Renal + Urology High Yield Flashcards
what are Renal stones and their types
AKA renal calculi, urolithiasis and nephrolithiasis
RF
- dehydration
- hypercalciuria, hyperparathyroidism, hypercalcaemia
- cystinuria
- high dietary oxalate + protein diet
- antacids
- renal tubular acidosis
Drug causes
- drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline
- thiazides can prevent calcium stones (increase distal tubular calcium resorption)
- May be asymptomatic until they irritate or get stuck in the ureters. Usually stuck a 3 junctionsCommonly at vesico-ureteric joint
- Can cause obstruction (AKI) and/or infection (pyelonephritis)
Types
- Calcium Oxalatae - Most common 85% - Radio-opaque on Xray.
- Calcium Phosphate - 10% - Radio-opaque on Xray
- Uric Acid - 5-10%, low pH, product of purine metabolism, cancers?, Radio-lucent
- Struvite 2 -20%, result of urease producing bacteria ( associated with chronic infections) - Radio-opaque
- Cysteine 1%, associated with cystinuria, an autosomal recessive disease - radio-dense
Staghorn Calculus stone forms in the shape of the renal pelvis. Common with Struvite stones where bacteria (from URTI or other infection) converts urine into ammonia. Infection with Proteus mirabilis accounts for 90% of all proteus infection
Presentation of Nephrolithiasis
Renal stones may be asymptomatic and never cause an issue.
When they do it leads to: Renal Colic
Renal Colic
- Unilateral loin to groin pain that can be excruciating (“worse than childbirth”)
- Colicky (fluctuating in severity) as the stone moves and settles
- Nausea or vomiting
Also
There may also be:
- Excessive movements
- Haematuria
- Reduced urine output
- Symptoms of sepsis, if infection is present
Management of Renal Colic
include investigations
- IM Diclofenac - IV paracetamol if NSAID contraindicated
- Alpha Blocker - Tamsulosin - If stone <10mm (smooth muscle relaxation and dilation)
Investigations
- Urine dipstick: checkking for haematauria and Infections
- Serum creatinine and electrolytes: check renal function
- FBC/CRP: looking for Infections
- Non Contrast CT-KUB within 24h of admission, if feverish or solitary kidney then investigate as soon as
- USS used in children and pregnant ladies - low sensitivity
Management of Confirmed Nephrolithiasis in Renal Vs Uretic
after managing renal colic and confirmed using CT-KUB
Shockwave lithotripsy
Ureteroscopy
nephrolithotomy
Renal
- If stone is <5mm = wait & watch
- 5mm-10mm - shockwave lithotripsy
- 10-20 mm shockwave lithotripsy OR ureteroscopy
- > 20 mm percutaneous nephrolithotomy
Uretic
- Stone <10mm Shockwave lithrotripsy + Tamsulosin
- 10-20 mm ureteroscopy
Severe Cases
- Infection presents with stones
- Needs Renal Decompression + abx
- Nephrostomy tube placement, insertion of ureteric catheters and ureteric stent placement.
Lithotripsy contraindicated in pregnancy
Prevention of future Nephrolithiasis occurence
Calcium stones
may be due to hypercalciuria, which is found in up to 5-10% of the general population.
high fluid intake
add lemon juice to drinking water
avoid carbonated drinks
limit salt intake
potassium citrate may be beneficial
thiazides diuretics (increase distal tubular calcium resorption)
Oxalate stones
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion
Uric acid stones
allopurinol
urinary alkalinization e.g. oral bicarbonate
Acute Kidney Injury Definition (incl. signs + symptoms)
common in acutely unwell patients
RF
- Older age (e.g., above 65 years)
- Sepsis
- Chronic kidney disease
- Heart failure
- Diabetes
- Liver disease
- Cognitive impairment (leading to reduced fluid intake)
- Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
- Radiocontrast agents (e.g., used during CT scans)
- Rise in creatinine of more than 25 micromol/L in 48 hours
- Rise in creatinine of more than 50% in 7 days
- Urine output of less than 0.5 ml/kg/hour over at least 6 hours
Symptoms - often not seen untill diseases progression
- pulmonary and peripheral oedema
- arrhythmias (secondary to changes in potassium and acid-base balance)
- features of uraemia (for example, pericarditis or encephalopathy)
Stage 1: 0.5 ml/kg/hour over at least 6 hours. Creatinine 2x baseline
Stage 2 0.5 ml/kg/hour over at least 12 hours Creatinine up to 3x baseline
Stage 3: 0.3 ml/kg/hour over at least 24h Creatinine more than 3x baseline
Causes of AKI
Divided into 3
Pre-Renal Insufficient blood supply (hypoperfusion) to kidneys reduces the filtration of blood. This may be due to:
- Hydration
- Shock (e.g., sepsis or acute blood loss)
- Heart failure
- Renal Artery stenosis
Renal (Intrinsic diease of kidney)
- Acute tubular necrosis
- Glomerulonephritis
- Acute interstitial nephritis
- Haemolytic uraemic syndrome
- Rhabdomyolysis
- Tumour Lysis Syndrome
Post-Renal causes involve obstruction to the outflow of urine away from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy. Obstruction may be caused by:
- kidney stone in ureter or bladder
- benign prostatic hyperplasia
- external compression of the ureter
- tumours
Management of AKI
Largely Supportive
What are the complications of unresolved AKI
- Stop Drugs with nephrotoxic potential
- Ok to continue with: Paracetamol, warfarin, aspirin (75mg), Clopidogrel, statins, B Blockers.
- Carefully moniotred Fluids
Specialist is reqd for when the cause is unknown or the AKI is severe.
Complications
Fluid overload, heart failure and pulmonary oedema
Hyperkalaemia
Metabolic acidosis
Uraemia (high urea), which can lead to encephalopathy and pericarditis
These indicate haemodialysis
Treating Hyperkalaemia in AKI
to avoid arrhythmias which may potentially be life-threatening
Stabilising Cardiac Membrane
- Calcium Gluconate
Shifting K+ from ECF to ICF
- Combined insulin/dextrose infusion
- Nebulised salbutamol
Removal of potassium from the body
- Calcium resonium (orally or enema)
- Loop diuretics
- Dialysis
When is Renal Replacement Therapy indicated in AKI
Renal replacement therapy (e.g. haemodialysis) is used when a patient is not responding to medical treatment of complications, for example hyperkalaemia, pulmonary oedema, acidosis or uraemia (e.g. pericarditis, encephalopathy).
Differentiating between AKI and CKD
- CKD: Bilateral small kidneys USS.
Except: ADPCKD, diabetic nepthropathy, amyloidosis, HIV - CKD: Hypocalcaemia due to no VitD.
Acute interstitial nephritis
Acute interstitial nephritis accounts for 25% of drug-induced AKI
Causes
Drugs: the most common cause, particularly antibiotics
- penicillin
- rifampicin
- NSAIDs
- allopurinol
- furosemide
Systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci
Histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules
Symptoms: Fever, Rash, Arthralgia, eosionophila (excess eosinophills), renal impairment, HTN
Ix: sterile pyuria + white cell casts
- RAISED EOSINOPHILS
Drugs with nephrotoxic potential
- NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
- Aminoglycosides
- ACE inhibitors
- Angiotensin II receptor antagonists
- Diuretics
Metformin, Lithium + Digoxin : NOT NEPHROTOXIC but stopped in AKI
Acute Tubular Necrosis
often due to: Ischaemia or Nephrotoxins
damage and death (necrosis) of the epithelial cells of the renal tubules. It is the most common intrinsic cause of acute kidney injury.
- Muddy brown casts on urinalysis confirm acute tubular necrosis
- Renal tubular epithelial cells may also be seen
- The epithelial cells can regenerate, making acute tubular necrosis reversible. Recovery usually takes 1-3 weeks.
Feautures and causes of CKD
Definition: Chronic reduction in kidney function sustained over three months. It tends to be permanent and progressive.
Feautures: oft asymptomatic, Fatigue, Pallor (due to anaemia), Foamy urine (proteinuria), Nausea, Loss of appetite, Pruritus (itching) , Oedema, Hypertension, Peripheral neuropathy, Polyuria
Causes: Diabetes, Hypertension, Medications (e.g., NSAIDs or lithium), Glomerulonephritis, Polycystic kidney disease
Classification of CKD
Factors which may affect the result
- pregnancy
- muscle mass (e.g. amputees, body-builders)
- eating red meat 12 hours prior to the sample being taken
- Estimated glomerular filtration rate (eGFR) is sustained below 60 mL/min/1.73 m2
- Urine albumin:creatinine ratio (ACR) is sustained above 3 mg/mmol
Staging
- 1 > 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
A diagnosis can be made when there are consistent results over 3 months
Most common eGFR used:
Modification of Diet in Renal Disease (MDRD) equation, which uses the following variables:
- serum creatinine
- age
- gender
- ethnicity
Complications of CKD
- Anaemia : reduced erythropoietin levels -> low RBC. normochromic normocytic anaemia.perform iron studies before commencing treatment
-
Bone Disease: High serum phosphate
Low vitamin D activity
Low serum calcium
These serum abnormalities lead to more parathyroid hormone release: Secondary Hyperparathyroidism
The following bone diseases seen due to this Osteitis fibrosa cysticae, Adynamic, Osteomalacia, Osteosclerosis, Osteoporosis - Hypertension: most require more than two drugs to treat hypertension
- Proteinuria: Proteinuria is an important marker of chronic kidney disease, especially for diabetic nephropathy. NICE recommend using the albumin:creatinine ratio (ACR)
the NICE guidelines state ‘regard a confirmed ACR of 3 mg/mmol or more as clinically important proteinuria’
Management of CKD
What can slow disease progression?
Treating the underlying cause involves:
Optimising diabetic control
Optimising hypertension control
Reducing or avoiding nephrotoxic drugs (where appropriate)
Treating glomerulonephritis (where this is the cause)
ACE inhibitors (or angiotensin II receptor blockers)
key in the management of proteinuria
they should be used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol
if the ACR > 70 mg/mmol they are indicated regardless of the patient’s blood pressure
SGLT-2 inhibitors (dapagliflozin)
patients who have proteinuric CKD (with or without diabetes) may benefit from treatment with SGLT2 inhibitors
they primarily act by blocking reabsorption of glucose in the proximal tubule → lowers the renal glucose threshold → glycosuria
by blocking the cotransporter, they also reduce sodium reabsorption → natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa → normalizes tubuloglomerular feedback and thereby reduces intraglomerular pressure
Management of end-stage renal disease involves:
- Special dietary advice
- Dialysis
- Renal transplant
Epididymo-orchitis
Epididymitis is inflammation of the epididymis. Orchitis is inflammation of the testicle. Epididymo-orchitis is usually the result of infection in the epididymis and testicle on one side.
- Gradual, unilateral Pain + swelling of testicle due to infection spread, commonly: chylamydia + gonorrhoea and e.coli elderly. and other cause could be mumps
- urethral discharge may be present, but urethritis is often asymptomatic
- Ix: young: STI screen Elderly: sexual history and MSU sample
- Elevation of the testis DOES ease the pain (Prehn’s sign)
- Tx: STI: ceftriaxone 500mg IM + oral doxycycline 100mg BDS for 10-14 days. Enteric Organism: oral quinolone for 2 weeks (e.g. ofloxacin) (co-amoxiclav if contraindicated)
most important differential diagnosis is testicular torsion - RULE OUT
Quinolone antibiotics such as ofloxacin, levofloxacin and ciprofloxacin are powerful broad-spectrum antibiotic with side effects:
1. Tendon damage and tendon rupture, notably in the Achilles tendon
2. Lower seizure threshold (caution in patients with epilepsy)
Testicular Cancer
Most common cancer in Males 20-30y
95% of cases of testicular cancer are germ-cell tumours.
Germ cell tumours may essentially be divided into:
1. Seminoma
2. Non Seminoma; Teratoma, embryonal, yolk sac, choriocarcinoma
Non Germ Cell include: Leydig cell tumours + sarcomas
RF: cryptorchidism, Klinefelter’s syndrome, Infertility
Symptoms: Hydrocele, painless testicular bump, Gynaecomastia (due to increased oestrogen:androgen ratio - Leydigs tumour)
Ix:
- seminomas: hCG may be elevated in around 20%
- non-seminomas: AFP and/or beta-hCG are elevated in 80-85%
- LDH is elevated in around 40% of germ cell tumours
Diagnosis: ultrasound is first-line
Management: treatment depends on whether the tumour is a seminoma or a non-seminoma
- orchidectomy
Seminomas have a better prognosis than teratoma
typical teenage boy presentation
Testicular Torsion
twisting of the spermatic cord with rotation of the testicle
If untreated can lead to ischaemia -> subfertility/infertility
- acute rapid onset of unilateral testicular pain +/- N&V
- Elevated (retracted) testicle
- Absent cremasteric reflex
- Elevation of the testis does not ease the pain (Prehn’s sign)
- Rotated Epididymis - abnormal testicular lie
- Bell-clapper deformity is where the fixation between the testicle and the tunica vaginalis is absent - correct this bilaterally when performing surgery for testicular torsion.
- USS: Whirlpool sign
Management
- Orchiopexy (correcting the position of the testicles and fixing them in place)
- Orchidectomy (removing the testicle) if the surgery is delayed or there is necrosis
Varicocele
veins in the pampiniform plexus
Varicoceles are the result of increased resistance in the testicular vein. Incompetent valves in the testicular vein allow blood to flow back from the testicular vein into the pampiniform plexus.
The right testicular vein drains directly into the inferior vena cava. The left testicular vein drains into the left renal vein.
- Abnormal enlargement of the testicular veins
- Usually asymptomatic but may be important as they are associated with infertility
- More common on the left side (> 80%). due to increased resistance in the left testicular vein.
- A left-sided varicocele can indicate an obstruction of the left testicular vein caused by a renal cell carcinoma.
- Diagnosis via USS
- Examination: Feels like bag of Worms
- Management: Usually conservative, occasionally surgery is required if the patient is troubled by pain
They may result in testicular atrophy, reducing the size and function of the testicle.
- Affected veins regulate the temperature of blood entering the testes by absorbing heat from the nearby testicular artery. The testicles need to be at an optimum temperature for producing sperm.
Hydrocele features and management
communicating vs non-communicating
the accumulation of fluid within the tunica vaginalis
Communicating: processus vaginalis allowing peritoneal fluid to drain down into the scrotum. are common in newborn males (5-10%) resolve within the first few months.
Non-communicating: caused by excessive fluid production within the tunica vaginalis
Features
- soft, non-tender swelling hemi scrotum
- swelling confined to scrotum
- Transilluminates when light shines
- testis may be diffcult to palpate if too large.
Ix
- Treat infant hydrocele if unresolved by 1-2y
- Adults Conservative
- USS if suspicious of alternative pathology
Hydroceles may develop secondary to:
* epididymo-orchitis
* testicular torsion
* testicular tumours
Epididymal cysts features and associated conditions
Epididymal cysts are the most common cause of scrotal swellings seen in primary care
- separate from the body of the testicle
- found posterior to the testicle
- Single or multiple cysts
- May contain clear or opalescent fluid (spermatoceles)
- Usually occur over 40 years of age
It is usually possible to ‘get above the lump’ on examination
Associated conditions
* polycystic kidney disease
* cystic fibrosis
* von Hippel-Lindau syndrome
