Overview of renal pathology and its importance in understanding kidney diseases.
Discussion of the basic histology of the kidney, which aids in diagnosing diseases.
Key Components of Renal Tissue
Glomerulus
Tuft of capillaries that filter blood.
Renal Tubules
Responsible for reabsorbing substances such as electrolytes.
Blood Vessels
Interstitium
Supports renal tissue, including the two poles.
Clinical Syndromes in Renal Diseases
Renal diseases exhibit a limited number of symptoms classified into clinical syndromes:
Nephrotic syndrome
Nephritic syndrome
Acute and chronic renal failure.
Importance of Knowledge in Diagnosis
Understanding normal kidney structure and functions is crucial in diagnosing renal diseases.
Correlation of light microscopy findings with immunofluorescence and electron microscopy is important, though only light microscopy will be observed in the pre-lab.
Glomerulus Structure
Vascular structure composed of specialized fenestrated capillaries.
Capillaries arranged in lobules and supported by a mesangium.
Bowman's space is the lumen surrounding the capillaries, lined by simple squamous epithelial cells.
Podocytes: Epithelial cells with tiny foot processes, seen on electron microscopy.
Hydropic Change of the Kidney
Definition: Reversible cell injury due to toxic damage.
Characterized by swollen renal tubules and accumulation of water inside the cells.
Reversible injury: nucleus is present with no necrosis features such as karyolysis.
Acute Kidney Infarct
Occurs when blood supply is diminished or cut off.
Commonly due to embolism, often from myocardial infarction.
Classification: White infarcts due to arterial occlusion.
Microscopic Features: Coagulative necrosis, preserved architecture, hypodemic areas due to congestion, absence of nuclei, and increased eosinophilia.
Acute Glomerulonephritis (Post-Streptococcal)
Characterized by diffuse endocapillary proliferation of glomerular cells due to immune complex deposition (type 3 hypersensitivity).
Common symptoms: hematuria, proteinuria, azotemia, hypertension.
Microscopic Features: Hypercellularity of glomeruli due to inflammatory cell infiltration and mesangial proliferation.
Immunofluorescence: Granular appearance of IgG and C3 deposits.
Electron Microscopy: Sub-epithelial electron dense deposits (humps).
Goodpasture Syndrome
An autoimmune disease with autoantibodies against the glomerular basement membrane.
Can also affect the lungs (pulmonary symptoms, hemoptysis).
Microscopic Features: Crescent formation within Bowman's space; proliferation of epithelial cells and macrophage infiltration.
Staining: Linear deposition of IgG and C3 along the basement membrane.
Membranous Nephropathy
Most common cause of nephrotic syndrome in adults, characterized by diffuse glomerular wall thickening.
Caused by immune complex deposition on the sub-epithelial side of the basement membrane.
Symptoms: heavy proteinuria, hypoproteinemia, edema, hypertension.
Microscopic Features: Absence of hypercellularity and inflammatory cells, thickened capillary walls.
Immunofluorescence: Granular appearance of immunoglobulins and complement.
Electron Microscopy: Sub-epithelial deposits with spikes (due to basement membrane deposits).
Membranoproliferative Glomerulonephritis (MPGN)
Characterized by hypercellularity due to mesangial activation and infiltration of inflammatory cells.
Microscopic Features: Double contour/tram track appearance of the basement membrane.
IgA Nephropathy (Berger's Disease)
Most common cause of glomerulonephritis worldwide.
Characterized by IgA deposits in mesangial regions, leading to mesangial proliferation.
Symptoms: Hematuria following infections in the respiratory or gastrointestinal tract.
Microscopic Features: Glomerular hypercellularity and hyalinosis in the mesangium.
Immunofluorescence: Mesangial deposition of IgA and C3.