrane (‘tram rails’ – metaphor)
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Membranoproliferative glomerulonephritis
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Clinical Manifestations
Uremia-specific findings Edemas Hypertension Jugular venous distension (if severe volume overload is present) Pulmonary rales (if pulmonary edema is present) Pericardial friction rub in pericarditis Tenderness in the epigastric region or blood in the stool (possible indicators for uremic gastritis or enteropathy) Decreased sensation and asterixis (indicators for advanced uremia)
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Characteristics of common glomerular diseases at presentation
Heavy proteinuria Proteinuria & haematuria Predominant haematuria Minimal changes Lupus nephritis Acute poststreptococcal glomerulonephritis Focal sclerosis Membranoproliferativeglomerulonephritis RPGN (crescentic) Membranous nephropathy Henoch-Schonlein purpura Haemolityc uraemic syndrome Diabetes mellitus Endocarditis Amyloidosis of kidney
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Acute Nephritic Syndrome
Syndrome characterised in typical cases by: Haematuria Proteinuria (1-3 g/l/24 hours) oliguria oedema hypertension reduced GFR fluid overload
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Nephrotic Syndrome Proteinuria > 3.5g / 24hrs , due to excessive permeability of glomerular capillary wall. Leads to hypoproteinemia, hypoalbuminemia, decreased colloid oncotic pressure and edema. Accompanied by sodium and water retention, hyperlipidemia, vulnerability to infection and thrombotic complications.
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Nephrotic syndrome biopsy histology in adults at different ages
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Indications to perform renal biopsy
Unexplained renal failure Acute nephritic syndrome Nephrotic syndrome Isolated nonnephrotic proteinuria Isolated glomerular hematuria Renal masses (primary or secondary) Renal transplant rejection Connective-tissue diseases (eg, systemic lupus erythematosus)
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Absolute contraindications to renal biopsy include the following:
Uncorrectable bleeding diathesis Uncontrollable severe hypertension Active renal or perirenal infection Skin infection at biopsy site The following are relative contraindications to renal biopsy: Uncooperative patient Anatomic abnormalities of the kidney which may increase risk Small kidneys Solitary kidney
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Treatment of nephrotic syndrome
General measures Dietary sodium restriction Normal protein intake is advisable. A high-protein diet (80–90 g protein daily) increases proteinuria and can be harmful in the long term Infusion of albumin produces only a transient effect. It is only given to diuretic-resistant patients and those with oliguria and uraemia in the absence of severe glomerular damage, e.g. in minimal-change nephropathy. Albumin infusion is combined with diuretic therapy and diuresis often continues with diuretic treatment alone.
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Treatment of nephrotic syndrome
The target pressure for patients with proteinuria greater than 1 g/d is less than 125/75 mm Hg; for patients with proteinuria less than 1 g/d, the target pressure is less than 130/80 mm Hg. Angiotensin-converting enzyme inhibitors (ACEIs) angiotensin II receptor blockers (ARBs) combination therapy with ACEIs and ARBs. Diuretics are often required because of decreased free-water clearance, and high doses may be required to control edema and hypertension when the GFR falls to less than 25 mL/min. Beta-blockers, calcium channel blockers, central alpha-2 agonists (eg, clonidine), alpha-1 antagonists, and direct vasodilators (eg, minoxidil, nitrates) may be used to achieve the target pressure.
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Treatment of nephrotic syndrome
Renal osteodystrophy can be managed early by replacing vitamin D and by administering phosphate binders. Seek and treat nonuremic causes of anemia, such as iron deficiency, before instituting therapy with erythropoietin. Discuss options for renal replacement therapy (eg, hemodialysis, peritoneal dialysis, renal transplantation). Treat hyperlipidemia (if present) Expose patients to educational programs for early rehabilitation from dialysis or transplantation.
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Treatment of edema Loop diuretics (furosemide, torsemide, bumetanide, ethacrynic acid) Secreted in the proximal tubules Have high saluretic effect (decrease sodium reabsorbtion, increase natriuresis) Quick diuretic effect Efficiency is reduced due to decreasing of external cellular fluid Side effects Hypovolemia, hypokalemia, metabolic alcalosis Impaired glucose tolerance Arterial hypotension, irregular heart beat Acute tubulointerstitial nephritis Aplastic anemia, nausea, vomiting Contraindications Hypokalemia, hyponatremia Hypovolemia with or without hypotension Interaction: Salycilates – increasing of toxic effects Cardiac hlycosides, corticosteroids, penicillin – the risk of hypokalemia, hypomagnesemia ACE-inhibitors – decreasing of blood pressure with impairment of renal function NSAIDs – decreasing of hypotension and diuretic effects Indirect anticoagulants – increasing diuresis and hypokalemia Appropriate to use with potassium-sparing diuretics
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Potassium-sparing diuretics (amiloride, triamterene, spironolactone)
Treatment of edema Potassium-sparing diuretics (amiloride, triamterene, spironolactone) Acting in the ultimate part of distal tubules Spironolactone structurrally similar to aldosterone Amiloride and triamterene are not aldosterone antagonists Side effects Vomiting, diarrhea Increasing of asotemia Menstrual disorders, amenorrhea Allergic dermatitis Hyperkalemia Contraindications Anuria Acute renal failure Chronic renal failure III-V st. Interaction: With other diuretics – potentiates their effect; It is recommended to reduce dose up to 50 %
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Treatment of edema Thiazide diuretics (benzothiadiazine, chlorothiazide, hydrochlorothiazide) Acting in the distal tubules Do not change concentration kidney ability Increasing potassium, magnesium, chloride, phosphate excretion with urine Delay the calcium in the body No depend on the acid-base balance of the organism Side effects Gout exacerbation Orthostatic hypotension, tachycardia Photosensitivity Necrotizing vasculitis Hypokalaemia, hyperglycemia Cholestatic jaundice Contraindications Gout Hypersensitivity to sulfonamides Liver insufficiency GFR less than 30 ml/min Diabetes mellitus Interaction: Not combined with potassium-sparing diuretics Ganglioplegic – increasedohypotension
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The most commonly used diuretics in nephrology
Medication Route of administration Initial single dose Maximal dose Top of effect Duration of effect Lasix (furosemide) i/v 0,5-1,0 mg/kg 2-4 mg/kg up to 200mg (in case of ARF mg/kg/24 hrs) 3-5 min 5-6 hours Per os 2-5 mg/kg 30-60 min 7-8 hours Hypothiazide (Hydrochloro- thiazide) 2,5 mg/kg 1 hour 8-12 hours Verospiron (spironolacton) 3-5 mg/kg/24 hours in 2-3 doses 10 mg/kg/24 hours 2-5 days Triamterene mg/24 hours 300 mg/24 hours 15-20 min 12-18 hours
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Treatment Minimal change glomerulonephritis (MCGN)
Acute glomerulonephritis: Prednisolone 1mg/kg/24 hours 4-6 weeks with next reduces of dose and addition of chlorbutin 0,2 mg/kg/24 hours or azathioprine 2 mg/kg/24 hours during of all period of prednisolone receiving In the ineffectiveness of this treatment – cyclosporine A 3-5 mg/kg/24 hours in combination with mild doses of corticosteroids 6-12 weeks Chronic glomerulonephritis: Prednisolone 1mg/kg/24 hours 6-8 weeks to the disappearance or stabilization at the minimum level of proteinuria, further - to 0.5 mg/kg for 4 weeks followed by 5 mg cancellation of in a month. Cytostatics appointed along prednisolone cancellation. Prognosis: 1% progress to ESRF.
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Treatment Focal segmental glomerulosclerosis
Prednisolone 1mg/kg/24 hours 4-16 weeks. If the full or partial remission achieved, cyclophosphamide added 2 mg/kg or chlorbutin 0.15 mg/kg. In the ineffectiveness of this treatment – prednisolone 0,5 mg/kg every other day and cyclosporine A 2-3 mg/kg during 12 monthes Prognosis: 30–50% progress to ESRF.
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Treatment Membranous nephropathy Prednisolone 1mg/kg/24 hours and chlorbutin 0.15 mg/kg or cyclophosphamide 2-3 mg/kg 6-8 weeks In case of relapce or in the ineffectivenes - cyclosporine A 2-3 mg/kg/24 hours 12 monthes in combination with prednisolone 0,5 mg/kg every other day Prognosis: Untreated, 15% complete remission, 9% ESRF at 2–5yrs and 41% at 15yrs
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Treatment Mesangiocapillary glomerulonephritis Treatment: None is of proven benefit Prognosis: 50% develop ESRF Mesangial proliferative GN Antibiotics, diuretics, and antihypertensives as necessary. Dialysis is rarely required. Prognosis: Good.
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Treatment In the absence of morphological verification of diagnosis Prednisolone 1mg/kg/24 hours 6-8 weeks with subsequent dose reduction and addition of chlorbutin 0.2 mg / kg / day or azathioprine 2 mg / kg / day
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