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Renal histology and glomerular disorders
- 1. The Kidney (Glomerulus) Dr.Vaheda K. M.D Associate Professor Dept. of Pathology, NMCH
- 3. Basic morphologic components: Four Glomeruli Tubules Blood vessels Interstitium
- 5. Glomeruli – Glomerulardisorders/ Glomerulo pathies Tubules – Tubular disorders Interstitium - Interstitial disorders Blood vessels - Vascular disorders
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- 7. Glomerular diseases • Primaryglomerular diseases • Secondary glomerular diseases
- 8. Primary glomerular diseases 1.Etiology 2.Mechanismof Injury ( pathogenesis) 3.Histological pattern 4.Clinical manifestations
- 9. • Etiology: ImmunologicalInsults • Mechanisms of Glomerular Injury (Pathogenesis) : Antibody-Mediated Injury ( Type - 2 ) Circulating Immune Complex Deposition ( Type – 3 ) Cell-Mediated Immune Injury ( Type – 4 )
- 10. Understanding The Languageof Glomerulus ..! Histological Features Of Glomerular Diseases
- 12. Basement Membrane Thickening Immunecomplex deposition Increased protein in GBM Additional layers of BM matrices Hypercellularity Infiltration of leukocytes Proliferation of mesangial or endothelial cells Formation of crescents Hyalinosis and Sclerosis Extracellular homogenous material Extracellular collagenous matrix
- 13. Basement Membrane Thickening Immunecomplex deposition Increased protein in GBM Additional layers of BM matrices Hypercellularity Infiltration of leukocytes Proliferation of mesangial or endothelial cells Formation of crescents Hyalinosis and Sclerosis Extracellular homogenous material Extracellular collagenous matrix
- 14. • Terminology • Diffuse-> Involving all of the glomeruli in the kidney • Focal -> Involving only a fraction of the glomeruli in the kidney • Global -> Involving the entirety of individual glomeruli • Segmental -> Affecting a part of each glomerulus
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- 18. • Mesangioproliferative glomerulonephritis •Membranoproliferative glomerulonephritis • Rapidly proliferating glomerulonephritis/Crescentic GN • Focal Segmental glomerulosclerosis
- 19. Understanding The Languageof Glomerulus ..! The Clinical manifestations
- 20. Clinical Manifestations ofGlomerular Diseases • Isolated urinary abnormalities • Nephrotic syndrome • Nephritic syndrome • Rapidly progressive glomerulonephritis • Chronic kidney disease
- 22. • Size barrier •Charge barrier • Different degree of injury to the filtration membrane presents with different features..! • Very mild injury: Smallest molecule will start leaking..! Albumin- albuminuria “Selective proteinuria”
- 23. • Mild injury: •Membrane is more leaky • Albumin+Globulin -> <3.5gms/day • Nonselective proteinuria • Moderate injury: • >3.5gms/day – Heavy proteinuria • AKA “Nephrotic range of proteinuria”
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- 25. Edema Low blood volume Renalhypo perfusion RAAA Na,H2O reabsorption-> but low oncotic pressure due to proteinuria, volume cant stay intravascularly..! Acc.Edema Hemoconcentrated -> Hypothalamus -> ADH -> Edema Lipoprotein levels -> disturbed LP -> Hyperlipidemia “Lipiduria”
- 26. • Heavy proteinuria •Hypoproteinaemia • Edema • Dyslipidemia • Lipiduria “Nephrotic Syndrome” Nephrotic syndrome is only “Clinical face”…! Different causes can lead to one common clinical picture / One clinical picture can be the result of different causes..!
- 27. • Other smallmolecular weight proteins that are lost: • Transferrin – IDA • Anti thrombin – “Pro coagulation” -> Renal vein thrombosis • Loss of Igs -> life threatening infections • Frothy urine- high protein loss
- 28. • Severe injury: Inflammatorylesions in the glomeruli Non selective proteinuria + RBC leak..! Blocked /Jammed tubules -> dysmorphic RBC Clogged glomeruli -> Decreased GFR-> Oliguria! Decreased excretion of Urea and Creatinine -> Azotemia..!
- 29. Decreased GFR Decreased filtration-> Decreased total loss of protein -> worsening injury infact..! RAAA -> Salt and water retention -> But now the volume can actually stay in intra vascular compartment…! -> HTN • Hematuria , Dysmorphic RBC • Oliguria, Azotemia • Hypertension • Proteinuria ( non Nephrotic range) “Nephritic syndrome”
- 31. • Very Severeinjury: • Albumin, globulin , RBC , RBC casts AND Fibrin molecules..! • Act as Growth factors -> proliferating epithelial cells -> urinary space is filled with cells cellular “CRESENTS” “Cresenteric Glomerulo Nephritis” Clinically: Presents as rapidly progressive loss of kidney function Uremia affecting all systems AKA “RPGN”
- 32. Glomerular Diseases Primary Glomerulopathies- classified by their histology..! Acute proliferative glomerulonephritis – APGN Rapidly progressive (Crescentic) glomerulonephritis – RPGN Minimal change disease- MCD Focal segmental glomerulosclerosis - FSGS Membranoproliferative glomerulonephritis - MPGN Systemic Diseases With Glomerular Involvement SLE DM Amyloidosis Heriditary
- 33. • Histological patternsthat present with Nephritic syndrome: • APGN • RPGN • Histological patterns that present with Nephrotic syndrome: • Membranous nephropathy • Minimal change disease • Focal segmental glomerulosclerosis • Dense deposit disease • IgA nephropathy
- 34. How do youApproach a Patient..? Determine the degree of injury Put him in a box of symptoms That degree of symptoms are offered by certain histological pictures only..! Confirm the histologic picture – Call “ME” Go back and search which etiological agents can likely cause this histologic picture..? Find the cause, Surrogate tests ,Give the Diagnosis , Treat..!