Internal Diseases and Therapy · MU Sofia

113. Kidney and diabetes

Covers how high blood glucose drives diabetic kidney damage, through reactive oxygen species, mesangial expansion, thickened glomerular basement membrane and glomerular sclerosis. It then describes the four stages of diabetic nephropathy in order, with their filtration, albuminuria and morphological features, followed by stage-specific treatment. A PAS-stained glomerulus image showing a Kimmelstiel-Wilson lesion is included, along with a short list of infection and vascular risks in diabetics.

Inside: 1 section · 1 labelled picture · 15 flashcards · 3 min

Topic 114 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 1 section, about 458 words (3 min of reading), with 15 flashcards.

In this note

  1. Kidney and diabetes

Kidney and diabetes

Diabetes mellitus is the single leading cause of end-stage renal disease. Of these, 90% have type 2 diabetes rather than insulinopenic type 1, this reflects how much more common type 2 is than type 1.

Hyperglycemia is responsible for significant changes in diabetic nephropathy via four mechanisms; Increased glucose in the blood causes increased generation of ROS, mesangial expansion, thickening of glomerular basement membrane and glomerular sclerosis due to intraglomerular hypertension (dilation of the afferent arteriole) or ischemic injury induced by hyaline narrowing of the vessels supplying the glomeruli.

Diabetics are especially susceptible to this due to a pathophysiological change found in all diabetics, hyperfiltration with greater relaxation of the afferent arteriole than the efferent. When diabetes is poorly controlled, we see glomerular hypertrophy with an increased glomerular capillary surface area. These structural changes contribute to the development and progression of diabetic renal injury.

Diabetic nephropathy has been divided into four stages:

  • Stage I
  • Begins with GFR increase up to 50%
  • Hypertension may present
  • Renal morphology shows kidney hypertrophy
  • No protein in urine as of yet
  • Stage II
  • 30% of type I patients advance to this stage. Characterised by fixed microalbuminuria of at least 30mg/24hrs. Generally occurs after a median of 10 years following diagnosis
  • Glomerular basement membrane thickening and mesangial matrix expansion are present
  • Stage III
  • Generally occurs about 5 years after stage II
  • Have overt proteinuria (>500mg/24hours) and macroalbuminuria (>300mg/24hours)
  • GFR begins dropping below expected levels (<100%)
  • Hypertension develops in most type I and worsens in type II patients
  • Kidney morphology shows focal glomerulosclerosis (with or without Kimmelstiel-Wilson lesions) additionally, afferent and efferent arteriolar hyalinosis is visible.
  • Stage IV
  • Advanced diabetic retinopathy. >3.5g/24hrs proteinuria.
  • All the extra renal symptoms of chronic renal insufficiency (see below, Q14)
  • Kidney often still enlarged, along with global glomerulosclerosis and tubulointerstitial fibrosis.
  • Stage IV patients should be monitored for hyperkalemia

PAS-stained glomerulus in diabetic nephropathy with a round, pink nodule of mesangial matrix (Kimmelstiel-Wilson lesion) on the left and a thickened Bowman capsule.

Image: “Diabetic glomerulosclerosis (4) PAS” by No machine-readable author provided. KGH assumed (based on copyright claims)., CC BY-SA 3.0, via Wikimedia Commons.

Treatment by stage:

  • Stage I
  • Tight glucose control with BP control (ACEI or ARBs)
  • Stage II
  • Tight glucose control with ACEI or ARB for BP. Smoking cessation, weight reduction, exercise and annual retinal screening
  • Stage III

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