Nephrology Flashcards
1.Pathophysiology of SIADH
Inappropriate release of ADH (Posterior pituitary gland) resulting in EUvolaemic Hyponatraemia (Dilutional)
ADH acts at the level of the collecting ducts to reabsord H20
5 Causes of SIADH
1) Malignancy - SCLC
2) Neurological - Stroke, SDH, SAH, Encephalitis/Meningitis
3) Infections - TB, Pneumonia
4) Drugs - SSRI, Tetracyclines, Carbamazepine, Sulphonylureas, Vincristine, Cyclophosphamide
5) Other - PEEP
Investigations for SIADH
Paired Urine and Plasma Osmolalit (Urine Osm >100 mOSm compared to plasma
Paired Urine and Plasma sodium - Urinary Na+ >40
Management of SIADH
1st line ) Fluid restriction
2nd line) Demeclocycline
3rd line) Vasopressin Receptor antagonists
Adverse outcome for rapid correction of Na+ during hyponatraemia
Central pontine myelinolysis
What are the post-op complications of renal transplant
Graft failure: Hyperacute, Acute (<6months), Chronic (>6Months)
Vascular thrombosis
UTI
Urine leakage
Causes of Hyperacute graft failure of renal transplant (Minutes-Hours)
IgG mediated antibody response usually due to prior sensitisation against HLA/ABO antigens on graft
Causes of acute graft failure of renal transplant (<6month
Cytoxic T cell mediated
- Could be due to CMV infection
NB - Rx with steroids/immunosuppression
Causes of chronic graft failure of renal transplant (>6motnhs)
Both cell and antibody mediated
How would you characterise Haematuria
Non-visible vs Visible Haematuria
How would you further characterise non-visible haematuria
Transient v persistent (Dipstick +ve on 2/3 tests 2-3 weeks apart)
Causes of transient Non-visible haematuria (Six)
Streaneous exercise (March haemoglobinuria)
UTI
Sexual intercourse
Menstruation
Non-UTI cuases - Beetroot
Iatrogenic - Rifampicin, Doxorubicin
Causes of persistent Non-visible haematuria (4)
Cancer - Renal, prostate, Bladder
Stones
Prostatis
BPH
Urethreitis
Renal causes - iGa NEPHROPATHY
Urgent 2 week wait referral criteria for haematuria
Age >45 with Visible haematuria and -ve UTI or after UTI treamtent
Age >60 and unexplained Visible haemturia with Dysuria/Raised WCC
Criteria for non urgent referral to Urology
Age >60 with recurrent UTI
Investigations for non-visible haematuria
Urine Dip
Protein:Creatinine ratio
Albumin:Creatinine ratio
+/- Urine for MCS
What is Minimal change disease
Usually a nephrotic syndrome that is idiopathic
Causes of Minimal change disease
Idiopathic - Mainly
Other:
-Hodgkins lymphma (Cytokine release from Reed-sternberg cells)
- Thymoma
- Infectious Mononucleosis (EBV virus)
Population affected by Minimal Change disease
75% Children
25% Adults
Presentation of Minimal Change disease
Nephrotic syndrome - Oedema - Facial, peripheral oedema
Normotensive
Investigations of Minimal change disease
Serum Albumin - <30
Urine Protein:Creatinine ration - >1000 9Very high
Light microscopy - NORMAL Nil immune complexes to be seen
Electron microscopy - Podocyte effacement
Complications of MCD
Low albumin - Pro-thrombotic state
(Consider Apixaban)
Managament of Minimal change disease
1st line - glucocorticoids - Prednisolone
2nd line - Cyclophosphamide
3rd line - Rituximab (CD 20 inhibitor)
Pathophysiology of Minimal change disease
T-Cell mediated and Cytokine mediated damage to podocytes
This increases the permeability of the glomerular basement membrane
Resulting in proteinurea
Hyperlipidaemia - Due to increase hepatic synthesis in response to hypoalbuminaemia
Characteristics of nephrotic syndrome
Oedema
Hypoalbuminaemia
Proteinuria >3.5g/day
Categorise the causes of nephrotic syndrome
Primary:
- Minimal change disease
- Focal segmental Glomerulosclerosis
Secondary:
- SLE
- Diabetes
Difference between focal segmental glomerulosclerosis and Minimal Change disease
Similarities - Nephrotic syndrome
Differences:
- FSGC is less steroid responsive and more common in adults with light microsopy showing changes to the glomeruli
- Hypertension often present
