Renal Flashcards
Causes of hypernatraemia? (4)
How may this present in an infant?
Rx?
Dehydration (e.g. D&V, high fever)
Osmotic diuresis (e.g. DKA)
Diabetes insipidus
Excessive saline infusion
In an infant: jittery, increased muscle tone, hyperreflexia, sunken fontanelles, drowsiness, eventually coma
Rx: Oral rehydration solution 1st line
Slow infusion IV 0.9% NaCl if cannot tolerate oral (D&V), sepsis/shock suspected, or if oral not working
Drugs to stop in AKI as they will cause worsening? (3)
DAAAMN
Diuretics
ACEI/Aminoglycoside/ARB
Metformin
NSAIDs
Drugs that may have to be stopped in AKI as they will build up?
Metformin
Digoxin
Lithium
Is aspirin safe in AKI?
At cardioprotective dose 75mg
Is paracetamol safe in AKI?
Yes
Is warfarin safe in AKI?
Yes
Are statins safe in AKI?
Yes
Is clopidogrel safe in AKI?
Yes
Are B Blockers safe in AKI?
Yes
Diagnosis of AKI?
4 symptoms, 3 bloods
Symptoms:
- oliguria
- oedema
- arrhythmias (from K/acid build up)
- features of uraemia (pericarditis, encephalopathy)
Bloods:
- rise in serum creatinine by 26 mol/l in 48 hours
- rise in serum creatinine by 50% in 7 days
- fall in urine output less than 0.5 ml/kg/hr for 6 hours
What usually increases during an AKI?
Things that the kidney normally excretes
- K
- Creatinine
- Urea
Also usually acidosis
SE of EPO therapy?
Why might someone not respond?
- Accelerated hypertension (encephalopathy and seizures)
- Bone ache
- Flu-like symptoms
- Pure red cell aplasia
- Iron deficiency due to increased erythropoiesis
Non-responsive:
- iron deficiency
- inadequate dose
- infection
- hyperparathyroid bone disease
Alport’s Syndrome:
- inheritance?
- presentation?
- diagnosis?
- why might a transplant fail in an alport’s pt?
X-linked dominant
In childhood:
- microscopic haematuria
- progressive renal failure
- bilateral sensorineural deafness
- Lenticonus: lens protrudes into anterior chamber (needs glasses)
- Retinitis pigmentosa
Diagnosis:
- genetic testing
- renal biopsy: EM - longitudinal splitting of lamina dense of GBM, causing ‘basket-weave’ appearance
Fail: due to anti-GBM antibodies against normal GBM
Minimal change disease:
- presentation? (1)
- renal biopsy? (2)
- Management?
- Nephrotic syndrome (normotension)
Biopsy:
- LM: normal glomeruli
- EM: fusion of podocytes, effacement of foot processes
Rx:
- Oral pred + urgent referral
- Cyclophosphamide if resistant
Why can nephrotic syndrome cause blood clots?
What must happen?
How can it cause infection?
How can it cause hypocalcaemia?
Clots:
- ATIII and plasminogen lost to urine
- Can cause DVT and renal vein thrombosis
- LMWH
Infection: Ig lost to urine
Hypocalcaemia: VitD and binding protein lost in urine
ADPKD:
- presentation? (4)
- extra-real manifestations? (4)
As a young adult:
- hypertension
- abdo pain
- CKD
- loin mass
- haematuria
Extra-renal:
- liver cysts (most common) - hepatomegaly
- berry aneurysm
- mitral/tricuspid incompetence
- pancreatinc/splenic cysts
IgA nephropathy vs post-strep glomerulonephritis?
IgA:
- 1-2 days after URTI
- haematuria
- caused by IgA
Post-strep:
- 1-2 weeks after URTI
- Proteinuria
- haematuria
- low complement count
- caused by IgG, IgM and C3 deposition in glomeruli
Caused by GAS
Renal biopsy of post-strep?
- Acute, diffuse, proliferative glomerulonephritis
- Endothelial proliferation with neurtophils
- EM: subaopithelial ‘humps’ caused by lumpy immune complex deposition
- IF: granular or ‘starry sky’ appearance
How to tell intrinsic AKI from pre/post renal?
Protein present in intrinsic
How to tell primary from secondary hyperaldosteronism?
Pt with refractory hypertension, low K and high Na (since high aldosterone)
Look at renin activity. If renal artery stenosis then low afferent blood flow will stimulate renon release and cause they hyperaldosteronism
3 things renal artery stenosis can cause?
Renal artery stenosis due to atherosclerosis is most common cause of renal vascular disease (90%), what is next most common cause?
- hypertension
- CKD
- flash pulmonary oedema
Fibromuscular dysplasia
50 y/o patient with progressive weakness, and dyspnoea, hepatomegaly, reduced renal function, T2DM, COPD, no FHx?
Diagnosis?
Amyloidosis
Rectal biopsy - congo red staining shows apple-green birefringence
What should you think of in young woman who develops AKI in response to ACEI?
What is seen on renal USS?
What is seen on duplex scan?
What is next Ix?
Fibromuscular dysplasia
USS: normal kidneys and urinary system
Duplex: stenotic arteries
MR angiography: ‘string of beads’ appearance
HSP:
- what is it?
- features? (4)
- treatment?
- IgA small-vessel vasculitis after URTI - degree of overlap with IgA nephropathy
- palpable purpuricrash with localised oedema over buttocks, extensors and legs
- abdo pain
- polyarthritis
- features of IgA nephropathy (haematuria, renal failure)
Rx: supportive. Good prognosis
If someone with CKD and low GFR needs contrast scan?
Offer Iv hydration before and after contrast infusion
Why is lupus nephritis different from other nephritic syndromes?
There are 6 different types of lupus nephritis - what is the most common?
What is seen on renal biopsy with this?
All patients with lupus nephritis will have proteinuria
Diffuse proliferative glomerulonephritis
endothelial and mesangial proliferation, ‘wire-loop’ appearance
EM: sub endothelial immune complex deposits
IF: granular appearance
Management of rhabdomyolysis causing myoglobinaemia?
What dangerous electrolyte disturbance may occur with this, and may appear before AKI?
Among other causes, e.g. prolonged collapse, seizure, ecstasy etc, what 2 common drugs may interact to cause this?
Lots of IV fluids to maintain good urine output, urinary alkalisation sometimes used
Hyperkalaemia
Statins with clarithromycin - don’t prescribe together
4 causes of transient non-visible haematuria?
5 causes of persistent non-visible haematuria?
2 causes of spurious red/orange urine where blood not present on dipstick?
- UTI
- menstruation
- vigorous exercise (settles after 3 days)
- sex
- cancer (kidney, renal, prostate)
- stones
- BPH
- prostatitis/urethritis (e.g. chlamydia)
- renal e.g. IgA nephropathy
Food: beetroot, rhubarb
Drugs: rifampicin, doxorubicin
Define persistent non-visible haematuria?
What else should be tested? (3)
Non-visible haematuria present on 2/3 samples tested 2-3 weeks apart
Renal function
ACR or PCR
BP
Who gets urgent cancer referral for haematuria?
Age 45+ AND:
- visible haematuria without UTI
- visible haematuroa that persists past UTI
Age 60+ AND:
- unexplained non-visible haematuria with dysuria/raised WBC on bloods
Who gets non-urgent cancer referral for haematuria?
Age 60+ AND:
- recurrent/persistent UTI
Acute interstitial nephritis:
- what is it?
- causes?
- features?
- Ix?
allergic-type reaction involving kidneys, causing interstitial oedema and infiltrates in the connective tissue between renal tubules - accounts for 25% of all drug-induced AKI
Most commonly drugs, usually antibiotics (penicillin, rifampicin) - also NSAIDs, allopurinol, furosemide
Features:
- fever, rash, arthralgia
- Eosinophilia
- mild renal impairment
- hypertension
Ix:
- sterile pyuria (WCC on dipstick but no culture)
- white cell casts
How long for fistulas to develop for dialysis?
3 complications?
6-8 weeks
- infection
- thrombosis (bruit)
- stenosis (limb pain, ischaemia)
What is the most common cause of nephrotic syndrome in adults?
What is seen on biopsy?
Causes?
Membranous glomerulonephritis
- LM: thickened basement membrane
- EM/silver staining: ‘spike and dome appearance’ due to sub epithelial deposits
Causes:
- anti-phospholipase A2 Ig
- hepB, malaria
- malignancy (prostate, lung, blood)
- autoimmune diseases
Management of membranous glomerulonephritis?
All its receive ACEI/ARB
Immunosuppression
Anticoagulation for high risk pts
Stages of CKD?
Definition of CKD?
1 - GFR >90 2 - GFR 60-90 3a - GFR 45-59 3b - GFR 30-44 2 - GFR 15-29 1 - GFR <15 - RRT if uraemia present
Reduced GFR and evidence of kidney damage for at least 3 months. Evidence:
proteinuria, haematuria, abnormal U&E, abnormal imaging. More proteinuria = more damage
6 things that can cause CKD
Diabetes - commonest Glomerulonephritis - 2nd Hypertension Chronic pyelonephritis Renovascular disease PKD Idiopathic - small, scarred kidneys unknown cause
At what GFR do symptoms usually become apparent for CKD?
Mild symptoms
Mod?
Sev?
GFR <20 - due to altered conc of electrolytes and urea
Mild - nocturia (unable to concentrate urine)
Mod - non-specific: fatigue, weakness, loss of appetite, nausea, abdominal cramps, gout, bad taste in mouth
Sev - Restless leg, yellow/brown tinge in skin, paraesthesia/cramps, encephalopathy, pericarditis,, itch, halitosis, seizures, uraemia frost
General management of CKD?
Slow progression with ACEI/ARB +/- Spironolactone
Aim for BP <130/80 to reduce proteinuria
Optimise glycaemia
Counsel on RRT once GFR <15
Anaemia of CKD - what type normally?
Management?
Normochromic normocytic (due to decreased EPO) - can also have malabsorption of Fe/B12/folate, decreased cel survival (dialysis), concurrent GI blood loss etc
Target Hb 10.5-12.5
Optimise Fe status - many require IV Fe
EPO injections weekly
How does renal bone disease occur?
What are the manifestations?
Management?
- high phosphate ‘drags’ Ca from bones –> osteomalacia
- Low vitD (no activation in kidney) causing low Ca –> secondary hyperparathyroidism
Manifest:
- osteoporosis
- osteomalacia
- osteitis fibrosa cystica (due to unchecked hyperparathyroidism)
- osteosclerosis
Rx:
- reduce dietary phosphate
- phosphate binders (calcium carbonate, sevelamer)
- VitD (calcitriol)
- parathyroidectomy in some cases
- Alendronic acid to prevent osteomalacia/osteoporosis
Calcium based phosphate binders risk hypercalcaemia and vascular calcification, so sevelamer may be better option
3 options of RRT?
Haemodialysis:
- most common, usually 3-4 sessions a week
- AV fistula
Peritoneal dialysis:
- filtration in patient’s abdo
- CAPD or APD (overnight)
Renal transplant
Life expectancy of renal transplant?
Anti-rejection meds?
What type of matching is best?
Risks of immunosuppression? (3)
10-12 years
ciclosporin/tacrolimus + MMF
Steroids in acute rejection
HLA most important (DR>A>B surface antigens)
CVD, renal failure, SCC of skin
3 types of transplant rejection?
Hyperacute - mins-hours - type II hypersensitivity from pre-existing Ig to HLA (rare - immediate removal)
Acute (<6 months) - HLA mismatching - Tc cell mediated - can be reversed with steroids
Chronic (>6 months) - chronic allograft nephropathy (renal fibrosis)
Peritoneal dialysis, fever, cloudy dialysis?
How does PD work?
Staph epidermidis
Inject high dextrose solution into abdominal cavity which draws out waste products from blood, drained after several hours dwell time and exchanged for new dialysis solution (so risk of hyperglycaemia as well)
What is seen on biopsy of diabetic nephropathy?
Does it cause nephritic/nephrotic syndrome?
What should be checked annually?
3 main management points in diabetic nephropathy?
Nodular glomerulosclerosis - kimmelstein-wilson lesions
Nephrotic syndrome
Urinary albumin:creatinine ratio
- Tight glycaemic control
- BP <130/80 (ACEI)
- Statin