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How are glomerular diseases mediated and how are tubular/interstitial diseases mediated?

Glomerular = immunologically mediated

Tubular/interstitial = toxic or infectious agents



↑ BUN and creatinine levels with ↓ GFR


Prerenal and postrenal azotemia

Prerenal = hypoperfusion of kidneys impairing renal function without parenchymal damage.

Postrenal = obstructed urine flow beyond level of kidney


Uremia and secondary manifestations

failure of renal excretory function, metabolic and endocrine alterations from renal damage.

secondary manifestations in: GI system, peripheral nerves, heart


Nephritic Syndrome

from glomerular disease.

from inflammation in glomeruli.

features: acute onset, hematuria, mild to mod proteinuria, HTN, red cell casts in urine, azotemia, oliguria.

classically: acute poststreptococcal glomerulonephritis


Rapidly progressive glomerulonephritis

nephritic syndrome with rapid decline in GFR.


Nephrotic Syndrome

  • from glomerular disease.
  • deranged capillary wall ⇒ ↑ permeability to plasma proteins (↑ proteinuria) ⇒ hypoalbuminemia and reversed albumin:globulin ratio.
  • ↓ colloid osmotic pressure and Na/water retention ⇒ edema
    • most markedly in periorbital regions.  also ascites and pleural effusions.
  • hypogammaglobulinemia ⇒ ↑ risk infection.
  • hypercoagulable state - from loss of antithrombin III.
  • ↑ synthesis lipoproteins in liver, abnormal transport of circulating lipid particles, and ↓ catabolism ⇒ hyperlipidemia and hypercholesterolemia may ⇒ fatty casts in urine, oval fat bodies or free fat in urine.
  • in kids: primary kidney lesion ⇒ minimal change disease, membranous GN (older adults), and FSGS (all ages).
  • in adults: from systemic diseases = SLE, diabetes, amyloidosis
  • features: heavy proteinuria (>3.5gm/day), hypoalbuminemia, severe generalized edema, hyperlipidemia, lipiduria, hypogammaglobulinemia


Asymptomatic Hematuria/Proteinuria

manifestation of subtle or mild glomerular abnormalities.


Acute Renal Failure

features: oliguria or anuria, recent onset azotemia from glomerular, interstitial, or vascular injury or acute tubular injury. frequently reversible.


Chronic Renal Failure

prolonged signs and symptoms of uremia. is end result of all chronic renal parenchymal diseases.

major cause of death from renal disease.


Renal Tubular Defects

features: polyuria, nocturia, electrolyte disorders (metabolic acidosis).

from direct effect on tubular structure or from defects in tubular functions (can be inherited or acquired).



features: bacteriuria and pyuria.

symptomatic or asymptomatic.

may affect kidney or bladder



aka renal stones

features: severe spasms of pain (renal colic) and hematuria.


Urinary Tract Obstruction

includes renal tumors.


4 Stages of Chronic Renal Failure

1. diminished renal reserve: GFR = 50%, serum BUN and creatinine are normal, patients asymptomatic but susceptible to azotemia.

2. renal insufficiency: GFR = 20-50%, azotemia with anemia and HTN, polyuria, nocturia. sudden stress can ⇒ uremia.

3. chronic renal failure: GFR < 20-25%, edema, metabolic acidosis, hyperkalemia. cannot regulate volume and solute composition. overt uremia with neurologic, GI, and cardiovascular complications.

4. end-stage renal disease: GFR < 5%. terminal stage of uremia.


Systemic Diseases Associated with Glomerular Disease

diabetes mellitus, SLE, vasculitis, amyloidosis, Goodpasture syndrome, microscopic polyarteritis/polyangiitis, Wegener granulomatosis, Henoch-Schonlein purpura, bacterial endocarditis


Glomerulus Anatomy


endothelium: thin, fenestrated.

glomerular basement membrane: thick electron-dense central layer (lamina densa), thinner electron-lucent peripheral layers (lamina rara externa and interna).  made of type IV collagen, laminin, proteoglycans (heparan sulfate), fibronectin, entactin, glycoproteins.

visceral epithelium: aka podocytes.  interdigitating processes adherent to lamina rara externa.  foot processes are separated by filtration slits which have a thin diaphragm.

mesangial cells: lies in mesangial matrix.  mesenchymal origin. contractile, phagocytic, and can proliferate, lay down matrix and collagen, and secrete mediators.


Normal Glomerular Filtration Barrier Characteristics

  • highly permeable to water and small solutes.  impermeable to proteins like albumin (70kD) or larger.
  • charge selector: more cationic can pass, anionic do not.  determined by proteoglycans of GBM and sialoglycoproteins of epithelial/endothelial cell coats (glycocalyx)
  • slit diaphragm allows for size selection.  important proteins in diaphragm: nephrin, podocin, CD2AP.
  • nephrin connects foot processes by attaching to podocin, CD2AP, and the actin cytoskeleton.



  • has PI of 4.5.
  • completely excluded from filtrate by size-charge barrier



  • part of the slit diaphragm.
  • connects foot processes by attaching to podocin, CD2AP, and the actin cytoskeleton.



  • part of the foot process of podocytes. 
  • via nephrin, helps link foot processes at slit diaphragm.



  • part of the foot process of podocytes.
  • via nephrin, helps link foot processes at slit diaphragm.



  • in inflammatory diseases of kidney.  
  • characterized by:  cellular proliferation of mesangial or endothelial cells, leukocytic inflitration (neutrophils, monocytes, lymphocytes), and/or formation of crescents



  • accumulations of cells composed of proliferating parietal epithelial cells and infiltrating leukocytes.  
  • fibrin may elicit the crescentic response.  find it in glomerular tufts and urinary spaces.  
  • others that elicit crescentic formation: tissue factor, IL-1, TNF, IFN-gamma


Basement Membrane Thickening

  • on PAS stain: see thickening of capillary walls
  • EM: has two forms:
  • 1. immune complex deposits on endothelial or epithelial side of GBM or within the GBM.  fibrin, amyloid, cryoglobulins, and fibrillary proteins can deposit in GBM.
  • 2. increased synthesis of protein components (see in diabetic glomerulosclerosis).



  • accumulation of material that is homogenous and eosinophilic by light microscopy.
  • EM: hyalin is extracellular and amorphous.  
  • made of plasma proteins insudated from circulation
  • extensive ⇒ obliteration of capillary lumens of glomerular tuft.
  • consequence of endothelial or capillary wall injury, end result of glomerular damage.  
  • found in focal segmental glomerulosclerosis



  • accumulations of extracelular collagenous matrix, confined to mesangial areas (diabetic glomerulosclerosis) or involving capillary loops.
  • can ⇒ obliteration of capillary lumens ⇒ form fibrous adhesions between sclerotic portions and parietal epithelium and Bowman capsules.


Primary Glomerulopathy Categories

  • diffuse = involving all glomeruli
  • global = involving entire glomerulus
  • focal = involves only a portion of the glomeruli
  • segmental = affects part of each glomerulus
  • capillary loop or mesangial = affects predominantly the capillary or mesangial regions.


Antibody-associated Injury

  • 1. antibodies reacting in situ within glomerulus, binding to insoluble fixed glomerular antigens or to molecules planted within glomerulus.
  • 2. deposition of circulating antigen-antibody complexes in glomerulus. 


Heymann Nephritis

  • on EM: presence of numerous discrete electron-dense deposits along subepithelial aspect of GBM.
  • IF: granular lumpy deposition.
  • results from rxn of antibody with antigen comlex on basal surface of visceral epithelial cells and cross-reacting with brush border antigen. then complement activation and shedding of aggregates to form subepithelial deposits.
  • antigen = megalin = lipoprotein receptor (in rats)
  • anti-GBM antibody induced disease = autoimmune.