Renal & Urology Flashcards
What is nephrotic syndrome?
Triad:
- Proteinuria (>3.5 g/24 hours)
- Hypoalbuminaemia (<30 g/L)
- Peripheral oedema
Hypercholesterolaemia also a common feature
What are the causes of nephrotic syndrome?
Most commonly caused by minimal change glomerulonephritis in children
However, all forms of glomerulonephritis can cause it
Other causes: DM SCD Amyloidosis Malignancy - lung and GI adenocarcinomas Drugs - NSAIDs Alport's syndrome HIV
What are the risk factors for nephrotic syndrome?
- Medical conditions that can damage your kidneys - DM, lupus, amyloidosis
- Drugs - NSAIDs, drugs used to fight infections
- Certain infections - HIV, hep B, hep C, malaria
Summarise the epidemiology of nephrotic syndrome
Usually adults
M:F = 2:1
What are the presenting symptoms of nephrotic syndrome?
FHx of atopy
FHx of renal disease
Swelling of face, abdo, limbs, genitalia (due to hypoAlb)
Weight gain - due to excessive fluid retention
Fatigue
Foamy urine
Loss of appetite
What are the signs of nephrotic syndrome?
Oedema: periorbital, peripheral, genital
Ascites: fluid thrill, shifting dullness
How is nephrotic syndrome investigated?
Urinanalysis - ++++ proteinuria > 3.5g over 24h
- protein looks frothy
Bloods - hypoalbuminaemia + hyperlipidaemia
Tests to identify cause:
- SLE: ANA, anti-dsDNA antibodies
- Infections: ASO titre for group A B-haemolytic streptococcal infection; HBV serology; Plasmodium malariae blood film
- Goodpasture’s syndrome: anti-glomerular basement antibodies
- vasculitides - polyangiitis w granulomatosis, microscopic polyarteritis (check ANCA)
Renal US
Renal biopsy
What is AKI?
An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes
Explain the aetiology of AKI
May be multifactorial
- Pre-renal:
- Decreased vascular volume: haemorrhage, D+V, burns, pancreatitis
- Decreased CO: cardiogenic shock, MI
- Systemic vasodilation: sepsis, drugs
- Renal vasoconstriction: NSAIDs, ACE-i, ARB, hepatorenal syndrome - Renal:
- Glomerular: glomerulonephritis, acute tubular necrosis
- Interstitial: drug reaction, infection, infiltration (eg sarcoid)
- Vessels: vasculitis, HUS, TTP, DIC - Post-renal:
- Within renal tract: stone, renal tract malignancy, stricture, clot
- Extrinsic compression: pelvic malignancy, prostatic hypertrophy, retroperitoneal fibrosis
What are the risk factors for AKI
Pre-existing CKD
Age
Male
Comorbidity - DM, CVD, malignancy, chronic liver disease, complex surgery
What are the presenting symptoms of AKI?
Depends on underlying cause
- Oliguria/anuria (abrupt anuria suggests post-renal obstruction)
- N+V
- Dehydration
- Confusion
What are the signs of AKI O/E?
- Hypertension
- Distended bladder
- Dehydration
- Postural hypotension
- Fluid overload (in HF, cirrhosis, nephrotic syndrome)
- Raised JVP
- Pulmonary and peripheral oedema
- Pallor, rash, bruising (vascular disease)
How is AKI investigated?
- Urinanalysis
- Blood - suggests nephritic cause
- Leucocyte esterase and nitrites - UTI
- Glucose
- Protein
- Urine osmolality - Bloods
FBC, film, U+Es, clotting, CRP, virology (hepatitis, HIV) - Immunology
- Serum Igs + protein electrophoresis for multiple myeloma - also look for Bence-Jones proteins in urine
- ANA, anti-dsDNA abs (active lupus) - SLE
- Low omplement levels - active lupus
- Anti-GBM antibodies - Goodpasture’s syndrome
- Antistreptolysin-O antibodies - high after Streptococcal infection - Ultrasound
- Check for post-renal cause
- Look for hydronephrosis - Other imaging
- CXR: pulm oedema
- AXR: renal stones
How is AKI managed?
Treat the cause
4 main components:
- Protect patient from hyperkalaemia (calcium gluconate)
- Optimise fluid balance
- Stop nephrotoxic drugs
- Consider for dialysis
- Monitor serum Cr, Na, K, Ca, phosphate, glucose
- Identify and treat infection
- Urgent relief of urinary tract obstruction
- Refer to nephrology if intrinsic renal disease suspected
- Renal replacement therapy (RRT) if:
- HyperK/pulm oedema refractory to medical Mx
- Severe metabolic acidaemia
- Uraemic complications
What are the possible complications of AKI?
Pulmonary oedema Acidaemia Uraemia Hyperkalaemia Bleeding
What are the indicators for poor prognosis of AKI?
Inpatient mortality varies depending on cause and comorbidities
Age Multiple organ failure Oliguria Hypotension CKD
What are the most common causes of AKI
- Sepsis
- Major surgery
- Cardiogenic shock
- Other hypovolaemia
- Drugs
- Hepatorenal syndrome
- Obstruction
What is the in the KDIGO classification of AKI?
Rise in creatinine > 26 micromol/L within 48h
Rise in creatinine > 1.5 x baseline (ie before AKI) within 7 days
Urine output <0.5mL/kg/h for >6 consecutive hours
What is the in the KDIGO classification of AKI?
Rise in creatinine > 26 micromol/L within 48h
Rise in creatinine > 1.5 x baseline (ie before AKI) within 7 days
Urine output <0.5mL/kg/h for >6 consecutive hours
What is amyloidosis?
A group of disorders characterised by extracellular deposits of a protein in abnormal fibrillar form, resistant to degradation
AL - primary
AA - secondary
Familial
Summarise the epidemiology of amyloidosis
UK:
- age-adjusted incidence = 5.1-12.8/million/yr
- 60 new cases annually
- Higher in males
- Mean age of diagnosis = 63
- Higher in Blacks, lower in Asians
- AA = 10% of systemic amyloidosis
What are the risk factors for amyloidosis?
- Monoclonal gammopathy of undetermined significance (MGUS)
- Inflammatory polyarthropathy - most common AA cause
- Chronic infections –> AA
- IBD (Crohn’s esp.) –> AA
- Familial periodic fever syndromes –> AA
(6. Castleman’s disease - non-cancerous tumours of lymphoid tissue - plasma cell variant –> AA)
What are the presenting symptoms of amyloidosis?
Fatigue
Extreme weight loss
Dyspnoea on exertion
What are the signs of amyloidosis O/E?
- Raised JVP
- Lower extremity peripheral oedema (due to hypoalbuminaemia from nephrotic syndrome)
Less so:
- Periorbital purpura (highly specific)
- Macroglossia (highly specific for AL primary)
How is amyloidosis investigated?
- Serum immunofixation
- positive for monoclonal protein in 60% of patients w immunoglobulin light chain amyloidosis - Urine immunofixation
- positive for monoclonal protein in 80% of patients w AL
- presence of light chain protein suggestive of multiple myeloma and amyloidosis - Immunoglobulin free light chain assay
- abnormal kappa:lambda
- extremely high sensitivity, >95%, for diagnosing AL - Bone marrow biopsy
- clonal plasma cells
How is amyloidosis investigated?
- Serum immunofixation
- positive for monoclonal protein in 60% of patients w immunoglobulin light chain amyloidosis - Urine immunofixation
- positive for monoclonal protein in 80% of patients w AL
- presence of light chain protein suggestive of multiple myeloma and amyloidosis - Immunoglobulin free light chain assay
- abnormal kappa:lambda
- extremely high sensitivity, >95%, for diagnosing AL - Bone marrow biopsy
- clonal plasma cells
What is benign prostatic hyperplasia?
Slowly progressive nodular hyperplasia of the periurethral (transitional) zone of the prostate gland
Summarise the epidemiology of benign prostatic hyperplasia
Common
70% of men > 70 yrs have histological BPH
50% of them experience symptoms
More common in West
More common in Afro-Caribbeans
What is the aetiology of benign prostatic hyperplasia?
UNKNOWN
Link with hormonal changed (androgens)
What are the risk factors for benign prostatic hyperplasia?
- Over 50
- FHx
- Non-Asian
- Smoking
What are the presenting symptoms of benign prostatic hyperplasia?
FUND HIPS - storage and voiding symptoms: Frequency Urgency Nocturia Dysuria/dribbling Hesitancy Incomplete voiding Poor stream Smell/odour
Acute retention symptoms:
- Sudden inability to pass urine
- Severe pain
Chronic retention symptoms:
- Painless
- Frequency - passage of small volumes
- Nocturia
What are the signs of benign prostatic hyperplasia O/E?
DRE: smoothly enlarged prostate w palpable midline groove
Signs of acute retention:
Suprapubic pain
Distended, palpable bladder
Signs of chronic retention:
Large distended painless bladder (vol > 1L)
Signs of renal failure
How is benign prostatic hyperplasia investigated?
- Urinanalysis - pyuria (white cells or pus) - complicated UTI
- Bloods
PSA - elevated - underlying prostate Ca or prostatitis
U+Es - impaired renal function - Midstream urine - MC&S
- International Prostate Symptom Score
- Global bother score
- Volume charting
How is benign prostatic hyperplasia managed?
In emergency (acute urinary retention): catheterisation
Conservative (if mild): watchful waiting
Medical:
- selective alpha blocker (tamsulosin) relax smooth muscle of internal sphincter and prostate capsule
- 5a-reductase inhibitors (finasteride) inhibit conversion of testosterone to DHT, can reduce prostate size by 20%
Surgery:
TURP
Open prostatectomy
What are the possible complications of benign prostatic hyperplasia?
Recurrent UTI Acute or chronic urinary retention Urinary stasis Bladder diverticula Stone development Obstructive renal failure Post-obstructive diuresis
What is the prognosis of benign prostatic hyperplasia?
- Mild symptoms usually well controlled medically
- Most patients get significant relief from surgery
What is TURP?
Transurethral resection of prostate
What are the indications for TURP?
BPH
What are the possible complications of TURP?
- Retrograde ejaculation (up into bladder bc internal sphincter is relaxed)
- Haemorrhage
- Incontinence
- TURP syndrome: seizures or CV collapse due to hypervolaemia and hypoNa due to absorption of glycine irrigation fluid)
- Urinary infection
- Erectile dysfunction
- Urethral stricture
What are epididymitis and orchitis?
Inflammation of the epididymis or testes
Summarise the epidemiology of epididymitis and orchitis
Common
Affects all age groups
Most common 20-30yo
What are the aetiologies of epididymitis and orchitis?
Most cases are INFECTIVE in origin
Bacterial:
If <35: Chlamydia, Gonococcus
If >35: mainly coliforms (Enterobacter, Klebsiella)
Rare: TB, syphilis
Viral: mumps
Fungal: Candida if immunocompromised
1/3 are idiopathic
What are the risk factors for epididymitis and orchitis?
Diabetes
Rare: vasculitis (eg Henoch-Scholein purpura)
What are the presenting symptoms of epididymitis and orchitis?
- Painful, swollen and tender testis or epididymis
- Penile discharge
What are the signs of epididymitis and orchitis O/E?
- Swollen and tender epididymis or testis
- Scrotum may be erythematous and oedematous
- Pyrexia
- Painful walking
- Eliciting cremasteric reflex may be painful
How are epididymitis and orchitis investigated?
- Urine: dipstick + early morning for Mc&S
- Bloods:
FBC - high WCC
High CRP
U+Es - Imaging: increased blood flow on duplex examination
How are epididymitis and orchitis managed?
Medical: ABx
Surgical:
- exploration of testicles if testicular torsion cannot be excluded clinically
- required if abscess develops
What are the possible complications of epididymitis and orchitis?
- Pain
- Abscess
- Fournier’s gangrene (if infection left untreated and spreads)
- Mumps orchitis could cause testicular atrophy and fertility issues
What are the prognoses of epididymitis and orchitis?
Good if treated
May take up to 2 months for swelling to resolve
How does the onset of epididymitis or orchitis differ from that of testicular torsion?
Less acute onset
What is chronic kidney disease?
Progressive loss of kidney function over a period of months or years
Summarise the epidemiology of CKD
Common
Risk increases with age
Often associated with other diseases, eg CVD
What is the aetiology of CKD?
Most common cause in adults = diabetes (1/3 develop KD within 5-10yrs of diagnosis)
HTN = 2nd most common cause
Less common causes = polycystic kidney disease obstructive uropathy glomerular nephrotic and nephritic syndromes membranous nephropathy lupus nephritis amyloidosis rapidly progressive glomerulonephritis
What are the risk factors for CKD?
DM
HTN
>50
Childhood kidney disease
What are the presenting symptoms of CKD?
Often asymptomatic
May be incidental finding of routine blood/urine test
Anorexia N+V Fatigue Pruritus Peripheral oedema Muscle cramps Sexual dysfunction
What are the signs of CKD O/E?
May show signs of underlying disease (eg SLE)
May show complications of CKD (eg anaemia)
Skin pigmentation Excoriation marks Pallor HTN Peripheral + pulmonary oedema Peripheral vascular disease
How is CKD investigated?
- Assessment of renal function: urea, creatinine, isotopic GFR (gold standard)
- Biochemistry:
- glucose: check for undiagnosed DM and diabetic control
- raised K
- also check Na, HCO3, Ca, PO4 - Serology:
- antibodies: ANA for SLE< c-ANCA for Wegener’s, anti-GBM for Goodpasture’s
- hepatitis serology
- HIV serology - Urinanalysis:
- check for proteinuria/haematuria
- 24h urine collection
- serum or urine protein electrophoresis - check for multiple myeloma - Imaging:
- US to check for structural abnormalities
- CT/MRI
- XR KUB - check for stones - Renal biopsy
What is a limitation of using creatinine to assess renal function?
Renal function can drop considerably with minimal change in serum creatinine
Why is looking at serum urea not ideal to assess renal function
Varies massively depending on hydration status and diet
What is glomerulonephritis?
An immunologically mediated inflammation of the renal glomeruli
Summarise the epidemiology of glomerulonephritis
Accounts for 25% of cases of chronic renal failure