Systemic diseases affecting the kidneys Flashcards
How do systemic diseases manifest in the kidneys?
- Acute kidney injury
- Chronic kidney disease
- Proteinuria
- Nephritic syndrome
- Nephrotic syndrome
Describe the process of diagnosing a systemic disease manifesting in the kidneys
- Renal impairment: work out if it is old or new, have they got any previous U+Es?
- Is there proteinuria? Urinalysis/uPCR
- Which type of manifestation? AKI, CKD, nephrotic, nephritic, proteinuria?
- What are the clues to systemic disease
- Other tests to diagnose
What is the association of eosinophils in blood/urine tests?
- Cholesterol emboli
- Drug induced interstitial nephritis
- Churg-strauss
What is the association of serum protein electrophoresis, serum free light chains, Bence Jones proteins in the context of systemic disease manifesting in the kidneys?
- Myeloma
- Light chain nephropathy
- Fibrillary glomerulonephritis
What is the association of anti-nuclear antigen, complements C3/4 or dsDNA antibodies in the serum/urine in the context of systemic disease manifesting in the kidneys?
- Lupus nephritis
* Systemic lupus erythematosus
What is the association of anti-neutrophil cytoplasmic antibody in the serum in the context of systemic disease manifesting in the kidneys?
ANCA-associated vasculitis
What is the pathophysiology of diabetes affecting the kidneys?
- Hyperglycaemia increases the osmotic load
- This leads to volume expansion of circulating blood volume
- Intra-glomerular hypertension
- Hyperfiltration of waste from blood into urine
- Proteinuria as more damage occurs: BM thickens, podocytes and their foot processes flatten, mesangial cells increase in number in the mesangial matrix
- Hypertension and renal failure
Describe the histology of diabetic nephropathy
- Kimmelsteil Wilson nodules
- Nodules of pink hyaline material form in regions of glomerular capillary loops in the glomerulus (due to increased mesangial matrix)
What must there be for it to be diabetic nephropathy
Proteinuria, glomerular disease results in proteinuria, if there is none then it isn’t diabetic nephropathy
Explain the model of the natural history of diabetic kidney disease
- From diagnosis: Hyperglycaemia, GFR high
- At 2 years: cellular injury
- From around 7 years: microalbuminuria , hypertension, GFR lowers to normal
- From 10 years: Cellular injury continues (mesangial expansion, glomerulosclerosis, tubulointerstitial fibrosis and inflammation), development to macroalbuminuria, GFR lowering
- 20+ years: all above, ESRD, Kidney complications
What is the classical presentation of diabetic nephropathy?
- Usually 20 years of diabetes mellitus (delayed in Type 2 diabetes)
- Always in association with other diabetic complications
- Always with proteinuria
- Kidney usually normal size on ultrasound
What is the approach to the management of diabetic nephropathy?
- Treat hypertension: ACEi/ARB, SGLT2
- Improve blood glucose control
- Education - DAFNE l
- Oral hypoglycaemic drugs: SGLT2i, insulin, glucose sensors and pumps
Describe tubular glomerular feedback in uncontrolled diabetes
- Increased glucose and Na+ reabsorption via SGLT1 and SGLT2
- This results in decreased Na+ delivery to the JGA resulting in an increase of renin and angiotensin
- Increased renin and angiotensin causes effect arteriole vasoconstriction
- Increased glucose excretion
name a SGLT2i
Empagliflozin
What is the pathogenesis of renovascular disease?
- Progressive narrowing of renal arteries with atheroma
- Perfusion falls by 20%, GFR falls but tissue oxygenation of cortex and medulla is maintained
- RA stenosis progresses to 70%, cortical hypoxia causes microvascular damage and activation of inflammatory and oxidative pathways
- Parenchymal inflammation and fibrosis progress and become irreversible
- Restoration of blood flow provides no benefit
