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![ May occur in typical form or
in association with nephritic
syndrome
Classification
Primary
Minimal-change
nephropathy
Focal glomerulosclerosis
Membranous nephropathy
Hereditary nephropathies
secondary
Diabetes mellitus
Lupus erythematosus
Viral infections (eg,
hepatitis B, hepatitis C,
human immunodeficiency
virus [HIV] )
Amyloidosis and
paraproteinemias
Preeclampsia
Allo-antibodies from
enzyme replacement
therapy](https://image.slidesharecdn.com/glomerulonephritis-240405024803-911b2a8d/85/GLOMERULONEPHRITIS-disease-description-pptx-28-320.jpg)
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GLOMERULONEPHRITIS disease description pptx
- 1.
- 2. AGN A specificset of kidney diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result to damage of the basement membrane or capillary endothelium Acute nephritic syndrome is the most serious of these syndromes AGN progresses to chronic GN in -30% APSGN is the archetype of AGN: incidences have fallen
- 3. GN associatedwith Staph aureus increasing due to increased antibiotic resistance to staph aureus
- 4. GN classification Immune-complexglomerulonephritis (including infection-related glomerulonephritis, IgA nephropathy, lupus nephritis) Antineutrophil cytoplasmic antibody (ANCA)–associated glomerulonephritis Anti-glomerular basement membrane glomerulonephritis C3 glomerulopathy Monoclonal immunoglobulin–associated glomerulonephritis – abnormal immunoglobulins
- 5. AGN Manifestswith sudden onset of haematuria , proteinuria, and RBC casts in urine Also usually accompanied by htn , edema, azotemia, renal salt and water retention Can be due to primary or sec renal disease
- 6. AGN Pathophysiology Resultfrom glomerular deposition or in situ formation of immune complexes : kidneys may be enlarged upto 50% of cases PSGN: Streptococcal protein neuraminidase may alter host IgG IgG/ antiIgG immune complexes form and collect in the glomeruli Other antibody titers to other antigens elevations (evidence of a recent poststreptococcal infection)=ASOT, antihyaluronidase, DNAase-B, streptokinase
- 7. Structural and functionalchanges Cellular proliferation of endothelial, mesangial and epithelial cells in the glomerular tuft Proliferation is in the glomerulus and bowman space Proliferation of parietal epithelial cells leads to the formation of crescents, a feature xstic of rapidly progressive GN Leukocytes proliferation within the glomerular capillary Thickening of basement memb Functional changes: proteinuria, hematuria, low GFR, urine sedments with RBCs and RBC casts
- 8. Etiology 1. Infectious Strepspp GABH Serotype 12: upper airway infection Serotype 49: skin infection Usually dvps 1-3 wks post infection Incidence 5-10% and 25% in pharyngitis and skin infection respectively Staph Other strep Mycobacteria Salmonella typhosa Brucella suis T.pllidum
- 9. CMC EBV COXSACKIE Hep b Rubella Mumps Hep A C. immitis P.Malariae Schistosoma mansoni Toxoplasma gondii Wuchereria bancrofti Trichinella Trypanasomes
- 10. Aetiology 2. Non infectious Primary kidney disease Membranoproliferative GN: Due to expansion & proliferation of mesangial cells as a consequence of complement deposition IgA Nephropathy:diffuse mesangial deposition of IgA and IgG Idiopathic rapidly progressive GN-xcterised by presence of glemerular crescents Sytemic diseases Vasculitis Collagen vascular disease e.g. SLE Polyarteritis nodosa Good pasture syndrome: autoantb against lungs and kidneys
- 11. Miscellaneous noninfectious AGN causes GBS Irradiation of wilms tumor DPT vaccine Covid 19 vaccine
- 12. Prognosis Most epidemiccases follow a course ending in complete recovery Sporadic cases of acute nephritis often progress to chronic In PSGN long term prognosis is generally good , more than 98% of individuals are asymptomatic after 5 yrs Within a week of onset , most PSGN patients experience spontaneous resolution of fluid retention, and HTN.Proteinuria may persist for 6 months and microscopic haematuria upto 1 yr Eventually, all urinary abnormalities should disappear, hypertension should subside, and kidney function should return to normal GN is the most common cause of CKD
- 13. The prognosisfor nonstreptococcal postinfectious glomerulonephritis depends on the underlying agent, which must be identified and addressed MRSA associated nephritis usually resolves after treatment
- 14. Patient education Saltrestriction during acute phase Bp monitoring Ongoing long term monitoring Consideration of protein restriction and ACE Early antibiotic rx for close contacts
- 15. Presentation History:Identification ofunderlying cause, abrupt onset, Usually a boy, 2-14 yrs, sudden puffiness,edema of face with hx of poststreptococcal infection. Dark urine, scanty, high BP,,,fevers, weakness,malaise, abdominal pains Anorexia Itching , easy bruising, nose bleeds, Sob , leg edema , dyspnoea Haematuria, oliguria, Flank pain- stretching of renal capsule
- 16. Symptoms specific tounderling diseases Triad of sinusitis, pulmonary infiltrates, and nephritis, suggesting granulomatosis with polyangiitis (Wegener granulomatosis)- a rare disorder where blood vessels become inflammed leading to damage in major organs Nausea and vomiting, abdominal pain, and purpura, observed with Henoch-Schönlein purpura-inflammation of the small blood vessels of the skin, joints, bowels and kidneys Arthralgias, associated with systemic lupus erythematosus (SLE) Hemoptysis, occurring with Goodpasture syndrome or idiopathic progressive glomerulonephritis Skin rashes, observed with SLE
- 17. PE Normal includingBP Often a combination of edema, HTN and oliguria Periorbital / pedal edema Crackles Elevated JVP Ascites and pleural effusion Rash pallor CVA tenderness Hematuria, microscopic or gross Abnormal neurological exam: HTN, Urea Arthritis Pharyngitis, impetigo, murmur Weight gain
- 18. Complications Kidney failure Severe proteinuria: anasarca and htn Hypertensive retinopathy Hypertensive encephalopathy CKD Nephrotic syndrome
- 19. DDX Renal syndromescommonly mimick early stage AGN Chronic GN with an acute exacerbation Idiopathic hematuria Familial nephritis –Alport syndrome(hearing loss/ocular abnormalities) AKI Goodpasture syndrome Lupus nephritis Membrenoproliferative GN PSGN
- 20. Workup Urinalysis Protein Blood Red blood cells (RBCs) White blood cells (WBCs) Cellular (ie, RBC,WBC) casts Oval fat bodies Presence of RBC casts is almost pathognomonic of GN Urine sodium CBC BUN/C/E Complement levels
- 21. The antistreptolysinO (ASO) titer is increased in 60-80% of patients. The increase begins in 1-3 weeks, peaks in 3-5 weeks, and returns to normal in 6 months.ASO titer is unrelated to severity, duration, or prognosis of kidney disease. Increasing ASO titers confirm recent infection. In patients with skin infection, anti-DNAase B (ADB) titers are more sensitive than ASO titers for infection with Streptococcus
- 22. Cultures throatand skin Blood culture: IVDU, iss, indwelling shunts Triglyceride levels Hepatitis B and C serologies Antineutrophil cytoplasmic antibody (ANCA)
- 23. u/s Kidneybiopsy
- 24. Treatment Treat theunderlying infection Antimicrobial therapy does not appear to prevent the development of glomerulonephritis, except if given within the first 36 hours. Antibiotic treatment of close contacts of the index case may help prevent development of PSGN. Loop diuretics Vasodilators in severe hypertension Glucocorticoids and cytotoxics are of no value except in severe cases of PSGN
- 25. Lifestyle changes Sodiumand water restriction Limit protein intake Calcium supplements Healthy diet and exercise Physiotherapy
- 26.
- 27. A combinationof Nephrotic range proteinuria >3g/day or on a single spot urine collection the presence of 2g/g of urine creatinine Low serum albumin Edema
- 28. May occurin typical form or in association with nephritic syndrome Classification Primary Minimal-change nephropathy Focal glomerulosclerosis Membranous nephropathy Hereditary nephropathies secondary Diabetes mellitus Lupus erythematosus Viral infections (eg, hepatitis B, hepatitis C, human immunodeficiency virus [HIV] ) Amyloidosis and paraproteinemias Preeclampsia Allo-antibodies from enzyme replacement therapy
- 29. From therapeuticperspective Steroid sensitive Steroid resistant Ssteroid dependent Frequently relapsing.
- 30. PATHOPHYSIOLOGY <0.1% plasmaalbumin pass glomerular filtration barrier in healthy persons Urine albumin in health is <50mg/day >500mg/day point to glomerular disease Glomerular caps endothelium are fenestrated Sits on GBM GBM covered by glomerular epithelium(podocytes) In nephrotic syndrome there is damage to endothelial surface, GBM or the podocytes Glomerular filtration barrier –filtration slits
- 31. Congenital nephroticsyndrome : Finnish type-mutated nephrin gene Podocin gene mutation
- 32. Theories foredema Underfill hypothesis –albuminuria- hypoalbuminaemia Overfill hypothesis-filtered intraluminal protein stimulate renal epithelial sodium reabsorption 2 facts favour this sodium retention is observed even before the serum albumin level starts falling Intravascular volume is normal or even increased in most patients with nephrotic syndrome.
- 33. Proteinuria consequences Infection Hyperlipidaemia and atherosclerosis Hypocalcemia and bone abnormalities Hypercoagulability Hypovolaemia Htn Gut edema Ascites and pleural effusion
- 34. 1. Infection Amajor concern in nephrotic syndrome Varicella infection common Most common infectious complications are bacterial sepsis, cellulitis, pneumonia, peritonitis Urinary immunoglobulin losses Edema fluid acting as a culture medium Protein deficiency Decreased bactericidal activity of the leukocytes Immunosuppressive therapy Decreased perfusion of the spleen caused by hypovolemia Urinary loss of a complement factor that opsonizes certain bacteria
- 35. 2. Hyperlipidaemia Hypoproteinaemialeads to reactive hepatic protein synthesis including of apolipoproteins and lipoproteins Reduced serum levels of lipoprotein lipase leads to reduced lipid catabolism Some lipoproteins filtered in kidneys :lipiduria and classic finding of oval fat bodies and fatty casts in urine
- 36. 3. Hypocalcaemia Lossof vitamin D binding proteins in urine Hypovitaminosis D Reduced intestinal calcium absorption
- 37. Hypercoagulability Risk forVTEs-renalven thrombosis Urinary loss of anticoagulants Loss of Antithrombin III and plasminogen Increase in clotting factors I,VII,VIII and X Protein C and S Altered levels and activity Hyperfibrinogenemia –increased hepatic synthesis Impaired fibrinolysis due to decreased plasminogen Increased plt aggregability Alteration in endothelial function
- 38.
- 39. Etiology Minimal changedisease, membraneous nephropathy, focal glomerulosclerosis StimulateT cells , release cytokines, damage podocytes Medications – NSAIDs, gold, penicillamine, lithium, anticancer drugs, Has been reported following Covid 19 infection and vaccination
- 40. Presentation History : Swelling of face Dependent edema Foamy urine Fatigue Loss of appetite Thrombotic event Recent start of a drug e.g NSAID
- 41. PE Ddx Edema Haematuria Htn Heart failure Cirrhosis Dm nephropathy HIV associated nephropathy Radiation nephropathy
- 42. Workup Urinalysis Urineprotein:urine creatine ration >2g/g corresponds to >3gram protein/day Urine sediment examination Urinary protein measurement Serum albumin Serologic studies for infection and immune abnormalities Renal ultrasonography Kidney biopsy
- 43. Important definitions Response:protein free urine on 3 consequtive days within 7 days Relapse: Protein +ve urine on 3 consequtive days within one week Frequent relapsing : steroid sensitive NS with 2 or more relapses in 6 months or > 3 in 1 year Steroid dependant:responders who relapses while steroid is being tapered or within 14 days of stopping steroid treatment Initial non responders: No response during initial 8 weeks of rx Late non responders:Initial steroid responder who fails to respond to 4 week treatment in relapse
- 44. Treatment Specific treatmentdepends on the cause Diuretics Anticoagulation Statins ARB/ACE for secondary nephrotic syndrome
- 45. Specific treatment Minimalchange nephropathy 70-80% of NS: Glucocorticoids e.g prednisolone It is Idiopathic loss of net negative charge in cap BM Sec causes:Infections , NSAIDs, Hodgkins lymphoma StimulateT cells-cytokines destroy podocytes Membraneous nephropathy:Primary:antiPLA2R receptor antibody. Attacks a protein in podocytes. Sec: HBA/B, syphillis,Gold, Penicillamine. Antibodies deposit in subepithelial region, inflammation, activation of compliment system, podocyte effacement Watchful waiting,Rituximab or cyclophosphamide+/- glucocorticoids
- 47. Focal segmental glomerulosclerosis Can be primary-idiopathic Sec: HIV,SCD, Heroin use Sclerosis of parts of the glomerulous leading to podocyte effacement Longterm immunosupressants In all treat the sec cause
- 48. In alltreat the sec cause In primary cause start on steroids Good response usually indicates MC disease.Bx may not be necessary Poor response ?FSGS Longterm immunosupressants
- 49. Diet Low sodium<2g/day (24hr urine<88mEq/day
- 50. LONGTERM MONITORING Adjustmentsfor diuretics Immunizations :Pneumococcal and influenza Monitoring corticosteroid toxicity every 3 months Supplemental vit D and Calcium may attenuate bone loss