RENAL Flashcards
what are the different types of stones in the urinary tract?
renal stones - nephrolithiasis
ureteral stones - urolithiasis
where are the 3 areas which renal stones classically form in?
the pelviureteric junction
pelvic brim
vesicoureteric junction
what is the presentation of renal stones?
- loin pain - typically severe intermittent colic pain
- renal colic is excruciating ureteric spasms - loin to groin with nausea/vomiting
- the patient is often restless and cannot lay still
- the site of pain often is determined by the site of the obstruction - renal obstruction will be felt in the loin, obstruction of the mid ureter will often mimic appendicitis/ diverticulitis, obstruction of the lower ureter will present with symptoms if bladder irratibitlty and pain in the scrotum, penile tip or labia majora, obstruction of the bladder or urethra will cause pelvic pain, dysuria
- dysuria
- fever
- they may have haematuria
what causes renal stones?
There are several risk factors which can increase the risk
there may be an increase of urinary solutes (calcium, uric acid, calcium oxalate and sodium) or there may be a decrease in stone forming inhibitors (citrate and magnesium)
these things lead to urine supersaturation which leads crystal formations
what are the risk factors for renal stones?
dehydration
hypercalciuria, hyperparathyroidism, hypercalcaemia
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, polycystic kidney disease
beryllium or cadmium exposure
Gout and ileostomy ( loss of bicarb and fluid results in acidic urine causing the precipitation of uric acid) - increase the risk of urate stones
Drugs :
drugs that promote calcium stones - loop diuretics, steroids, acetazolamide, theophylline
thiazides can prevent calcium stones as they increase distal tubular calcium
what are the different types of renal stones?
calcium oxalate (85%) cystine uric acid - 5-10% calcium phosphate - 10% struvite - 2-20%
what are the features of calcium oxalate stones?
Hypercalciuria is a major risk factor (various causes)
Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms complexes with calcium making it more soluble
Stones are radio-opaque (though less than calcium phosphate stones)
Hyperuricosuria may cause uric acid stones to which calcium oxalate binds
what are the features of calcium phosphate stones
May occur in renal tubular acidosis, high urinary pH increases supersaturation of urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone formation (types 2 and 4 do not)
Radio-opaque stones (composition similar to bone)
what are the features of cystine stones?
Inherited recessive disorder of transmembrane cystine transport leading to decreased absorption of cystine from intestine and renal tubule
Multiple stones may form
Relatively radiodense because they contain sulphur
Semi-opaque, ‘ground-glass’ appearance
what are the features of uric acid stones?
Uric acid is a product of purine metabolism
May precipitate when urinary pH low
May be caused by diseases with extensive tissue breakdown e.g. malignancy
More common in children with inborn errors of metabolism
Radiolucent
urine will be acidic
what are the features of struvite stones?
Stones formed from magnesium, ammonium and phosphate
Occur as a result of urease producing bacteria (and are thus associated with chronic infections)
Under the alkaline conditions produced, the crystals can precipitate
Slightly radio-opaque
urine will be alkaline
what investigations would you perform for renal stones?
urinalysis FBC serum electrolytes, urea and creatinine urine pregnancy test non contrast helical CT of KUB stone analysis KUB x ray renal USS 24 hour urine monitoring
how do you manage renal stones?
NSAID is the analgesia of choice for renal colic
for patients who require admitting give IM diclofenac for rapid relief of severe pain
stones less than 5mm will usually pass spontaneously within 4 weeks of symptom onset
ureteric obstruction due to stones together with infection is a surgical emergency and the system must be decompressed - options include nephrostomy tube placement, insertion of ureteric catheters and ureteric stent placement
in the non emergency setting the preferred options for treatment of stone disease include the
shock wave lithotripsy, percutaneous nephrolithotomy,
utereroscopy,
open surgery remains an option for selected cases
how can calcium stones be prevented?
Calcium stones may be due to hypercalciuria, which is found in up to 5-10% of the general population.
high fluid intake
low animal protein, low salt diet (a low calcium diet has not been shown to be superior to a normocalcaemic diet)
thiazides diuretics (increase distal tubular calcium resorption)
how can oxalate stones be prevented?
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion
how can uric acid stones be prevented?
allopurinol
urinary alkalinization e.g. oral bicarbonate
what are the criteria for AKI?
> Rise in creatinine of ≥ 25 micromol/L in 48 hours
> Rise in creatinine of ≥ 50% in 7 days
> Urine output of <0.5ml/kg/hour for > 6 hours
what are the risk factors for AKI?
CKD Heart failure diabetes liver disease older age (above 65) cognitive impairment nephrotoxic medications such as NSAIDS and ACE inhibitors the use of contrast medium during CT scanning post op previous AKI
what are the causes of acute kidney injury?
PRE RENAL CAUSES - pre-renal pathology is the most common cause of acute kidney injury, it is due to inadequate blood supply to the kidney reducing the filtration of the blood. Inadequate blood supply may be due to:
- dehydration
- hypotension
- heart failure
- renal artery stenosis
- sepsis
RENAL CAUSES - this is where intrinsic disease in the kidney is leading to reduced filtration of blood. It may be due to:
- glomerulonephritis
- interstitial nephritis
- tubular - acute tubular necrosis, rhabdomyolysis, myeloma, radio contrast, drugs
- vascular -e.g. vasculitis
POST RENAL CAUSES - post renal acute kidney injury is caused by obstruction to outflow of urine from the kidney causing back pressure into the kidney and reduced kidney function. The obstruction may be caused by:
- kidney stones
- masses such as cancer in the abdomen or pelvis
- ureter or urethral strictures
- enlarged prostate or prostate cancer
what investigations would you perform for AKI?
urea and electrolytes
urinalysis
imaging - renal USS
how do you manage AKI?
management is largely supportive
review medication
fluid rehydration in pre-renal AKI
Relieve obstruction
Hyperkalaemia also needs prompt treatment to avoid arrhythmias which may potentially be life-threatening.
what drugs Should be stopped in AKI as may worsen renal function
- NSAIDs
- Aminoglycosides
- ACE inhibitors
- Angiotensin II receptor antagonists
- Diuretics
what May have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)?
- Metformin
- Lithium
- Digoxin
what are the complications of AKI?
Hyperkalaemia
Fluid overload, heart failure and pulmonary oedema
Metabolic acidosis
Uraemia (high urea) can lead to encephalopathy or pericarditis
what is AKI?
sudden decline in a renal function
what is the diagnosis of AKI based on?
changes in creatinine and urine output
what medications affect the kidneys?
DIRECT EFFECT ON KIDNEYS
- NSAIDS and antibiotics
Accumulation during renal dysfunction
- metformin
EFFECTS ON RENAL/FLUID/ELECTROLYTE PHYSIOLOGY
- ACEi and diuretics
how do patients with AKI present?
it depends on the underlying cause
it may be an incidental finding of raised creatinine
more severe the are they may get clinical symptoms of AKI
If there is increased urea they may have nausea, vomiting, decreased consciousness
If they is hyponatraemia there may be peripheral and pulmonary oedema, ascites, pleural effusion
Hyperkalaemia - muscle weakness, ECG changes
Metabolic acidosis - kussmaul breathing
what is the role of creatinine in diagnosing AKI?
it is a waste product of normal muscle breakdown
it is an endogenous marker of GFR
- it is excreted really
- it is freely filtered at the glomerulus
- not reabsorbed, small amount secreted by proemial tubule
- generally remains consistent
creatinine measurement used in eGFR calculations however eGFR is not valid when creatinine is changing rapidly i.e. AKI
what is the absolute creatinine affected by other than AKI?
muscle mass
ethnicity
gender
age
this is why we are bothered about change in creatinine not the value as it is in relation to the previous results as people have different baselines
what may be the first sign of AKI?
urine output
sometimes there is a lag between the onset of kidney injury and increase in creatinine
how many stages of AKI are there?
3 stages - KDIGO
stage one: Cr increase 1.5x in 7 days or Cr increase greater than 26.5umol/L in 48 hours or le ss than 0.5mL/kg/h urine out put for 6 hours
stage 2 - Cr increase 2x in 7 days or less than 0.5mL/kg/h urine output for 12 hours
stage 3: Cr increase 3x in 7 days, or Cr greater than 354umol/L and increased by 1.5x or initiation or renal replacement therapy irrespective of the stage or less than 0.3mL/kg/h for 24 hours or anuria for 12 hours
