Diabetic nephropathy
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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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  • a glomerulonephropathy is defined by characteristic structural and functional changes

    • Structural: mesangial expansion, GBM thickening and glomelularsclerosis.

    • Functional: hyperfiltration and albuminuria.


  • 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.

Risk factors
Risk Factors

  • Type I = Type II (we think. Start time dubious)


  • 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


  • earliest detectable sign is microalbuminuria.

  • Macroalbominuriais more predictive for future developmet of severe nephropathy and decreased GFR.

Pathophysiology and pathology
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

Pathophysiology and pathology 2
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)

Pathophysiology and pathology 3
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.

Tx and management
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.