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Diabetic Nephropathy

Diabetic Nephropathy. Rick Allen. Definition. a glomerulonephropathy is defined by characteristic structural and functional changes Structural : mesangial expansion, GBM thickening and glomelular sclerosis. Functional : hyperfiltration and albuminuria. Epidemiology.

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Diabetic Nephropathy

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  1. Diabetic Nephropathy Rick Allen

  2. Definition • a glomerulonephropathy is defined by characteristic structural and functional changes • Structural: mesangial expansion, GBM thickening and glomelularsclerosis. • Functional: hyperfiltration and albuminuria.

  3. Epidemiology • DM type I – 20-30% develop microalbuminuria after 15 years. <1/2 of these  overt nephropathy. Can regress or remain stable. Now dropping due to effective control methods. • DM type II – As above? Rates on the rise due to increased fatty numbers. • Leading cause of premature death in young diabetics. Second to MI overall.

  4. Risk Factors • Type I = Type II (we think. Start time dubious) • GENETICS (AT2, ACE) • HTN • High GFR • Poor hyperglycaemic control (high HbA1c) • Obesity • Smoking • OCP • Race (blacks 3-6x > whites)…SES? + above. • Age…unknown, however DM I Dx <5y.o. is good

  5. Ix • earliest detectable sign is microalbuminuria. • Macroalbominuriais more predictive for future developmet of severe nephropathy and decreased GFR.

  6. Pathophysiology and Pathology • Glomerular sclerosis/damage • Metabolic defect; insulin deficiency  hyperglycaemia biochemical alterations in GBM (increased collagen type IV and fibronectin, decreased proteoglycan) and increased ROS ( damage) • Nonenzymatic glycosylation  inflammatory cytokines and GF released from macrophages, ROs generation in endothelial cells, increased procoagulant activity in endothelial cells and macrophages, ECM synthesis and SM prolif. • Haemodynamic changes  increased GFR, glomerular capillary pressure, glomerular filtration area, and glomerular hypertrophy. • Afferent arteriole is damaged  bigger afferent than efferent  increased GFR and pressure, causing further damage and increased shearing forces mesangial cell hypertrophy and excretion of ECM products  glomerular sclerosis

  7. Pathophysiology and Pathology 2 • Ischaemia (due to hypertrophy of afferent and efferent arterioles) • hypertrophy and hylanization of vessels  ischaemic kidney damage • Ascending infection • Occur more in women with diabetes than without. No difference for men. Causes: bladder stasis (neuropathy), infections like to live in damaged kidney (easier to get established)

  8. Pathophysiology and Pathology 3 • Under the microscope we get • Glomerular lesions: GBM thickening, diffuse mesangial sclerosis (PAS positive for stain) and nodular glomerulosclerosis (Kimmelstiel-Wilson lesion, + hyaline accumulations in fibrin caps [in capillary loops] and capsular drops [adhere to Bowman’s capsule]. 15-30% of long term diabetics get this, most associated with renal failure.) • Vascular lesions: arteriosclerosis/hylanisation of afferent and efferent arterioles • Pyelonephritis, including necrotising papillitis. • Glomerular and vascular lesions ischaemia tubular atrophy and interstitial fibrosis  overall contraction in size.

  9. Tx and management • Same as any other chronic renal disease, however; • Use an ACEI or AT2 inhibitor to get that BP down! • Avoid oral hypoglycaemics excreted by the kidney (metformin) • Assess insulin dose and effectiveness • Retinopathy may cause issues with treatment (blind, can’t see what doing) • Haemodialysis may be difficult as fistulas calcify rapidly. Peritoneal. • Kidney transplant failure is higher than pt. without DM.

  10. The End!

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