Jan 15, 2016
Dr. Francisco G. La Rosa [email protected] Page
Embriology of the Kidney and Collecting SystemHome Page
Anatomy of the KidneyHome Page
KIDNEYFunctions: Excretion of waste products Regulation of water and salt Maintenance of acid balance Secretion of hormones and by-productsStructures and Diseases: Glomeruli (immune damage) Tubuli (toxic or infections) Interstitium (toxic or infections) Blood vessels (metabolic)
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CLINICAL MANIFESTATIONS OF RENAL DISEASE Syndromes:Acute Nephritic syndrome Nephrotic syndrome Asymptomatic hematuria Asymptomatic proteinuria Acute renal failure Chronic renal failure Urinary tract infection (UTI) Nephrolitiasis TumorsHome Page
GLOMERULAR DISEASES Primary Glomerulonephritis Acute diffuse proliferative GN Rapidly progressive GN Membranous GN Lipoid nephrosis (minimal change disease) Focal segmental glomerulosclerosis Membranoproliferative GN IgA Nephropathy Chronic GN Secondary (Systemic) Diseases Systemic lupus erythematosus Diabetes mellitus Amyloidosis Goodpastures syndrome Polyarteritis nodosa Wageners granulomatosis Henoch-Scholein purpura Bacterial endocarditis Hereditary Disorders Alports syndrome Fabrys disease Home Page
Ischemia / ToxinsIntrarenal Vasoconstriction(Increased Endothelin; decreased NO)Tubular InjuryReduced GlomerularPlasma FlowReduced O2 delivery toOuter Medulla? Direct GlomerularEffect Reduced GFR Oliguria TubuleObstructionBack-LeakageIncreasedIntratubular PressureAcute Renal FailureHome Page
Schematic Representation of a Glomerular LobeHome Page
Low-power electron micrograph of rat glomerulus: CL, capillary lumen; End, endotheliumMes, mesangium; B, basement membrane; Ep, visceral epithelial cells with foot processes; US, urinary space.Home Page
Antibody-mediated glomerular injury: (A) Circulating Ag-Ab complexes, (B) Anti-basement membrane, (C) In situ Ag-Ab complexes.Home Page
Epithelial cell injury and destruction of the basement membrane as a result of immune complex in the glomerulus. Normally, the basement cell membrane does not filter large molecules such as albumin (70,000 kD), which is present in urine if the membrane is damaged.Home PageAlbumin
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NEPHROTIC SYNDROME
Proteinuria (>3.5 g/day)General edemaHypoalbuminemia (
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Lipoid Nephrosis (A and C) and Membranous Glomerulonephritis (B and D).Home Page
Nephrotic syndrome:Home Page
IgAIgA NephropathyFocal mesangial proliferative glomerulonephritisImmunofluorescence in the glomeruli: IgG +, IgA +++ (shown here), IgM Negative, and C3 ++.Home Page
IgA NephropathyHome Page
C3Acute Nephritic Syndrome Home Page
Acute Nephritic Syndrome Home Page
Acute nephritic syndrome Goodpasture's syndromeIgG linear patternFibrinogenCastProliferation, glomerular crescents, necrosisHome Page
Membranoproliferative Glomerulonephritis (MGN): Mesangial proliferation, basement membranethickening, leukocyte infiltration and accentuation of lobular architecture.(B) Type I and Type II MGN .Home Page
Proliferative Glomerulonephritis Systemic LupusIgGHome Page
Tubular and Interstitial Diseases Tubulointerstitial Nephritis Acute pyelonephritis Chronic pyelonephritis Drug-Induced interstitial nephritis Acute tubular necrosis Home Page
Pathways of Renal InfectionHome Page
Acute CystitisHome Page
Hydronephrosis and chronic obstructive pyelonephritis Home Page
Chronic pyelonephritisHome Page
Vascular Diseases Benign nephrosclerosisMalignant hypertension/ Malignant nephrosclerosisThrombotic microangiopathiesHome Page
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Thickening of the arterial wall with malignant hypertension produces a hyperplastic arteriolitis. The arteriole has an "onion skin" appearanceMalignant hypertension leads to fibrinoid necrosis of small arteries. The damage to the arteries leads to formation of pink fibrin -- hence the term "fibrinoid".Home Page
CONTINUE IN LECTURE 2Home Page