CAM202 Lecture Notes - Lecture 7: Pyelonephritis, Hypertensive Kidney Disease, Immune Complex
Document Summary
Learning objectives: describe the aetiology and pathogenesis of, glomerulonephritis, tubulointerstitial diseases, tubulointerstitial nephritis, pyelonephritis acute & chronic, & how they may present clinically, pathogenesis and micro appearances of diabetic and hypertensive nephropathy. Infections of the kidney and ut, including cystitis, acute and chronic pyelonephritis. Aetiology/pathogenesis: most gn forms are immunologically mediated, antibodies reacting with glomerulus. Intrinsic glomerular antigens or "planted" antigens: glomerular deposition of circulating immune complexes, endogenous or exogenous antigens. Soluble mediators eg cytokines, chemokines, coagulation factors etc: may be primary or associated with systemic disease. Focal: involving only some glomeruli: proliferative or non-proliferative, diffuse: involving most (usually all) glomeruli. Segmental: involving part of the glomerulus: global: involving the entire glomerulus. Segmental/global: basement membrane thickening, crescent formation - reflects severe glomerular injury. Major clinical syndromes: nephritic syndrome: haematuria, proteinuria, impaired rf (increased creatinine), oedema, ht, nephrotic syndrome: heavy proteinuria, reduced serum albumin, elevated serum lipids, oedema. Isolated proteinuria (subnephrotic: acute renal failure (rapidly progressive gn, chronic renal failure.
