Renal & Urology Flashcards
Contraindications to renal transplant
Active sepsis
Malignant disease within last 2 years
Common sites for kidney stones to be trapped
Where renal pelvis becomes ureter
Where ureter enters the pelvis (at bifurcation of the common iliac vessels and the sacroiliac join)
Where ureter enters the bladder (ureterovesical valve)
Bladder sphincter control
Internal urethral sphincter (sphincter vesicae)
- At neck of the bladder
- PNS control - relaxes when bladder wall tension increases = INVOLUNTARY
- Continuation of detrussor muscle
- In men it is between bladder and prostate
External urethral sphincter (sphincter urethrae)
- In perineum
- Skeletal muscle = VOLUNTARY
- Innervated by pudendal nerve (arising from S2-S4)
- In men it is after the prostate
Renal function
Excretion of water-soluble waste Water balance Electrolyte homeostasis Acid-base homeostasis Endocrine: EPO, RAS, vit D Regulate BP
Nephron filtration through various parts
1) PCT: Active reabsorption Na, also glucose, AA Phosphate, K
2) LOH
- D/thin limb: Only permeable to water
- Asc limb: Active reabsorption of Sodium and chloride
3) PCT:
- pH balance - active transport H+/HCO3-
- Na, K regulation - active transport (aldosterone)
- Calcium regulation (PTH, 1,25 vit D)
4) CD
- water reabsorption (ADH)
- pH regulation (proton excretion)
Drugs to avoid in renal failure
Drugs likely to accumulate in renal failure (need dose adjusting)
NSAIDs
Antibiotics: tetracycline, nitrofurantoin
Lithium
Metformin
Dose adjusting needed
- Most antibiotics including penicillins, cephalosporins, vancomycin, gentamicin, streptomycin
- Digoxin, atenolol
- Methotrexate
- Sulphonylureas
- Furosemide
- Opioids - Oxycodone is mainly metabolised in the liver and thus SAFER to use in patients with moderate to end-stage renal failure with dose reductions.
AKI criteria to define
KDIGO - any of:
1) Rise in Cr 26 micromol/L in 48h
2) Rise in Cr 1.3 x baseline within 7 days
3) UO <0.5ml/kg/hr for 6 hours
Stage 1 - 1.5 -1.9 x baseline sCr or - 26 or more micro mol/L \+ - UO <0.5ml/kg/h for 6 h
Stage 2
- 2-2.9 x baseline sCr
+
- UO <0.5ml/kg/h for 12 h
Stage 3 - 3 x baseline sCr or -354 or more micromol/L \+ - Anuria for 12 h
Causes of AKI
1) Pre-renal
HYPOVOLAEMIA: Sepsis, haemorrhage, GI loss, RAS +/- ACEi, CCF (low CO), Liver failure, NSAIDs
–> cause renal ischaemia
2) Renal Glomerulonephritis Acute Tubular Necrosis Interstitial disease Iatrogenic (contrast, nephrotoxins e.g. aminoglycosides) Vasculitis Rhabdomyoloysis
3) Post-renal Stones Neoplasm Inflammation - stricture, retroperitoneal fibrosis Prostate Posterior urethral valves Infection Neuropathic
Indications for acute dialysis
1) Persistent acidosis (ph <7.2 or BE <10)
2) Persistent hyperkalaemia >7
3) Fluid overload, refractive pulmonary oedema
4) Symptomatic uraemia e.g. pericarditis, encephalopathy
Drug OD: (BLAST)
- Barbituates
- Lithium
- Alcohol
- Salicyclates
- Theophylinne
Presentation of renal failure
Anaaemia
- Breathlessness Lethargy Faintness Tinnitus
- Pallor Tachycardia Flow mumurs (ESM @ apex)
Acidosis
- Breathlessness Confusion
- Signs: Kussmaul breathing
Bone (Vit D deficiency
- Bone pain #s
- Signs: Osteomalacia, Looser’s zones (pseudo#s) - Cupped mataphyses
Clearance (Uraemia)
Pruritus, n/v, anorexia, wt. loss Lethargy, Confusion, Restless legs, Metallic taste Paraesthesia: neuropathy, Bleeding, Chest pain: serositis Hiccoughs
- Signs: Pale, sallow skin, Striae, Pericardial or plueral rub, Fits, Coma
Electrolytes - hyperkalaemia
- Palpitations, Chest pain, Weakness
- Signs: Peaked T waves Flattened P waves, ↑ PR interval, Widened QRS Sine-wave pattern → VF
Fluid balance
- Polyuria, polydipsia Oliguria, anuria Breathlessness
- Signs: Oedema, ↑ JVP, HTN (or ↓BP)
AKI presentation
- Uraemia / Azotaemia
- Acidosis
- Hyperkalaemia
- Fluid overload
- Oedema, inc. pulmonary ↑BP(or↓)
- S3 gallop
- ↑ JVP
AKI
Clinical assessment
Investigations
- Acute or chronic?
- Can’t tell for sure: Rx as acute
- Chronic features: Hx of comorbidity: DM, HTN; Long duration of symptoms; Previously abnormal bloods (GP records) - Volume depleted?
- Postural hypotension
- ↓ JVP
- ↑ pulse
- Poor skin turgor, dry mucus membranes - GU tract obstruction?
- Suprapubic discomfort
- Palpable bladder
- Enlarged prostate
- Catheter
- Complete anuria (rare in ARF) - Rare cause?
- Assoc. ̄c proteinuria ± haematuria
- Vasculitis: rash, arthralgia, nosebleed
INVESTIGATIONS Bloods: FBC, U+E, LFT, glucose, clotting, Ca, ESR ABG: hypoxia (oedema), acidosis, ↑K+ GN screen: if cause unclear Urine: dip, MCS, chemistry (U+E, PCR, osmolality, BJP) ECG: hyperkalaemia CXR: pulmonary oedema Renal US: Renal size, hydronephrosis
What does a specialist renal screen involve
Vasculitis screen: ANA, ANCA, Anti-GBM Complement; dsDNA (SLE) Viral HIV, Hep B/C Protein electrophoresis CK
Hyperkalaemai mangament
10 ml 10% Calcium Chloride IV
50 ml 50% Glucose with 10U insulin
Salbutamol - Give 10 mg if history of IHD. Avoid if tachyarrhythmia present
Other
Calcium resonium (orally or enema)
- enemas are more effective than oral as potassium is secreted by the rectum
Loop diuretics
Dialysis
- haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia
Acute interstitial nephritis
Causes
Features
Causes drugs: the most common cause, particularly antibiotics - penicillin - rifampicin - NSAIDs - allopurinol - furosemide Systemic disease: SLE, sarcoidosis, and Sjögren's syndrome Infection: Hanta virus , staphylococci
Features fever, rash, arthralgia eosinophilia mild renal impairment hypertension
Complications of being on long term immunosuppression for organ transplantation
Cardiovascular disease - tacrolimus and ciclosporin can cause hypertension and hyperglycaemia. Tacrolimus can also cause hyperlipidaemia. Patients must be monitored for accelerated cardiovascular disease.
Renal failure - due to nephrotoxic effects of tacrolimus and ciclosporin/graft rejection/recurrence of original disease in transplanted kidney
Malignancy - patients should be educated about minimising sun exposure to reduce the risk of squamous cell carcinomas and basal cell carcinoma
Nephrotic syndrome
RISK
Causes
Triad of:
- Proteinuria (> 3g/24hr) causing
- Hypoalbuminaemia (< 30g/L) and
- Oedema
Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis. Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels.
Causes
- DM
- Amyloidosis
- Minimal change disease
- Membranous GN (can be associated with SLE)
- FSGS
Both nephrotic + nephritic
- Diffuse proliferative GN
- Membranoproliferation GN
- Post strep GN
Minimal change disease
Causes
Features
Management
Prognosis
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis
Features - Nephrotic syndrome - Normotension - hypertension is rare - Highly selective proteinuria only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus renal biopsy - Normal glomeruli on light microscopy - Electron microscopy shows fusion of podocytes and effacement of foot processes
Management
Majority of cases (80%) are steroid-responsive
Cyclophosphamide is the next step for steroid-resistant cases
Prognosis
Prognosis is overall good, although relapse is common. Roughly:
1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood
DI define
Causes
Features
Investigation
Either a deficiency of antidiuretic hormone, ADH, (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).
Causes of cranial DI idiopathic post head injury pituitary surgery craniopharyngiomas histiocytosis X DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome) haemochromatosis
Causes of nephrogenic DI
genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
- electrolytes: HYPERcalcaemia, hypokalaemia
- drugs: demeclocycline, LITHIUM
- tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
Features
polyuria
polydipsia
Investigation
High plasma osmolality, Low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test
Management
nephrogenic diabetes insipidus: thiazides, low salt/protein diet
central diabetes insipidus can be treated with desmopressin
ADPKD
Features
Extra-renal manifestatiomns
Features hypertension recurrent UTIs abdominal pain renal stones haematuria chronic kidney disease
Extra-renal manifestations
liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly
berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
CKD Stagea
CKD stages -
1 Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a 45-59 ml/min, a moderate reduction in kidney function
3b 30-44 ml/min, a moderate reduction in kidney function
4 15-29 ml/min, a severe reduction in kidney function
5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
Hypokalaemia
Causes
Management
Causes can be secondary to:
1.) Increased potassium loss:
Drugs: thiazides, loop diuretics, laxatives, glucocorticoids, antibiotics
GI losses: diarrhoea, vomiting, ileostomy
Renal causes: dialysis
Endocrine disorders: hyperaldosteronism, Cushing’s syndrome
2.) Trans-cellular shift Insulin/glucose therapy Salbutamol Theophylline Metabolic alkalosis
- ) Decreased potassium intake
- ) Magnesium depletion (associated with increased potassium loss)
ECG changes seen in hypokalaemia include:
U waves
T wave flattening
ST segment changes
Treatment of hypokalaemia depends on severity. Any causative agents should be removed. Gradual replacement of potassium via the oral route is preferred if possible.
Mild to moderate hypokalaemia 2.5 - 3.4 mmol/l can be treated with oral potassium provided the patient is not symptomatic and there are no ECG changes.
Severe hypokalaemia (<2.5mmol/l) or symptomatic hypokalaemia should be managed with IV replacement. The patient should be managed in an area where cardiac monitoring can take place. If there are no contraindications to fluid therapy (e.g. volume overload, heart failure) potassium should be diluted to low concentrations as higher concentrations can be phlebitic. The infusion rate should not exceed 20mmol/hr.
HUS
Cause
Investigations
Management
Haemolytic uraemic syndrome is generally seen in young children and produces a triad of:
1) acute kidney injury
2) microangiopathic haemolytic anaemia
3) thrombocytopenia
Most cases are secondary (termed ‘typical HUS’):
classically Shiga toxin-producing Escherichia coli (STEC) 0157:H7 (‘verotoxigenic’, ‘enterohaemorrhagic’). This is the most common cause in children, accounting for over 90% of cases
pneumococcal infection
HIV
rare: systemic lupus erythematosus, drugs, cancer
Primary HUS (‘atypical’) is due to complement dysregulation.
Investigations
full blood count: anaemia, thrombocytopaenia, fragmented blood film
U&E: acute kidney injury
stool culture
Management
treatment is supportive e.g. Fluids, blood transfusion and dialysis if required
there is no role for antibiotics, despite the preceding diarrhoeal illness in many patients
Indications for plasma exchange in HUS are complicated. As a general rule plasma exchange is reserved for severe cases of HUS not associated with diarrhoea
Eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS
Rhabdomyolysis
Features
Causes
Management
Rhabdomyolysis will typically feature in the exam as a patient who has had a fall or prolonged epileptic seizure and is found to have an acute kidney injury on admission.
Features
acute kidney injury with disproportionately raised creatinine
elevated creatine kinase (CK)
myoglobinuria
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia (may develop before renal failure)
metabolic acidosis
Causes
seizure
collapse/coma (e.g. elderly patients collapses at home, found 8 hours later)
ecstasy
crush injury
McArdle’s syndrome
drugs: statins (especially if co-prescribed with clarithromycin)
Management
IV fluids to maintain good urine output
urinary alkalinization is sometimes used
What are Arteriovenous fistulas
How are they made
Time to develop
Potential complications
Arteriovenous fistulas are direct connections between arteries and veins. They may occur pathologically but are generally formed surgically to allow access for haemodialysis.
They are now regarded as the preferred method of access for haemodialysis due to the lower rates of complications.
The time taken for an arteriovenous fistula to develop is 6 to 8 weeks.
Potential complications include: Infection Thrombosis May be detected by the absence of a bruit Stenosis May present with acute limb pain Steal syndrome
Causes of a normal anion gap or hyperchloraemic metabolic acidosis
What is a normal anion gap
Causes of a normal anion gap or hyperchloraemic metabolic acidosis
GI bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula Renal tubular acidosis Drugs: e.g. acetazolamide ammonium chloride injection Addison's disease
A normal anion gap is 8-14 mmol/L
Calculation: (sodium + potassium) - (bicarbonate + chloride)
Causes of a raised anion gap metabolic acidosis
What is a normal anion gap
Causes of a raised anion gap metabolic acidosis
Lactate: shock, hypoxia Ketones: diabetic ketoacidosis, alcohol Urate: renal failure Acid poisoning: salicylates, methanol 5-oxoproline: chronic paracetamol use
A normal anion gap is 8-14 mmol/L
