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
when should you refer patient with AKI to renal?
persistent oliguria serum creatinine >350umol/L indications for dialysis (hyperkalaemia, severe acidosis, pulmonary oedema) need for iodinated contrast blood and protein in urine no clear cause for AKI
what is nephritis?
what is nephritic syndrome?
nephritis is a very generic term which means inflammation of the kidneys
nephritic syndrome or acute nephritic syndrome refers to a group of symptoms, not a diagnosis.
what are the features of nephritic syndrome?
haematuria - may be microscopic or macroscopic
oliguria
proteinuria (less than 3g/24hours - any more anti starts to be classified as nephrotic syndrome)
fluid retention
what is nephrotic syndrome?
nephrotic syndrome refers to a group of symptoms without specifying the underlying cause
to have nephrotic syndrome the patient must fulfil the following criteria:
- peripheral oedema
- proteinuria more than 3g/24 hours
- serum albumin less than 25g/L
- hypercholesterolaemia
what is glomerulonephritis?
Glomerulonephritis is an umbrella term applied to conditions that cause inflammation of or around the glomerulus.
what is interstitial nephritis?
Interstitial nephritis is term to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney. It is important not to confuse this with glomerulonephritis. Under the umbrella term of interstitial nephritis there are two key specific diagnoses: acute interstitial nephritis and chronic tubulointerstitial nephritis.
what is glomerulosclerosis?
Glomerulosclerosis is a term to describe the pathological process of scarring of the tissue in the glomerulus. It is not a diagnosis in itself and is more a term used to describe the damage and scarring done by other diagnoses. Glomerulosclerosis can be caused by any type of glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a disease called focal segmental glomerulosclerosis.
what are the different types of glomerulonephritis?
Minimal change disease Focal segmental glomerulosclerosis Membranous glomerulonephritis IgA nephropathy (AKA mesangioproliferative glomerulonephritis or Berger’s disease) Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis) Mesangiocapillary glomerulonephritis Rapidly progressive glomerulonephritis Goodpasture Syndrome
how are most types of glomerulonephritis treated?
Immunosuppression (e.g. steroids)
Blood pressure control by blocking renin-angiotensin system (i.e. ACEi or ARBs)
what is the most common case of nephrotic syndrome in children?
minimal change disease
this is usually idiopathic and is treated with steroids
what is the most common case of nephrotic syndrome in adults??
focal segmental glomerulosclerosis
how does nephrotic syndrome usually present?
Nephrotic syndrome usually presents with oedema. Patients might notice frothy urine (proteinuria). Nephrotic syndrome predisposes patients to thrombosis, hypertension and high cholesterol.
what is IgA nephropathy?
AKA berger’s disease
it is the most common cause of primary glomerulonephritis
peak age at presentation is in the 20s
usually following an URTI
classically macroscopic haematuria
associated with: alcoholic cirrhosis, coeliac disease/dermatitis herpetiformis, HSP
what is membranous glomerulonephritis?
it is the most common type of glomerulonephritis overall
there s a bimodal peak in age in the 20s and 60s
histology shows IgG and complement deposits on the basement membrane
the majority are idiopathic
can be secondary to malignancy, rheumatoid disorders and drugs e.g. NSAIDs
it usually presents with nephrotic syndrome and proteinuria
what is post-streptococcal glomerulonephritis?
aka diffuse proliferative glomerulonephritis
it is caused by immune complex deposition in the glomeruli.
patients are typically under 30 it presents as: 1-3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo) they develop a nephritic syndrome they usually recover fully
what is good pasture syndrome?
Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes. This causes glomerulonephritis and pulmonary haemorrhage.
there may be a patient that presents with acute kidney failure and haemoptysis (coughing up blood).
what is rapidly progressive glomerulonephritis?
Rapidly progressive glomerulonephritis is a term used to describe a rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli.
Histology shows “crescentic glomerulonephritis”
It presents with a very acute illness with sick patients but it responds well to treatment
Often secondary to Goodpasture syndrome, and ANCA positive vasculitis
what are the causes of membranous glomerulonephritis?
idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy: lung cancer, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
how do you manage membranous glomerulonephritis?
all patients should receive an ACE inhibitor or an angiotensin II receptor blocker
immunosupression
what is focal segmental glomerulosclerosis? and what are the causes?
Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.
Causes idiopathic secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy HIV heroin Alport's syndrome sickle-cell
how do you manage focal segmental glomerulosclerosis?
steroid +/- immunosuppressants
what are the features of post-streptococcal glomerulonephritis?
headache, malaise haematuria proteinuria hyertension low C3 raised ASO titre
what is membranoproliferazive glomerulonephritis?
aka mesangiocapillary glomerulonephritis
may present as nephrotic syndrome, haematuria or proteinuria
poor prognosis
three types
type 1: most common - caused by cryoglobulinaemia and hepatitis C
Type 2 - dense deposit disease
type 3 - caused by hepatitis B and C
steroids may help
how does IgA nephropathy present?
- young male, recurrent episodes of macroscopic haematuria
- typically associated with a recent respiratory tract infection
- nephrotic range proteinuria is rare
- renal failure is unusual and seen in a minority of patients
what are the causes of minimal change disease?
most are idiopathic
drugs -NSAIDs, rifampicin
hodgkins lymphoma
thymoma
infectious mononucleosis
how do you manage minimal change disease?
majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases
what investigations would you perform for glomerular disease?
baseline measurements - eGFR, urinary protein, serum U&Es, serum albumin
urine microscopy and culture serum ASO titre blood glucose antinuclear andante-DNA antibodies - present in significant titre is SLE ANCA - present in vasculitis anti GBM antibody - good pastures HEP B and C screening cryoglobins - increased in cryoglobuninaemia
CXR
Kidney USS
renal biopsy
what is polycystic kidney disease?
it is a genetic condition where the kidneys develop multiple fluid filled cysts and kidney function is significantly impaired
what are the two types of polycystic kidney disease?
Autosomal dominant and autosomal recessive
what are the two types of AD PKD?
PKD-1: chromosome 16 (85% of cases)
PKD-2: chromosome 4 (15% of cases)
what are the extra- renal manifestations of ADPKD?
Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Cardiac valve disease (mitral regurgitation)
Colonic diverticula
Aortic root dilatation
what are the complications of AD PKD?
Chronic loin pain
Hypertension
Cardiovascular disease
Gross haematuria can occur with cyst rupture. This usually resolves within a few days.
Renal stones are more common in patients with PKD
End stage renal failure occurs at a mean age of 50 years
what chromosome does AR PKD affect?
chromosome 6
how is AR PKD diagnosed?
Diagnosis may be made on prenatal ultrasound or in early infancy with abdominal masses and renal failure. Newborns may also have features consistent with Potter’s syndrome secondary to oligohydramnios. End-stage renal failure develops in childhood. Patients also typically have liver involvement, for example portal and interlobular fibrosis.
how is PKD managed?
Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease.
mainly supportive management of the complications:
Antihypertensives for hypertension.
Analgesia for renal colic related to stones or cysts.
Antibiotics for infection. Drainage of infected cysts may be required.
Dialysis for end stage renal failure.
Renal transplant for end stage renal failure.
what is the USS diagnostic criteria for AD PKD?
Ultrasound diagnostic criteria (in patients with positive family history)
two cysts, unilateral or bilateral, if aged < 30 years
two cysts in both kidneys if aged 30-59 years
four cysts in both kidneys if aged > 60 years
what causes interstitial nephritis?
- drugs: the most common cause, particularly antibiotics penicillin rifampicin NSAIDs allopurinol furosemide - systemic disease: SLE, -sarcoidosis, and Sjögren's syndrome - infection: Hanta virus , staphylococci
what are the features of interstitial nephritis?
fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension
what would investigations show in interstitial nephritis ?
sterile pyuria
white cell casts
who is Tubulointerstitial nephritis with uveitis common in and what are the symptoms?
Tubulointerstitial nephritis with uveitis (TINU) usually occurs in young females. Symptoms include fever, weight loss and painful, red eyes. Urinalysis is positive for leukocytes and protein.
what is acute tubular necrosis?
Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI) seen in clinical practice. Necrosis of renal tubular epithelial cells severely affects the functioning of the kidney. In the early stages ATN is reversible if the cause if removed.
what are the causes of acute tubular necrosis?
> ischaemia shock sepsis > nephrotoxins aminoglycosides myoglobin secondary to rhabdomyolysis radiocontrast agents lead
what are the features of acute tubular necrosis?
features of AKI: raised urea, creatinine and potassium
muddy brown casts in the urine
what are the histopathological features of acute tubular necrosis?
tubular epithelium necrosis: loss of nuclei and detachment of tubular cells from the basement membrane
dilatation of the tubules may occur
necrotic cells obstruct the tubule lumen
what is haemolytic uraemia syndrome?
Haemolytic uraemic syndrome is generally seen in young children and produces a triad of:
acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia
what are most causes of haemolytic uraemia syndrome secondary too?
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
sometimes you can get primary HUS (atypical) which is due to compliment dysregulation
what investigations would you perform for haemolytic uraemia syndrome?
full blood count: anaemia, thrombocytopaenia, fragmented blood film
U&E: acute kidney injury
stool culture
how would you manage haemolytic uraemic syndrome?
supportive - fluids, blood transfusion and dialysis if required
