Renal/Uro Flashcards
Define AKI in terms of Creatinine/UO/GFR
* Stage 1 (Risk)
* Stage 2 (Injury)
* Stage 3 (Failure)
* (Loss of Function)
* (End-stage)
- > 1.5x baseline Cr (7 days) or rise >26 (2days), UO 0.5ml/kg/hr in 6 hrs, >25% decline
- 2x baseline Cr, UO 0.5 in 12 hrs, >50% decline
- 3x baseline Cr, UO Anuria in 12 hrs/0.3 in 24 hrs, >75% decline
- Loss of function for >4 weeks; req dialysis
- > 3mo, req dialysis
Investigations - AKI
Bedside (obs, urinalysis, ECG)
Bloods (U&E + eGFR, LFTs, FBS, CRP) + cultures
Imaging (renal u/s / CT KUB / XR KUB / Doppler)
Special tests (renal biopsy / immune or virology screen)
Urinalysis to distinguish pre-renal from intra-renal
- Casts
- Urine Na
- Urine FeNA (fraction of excreted Na+ compared to amount reabsorbed)
- Serum Urea:Creatinine ratio
- Urine osmolarity
Pre-renal:
hyaline casts, Low Na+ & Low FeNA, high Urea:Creatinine, high urine osmolarity
Kidneys preserve Na+ - hence don;t secrete Na+ in urine - to maintain blood volume/treat hypovolaemia
Intra-renal:
brown granular casts, High Na+, Normal Urea:Creatinine, Low osmolality (dilute)
High Urea:Creatinine ratio in Pre-renal because Cr isn’t being re-absorbed due to reduced GFR.
Mx of AKI - fluid balance and electrolyte monitoring, stop nephrotoxics, treat underlying cause.
List nephrotoxic drugs (DAMN my PCL)
Which of these are not technically nephrotoxic but need to be stopped in AKI due to increased risk of toxicity?
- Diureitcs
- Aminogycosides, ACE-I, ARBs
- Meformin, Morphine
- Nitrates and NSAIDs
- Phenytoin
- Contrast media
- Lithium –> diabetes insipidus
Increased risk of toxicity - digoxin, metformin, lithium
NSAIDs and ACE-Inhbs effect on renal blood flow:
Reduction in GFR - worsening or causing AKI.
NSAIDs cause vasconstriction of afferent arteriole.
ACE-Inhbs cause vasoldilation of efferent arteriole.
The combination together reduces blood flow into the glomerulus and increases blood flow out of it - aka reducing the GFR
Define CKD and the 3 ways it can be classified?
Abnormal kidney function present for >3 months with significant health implications:
* GFR 1, 2, 3a/b, 4, 5: >90, 60, (45, 30) 15, <15
* ACR (Albuminuria) 1-3: <30, 30-300, >300
* Underlying disease
Top 3 Causes in UK for CKD
- Diabetes
- HTN
- Glomerularnephritis
General mx for CKD:
* Treat underlying cause; optimise modifiable RF
* Slow disease progression
* Treat complications
* Nephrology referral for RRT
Conservative measures include lifestyle modifications, stopping nephrotoxics - what diet is recommended?
Low K+ and PO42-
Fluid restriction
Complications of CKD
- Uraemia
- Electrolyte imbalance - hyperkalaemia
- Anaemia of chronic disease (normocytic)
- Acid-base imbalance: Acidosis
- Reduced synthesis of 1,25-dihydroxycholecalciferol –> Hypocalcaemia, renal osteodystrophy, secondary hyperparathyroidism
- Fluid overload, oedema
- Gout
Nephrotic vs nephritic syndrome
* Nephrotic = proteinuria (>3g/day), hypoalbuminaemia (<30g/l), oedema (reduced oncotic pressure) +/- hypercholesterolaemia
* Nephritic= haematuria, HTN, oliguria +/- proteinuria/oedema
EPO injections are not effective if…
Iron deficient.
One of their side effects is IDA (brittle hair, glossitis, oncholysis etc)
Extra-renal features of autosomal dominant polycystic kidney disease
Screening investigation
- Liver cyst (most common)
- Berry aneursym –> SAH
- CVS - mitral valve prolapse
- Other GI cysts
Screening: ultrasound abdomen
Paediatric Glomerulonephritides: nephrtic px. Disease and typical causative organism.
* 1-2 wks post URTI/skin inf with raised anti-streptolysin O, immune complex deposition, and starry sky appearnace on bx.
* AKI, haemolytic anaemia and low Plt, following bloody diarrhoea. Shistocystes on blood film.
* Throat infection followed by purpuric rash on buttocks and extensor surfaces, abdominal pain, haematuria & polyarthritis.
* Inherited connective tissue disorder causing eye problems (retinitis pigmentosa and lenticonus), ear problems (sensorineural deafness) and nephritic syndrome. Basket weave on bx.
- Post-strep GN (after strep pyogenes URTI or skin infection)
- Haemolytic uraemic syndrome (after shiga-producing E-Coli)
- Henoch-Shonlein Purpura (various causative organisms)
- Alport’s syndrome;need a basket for transport
Generally managed conservatively. HUS may require IV Fluids and HSP NSAIDs for arthralgia. Alport’s with BP management (ACE-Inhb).
Paediatric Glomerulonephritides - nephrotic px
* Kid with loss of albumin & transferrin in urine, podocyte effusion on electron microscopy, requiring Prednisolone.
* Can present in teens but most common nephrotic presentation in adults. Scarring on bx. Normally 2ndary to other renal disease, req steroids +/- I/s.
- Minimal change disease (no changes seen on light microscopy)
- Focal segmental glomerulosclerosis
Adult glomerulonephritides - nephritic sx:
* Young male with reucrrent eps of recurrent macroscopic haematuria; note 1-2 days post URTI. Immune complex deposition; association with HSP and other autoimmune dx.
* * HLA-DR2 associatied disease with bimodal presentation (20s & 60s) affecting connective tissue of lungs & kidneys
* P-ANCA associated small vessel vasculitis presenting with haematuria & haemopytisis
* C-ANCA associated “ following an URTI/LRTI
* P-ANCA associated “ presenting with severe asthma
- IgA Nephropathy (diffuse proliferative) - monitor proteinuria (No treatment –> ACE-I –> CS)
- Anti-GBM disease (Good-pasture’s)
- Microscopic polyangitis
- Granulomatosis with polyangitis (wegners)
- Eosinophilic granulomatosis with polyangitis (Churg Strauss)
Adult glomerulonephritides - nephrotic sx
* Common cause of ESRD. Rule of 1/3 (recover, relapse, chronic). Spike & dome appearance (thickened GBM) on bx.
* Rare disease with poor prognosis.Tramline of double BM on bx. Type 1 - low C4, type 2 - low C3.
- Membranous nephropathy
- Membranoproliferative GN (mesangiocapillary)
Renal transplant - underlying cause & mx.
1. Hyperacute (mins -hrs)
2. Acute/ T-cell mediated (<6 mo)
3. CHronic (>6mo)
- Existing antibodies to ABO/HLA causing necrosis. Reqs Graft removal.
- Mismatched HLA. Asx/ raised CR/proteinuria. Reversible with steroids/IS.
- Antibody & T-cell mediated, causing fiborosis. Note recurrence of renal disease e.g. MCGN, IgA, FSGS.
Prostate cancer - after doing a PR exam & PSA test:
* First line investigation
* Next investigation to establish diagnosis (two methods)
* Scan for bony mets?
-
Multiparametric MRI
(results reported as Likert scale 1-5 from very low suspicion to definite cancer) - Prostate biopsy e.g. Likert scale 3+ and clinical suspicion etither transrectal (TRUS; ultrasound probe) or transperineal (needle)
- Isotope bone scan / radionucleide/bone scintigraphy (injection into bone - cancer cells take up more isotope so stand out)