Diabetic Nephropathy
Diabetic nephropathy is the most common cause of end-stage renal disease (ESRD) in the developed world. It results from long-standing hyperglycemia, causing damage to the glomerular microvasculature.
1. Pathogenesis and Morphology
- Early Stage: Hyperfiltration (increased GFR) and microalbuminuria.
- Glomerular Basement Membrane (GBM): Hyperglycemia leads to non-enzymatic glycosylation of the GBM, causing thickening and increased permeability.
- Mesangial Expansion: Non-enzymatic glycosylation of efferent arterioles (and potentially afferent) increases glomerular capillary pressure, leading to mesangial matrix deposition.
2. Classic Histological Findings
| Finding | Description |
|---|---|
| Kimmelstiel-Wilson Nodules | Pathognomonic nodular glomerulosclerosis (mesangial matrix deposition). |
| Hyaline Arteriolosclerosis | Affects both afferent and efferent arterioles (efferent is more specific to DM). |
3. Exam Must-Knows
- Treatment Priority: The first-line pharmacological intervention to slow progression is an ACE inhibitor or ARB, which reduces intraglomerular pressure by dilating the efferent arteriole.
- Screening: Annual screening for microalbuminuria (urine albumin-to-creatinine ratio) is standard for all diabetic patients.
Pathology Board Hint: For board exams, “Kimmelstiel-Wilson” = Diabetic Nephropathy. Remember that this condition can lead to both Nephrotic syndrome (initially) and chronic kidney disease as the glomeruli become progressively sclerotic.