Dr. Francisco G. La Rosa Francisco.LaRosa@UCHSC.eduHome 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