XIV - The Kidneys and Its Collecting System Flashcards
A glomerular syndrome dominated by the acute onset of usually grossly visible hematuria, mildly moderate proteinuria, azotemia, edema and hypertension.
Acute nephritic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
A glomerular syndrome characterized by heavy proteinuria, hypoalbunemia, severe edema, hyperlipidemia and lipiduria.
Nephrotic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
Characterized by bacteriuria and pyuria, which may be asymptomatic.
Urinary tract infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
Most common type of collagen found in glomerular basement membrane.
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 543
Most frequent cause nephrotic syndrome in children. Under light microscope, the glomerular basement membrane appears normal, but on electron microscopy, GBM shows uniform and diffuse effacement of foot processes of the podocytes. Good response to corticosteroid therapy.
Minimal change disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550
A lesion characterized histologically by sclerosis affecting some but not all glomeruli and involving only segments of each affected glomerulus.
Focal segmental glomerulosclerosis (FSGS)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550
Slowly progressive disease characterized by the presence of subepithelial immunoglobulin-containing deposits along the glomerular basement membrane. Histologically, there is diffuse thickening of the BM. (+) spike and dome pattern on electron microscopy. Often resistant to steroid therapy.
Membranous glomerulonephritis (Membranous Nephropathy)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 551
Characterized by discrete SUBENDOTHELIAL electron-dense deposits in irregular granular pattern.
Type I MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553
GBM is thickened, showing a “tram-track” appearance on PAS stains. There is proliferation of mesangial and endothelial cells as well as infiltrating leukocytes.
MPGN(Membranoproliferative Glomerulonephritis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553
MPGN wherein the lamina densa and the SUBENDOTHELIAL space of the GBM are transformed into an irregular, ribbon-like extremely electron dense structure.
Type II MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 554
Caused by glomerular deposition of immune complexes resulting in diffuse proliferation and swelling of resident glomerular cells. There is uniformly increased cellularity of glomerular tufts. Electron microscopy show subepithelial “humps” against the GBM, with granular deposits of IgG and complement.
Acute postinfectious (poststreptococcal) Glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555
Most common cause of recurrent microscopic or gross hematuria and is the most common glomerular disease revealed by renal biopsies.
IgA Nephropathy (Berger disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555
Pathologic hallmark of this disease is the deposition of IgA in the mesangium.
IgA nephropathy (Berger Disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 556
Nephritis accompanied by nerve deafness, lens dislocation, posterior cataracts and corneal dystrophy.
Alport syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 556
Caused by mutations in genes encoding GBM collagen, manifest as hematuria and slowly progressing proteinuria and declining renal function. GBM has “basket-weave” appearance due to splitting and lamination of the lamina densa.
Hereditay nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
A clinical syndrome characterized by rapid and progressive lossof renal function with features of nephritic syndrome,often with severe oliguria. Histologic feature is the presence of crescents.
Rapidly Progressive Glomerulonephritis (Crescentic GN)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
CrGN characterized by linear deposits of IgG and C3 on the GBM. anti-GBM Ab also bind to pulmonary alveolar capillary basement membranes to produce pulmonary hemorrhages associated with renal failure.
Anti-Glomerular Basement Membrance Antibody (Type I) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
CrGN which are immune complex-mediated disorders, as a complication of any of the IC nephritides including PSGN, IgA Nephropathy and HSP. There is segmental necrosis and characteristic granular pattern of the underlying immune complex disease.
Immune Complex-Mediated (Type II) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558
CrGN defined by the lack of anti-GBM Ab and immune complex deposition. Glomeruli show segmental necrosis, negative immunofluorescence.
Pauci-immune (Type III) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558
An important cause of end-stage renal disease presenting as chronic renal failure. Kidneys are symmetrically contracted, surfaces are red-brown and diffusely granular. Glomeruli are obliterated with marked interstitial fibrosis.
Chronic glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 559
A common suppurative inflammation of the kidney and renal pelvis caused by bacterial infection, either by hematogenous spread or through ascending infection.
Pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 560
Hallmark of this disease is scarring involving the pelvis or calyces, or both, leading to papillary blunting and marked calyceal deformities.
Chronic pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 562
Nephritis with prominent eosinophilic and mononuclear inflitrate, with pronounced edema.
Acute Drug-Induced Interstitial Nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 563
A clinicopatholigic entity characterized by damaged tubular epithelial cells and clinically by acute suppression of renal function.Most common cause of acute renal failure.
Acute tubular necrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564