Renal colic Flashcards
What is renal colic?
Refers to acute severe loin pain that occurs secondary to a urinary stone.
What is another name for urinary stones?
urolithiasis
What is the peak incidence age for symptomatic urinary stones in men and women?
Between 40-60 years in males and late 20’s in females
Why do patients experience pain (renal colic) when they have a urinary stones?
Obstruction to urinary flow within the ureter due to the urinary stones. Also spasms that occur in ureter
What are the signs and symptoms of renal stones?
Symptoms
Loin-to-groin pain (sever, sudden onset pain not relived by pain medication- pain is constant but can vary in severity)
(this means pain can radiate from the flank to groin)
Nausea and vomiting
Haematuria
Dysuria (painful urination)
Urgency
Patient is restless to obtain relief from pain
Some are asymptomatic
Signs Flank tenderness Haematuria (typically microscopic) Fever chills, Rigors
List the different types of renal stones
Calcium Oxalate Calcium phosphate Urate Magnesium Ammonium Phosphate (Struvite) Cysteine
Others
- Xanthine
- Idinavir
- Matrix
Describe the properties of calcium oxalate stones and how they are formed
- Most common type of stone
- Calcium oxalate is insoluble.
- Not forming this type of stone depend upon
inhibitors (citrate, magnesium) Loss of these inhibitors can promote stone formation - Shows up on Xrays
Formation -
- Calcium phosphate crystals accumulate in the Interstitium
- This leads to the formation of Randall’s plaques (calcification) at the loop of Henle
- This creates a surface for renal stones to form
- Renal stones formed in the tubules get stuck at the ducts of Bellini (collecting duct) at the papillary surface (most distal part of the duct)
There are 2 types of calcium oxalate stones what are they?
Dihydrate which are softer (700HU)
Monohydrate which are extremely hard (1500 HU)
Describe the properties of calcium phosphate crystals
Associated with 3 conditions:
- Hyperparathyroidism
- Distal Renal Tubular Acidosis (Type1)
• Medullar Sponge Kidney
(MSK)
Also associated with urinary stasis & partly with infection
Show up reasonably well on x ray, and are usually quite hard (1200HU)
Describe the properties of urate crystals. Colour, shape, urinary conditions for production.
- Bright yellow stones formed from uric acid in the urine
- Needle shaped
- Formation is strongly associated with low PH and high uric acid concentration in the kidneys (idiopathic gout, increased cell turnover in myeloproliferative disease, dehydration)
- So (400HU) and, dissolvable
What are the different causes of uric acid stones?
Metabolic syndromes e.g diabetes
Gout
Dehydration due to malabsorption or chronic diarrhoea
Hyperuricaemia and, therefore, hyperuricosuria which can be caused by -
Myeloproliferative disorders such as leukaemia (increased cell turn over)
Chemotherapy (increased cell turn over)
Haemolytic anaemia (increased cell turn over
Describe the properties of Magnesium Ammonium Phosphate crystals (struvite)?
- Associated with infections
- Shows up slightly on X rays
- Usually relatively soft
(200-‐600HU) - Often has associations with calcium phosphate crystals
- usually associated with Staghorn Calculi (due to growing rapidly)
- Coffine lid appearance
Which microorganisms are associated with Magnesium Ammonium Phosphate crystals (struvite) and how?
Protease-producing microorganisms including Proteus and Klebsiella.
microorganisms are able to convert urea into ammonia which reacts with water increasing the pH of the urine. Increased ammonia and alkaline urine promote stone formation.
What are the properties of Cysteine crystals?
- Associated with Cysteinuria
– gene disease - Poorly visible on x-‐ray & are Hard (1400HU)
- Produce a white smoke and rotten egg smell when lasered (Hydrogen sulphide)
- Hexegan shape
How are Cysteine crystals treated?
medical dissolution
therapy
What is a key feature of the matrix urinary stones?
Proteinaceous material - a lot like chewing gum
What is a key feature of the Idinavir urinary stones?
Do not show up on CT
What is the free theory associated the stone formation?
The presence of stone constituents in the right amount, and without enough inhibitors, will form stones . Formation is effected by: - Concentration of solutes - Urine acidity - Presence of formation inhibitors
What is the fixed theory regarding renal stone formation?
The energy to form a crystal lattice is lower if there is a surface to form them on
Formation effected by:
- Surface to form lattice on
- Crystals (other crystals like urate can form a surface)
- Randall’s plaques (sub urothelial deposits which form a surface)
What are the main inhibitors in renal stone formation? (5)
Citrate (calcium citrate is soluble)
Magnesium (magnesium oxalate is soluble)
They prevent calcium oxalate crystals from forming
osteopontin
Nephrocalcin
Tamm Horsfall Protein (THP) (uromodulin)
From where does the body obtain oxalate?
- The diet
- endogenous sources in the
liver as part of glycolate
metabolism - Vitamin C is converted to oxalate
Where is oxalate absorbed from and how is absorption prevented? Why is it important for absorption to be inhibited?
Oxalate is absorbed mainly from the gut
When calcium binds to oxalate it prevents it from being absorbed
Enhanced intestinal absorption of dietary oxalate leads to elevated renal oxalate excretion
What is enteric hyperoxaluria and which conditions can cause it?
Enhanced intestinal absorption of dietary oxalate
- Crohns disease
- jejunoileal bypass surgery
How would calcium supplements help to prevent high levels of oxalate?
Very little oxalate is stored so if not bound to calcium it will be absorbed and can lead to hyperoxaluria.
Calcium can be stored in the bones so it is important to ensure there is enough circulating to bind to oxalate
List 4 dietary sources of oxalate?
Rhubarb, spinach, beetroot, swiss chard, okra, sweet potato, nuts
Tamm Horsfall protein acts to prevent renal stones and also prevent infections and UTI’s. How does it accomplish this?
It covers crystal structures and prevents them from binding to the renal epithelial cells
Prevents bacteria from binding to epithelium preventing UTI from E.coli
What is caused by a mutation in the Tamm Horsfall protein gene?
familial juvenile hyperuremic nephropathy
medullary cystic kidney disease 2
both have increased stone
formation/ nephrocalcinosis
Which tests would you conduct if someone suspected of having Renal stones?
Bedside- Observations ECG Urinanalysis (blood urine) Urine dip - WBc/ nitrates/PH Urine MC & S
Blood test- FBC (normal) Urine analysis and urine Dip U and E's (creatine elevated) Calcium CRP - used to assess for infection LFT Renal function test - AKI Amylase (rule out pancreatitis) Bone profile (loss in calcium) Uric acid ( urate) Pregnancy test (ectopic pregnancy)
Diagnostic
X ray
CT KUB (kidneys-ureters-bladder) Non contrast as patient may be nephrotoxic - first line gold standard
If CTKUB is positive - perform KUB to look at stone postion
Ultrasound for those who cant use CTKUB (pregnant women, children, adolescence)
Which stones can not be detected on X ray?
uric acid, indinavir-induced, cystine, matrix
Which drugs can lead promote calcium stone formation?(9) Which if these causes the formation of urate stones and calcium stones
Saltcat - G
S - Salicylate
A- Acetozolamide (carbonic anhydrase inhibitor used in glaucoma and epilepsy. Also a good diuretic which causes excretion of potassium and biocarbonate (carbonic anhydrase catalysis conversion of CO2 to biocarbonate) - used in metabolic acidosis )
L - Loop diuretics (Inhibits sodium/potassium/chloride transporter in the loop of Henle)
T- Thiazides (Inhibits reabsorption of sodium and chloride, inhibits sodium reabsorption and increases fluid excretion)
C - Vitamin C and D
A- Antacids
T- Theophylline (phosphodiesterase inhibiting used for COPD and asthma)
G- Glucocorticoids
U rate = Salicylate and Thiazides
What are some potential differential diagnosis for renal colic?
Abdominal -
- leaking AAA, bowel colic (goes and comes completely with uteric colic pain is in background)
- Ectopic pregnancy
- Pancreatitis
Chest and heart-
Pneumonia
MI
Urinary -
- pyelonephritis
- Bleeding tumours (renal call carcinoma)
- Cystitis
What about a kidney stones does the CTKUB assess?
Position, Size, Hardness
Which imaging test is used to assess kidney stones in women who are in their second or third trimester of pregnancy?
MRI
Poor for stones
Which factors dictate the management of renal colic?
Size and location of the renal stone
A stone <4mmm has a 80% chance of passing spontaneously
- > 8mm less likely to pass alone
How is renal colic medically managed?
Monitor and expulsion
Analgesia
NSAIDS- usually in acute situations but may effect renal function. Help reduce uretal spasm especially when given by the rectal route
Opiates - sometimes
Antiemetics
ondansetron or cyclizine
Hydration
Iv if patient is vomiting but this wont push out the stone
Medical expulsive therapy - Tamsulosin - relaxes lower ureter and increases stone passage
Stone removal
In which kinds of patients should NSAIDS not be used and what should patients be offered instead?
AKI
History of Peptic ulcer or Gastritis
Give paracetamol
How is renal colic surgically managed
Shockwave lithotripsy- shock wave is used to break down stone. Used in stones under 20mm
Ureteroscopy - energy devices e.g. lasers used to break down stone. Used in stones 10-20mm
Can be flexible or semi ridged
Percutaneous nephrolithotomy - nephroscope is passed into the collecting system and used to break up stones. used in stones >20mm
Used in other stones when other measures have failed
What are the metabolic tests done for those with renal stones? (5)
2 x 24h urine collection: test for Calcium, Oxalate, Urate, Volume, Sodium Citrate
Spot Nitroprusside test for Cysteine
Stone analysis
Blood tests - calcium, urate, bicarbonate, U and E’s
Parathyroid hormone test
What are the indications for a metabolic test?
- Multiple stones attacks
- Bilateral stone disease
- Solitary kidney (increased risk)
- Urate, cysteine, calcium stones
How are renal stones be prevented non medically?
Increase fluid intake - >2l a day Reduce sodium intake Increase potassium intake restrict high oxalate foods reduce fatty acids take calcium with high protein meals Reduce animal protein intake Not more than 1000% - one tablet of vitamin C daily
Which drugs are used to treat/prevent renal stones?
Calcium oxalate stones-
Thiazides- bendroflumethazide (hypercalciuria stones to reduce calcium excretion)
Renal tubular acidosis Potassium citrate (alkalines urine)
Sodium bicarbonate - alkalines urine
Cystein stones - Tiopronin
Struvite - Antibiotics for UTI
Urate stones-
Allopurinol
Cystein stones- Penicillamine & Thiola for Cysteinuria
Which tests are used to monitor the treatment of renal stones?
24h urine (assess for volume (patient drinking enough), sodium and to ensure specific therapy is working - citrate, oxalate, restriction)
Spot urine for Na/K as an alternative,
Blood urate in users of allopurinol
Give examples of the type of metabolic conditions being assessed in the metabolic test? - you can only mention 2 here
hyperparathyiodsm and distal renal tubular acidosis
How are patients with renal stones followed up?
50% chance another stone will present in 10 years if no dietary changes are made
Consider a 6 monthly KUB to follow unknown or asymptomatic stones
Which factors effect the formation of calcium oxalate crystals?
High oxalate concentration in urine
Loss of stone inhibitors
High urinary PH (alkaline)
What are the non- modifiable risk factors for renal stone development?
- Male
- Infection
- Crohns disease
- Family history
- Metabolic disorder
- anatomic abnormalities
- primary renal diseases (polycystic kidneys, medullary sponge kidneys, renal tubular acidosis)
What are the modifiable risk factors for renal stone development?
- Dehydration - concentrated urine
- Increased BMI
- High salt diet
- High meat diet
Which complications of renal stones causes lasting damage?
Infection
Obstruction leading to hydro nephrosis
Which metabolic conditions lead to kidney stone formation and how? What are the potential causes of these conditions
Hypercalcaemia
If the GFR is low then it can cause hypercalciuria. Causes include hyperparathyroidism, vitamin D ingestion and sarcoidosis
Hypercalciuria (high calcium in urine) - 24h urine calcium excretion of >7.5mmol for men and 6.5mmol form women.
Causes, Hypercalcaemia, increased calcium ingestion, idiopathic (enhanced gut uptake and urine excretion)
Hyperoxaluria - increase oxalate in urine. For oxalate to make stones with.
Causes -
Increased ingestion of food with oxalate in them
Dietary calcium restriction which causes increased absorption of oxalate
GI diseases like Crohns -increased absorption of oxalate from colon
Cystinuria
causes - polycystic kidney disease, medullary sponge kidney, renal tubular acidosis
How do infections such as a urinary tract infection lead to renal stone formation?
UTI causes the formation of mixed infective stones (struvite + calcium)
These stones are large forming staghorn calculus,
Cause of UTI in this case is Proteus mirabilis
