Nephrotic syndrome Undergaraduate
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The document discusses nephrotic syndrome, characterized by significant proteinuria, hypoalbuminemia, edema, hyperlipidemia, and hypercoagulability. It outlines diagnosis criteria, common causes, and treatment options, emphasizing the importance of managing underlying conditions and complications. Various types of nephrotic syndrome are highlighted, along with their incidence rates and treatment responsiveness.
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Nephrotic syndrome Undergaraduate
- 1. Dr Ashutosh Ojha Reader, Internal Medicine 17 Feb2016Dr A Ojha
- 2. Clinical complex characterized by a number of renal and extra renal features.The most prominent being. Proteinuria of > 3.5 g/d Hypoalbuminaemia Oedema Hyperlipidaemia Hypercoagulability. 17 Feb2016Dr A Ojha
- 3. Key component is proteinuria ◦ Results from altered permeability of glomerular filtration barrier(GBM,podocytes& their slit diaphragm) for proteins ◦ All other metabolic complications are secondary to urine protein loss. 17 Feb2016Dr A Ojha
- 4. Proteinuria Loss of lipid metabolism Sr Albumin regulating protein Oncotic pressure Oedema Hepatic lipoprotein synthesis Hyperlipdaemia 17 Feb2016Dr A Ojha
- 5. Altered level of Urinary loss of protein C and S Antithrombin III Hyperfibrinogenaemia Impaired fibrinolysis Platelet aggregability Hypercoagulability Peripheral arterial and venous thrombosis Renal vein thrombosis Pulmonary embolism 17 Feb2016Dr A Ojha
- 6. Other metabolic complications. ◦ Protein malnutrition ◦ Iron resistant microcytic hypochromic anaemia ◦ Hypocalcaemia ◦ Vit D deficiency ◦ Secondary hypoparathyroidism ◦ thyroxin levels ◦ IgG 17 Feb2016Dr A Ojha
- 7. Damage to GBM o Number & size of pores Passage of more and larger proteins o in fixed negatively charged components ( Repel negatively charged protein molecules ) 17 Feb2016Dr A Ojha
- 8. 17 Feb2016Dr A Ojha
- 9. 6 entities account for >90% in adults ◦ Minimal change disease(MCD) ◦ Focal & segmental glomerulosclerosis(FSGS) ◦ Membranous glomerulopathy. ◦ Membrnoproliferative GN (MPGN). ◦ Diabetic nephropathy. ◦ Amyloidosis 17 Feb2016Dr A Ojha
- 10. Systemic vasculitis eg-SLE Drugs ◦ Penicillamine ◦ Captopril ◦ Gold ◦ Cadmium Allergic reactions ◦ Pollens ◦ Bee sting 17 Feb2016Dr A Ojha
- 11. History. ◦ Frothy urine –heavy proteinuria ◦ Oedema-Periorbital,arms.ascites,genital oedema. ◦ BP in some. ◦ Features of underlying disease viz SLE,DM ◦ Rule out Primary cardiac failure Chronic liver disease 17 Feb2016Dr A Ojha
- 12. Diagnosis established by ◦ 24 hr urinary protein >3.5g/day ◦ Sr Albumin <3g/dl 17 Feb2016Dr A Ojha
- 13. Cholesterol, LDL, triglycerides Urea, Creatinine ---- progressive disease Urine microscopy—RBC,RBC casts Throat swab Streptococcal infection ASO titer C3 level-immune complex mediated ANA HBsAg&HCAntibodies Cryoglbulinaemia 17 Feb2016Dr A Ojha
- 14. Sr electrophoresis - MM Blood glucose.—DM Selective proteinuria—MCD,diabetic nephropathy,amyloidosis. Non selective proteinuria—Diffuse proliferative GN 17 Feb2016Dr A Ojha
- 15. Gradual onset of acute renal failure No obvious cause of acute renal failure Heavy proteinuria Significant haematuria Clinical evidence or history of systemic disease Prolonged oliguria 17 Feb2016Dr A Ojha
- 16. Not required in ◦ Young children with highly selective proteinuria,no HTN,no red cells or red cell casts in urine ◦ Long standing insulin dependent diabetes mellitus ◦ On drugs like penicillamine. 17 Feb2016Dr A Ojha
- 17. Specific treatment of underlying cause. Drugs- immunosuppressive therapy. General measures to control proteinuria. General measures to control complications. 17 Feb2016Dr A Ojha
- 18. 80% cases < 16yrs, 20% cases in adults. Peak incidence 6-8yrs Idiopathic. Occurrence after URTI, immunization. incidence in HLA B12. May be associated with interstitial nephritis, lymphomas. 17 Feb2016Dr A Ojha
- 19. High mol wt proteinuria. Benign urinary sediment. Microscopic haematuria in 20-30% cases. HTN & RF -----rare 17 Feb2016Dr A Ojha
- 20. Glomerular size & structure – normal in light microscopy. Immunoflorescense studies –neg for Ig & C3 Electron microscopy Diffuse effacement of foot processes of visceral epithelial cells. 17 Feb2016Dr A Ojha
- 21. 17 Feb2016Dr A Ojha
- 22. Highly steroid responsive . Excellent prognosis. Spontaneous remission in 30-40% children. Remission with 8 wks of high dose glucocorticoids in 90% of children, 50% of adults. 17 Feb2016Dr A Ojha
- 23. Dose Children: 60 mg/mt2/day x 4 wks 40 mg/mt2/day x 4 wks Adults: 1.15mg/kg/day x 4 wks 1mg/kg/day x 4 wks 50% relapse fallowing withdrawal. 17 Feb2016Dr A Ojha
- 24. Relapse during / shortly after withdrawal Relapse - >3 / yr Cyclophosphamide- 2-3 mg/ kg /day 8 –12 wks or Chlormabucil- 0.1-0.2 mg/ kg /day 8 –12 wks Side effects-infertility, cystitis, alopecia, infections, sec malignancies. Cyclosporin can be tried in those resistant to above . 17 Feb2016Dr A Ojha
- 25. Sclerosis with hyalinosis involving portions of < 50% glomeruli in a tissue section. 1/3 cases of nephrotic syndrome in males. Proteinuria with HTN and mild renal insufficiency. 17 Feb2016Dr A Ojha
- 26. 17 Feb2016Dr A Ojha
- 27. Spontaneous remission rare. Prognosis poor. Drug therapy unsatisfactory. Renal transplant. 17 Feb2016Dr A Ojha
- 28. 30-40% of NS in adults. Rare in children. Peak incidence 30-50 yrs. 1/3 rd assocition with systemic diseases like SLE, infections, malignancy, HBV, drugs. 17 Feb2016Dr A Ojha
- 29. 17 Feb2016Dr A Ojha
- 30. Light microscopy- diffuse thickening of GBM with e/o cellular infiltration. Electron microscopy- immune deposits of IgG & C3 17 Feb2016Dr A Ojha
- 31. Proteinuria- non selective Microscopic hematuria in 50%. RBC casts, leukocytes, macroscopic hematuria are rare. HTN 10-30%. 40% remit spontaneously, 10-20% slowly progressive ESRD, others remit & relapse. 17 Feb2016Dr A Ojha
- 32. Steroids- unsatisfactory. Cytotoxic drugs- some benefit. 17 Feb2016Dr A Ojha
- 33. Features -Thickening of GBM - proliferative changes. -diffuse increase in mesangial cells and matrix. -immune deposits- C3, IgG, IgM, IgA. 17 Feb2016Dr A Ojha
- 34. In association with -IE -HIV -HBV, HCV -Cryoglobulinaemia -Lymphoma 17 Feb2016Dr A Ojha
- 35. Heavy proteinuria Active urinary sediment Normal to mildly impaired renal function. Course- benign to ESRD. No effective treatment. 17 Feb2016Dr A Ojha
- 36. ACE inhibitors- act by ↓ intraglomerular pressure and prevent hemodynamically mediated focal segmental glomerulosclerosis. Specially in DM, FSGS. NSAIDS- act by altering glomerular hemodynamics& permeability. 17 Feb2016Dr A Ojha
- 37. Edema- salt restriction 1-2 gms/ day Loop diuretics Hyperlipidaemia- statins Thromboembolism- anticoagulation. Malnutrition- ? High protein diet. Vitamins D supplements 17 Feb2016Dr A Ojha
- 38. Thank You 17 Feb2016Dr A Ojha
- 39. Contact-9719713786 [email protected] [email protected] 17 Feb2016Dr A Ojha