Acute Kidney Injury Flashcards
What can the causes of AKI be classified into?
pre-renal
renal
post renal
give examples of pre renal causes of AKI?
dehydration circulatory collapse hypovolemia blood loss RAS dehydration heart failure medications liver failure (albumin low, low oncotic pressure) CLD HYPOPERFUSION OF KIDNEYS! [fluid overload; oedema, ascites, increased RR, decrease oncotic pressure so fluid moves out and less fluid intravascularly so decreased BP and RAS to compensate and maintain perfusion.]
give examples of renal causes of AKI?
acute tubular necrosis acute glomerulonephritis acute cortical necrosis renal vascular damage necrotising papillitis
give examples of post renal causes of AKI?
intratubular
uretal
urethral
stones, tumours, prostatitis, pelvic tumours, retroperitoneal pelvic tumour , strictures,
what is the most common cause of acquired AKI?
‘surgical triad’
- post operative volume depletion
- infection
- nephrotoxic drugs
describe the presentation of renal syndromes?
acutely, insidious slow progression, symptoms relating to aetiology (proteinuria), signs (nephrotic-rash), haematuria, hypertension
what groups are at risk of AKI?
elderly diabetics vasculopaths known chronic renal impairment significant cardiac dysfunction chronic liver disease drugs (ACE inhibitors (efferent vasodilation), NSAIDS (afferent vasodilation, aminoglycosides, contrast mediums)
what are the ways of screening for AKI?
urinalysis for proteinuria and non visible haematuria
blood pressure
prostate examination
what investigations are of use in patients with suspected AKI?
haematology (FBC, coagulation profile)
biochemistry (profile, CRP, glucose)
microbiology/virology (hepatits, blood cultures)
radiology (ultrasound, CXR)
immunology (ANA, ANCA, C3, C4) others (myeloma screen-presents as hypercalcaemia, anaemia and kidney failure), ECG
describe the relationship between creatinine and actual GFR?
As GFR falls, creatinine rises
Normal serum creatinine is not synonymous with normal GFR
Creatinine level not a good indicator of kidney function (don’t rely on it)
describe the patient pathway for a patient with AKI?
GP -> nephrologist and MDT (low clearance clinic for advice about dialysis) -> dialysis (haemodyalisis, peritoneal dialysis) -> transplant (sometimes patients go straight from clinic to transplantation avoiding dialysis)
what are the life threatening complications of AKI?
Hyperkalaemia Pulmonary oedema Intravascular volume depletion Uraemic encephalopathy Pericardial fluid
what are the functions of the kidneys?
Excretory-elimination of waste products of metabolism (water soluble drugs)
Regulatory (electrolyte homeostasis, acid base balance, fluid balance, blood pressure control
Metabolic-metabolism of vitamin D
Endocrine-erythrpoetin, vitamin D RAAS
what is the classification of AKI?
stage 1 RISK
stage 2 INJURY
stage 3 FAILURE
describe stage 1 AKI?
actual/rise in serum creatinine >25
% rise from baseline >150%
urine output <0.5ml/kg/h for 6 hours
describe stage 2 AKI?
% rise from baseline >200% / urine output <0.5ml/kg/h for 12 hours
describe stage 3 AKI?
actual/rise in serum creatinine >354
% rise from baseline >300%
urine output <0.3ml/kg/h for 24 hours or anuria for 12 hours
define oliguria?
Volume of urine below which at maximum urinary concentrations the body cannot excrete the products of metabolism
why might a sick patient be acidotic?
Failure to remove acid by renal system
Overload of buffering system
Production of other acids eg lactic acid from tissue hypoxia
what would an ECG show in patients with hyperkalaemia?
Tenting of T waves
Widening QRS complex
Disappearnce of p waves
Sine wave pattern
what clinical methods are used to assess intravascular volume?
Body weight Skin turgor Postural blood pressure Mucous membrane JVP-elevated=overload Lung bases, peripheries
what methods are used in patients with AKI in ICU for monitoring progress?
Observation CVP line BP and pulse Arterial line for blood gas Blood test Urine output and fluid balance chart
what are the main complications in chronic renal failure?
Anaemia -EPO Renal bone disease-Vit D Acidosis –acid base balance Malnutrition Uraemia
what is chronic renal dysfunction?
Permanent usually progressive reduction in renal function
until proven otherwise what should absolute anuria be assumed to be?
urinary tract obstruction
what is the most common way of measuring kidney function?
GFR
what is GFR?
equivalent to kidney function, above 90-120ml/min/1.73m2 (volume, time and body surface area). difference In male and females.
mGFR
eGFR
what is mGFR?
(measured)(inulin)-not used often in clinical practice. Inulin used for research and numerous samples are needed. Nuclear scans eg DTPA, MPG3.
what is eGFR?
what are the different methods to calculate eGFR?
estimated) (used in clinical practice), urea and creatinine and cystatin C (new). Ideal marker need to be substance kidney freely filters doesn’t excrete or absorb.
- Mainly creatinine (from muscles, everyone has different muscle mass (60-110 normal) low muscle mass /pregnancy is the only cause of low creatinine,
- urea no longer used as small molecule so passes across membrane, produced by liver so urea levels affected by liver disease)
- Cystatin C production over 24 hours and is similar across everyone
define AKI?
Reversible loss of kidney function (GFR) within hours to days. If deranged kidney function for more than 6 weeks-chronic
Sepsis with AKI has a much larger mortality rate than sepsis on its own
what classification systems can be used for AKI and what measurements do they use?
RIFLE
AKIN
creatinine and urine output
how many stages are in the AKIN classification system?
stages 1-3
what are the stages in the RIFLE classification system of AKI?
risk injury failure loss ERSD (end stage renal disease)
what is the urine output;
- normally
- anurea
- oliguria
- polyuria
- 1-1.5L (0.5/weight in Kg x24)
- <200mL over 24 hours
- 200-1L over 24 hours
- > 2L
what information can be gained from 24 hour urine collection?
Proteinuria Hormones Hypertension follow up Adrenal tumours Electrolytes Creatinine clearance
what is the gold standard for getting a protein urine sample?
24 hour urine collection
how can a patient with AKI be identified?
- Blood test-creatinine
- Can be asymptomatic depending on degree of renal failure
- History (BP symptoms-headaches, visual disturbances, Volume-hypervolaemia, hypovolaema, thirst, nausea, vomiting, oedema, Drugs)
if the afferent and efferent arterioles are even what is the GFR?
normal
if the afferent arteriole and efferent arteriole are both constricted what is the effect on GFR?
reduced GFR
if the afferent arteriole is normal and the efferent is constricted what is the GFR?
increased GFR
if the afferent arteriole is constricted and the efferent is normal what is the affect on GFR?
decreased GFR
- what is the main cause of inpatient AKI?
in which of these scenarios is AKI likely/unlikely to develop
- missing one kidney
- blockages of both ureters
- blockage of urethra
- kidney stones in one ureter
- volume related
- unlikely
- likely
- likely
- unlikely
how is a diagnosis of AKI confirmed?
- Blood tests (U&E, creatinine, electrolytes, FBC, Hb, HCT, WCC, CRP)
- Urine dip (protein, blood. Nit, leu
- Ultrasound imaging- structure, size (usually 9-12cm enlarged in diabetes, smaller in scarring, fibrosis, hypperfusion), stones, obstruction (enlarged), number of kidneys
- ABG – potassium, metabolic acidosis
- Immune screen- ANCA, anti GBM, ANA, anti-dsDNA, protein electrophoresis, complement
- what is glomerulonephritis?
2. what are the 3 cell types of the glomerulus?
- inflammation of the glomerulus
2. endothelial, epithelial, mesangial
describe the histology of a normal glomerulus?
capilliary loop
bowmans space (urine collects)
mesangium (holds capillary loop in place)
podocytes with foot like processes
what are the different histological patterns in glomerulonephritis?
minimal change membranous GN mesangial proliferative focal segmental GN, focal segmental glomeruloclerosis, diffuse endothelial proliferative, mesangiocapillary, crescentic
what makes up the filtration barrier of the glomerulus?
endothelial cells fenestrated, glomerular basement membrane trilaminar, podocyte with foot like processes
- what is primary glomerulonephritis?
2. what is secondary glomerulonephritis?
- disease originates or only affects the kidney
2. kidney damage is result of another disease such as type 1 diabetes
what are the consequences to the loss of function of the glomerular basement membrane?
blood loss
protein loss
describe blood loss in patients with GMB loss of function?
Non visible/visible
Nephritic syndrome
Due to IgA nephropathy
-Visible haematuria, 1-2 days following URTI in younger patients
-Worse prognosis if; proteinuria, hypertension, scarring on biopsy, male, abnormal renal function
-36% progress to ESFR
describe protein loss in patients with GMB loss of function?
Asymptomatic
Nephrotic syndrome: peripheral oedema, proteinuria, hypoalbuminaemia, hypercholesterolaemia (increased infection and thromboembolic risk). >3.5 grams/day.
-Get oedema due to capillary hydrostatic pressure forcing fluid out of capillaries and interstitial hydrostatic pressure causing fluid to move into capillaries, capillary oncotic pressure (albumin) and maintain fluid in capillary, interstitial oncotic pressure-keep fluid in interstitial space. In nephrotic syndrome due to albumin being low there is balance so fluid into interstital space and secondary hyperaldosteonism and salt and water retention
what is minimal change glomerulonephritis?
Nephrotic syndrome but normal microscopy
describe steroid responsive nephrotic syndrome?
Most children with nephrotic syndrome will have minimal change disease and most will respond to steroids so treat without biopsy=steroid responsive nephrotic syndrome
Some relapse on steroid withdrawal (relapsing nephrotic syndrome)
describe steroid dependent nephrotic syndrome?
Some never respond to steroid (steroid resistant nephrotic syndrome-need biopsy showing either inherited abnormality of podocyte proteins or other cause such as FSGS.
what is FSGS (focal segmental glomerular sclerosis)?
some of glomerulus normal and some is sclerosed
describe membranous glomerulonephritis?
- thickening of capillary loops
- Proteinuris with or without renal impairment
- 1/3 spontaneous recovery, 1/3 persistant proteinuria, 1/3 ESFR
- Mainly autoimmune
- Associations with adenocarcinoma of lung and GI, hepatitis B, SLE, drugs
- Treatment-immunosuppression if progressive disease
what is Alports syndrome?
- Cause of non visible haematuria
- X linked autosomal recessive
- Males
- Haematuria, proteinuria, progressive renal failure, sensorineural deafness, anterior lenticonus
- Female carriers-non visible haematuria
give examples of secondary glomerulonephritis?
diabetic nephropathy (kimmelsteil wilson lesion0 amyloidosis cryoglobulinaemia subacute bacterial endocarditis systemic lupus erythematosus shunt nephritis
describe secondary amyloidosis?
AA amyloid: serum amyloid component A, acute phase protein, due to chronic inflammation (RA, ankylosing spondylitis, psoriatic arthritis, crohns), hereditary (familial Mediterranean fever), chronic pyogenic infection (bronchiectasis, osteomyelitis). Present with kidney disease
describe primary amyloidosis?
AL amyloid; serum amyloid A component + light chain fragments.
Causes; myeloma, lymphoma, MGUS, waldenstroms. Paraprotein in blood or urine 90%.
Affects kidney and heart
what staining is used for amyloidosis?
congo red
describe the features of nephritic syndrome?
Haematuria Hypertension AKI Oliguric Proteinuria Oedema (due to oliguria causing salt and water retention not due to protein retention in nephrotic syndrome
what are the causes of nephritic syndrome in adults?
good pastures ANCA associated vasculitis SLE primary or secondary mesangiocapillary GM rapid progressive GN
describe good pastures syndrome?
(antiglomerular basement membrane antibody disease): AKI, pulmonary haemorrhage (crescenteric GN, linearg IgG deposition due to anti-GBM antibody. Treatment with steroids, cyclophosphamide, plasma exchange.
what are the causes of mesangiocapillary GN?
infections, collagen vascular disease, genetic/acquired, monoclonal gammopathies)
describe rapid progressive GN?
(AKI developing over days to weeks. Histology: crescentic glomerulonephritis, vascular necrosis. Serology: ANCA (cANCA (wegeners), pANCA (microscopic polyangiitis)). Early treatment=better outcome, steroids, cyclophosphamide with or without plasma exchange, rituximab
what are the causes of nephritic syndrome in children?
haemolytic uraemic syndrome
henoch schonlein purpura
post streptococcal GN
describe henoch schonlein purpura?
presents with rash on back of legs, extensor surfaces, joint, abdominal pain, GI haemorhage
describe post streptococcal GN?
presents as diffuse proliferative GN/ 10-14 days after streptococcal throat infection, supportive care, spontaneous recovery
name important plasma electrolytes?
sodium potassium chloride bicarbonate calcium phosphate
what is the major extracellular cation?
sodium
describe hypernatraemia?
can be due to water loss from the blood causing hemoconcentration of blood constituents. Hormonal inbalances (ADH and aldosterone) can be a cause
describe hyponatraemia?
- usually associated with excess water accumulation.
- Absolute loss of sodium may be due to: decreased intake of ion coupled with continual excretion
- Abnormal loss of sodium: excessive sweating, vomiting, diarrhea, diuretic use, excess urine production (diabetes, acidosis either metabolic acidosis of diabetic ketoacidosis)
- Relative decrease: imbalance of sodium in one of the body’s fluid compartment (from dilatation of sodium due to water retention related to oedema of CHF.
- At cellular level; hyponatraemia results in increased entry of water into cells by osmosis because concentration of solutes in cell exceeds concentrations of solutes in dilute ECF. Excess water causes swelling of cells, swelling of RBC (decreased oxygen carrying capacity and too large to fit through capillaries), swelling of neurons in brain causing damage
- what is the major intracellular cation?
2. what is the predominant extracellular anion?
- potassium
2. chloride
describe hyperkalaemia?
Due to increased dietary intake of potassium (potassium from blood ends up in ECF in high concentrations causing partial depolarization of plasma membranes and can lead to inability to repolarize. Heart won’t be able to relax after contraction and will ‘seize’.) may have confusion, numbness and weakened respiratory muscles.
describe hypokalaemia?
Can occur because of absolute reduction or relative reduction
Absolute loss: decreased intake, frequency related to starvation, vomiting, diarrhea, alkalosis
Relative reduction: insulin dependent diabetic patients (when insulin is administered and glucose taken up by cells potassium passes along with glucose.
describe hyperchloremia?
Due to dehydration, excessive dietary salt , aspirin intoxification, CHF, lung disease, CF
describe hypochloremia?
Occur due to defective renal tubular absorption, vomiting, diarrhea, metabolic acidosis
describe hypocalcaemia?
hypoparathyroidism (removal of thyroid gland)
describe hypercalacemia?
primary hyperparathyrodisim, malignancies
describe hypophophatemia?
due to heavy use of antacids, during alcohol withdrawal and malnourishment. In phosphate depletion the kidneys usually conserve phosphate but during starvation this is impaired
describe hyperphosphatemia?
due to decreased renal function or acute lymphocytic leukemia
describe creatinine?
- Produced from breakdown of creatinine and phosphocreatine and serves as indicator of renal function
- Synthesised in liver, pancreas, kidneys.
- Mosty produced in muscles so is influenced by muscle mass
describe urea (blood urea nitrogen-BUN)
- is a product of protein metabolism
- Concentration of urea is dependent on protein intake, body’s capacity to catabolise protein and adequate excretion of urea by renal system
- The body depends on the renal system to excrete urea means it can be used to evaluate renal function
- Increase can be a result of diet high in protein or decreased renal excretion
what is a low BUN: creatinine ratio suggestive of?
acute tubular necrosis
low protein intake
starvation
severe liver disease
what is a high BUN:creatinine ratio suggestive of?
pre renal uraemia
high protein intake
after GI bleeding
what is a high BUN: creatinine ratio w/ raised creatinine suggestive of?
post renal obstruction
pre renal uremia with renal disease
what are the causes of hyperamylasemia?
Pancreatitis Tumours Gall bladder infection Kidney failure ERCP Medications
describe the renin angiotensin aldosterone system?
Hormone system important for the regulation of blood pressure and fluid balance
Hormones: renin, angiotensin II, aldosterone
Regulated by renal blood flow
Renin release
-From granular cells of juxtaglomerular apparatus in response to: reduced NaCl delivery to distal tubule and detected by macula densa, reduced perfusion pressure in kidney detected by baroreceptors in afferent arteriole, systemic stimulation of JGA
describe angiotensin II production?
Angiotensinogen is a precursor protein produced in the liver and cleaved by renin to form angiotensinogen
Angiotensin I is converted to angiotensin II by ACE (in renal endothelium, lungs and capillary endothelium)
Angiotensin II binds to receptors (most action via AT1 receptors), acts on; arterioles (vasoconstriction), kidney (sodium reabsorption), sympathetic nervous system (increased noradrenaline release), adrenal cortex (aldosterone release), hypothalamus (thirst, ADH release)
give examples of drug induced pre renal impairment?
due to impaired perfusion of kidneys
- Hypovolaemia: loop diuretics such as furosemide, renal salt and water loss from hypercalcaemia induced by vit D therapy
- Decrease in cardiac output: such as beta blockers
- Decreased renal blood flow such as ACE inhibitors especially in renovascular disease
give examples of drug induced renal impairment?
- Acute tubular necrosis produced by direct nephrotoxicity: prolonged, excessive aminoglycoside treatment, amphotericin b, heavy metals or carbon tetrachloride. Aminoglycosides plus furosemide is particularly nephrotoxic
- Acute tubulointerstitial nephritis: cell mediated hypersensitivity nephritis occurs with penicillins, sulphonamides, NSAIDs
- Chronic tubulointerstitial nephritis
- Membranous glomerulonephritis such as penicillamine, gold, anti-TNF
give examples of drug induced post renal impairment?
Retroperitoneal fibrosis with urinary tract obstruction can result from use of drugs
what problems can NSAIDs cause in the kidneys?
- Sodium and water retention due to Reduced prostaglandin production
- Acute tubulointerstitial nephritis due to hypersensitivity reaction
- Nephrotic syndrome due to membranous glomerulopathy
- Analgesic nephropathy due to papillary necrosis after chronic use
- AKI due to acute tubular necrosis
- Hyperkalaema due to decreased renal excretion of potassium
what questions should be asked in relation to safe prescribing with the potential for kidney injury?
Is treatment mandatory?
Can drug reach the site of action?
Is the drug metabolism altered in uraemia?
will accumulation of drug or metabolites occur?
Is the drug toxic to the kidneys?
Are the effective concentration of the drug similar to toxic concentrations?
Will the drug worsen uraemic state?
Is the drug a sodium or potassium salt?
how can impaired renal function affect absorption of drugs ?
unpredictable in uraemia due to nausea and vomiting
how can impaired renal function affect metabolism of drugs?
oxidative metabolism of drugs by liver is altered in uraemia. Rate of drug metabolism by the kidney is reduced as a result of 2 factors
- Reduced drug catabolism: insulin
- Reduced conversion of precursor to more active metabolite: 1 alpha hydroxylase enzyme located in the kidney needed for vitamin D synthesis
how can impaired renal function affect protein binding of drugs?
reduced protein binding of a drug potentiates its activity and increases toxic side effects. Eg serum concetration of phenytoin required to produce antiepileptic effect is higher in normal patients than those with CKD. Some patients with renal disease are hypoproteinaemic and so less drug binding to protein. Eg hydrogen ions retained in CKD bind to receptors for acidic drugs such as sulphonamides, penicillin and salicylate so increases potential for toxicity
how can impaired renal function affect volume of distribution of drugs?
Salt and water overload or depletion may occur in patients with renal disease and can affect the concentration of drug obtained from a given dose
how can impaired renal function affect end organ sensitivity to drugs?
renal response to drug treatment may be reduced in renal disease eg. Mild thiazide diuretics have little diuretic effects in patients with severe CKD
how can impaired renal function affect renal elimination of drugs?
major problem with drug use in patients with CKD. Water soluble (gentamycin) are poorly absorbed from the gut, typically given by injection and not metabolized by the liver cause more problem than lipid soluble (propranolol) which are well absorbed and metabolized by the liver but metabolites of lipid soluble drugs may be water soluble and therefore toxic
what drugs can cause uraemia by their effects on protein anabolism and catabolism?
tetracyclines (not doxycycline) have catabolic effect and increase concentration of nitrogenous waste. May also cause direct impairment of GFR. Corticosteroids have a catabolic effect and do the same. Moderate impairment of renal function may become severely uraemic if given these drugs
give examples of drugs and toxic agents that cause specific renal tubular syndromes?
mercury, lead, cadmium, vitamin D
describe the pathophysiology of essential hypertension?
Benign essential hypertension-arterioscleorosis of major renal arteries and changes in intrarenal vasculature (nephrosclerosis) occurs as follows:
- small vessels/arterioles - intimal thickening and hyalinized vessel
- large vessels - concentric reduplication of internal elastic lamina and endothelial prolifetation cause ‘onion skin’appearance
- Reduction in size or both kidneys-asysmetrical if one major renal artery is more affected than the other
- Proportion of sclerotic glomeruli is increased compare with age matched controls
- These changes are accompanied by deterioration in excretory function
- Severe CKD more common in black africans. APOL1 gene assosciated (this gene gives protection against trypanosomal infection and African sleeping sickness
describe the features of accelerated or malignant phase hypertension?
- Arteriolar fibrinoid necrosis occurs, probably as a result of plasma entering the media of the vessel through splits in the intima. It is prominent in afferent glomerular arterioles
- Fibrin deposition within small vessels associated with thrombocytopenia and red cell fragmentation seen in peripheral blood film
- Microscopic haematuria, proteinuria, progressive uremia. Poor prognosis untreated
what are the mechanisms of renal hypertension?
- Activation of RAAS
- Salt and water retention leading to increase in blood volume and BP (greater influence as renal function deteriorates
describe renal hypertension?
Hypertension commonly complicates bilateral renal disease such as chronic glomerulonephritis, bilateral reflux nephropathy, polycystic disease and analgesic nephropathy
Hypertension occurs earlier, is more common and tends to be more severe in patients with renal cortical disorders, such as glomerulonephritis, than in those with disorders affecting primarily the renal interstitium such as reflux or analgesic nephropathy
what is the mechanism of hypertension in renovascular disease?
Mechanism of hypertension: renal ischaemia results in reduction in pressure in afferent glomerular arterioles leading to increased production and released of renin from JGA and increase in angiotensin II (vasoconstrictor and upregulates NADPH oxidase enzymes so reduced vasodilator activity)
what are the physiological changes in renal artery stenosis?
In renal artery stenosis renal perfusion is reduced and nephron transit time prolonged on side of stenosis so salt and water reabsorption is increased. Urine from ischamemic kidney is more concentration than urine from contralateral kidney and creatinine clearance is decreased on the iscahemic side
Pathology: narrowing of the renal arteries (renal artery stenosis) is caused by one of two pathological entities: fibromuscular disease or atherosclerotic renovascular disease
what are the types of firbomuscular disease of the renal arteries?
20-40% of renal vascular disease and has 4 types
- Medial fibroplasia-usually follows benign course, never follows progressive course after 40 yrs
- Perimedial fbroplasia-progressive course and may lead to complete occlusion
- Intimal fibroplasia –progressive course and may lead to complete occlusion
- Medial hyperplasia-rare, affects young women with high blood pressure with well preserved renal function
what investigations are useful in fibromuscular disease of the renal arteries?
MR angiography reveals string of beads appearance in fibroplasia
Angioplasty
describe atherosclerotic renovascular disease and patients it should be looke for in?
Common cause of hypertension and CKD due to ischaemic nephropathy
Associated with symptomatic atherosclerotic vascular disease elsewhere
Patients with PVD, CAD, congestive cardic failure and AA are at high risk of developing renal artery stenosis
Renovascular disease should be looked for in the following; patients with hypertension, CKD, abdominal audible bruits, doppler showing renal asymmetry, recurrent flash pulmonary oedema without cardiopulmonary diseases and progressive CKD with evidence of atherosclerosis
what are the aims in treating renovascular disease and why is it important to treat?
Aim is to correct hypertension and improve renal perfusion and excretory function
Renal artery stenosis can progress to occlusion
what are the treatment options in renal artery stenosis?
transluminal angioplasty to dilate stenotic region, stent insertion across stenosis, reconstructive vascular surgery, nephrectomy
what are the indications for revascularisation in patients with renovascular disease?
vessels with stenosis >75% and recurrent flash pulmonary oedema, drug resistant severe hypertension, ARVD affecting solitary functioning kidney, patients with cardiac failure needing ACE inhibitors, unexplained progressive CKD and dialysis dependent renal failure. Endovascular procedures considered better than medical therapy alone.
what medications should be given to patients with atherosclerotic renal vascular disease (ARVD)?
all patients with ARVD should be treated with combination of aspirin, statins, optimal control of blood pressure as prophylaxis against progression of atherosclerosis
what is the prognosis for patients with renovascular disease?
High mortality due to co-morbidities and ARVD patients have generalized endothelial dysfunction
ARVD patients with ESKD have higher rates than those with good renal function
what are the methods for screening for renovascular disease?
radionuclide studies doppler ultrasound magnetic resonance angiography CT scanning renal arteriography
what is the role of angiotensin 2 in the kidneys?
Angiotensin II stimulates adrenal cortex to produce aldosterione and is a powerful vasoconstrictor. It forms part of the renal autoregulation of glomerular perfusion mechanism. The preglomerular arteriolar tone is reduced when renal perfusion falls and increases glomerular blood flow and maintaining glomerular filtration
Afferent pressure reduced by narrowed vessel so autoregulation is dependent on changes in glomerular arteriolar tone
describe the role of ACE inhibitors in renovascular disease?
ACE inhibitors interfere with Angiotensin II production so autoregulation is impaired, glomerular perfusion falls, renal ischamic nephropathy develops and renal failure ensues
ACE inhibitors are effective when treating renovascular hypertension especially with diuretics as long as eGFR isn’t deteriorating, renal function and potassium should be checked before staring an ACE inhibitor
what are the major causes of oedema?
- heart failure
- hepatic cirrhosis
- nephrotic syndrome
- sodium retention
- others: insulin treatment, increased capillary pressure, increased interstitial oncotic pressure due to increased capillary permeability to proteins
how does heart failure cause oedema?
Reduction in cardiac output and fall in effective circulatory volume, RAAS activation, ADH release and increased activity of renal sympathetic nerves. Increased peripheral and renal arteriolar resistance and water and sodium retention. Causing extracellular volume expansion and increased venous pressure.
how does hepatic cirrhosis cause oedema?
Peripheral vasodilatation, reduced effective arterial blood volume and arterial filling leading to activation of events similar to cardiac failure and other conditions with marked peripheral vasodilatation. Increased peripheral and renal resistance, water and sodium retention and oedema
how does nephrotic syndrome cause oedema?
Interstitial oedema common with hypoalbuminaemia esprcially nephrotic syndrome. Expansion of interstitial compartment is secondary to sodium accumulation in extracellular space due to imbalance between oral sodium intake and urinary output
how does sodium retention lead to oedema?
Decreased GFR decreases renal capacity to excrete sodium. This can be due to drugs such as; oestrogens, mineralocorticoids ans liquorice, NSAIDs, thiazolidinediones
give a physiological example of a cause of proteinuria?
fever
exercise
orthostatic proteinuria
give a renal example of a cause of proteinuria?
glomerular disease
amyloidosis
pyelonephritis
acute tubular necrosis
give a lower urinary tract example of proteinuria?
cystitis
obstructive uropathy
give extra-renal causes of proteinuria?
diabetes mellitus pre-eclampsia hypertension congestive cardiac failure myeloma
describe the monitoring and prevention of AKI in patients at high risk?
- electronic clinical decision support systems to support clinical decision making and prescribing (ensure they can; interact with lab systems, recommend drug dosing, store and update data on patients history, include alerts)
- pharmacist advice
- stop ACE inhibitor and ARBs temporarily
how is AKI prevented in hospital?
at risk patients have systems in place to recognise it such as oliguria
how is the risk of AKI assessed in adults having surgery?
increased risk: emergency surgery intraperitoneal surgery CKD diabetes heart failure over 65 yrs liver disease drugs in perioperative period such as NSAIDs
what are the basic investigations in a patient with AKI?
- basic metabolic profile (U&Es)-acutely elevated serum creatinine may be initial only sign of renal function decline
- Serum urea to creatinine ratio-consider other causes of raised urea. >20:1 suggests pre-renal azoteamia
- Urinalysis
- Urine culture
- FBC- anaemia suggest possible CKD, blood loss. Leukocytsis, thrombocytopenia
- Fractional excretion of sodium- <1% suggests pre-renal azotaemia
- Fractional excretion of urea <35% suggests pre renal azotaemia
- Urinary eosinophil count->5% to 7% supports diagnosis of interstitial nephritis
- Venous blood gases-anion gap acidosis in renal failure
- Fluid challenge-diagnostic and therapeutic in pre-renal azotaemia
- Bladder catheterization- diagnostic/therapeutic for bladder neck obstruction. Assessment of residual urine
- Urine osmorality – evaluate normal tubular function and response to ADH
- Urine sodium concentration- high levels in acute tubular necrosis not exclusive to diagnosis
- Renal ultrasound-assess post obstructive causes
- CXR-if associated with heart failure
- ECG- changes with severe hyperkalaemia
what is the management for pre-renal failure?
techniques to improve the haemodynamic status of the patient.
Volume contracted patient: need volume expansion with crystalloid or colloid. HES solutions for infusion
Vasopressors recommended if hypotension is severe to augment BP whilst optimizing volume status
Management difficult if renal hypoperfusion due to impaired cardiac function
Renal replacement therapy may be neededif severe acid/base, electrolyte or uraemic complications are present
describe the management for patients with intrinsic renal failure?
Management varies according to aetiology
Volume expansion needed when co-exsting pre-renal azotaemia
Patients with volume overload require sodium restriction, may be managed with diuretics
Remove offending drugs
Accute GMN and vasculitis management-may need corticosteroids, cytotoxic drugs or other immune modifying drugs depending on specific diagnosis
Acute glomerulonephritis- cytotoxic and immunemodifying agents
describe the management for patients with obstructive renal failure?
Bladder catheter placement if bladder outlet obstruction cannot be quickly ruled out
Urological or surgical assistance for ureteral stenting, urinary diversion, debulking procedures
renal replacement therapy if severe acidosis, volume overload unresponsive to diuretics or electrolyte or uraemic complications while underlying obstructive issue is being addressed.
what is the management for pre-renal failure?
techniques to improve the haemodynamic status of the patient.
Volume contracted patient: need volume expansion with crystalloid or colloid. HES solutions for infusion
Vasopressors recommended if hypotension is severe to augment BP whilst optimizing volume status
Management difficult if renal hypoperfusion due to impaired cardiac function
Renal replacement therapy may be neededif severe acid/base, electrolyte or uraemic complications are present
describe the management for patients with intrinsic renal failure?
Management varies according to aetiology
Volume expansion needed when co-exsting pre-renal azotaemia
Patients with volume overload require sodium restriction, may be managed with diuretics
Remove offending drugs
Accute GMN and vasculitis management-may need corticosteroids, cytotoxic drugs or other immune modifying drugs depending on specific diagnosis
Acute glomerulonephritis- cytotoxic and immunemodifying agents
describe the management for patients with obstructive renal failure?
Bladder catheter placement if bladder outlet obstruction cannot be quickly ruled out
Urological or surgical assistance for ureteral stenting, urinary diversion, debulking procedures
renal replacement therapy if severe acidosis, volume overload unresponsive to diuretics or electrolyte or uraemic complications while underlying obstructive issue is being addressed.
describe renal repacement therapy?
Indicated for refractory severe hyperkalaemia acidosis, volume overload or uraemia
Conventional haemodialysis often used when indications for dialysis arise
CRRT mostly used in haemodynamically unstable patients
Early dialysis
Peritoneal dialysis
