Nephrology Flashcards
Contrast-induced nephropathy
- definition
- common interventions
- prevention
- drug to hold to avoid
25% increase in creatinine occurring 2 -5 days after administration.
Common interventions: CT, angiography, PCI
Prevention
the evidence base currently supports the use of intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure. There is also evidence to support the use of isotonic sodium bicarbonate
high-risk for contrast-induced nephropathy should have metformin withheld for a minimum of 48 hours and until the renal function has been shown to be normal
acute interstitial nephritis
- causes
- common drugs causing
- symptoms and signs
- diagnosis
- management
Acute interstitial nephritis (AIN) typically arises following drug therapy in the majority of cases (~75%), with infections and systemic vasculitides (SLE, sarcoidosis) forming the rest
Common drugs - NSAIDs, penicillins, allopurinol, PPIs, ciprofloxacin
Signs - Sterile pyuria and white cell casts in the setting of rash and fever and joint pain
Diagnosis - renal biopsy
Management - stop drug, steroids, dialysis
Common nephrotoxic drugs
NSAIDs, aminoglycosides (amikacin, gentamicin) ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics
Definition of AKI
a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
Drugs that may have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)
Metformin
Digoxin
Lithium
Should be stopped in AKI as may worsen renal function
NSAIDs
High dose aspirin 300mg (the cardio protective 75mg dose is safe to continue)
Aminoglycosides (amik, gent)
• ACE inhibitors
• Angiotensin II receptor antagonists
• Diuretics
Indications for dialysis
Acidosis
Excess - hyperkalaemia
O- pulmonary oedema
Ureaemia (e.g. pericarditis, encephalopathy)
prevent the formation of ascites in patients with chronic liver disease
- Aldosterone antagonists such as spironolactone
- Loop diuretics
Prostate cancer management
T1/2
- watchful wait
- radical prostatectomy (side effect - erectile dysfunction)
- external beam radiotherapy/ brachytherapy (risk of proctitis, increased risk bladder colon cancer)
T3/t4 metastic prostate cancer
- we need to reduce androgen levels
- given GnRH agonists (eg. Zoladex Goserelin) paradoxically decrease LH levels overtime by causing increase overstimulation that disrupts the negative feedback mechanism
- to counteract the initial increase in LH which results in crease in testosterone and tumour flare (pain) we give anti-androgen eg. bicalutamide, cyproterone acetate
Or androgen synthesis inhibitor eg. abiraterone
- severe cases may benefit from bilateral orchidectomy
Renal transplant HLA matching - which is most important
DR is the most important
relative importance of the HLA antigens are as follows DR > B > A
Post kidney transplant problems
ATN of graft
vascular thrombosis
urine leakage
UTI
Renal transplantation rejection types
Hyperacute rejection (minutes to hours)
- due to pre-existing antibodies against ABO or HLA antigens
- a type II hypersensitivity reaction
- leads to widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
- no treatment is possible and the graft must be removed
Acute graft failure (< 6 months)
- due to mismatched HLA —> Cell-mediated (cytotoxic T cells)
- asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
- other causes include cytomegalovirus infection
- may be reversible with steroids and immunosuppressants
Causes of chronic graft failure (> 6 months)
- both antibody and cell-mediated mechanisms —> fibrosis to the transplanted kidney (chronic allograft nephropathy)
- recurrence of original renal disease (MCGN > IgA > FSGS)
Henoch-Schonlein purpura (HSP)
- causes
- symptoms / signs
- treatment
- prognosis
IgA mediated vasculitis
Children - triggered by infection
Symptoms: palpable purpuric rash over buttocks, backs of limbs, localised oedema, haematuria, arthralgia
Treatment: supportive
Prognosis- one third get relapse, majority return to normal renal function
Diabetes insipidus
Inability to produce (cranial) or respond (nephrogenic) to anti diuretic hormone (vasopressin)
Cranial DI causes
- idiopathic
- pituitary gland surgery
- infiltration: sarcoidosis, haemochromarosis
- tumour
- head injury
Nephrogenic causes
- lithium
- genetic mutations in the ADH receptor
- tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
- hypercalcaemia, hypokalaemia
Features - polyuria, polydipsia
Investigation - water deprivation test, plasma:urine osmolality (high urine osmolality automatically excludes)
Management
nephrogenic diabetes insipidus
- thiazides
- low salt/protein diet
central diabetes insipidus can be treated with desmopressin (Vasopressin receptor 2 agonist)
Autosomal dominant polystic kidney disease
ADPKD type 1 ADPKD type 2
85% of cases 15% of cases
Chromosome 16 Chromosome 4
renal failure earlier
Diagnostics: ultrasound
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
Management: if already developed CKD - tolvaptan (vasopressin receptor 2 antagonist) which also slows cyst development
Most common cause of nephrotic syndrome in children
Minimal change >80%
Minimal change disease
- causes
- signs
- pathophysiology
- diagnosis by microscopy
- treatment
- prognosis
Causes nephrotic syndrome
Signs: peripheral oedema, hypoalbuminaemia, proteinuria
Causes: idiopathic (80-90%)
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis
Pathophysiology - T cell and cytokine mediated —> effacement of foot processes and podocyte loss —> permeability of glomerular basement membrane
renal biopsy
normal glomeruli on light microscopy
electron microscopy shows fusion of podocytes and effacement of foot processes
Treatment
1. Oral steroids
2. Cyclophosphamide
Prognosis: thirds
1/3 have one episode
1/3 have infrequent episodes
1/3 have frequent relapses which cease by adulthood
Causes of nephrogenic Diabetes insipidus
Genetic - mutation to ADH receptor
Electrolytes - hypoK, hyperCa
Lithium demeclocycline
Tubulo-interstitial disease - obstruction, sickle cell, pyelonephritis
most common histological pattern seen in lupus nephritis
diffuse proliferative glomerulonephritis
which chromosome is implicated in ADPKD
type 1 - chr 16
type 2 - chr 4
what clotting factor is lost in nephrotic/nephritic syndrome resulting in clot formation?
antithrombin III and plasminogen
normal anion gap
8-14
antibody for
Idiopathic membranous glomerulonephritis
anti-phospholipase A2 antibodies
stones produced by Proteus mirabilis bacteria in UTI
magnesium ammonium phosphate stones
staghorn calculi
Young female, hypertension and asymmetric kidneys
fibromuscular dysplasia
drug treatment for polycystic kidney disease
tolvaptan (vasopressin receptor 2 antagonist)
— to slow the progression of cyst development
What is Fanconi syndrome
disorder of PCT in tubules
loss of potassium, glucose, bicarbonate, amino acids
–> bone demineralisation (osteomalacia in adults, or rickets in children) due to phosphate wasting
–> polyuria, polydipsia and dehydration, growth failure, acidosis, hypokalaemia and hyperchloraemia
caused by congenital (inborn errors of metabolism) or acquired with other autoimmune disease
three main antigens responsible for graft vs host disease;
HLA-A, HLA-B, and HLA-DR
most important HLA antigen to match in renal transplant
HLA-DR
which vitamin D supplement in end-stage renal disease
Alfacalcidol is used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys
time taken for an arteriovenous fistula to develop is?
6 to 8 weeks
which skin cancer is common in renal transplant patients
scc
red congo stain
amyloid
Alport’s syndrome
- haemorrhagic nephritis renal failure - glomerular basement membrane problem
renal biopsy: splitting of lamina densa seen on electron microscopy - sensorineural deafness
- visual problems
x linked dominant - inherited defect in type IV collagen
most common cause of peritonitis secondary to peritoneal dialysis
Coagulase-negative Staphylococcus
e.g. Staphylococcus epidermidis and Staphylococcus capitis peritonitis
how do aminoglycosides (gent/vanc/amik) cause AKI?
acute tubular necrosis
ADPKD is associated with which heart defect?
mitral valve prolaspe
renal transplant, most likely infection?
CMV
what renal disease causes hyperlipidaemia specifically hypercholesterolaemia, as opposed to hypertriglyceridaemia?
nephrotic syndrome
This results in low levels of albumin and increased lipoprotein production, leading to hypercholesterolaemia (high cholesterol).
most common cause of peritonitis secondary to peritoneal dialysis
Coagulase-negative Staphylococcus
eg. Staphylococcus epidermidis
what type of glomerulonephritis is caused by HIV?
HIV-associated nephropathy (HIVAN) causes collapsing FSGS and usually presents as nephrotic syndrome
what type of glomerulonephritis is caused by malignancy?
Membranous nephropathy is frequently associated with malignancy
How can CKD result in neuropathy
Uraemic nephropathy = sensory
where is Phosphate reabsorbed?
Phosphate is reabsorbed in the proximal tubule
trimethoprim vs the kidneys (creatinine)
moderate risk in creatinine
- trimethoprim competitively inhibits the tubular secretion of creatinine
- reversible when drug stops
Interstitial nephritis secondary to trimethoprim
- more dramatic rise in creatinine
-haematuria, proteinuria or eosinophiluria and systemic symptoms like rash or fever
How does nephrotic syndrome cause clots
increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
screening test for adult polycystic kidney disease
Ultrasound is the screening test for adult polycystic kidney disease
Medications to prevent renal stones
High calcium = thiazides
Oxalate = cholesyramine or pyridoxine
Utica stones =allopurinol
Acute interstitial nephritis vs acute tubular necrosis
Acute interstitial nephritis is an inflammatory process so there is a higher white cell content in the urine, while acute tubular necrosis is not so the urine has no cellular component.
On CT imaging, actue vs chronic haematomas
On CT imaging, acute haematomas appear bright (hyperdense) whereas chronic haematomas appear dark (hypodense).
Complications of nephrotic syndrome
increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
deep vein thrombosis, pulmonary embolism
renal vein thrombosis, resulting in a sudden deterioration in renal function
hyperlipidaemia
increasing risk of acute coronary syndrome, stroke etc
chronic kidney disease
increased risk of infection due to urinary immunoglobulin loss
hypocalcaemia (vitamin D and binding protein lost in urine)
CKD on haemodialysis - most likely cause of death is ?
IHD
What is the most useful marker of prognosis in myeloma?
B2-microglobulin
what is calciphylaxis
rare complication of end-stage renal failure.
linked with hypercalcaemia, hyperphophataemia and hyperparathyroidism.
results in deposition of calcium within arterioles causing microvascular occlusion and necrosis of the supplied tissue. It most commonly affects the skin and presents with painful necrotic skin lesions.
warfarin increases risk.
link between hepcidin and CKD
hepcidin is an acute phase protein, so increased in CKD
furthermore there is reduced hepcidin clearance in CKD
elevated hepcidin levels lead to decreased iron absorption from the gut
link between metabolic acidosis and CKD and anaemia
metabolic acidosis, a common condition in CKD, can inhibit the conversion of ferric iron (Fe³º) to its absorbable form, ferrous iron (Fe²º), in the duodenum → reduced iron absorption.
ATN vs AIN
Acute tubular necrosis is associated with granular, muddy-brown urinary casts
acute interstitial nephritis - triad of rash, fever and eosinophilia are all not present
The urine sediment, if present, is more likely to be white cell (and/or red cell) casts/pyuria.
ATN or prerenal uraemia?
In prerenal uraemia think of the kidneys holding on to sodium to preserve volume
a FENa (fractional sodium excretion) greater than 1% suggests ATN rather than pre-renal uraemia
lithium desensitizes the kidney’s ability to respond to ADH in which part of the nephron?
the collecting ducts
Flash pulmonary oedema, U&Es worse on ACE inhibitor, asymmetrical kidneys
diagnosis and investigation
renal artery stenosis - do MR angiography
Bendroflumethiazide and effect on kidney stones
Bendroflumethiazide may help prevent the formation of calcium based renal stones.
theoretically increase the risk of urate based stones
drugs that prevent each of the different kidney stone types
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
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
diuretics mechanism of action
Amiloride inhibits the epithelial sodium transporter in the distal convoluted tubules.
Carbonic anhydrase inhibitors include dorzolamide and act in the proximal tubules.
Loop diuretics such as furosemide act to block the sodium/potassium/chloride transporter in the loop of Henle.
Thiazide diuretics such as bendroflumethiazide block the sodium/chloride transporter in the distal convoluted tubules.
Spironolactone is an aldosterone antagonist, therefore, acts to inhibit the mineralocorticoid receptor in the cortical collecting ducts.
how does alcohol impact ADH
suppresses it –> polyuria
Urinalysis with ‘muddy brown casts’ is indicative of
acute tubular necrosis.
