Week 13 - Renal Disease Flashcards
What are the three groups of causes of AKI?
Pre-Renal (Hypovolaemia)
Renal
Post-Renal (Obstructive)
What causes 90% of AKIs?
Pre-renal (most common) or Post-renal causes
How is AKI staged?
By rise in serum creatinine or reduction in urine output.
What is the mortality of AKI Stage 3 in hospital?
30%
What is a pre-renal cause of AKI?
Inadequate blood supply to the kidney - can be due to
hypovolaemia,
decreased CO,
dehydration,
hypotension,
arterial occlusion (atherosclerosis, thromboembolic disease, renal artery dissection),
ACEIs, ARBs or NSAIDs,
renal vasoconstriction (NOR)
Which Ps are more at risk of AKI?
What are the intrinsic renal causes of AKI?
Glomerulonephritis
Small Vessel Vasculitis
Interstitial Nephritis
Acute Tubular Necrosis (Ischaemic or Nephrotoxic)
Renal Vascular Disease (rare)
Also -
Myeloma
Rhabdomyoloysis
What investigations should you do for an AKI assessment?
BP = are they hypo / hyper perfused?
Fluid status - dry / overloaded?
Urine dipstick - look for blood or protein - can indicate intrinsic cause
Imaging - USS or CT
Renal Screening -
Serum & Urine Electrophoresis - looking for amyloid
Immunoglobulins
Blood film - look for haemolysis
Calcium - Ps will often have high calcium
ANA, ANCA, GBM ABs
Complement levels - if you suspect lupus or infection
Cryoglobulins
Which guidelines are used for diagnosing and treating AKI?
STOP AKI
What is ANA antibody used to indicate?
Lupus
What disease is diagnosed with ANCA antibodies?
Vasculitis
What are the management steps you can take for AKI?
Fluid rehydration if pre-renal AKI
Stop nephrotoxic medications (ACEIs, ARBs, Abx = penicillin, gent, vanc, NSAIDs
Relieve obstruction if post-renal cause
What complications can result from AKI?
Hyperkalaemia
Fluid overload, HF, pul oedema
Metabolic acidosis
Uraemia -> encephalopathy or pericarditis
What can lots of blood but nothing else on dipstick indicate?
Post-renal obstruction or myoglobinuria (rhabdomyolysis)
What would a pre-renal cause of AKI show on urine dipstick?
No substantial blood or protein
How can you differentiate between glomerulonephritis and interstitial nephritis by dipstick?
GN = lots of blood and protein, no WBCs
IN = less blood + protein, WBCs present
What can cause lots of blood and protein but not WBCs on urine dipstick?
Glomerulonephritis
ANCA Vasculitis
Anti-GBM Lupus
Infections - Hep B/C, HIV
What is nephritic syndrome?
Symptoms of an inflamed kidney that has
- blood in urine (microscopic or macroscopic)
- protein in urine (less than 3g per 24hr)
- oliguria
What are the causes of glomerulonephritis?
Also minimal change disease
Goodpasture syndrome
What is a life threatening complication of vasculitis?
Pulmonary-renal syndrome - can get pulmonary haemorrhage and AKI
Which disease has anti-glomerular basement membrane antibodies that attack the glomerulus and pulmonary basement membranes? Can cause glomerulonephritis and pulmonary haemorrhage? - i.e. Acute AKI and haemoptysis
Goodpasture Syndrome
What will histology show for rapidly progressive glomerulonephritis?
Crescentic glomerulonephritis
Which antibody is associated with vasculitis?
ANCA antibody
What is an umbrella term for conditions that cause inflammation of or around the glomerulus.
Glomerulonephritis
What is the term of inflammation of the space between the cells and the tubules within the kidney?
Interstitial nephritis
What is pathological scarring of the tissue in the glomerulus called?
Glomerulosclerosis
What can hyperkalaemia do to ECGs?
Can caused depressed ST segment, biphasic T waves, Tall Waves, Long PR interval and wide QRS duration
When should urgent treatment for hyperkalaemia be carried out?
K > 6 + ECG changes
OR
K > 6.5 regardless of ECG
In urgent hyperkalaemia what is the Rx that should be given?
First give calcium gluconate/chloride - is cardioprotective and stabilises the membranes of the heart cells.
Then give Insulin + Dextrose + Salbutamol - drives K into cells.
If acidotic - correct with bicarbonate
Stop any medications exacerbating the hyperkalaemia
Furosemide if overloaded
Dialysis
Can give K binders (Lokelma)
When should dialysis or haemofiltration be given for AKI?
If there is refractory hyperkalaemia (>7)
If ph <7.2 & bicarb <12
If pulmonary oedema & persistent anuria
If uraemia >30mmol
AEIOU
A = Acidosis (severe and not responding)
E = Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I = intoxication (OD certain medications)
O = oedema (severe and unresponsive pul oedema)
U = uraemia Sx - seizures or reduced consciousness
What is the definition of CKD?
Abnormal kidney function for >3m
Which Ps are at risk of CKD?
DM = biggest cause of CKD
HT = second largest cause of CKD
Age related decline
Glomerulonephritis
PKD
Meds - NSAIDs, PPIs, Lithium
Which is better for proteinuria measurement - ACR or PCR?
ACR - detects early stages of CKD better. Measures albumin:creatinine rather than protein:creatinine
What are possible S&S of CKD?
Normally asymptomatic and diagnosed incidentally.
Can also get
- itching
- loss of appetite
- nausea
- oedema
- muscle cramps
- peripheral neuropathy
- pallor
- HT
What are the different GFRs for staging CKD?
Stage 1 = >90
Stage 2 = 60-90
Stage 3a = 45-60
Stage 3b = 30-45
Stage 4 = 15-30
Stage 5 = <15
If a diabetic patient has diabetic retinopathy, what is it also likely that they have?
Diabetic nephropathy
This is because high levels of glucose passing through the glomerulus causes scarring (glomerulosclerosis).
=> Proteinuria - due to damage to the glomerulus allowing protein to pass through the barrier into the urine.
What are the possible complications of CKD?
Anaemia
Renal bone disease
CVD
Peripheral neuropathy
What are the aims of management of CKD?
Slow progression of disease
Reduce risk of CVD
Reduce risk of complications & treat any
Optimise diabetic control and hypertensive control if needed
Treat glomerulonephritis
What drug is used to treat metabolic acidosis?
Sodium bicarbonate
What is used to treat anaemia in CKD?
Iron supplementation + erythropoietin
EPO given because damaged kidney cells = drop in EPO production.
What is used to treat renal bone disease?
Vitamin D
How can renal bone disease show on Xray?
Can get sclerosis of the ends of vertebrae (denser white) and osteomalacia in the centre of the vertebra (rugger jersey spine)
What happens to P in CKD?
Can get high serum P due to reduced excretion
Why can CKD lead to secondary hyperparathyroidism?
Damaged kidneys = less Vit D converted => low serum calcium.
Parathyroid gland react to this (and the high P levels) by excreting more parathyroid hormone => inc osteoclastic activity.
What Rx can be given for renal bone disease?
Active forms of Vit D
Low P diet
Bisphosphonates can be used to Rx any osteoporosis.
What Sx does nephrotic syndrome usually present with?
Oedema
Proteinuria - may get frothy urine - >3.5h of protein
Hypoalbuinaemia (<30g)
May get associated high cholesterol (as liver tries to produce more albumin) and inc tendency to thrombus
What is the most common cause of nephrotic syndrome in children?
Minimal change disease
What hereditary renal diseases can cause CKD?
What is the most common treatment for most types of glomerulonephritis?
Immunosuppression
Blood pressure control
What mechanisms in the body can CKD interfere with?
Sodium and water balance -> HT and HF
Potassium balance
Elimination of nitrogenous waste stopped = uraemia
Erythropoietin -> anaemia
Acid-base balance - no buffering = acidosis
Activation of Vit D & decreased P elimination = renal bone disease
What are the options for renal replacement therapy?
Transplantation
Peritoneal dialysis
Haemodialysis
At what GFR would you start looking at renal replacement therapy?
GFR <20
If you have hypoalbuminaemia but no proteinuria - what are the possible causes?
HF
Thyroid disease
Cirrhosis
Infections
IBD
Malnutrition
What are the associated features with nephrotic syndrome?
What are the most common causes of nephrotic syndrome in adults?
Glomerulosclerosis
Membranous Nephropathy
Can also be associated with AI conditions such as Lupus and Sarcoidosis
How is nephrotic syndrome treated?
ARBs or ACEIs
Statins
Diuretics
Treat infection
If albumin <35, dose with anticoagulation
May need high dose steroids / immunosuppressants
When should ACEIs be started in Ps with diabetic nephropathy?
Immediately = even if they have normal BP
What causes acute tubular necrosis?
Ischaemia or toxins - damage the kidney cells.
ATN can be reversible - how long does it take for cells to regenerate?
7-21 days
Which drugs are nephrotoxic and can cause ATN?
Contrast
Gentamicin
NSAIDs
Lithium
Heroin
How is ATN managed?
Same as any other AKI - fluids, stop nephrotoxic meds and treat complications
Which disease causes thrombosis in the small blood vessels in the body -> haemolytic anaemia, AKI & low platelet count (thrombocytopenia)?
What causes this?
Haemolytic uraemic syndrome
Caused by shiga toxin from E.coli 0157 or from shigella
When myocytes die in rhabdomyolysis - what is released into the blood stream?
Myoglobin (toxic to kidney -> AKI)
K (-> cardiac arrhythmias)
P
CK
What are the S&S of rhabdomyolysis?
Muscle aches and pain
Oedema
Fatigue
Confusion
Red-brown urine (from myoglobulin)
What is the Rx of rhabdo?
IV fluids - encourage filtration of breakdown products
IV sodium bicarb - make urine more alkaline and reduce toxicity of myoglobin on kidneys
IV mannitol - can inc GFR and reduce oedema
Why do ARBs cause pre-renal injury?
ARBs block the action of angiotensin II by binding to the angiotensin II type 1 (AT1) receptors.
Normally, angiotensin II constricts the efferent arterioles (the blood vessels exiting the glomeruli) more than the afferent arterioles (the blood vessels entering the glomeruli), which helps maintain glomerular filtration pressure and thus the glomerular filtration rate (GFR).
By blocking the effect of angiotensin II, ARBs cause dilation of the efferent arterioles. This can lead to a reduction in the intraglomerular pressure, thereby decreasing the GFR.
In patients with conditions that already compromise renal perfusion (e.g., dehydration, heart failure, or significant renal artery stenosis), this reduction in GFR can be substantial enough to precipitate pre-renal AKI.
In situations where renal perfusion is compromised, the body typically increases angiotensin II levels to help maintain GFR by preferentially constricting efferent arterioles.
When ARBs inhibit this compensatory mechanism, the kidneys’ ability to maintain adequate GFR in the face of reduced renal blood flow is impaired, leading to pre-renal AKI.
What is the most common renal cause of AKI? (not pre or post renal cause)
ATN
What is the most common causes of acute interstitial nephritis?
Drugs - NSAIDs / penicillins
Infection - TB
Immune mediate - SLE, sarcoidosis
What are the Sx of a pre-renal AKI?
Severe dehydration Sx
Which antibody should you test for for Lupus?
Serum dsDNA antibody
What is visible blood in the urine more indicative of?
A post renal AKI
What do red casts on urine microscopy indicate?
Glomerular disease
What can Coca Cola urine indicate?
Nephritic syndrome - protein and fat present in the blood
What is the difference between nephrotic and nephritic syndrome?
Nephrotic syndrome = high proteinuria (>3.5g/day) + oedema + hypoalbuminemia + hyperlipidemia (The liver increases lipoprotein synthesis in response to hypoalbuminemia.)
Nephrotic syndrome results from damage to the glomerular filtration barrier, which includes the endothelial cells, glomerular basement membrane, and podocytes (specialized epithelial cells). This damage leads to increased permeability and excessive loss of proteins in the urine.
Causes = minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, DM, SLE, amyloidosis, infections (HIV & Hep B&C).
Nephritic syndrome = haematuria (Blood in the urine is a hallmark due to the rupture of glomerular capillaries), proteinuria (less than nephrotic), HT, reduced GFR.
Nephritic syndrome results from inflammatory damage to the glomeruli, leading to hematuria and a reduced glomerular filtration rate (GFR).
Causes inc post-infectious glomerulonephritis (often following strep - immune complexes deposit in the glomeruli), IgA Nephropathy (Berger’s disease), rapidly progressive glomerulonephritis (Goodpastures, systemic vasculitis), Lupus.
How are podocytes in the glomerulus damaged?
Damage to podocytes can come from release of inflammatory mediators, pressure & immunoglobulin deposition
Damage by release of factors from T-cells causes effacement - the podocytes flatten out - barrier breaks down and allows proteins and RBCs to appear in Bowman’s capsule.
What causes hypertensive nephropathy?
Atherosclerosis = arteries into kidney become thickened and narrowed - less blood reaches the glomerulus.
Over time - causes immune cells within mesangium (macs & foam) to secrete growth factors -> mesangial proliferation. Mesangial cells regress to mesangioblasts - secrete ECM (collagen etc) -> glomerulosclerosis
How does diabetes affect the glomerulus?
Excess glucose in blood = non-enzymatic glycation
Glucose sticks to plasma proteins - causes toxicity and thickening of BM esp in efferent arteriole -> obstruction -> response is dilation of afferent arteriole - incs pressure in glomerulus -> over time leads to hyperfiltration injury.
Mesangial cells proliferate - secrete ECM - glomerulus becomes thickened and end up with nodular glomerulosclerosis.
Difference between hypertensive and diabetic glomerulonephropathy = diabetic is more nodular - doesn’t affect the whole of the glomerulus.
What is the pathophysiology of ATN?
Cells die - end up with leakage of filtrate into substance of kidney - causes inflammatory reaction.
As the cells die = debris = obstruction to tubules - causes backleak into glomerulus and leakage from there into interstitium.
Inducting event = MI, bleed, - lowers BP - lowers GFR = hypoxic changes in tubules - extends by inflammatory response.
Corticomedullary nephrons affected the most - have the most precarious blood supply.
Maintenance = fix underlying problem, reverse hypoxia - give cells a chance to repair and proliferate - can restore renal function.
What can cause interstitial nephritis?
Most common = drugs - NSAIDs, diuretics, ABx
What are the stages of AKI in terms of creatinine baseline?
Stage 1 = Creatinine 1-2 x baseline
Stage 2 - 2-3
Stage 3 - >3
When should you think about renal replacement therapy?
How can you tell whether a P has acute or chronic CKD?
Acute - acidotic, unwell, normal Ca and normal kidney size
Chronic = well, low Ca, high PTH, small kidneys
What lifestyle advice should Ps with CKD be given?
When do Ps with ADPKD tend to become symptomatic?
30s - 40s
When do Ps with ARPKD become symptomatic?
Infancy
From which part of the kidney is classified as post-renal?
Anything beyond the nephron
What is a dilated intrarenal collecting system called?
Hydronephrosis
What causes hydropnephrosis and hydroureter?
Obstruction
Why is urinary tract obstruction an emergency?
Because you get obstructive atrophy in a relatively short amount of time - which can lead to unrecoverable renal function.
Glomeruli can survive but the nephrons become scarred and non-functioning.
What are the symptoms of urinary tract obstruction?
Which mode of imaging is best for looking for stones?
CT
What is dynamic renography of the kidneys called?
MAG3 Renography
How is acute kidney obstruction treated?
Percutaneous nephrostomy
Radiologists pass needle to inside of kidney - can feed guide wire and leave tube hanging out - decompress kidney, let infection settle and let it recover.
What can cause obstructions in the urinary system?
What is the most common type of urinary tract stone?
Calcium oxalate and phosphate
What composition are staghorn stones?
Ca, Mg & ammonium phosphate
What are stones made from when associated with gout?
Uric acid
What are the symptoms of ureteric colic?
What is the commonest cancer of the bladder and ureter?
What treatments can be given for urinary retention?
What type of medication is tamsulosin?
α blocker
What type of medications are finasteride and dutasteride?
5 α reductase inhibitors
inhibit further growth of BPH, reduce rate of growth by blocking conversion of testosterone.
What procedures can be carried out for BPH?
HoLEP
TURP
What are possible Sx of prostate cancer?
Haematuria
LUTS
Haematospermia
Bone pain if mets
Bladder outflow obstruction with AKI (rare)
Elevated PSA
Do urethral strictures cause obstructive nephropathy?
Rarely
Can cause difficulty emptying but rarely cause high pressures in the bladder.
What is the most common cause of end stage renal disease?
Diabetic nephropathy
What term is used to define clinical conditions in which heart and kidney dysfunction overlap?
Cardio-renal syndrome
How can dysfunction in the heart cause dysfunction in the kidney?
Type 1: Acute Cardio-Renal Syndrome
○ Primary Issue: Acute heart dysfunction (e.g., acute heart failure, acute myocardial infarction)
○ Secondary Effect: Acute kidney injury (AKI)
○ Mechanism: Reduced cardiac output leads to decreased renal perfusion, causing AKI. Additionally, high central venous pressure due to heart failure can increase renal venous pressure, impairing kidney function.
Type 2: Chronic Cardio-Renal Syndrome
○ Primary Issue: Chronic heart dysfunction (e.g., chronic heart failure)
○ Secondary Effect: Chronic kidney disease (CKD)
○ Mechanism: Chronic reduction in cardiac output leads to long-term decreased renal perfusion and progressive kidney damage. Neurohormonal activation (e.g., RAAS, sympathetic nervous system) exacerbates renal dysfunction.
How can kidney dysfunction cause heart dysfunction?
Type 3: Acute Reno-Cardiac Syndrome
○ Primary Issue: Acute kidney injury
○ Secondary Effect: Acute heart dysfunction (e.g., acute heart failure, arrhythmias)
○ Mechanism: AKI leads to fluid overload, electrolyte imbalances (e.g., hyperkalemia), and increased levels of uremic toxins, all of which can adversely affect cardiac function.
Type 4: Chronic Reno-Cardiac Syndrome
○ Primary Issue: Chronic kidney disease
○ Secondary Effect: Chronic heart dysfunction (e.g., chronic heart failure)
○ Mechanism: CKD leads to chronic volume overload, hypertension, anemia, and mineral metabolism disorders, all of which can contribute to cardiac remodeling and heart failure.
Renal dysfunction can lead to metabolic derangements -> systemic inflammation and microvascular dysfunction = can cause cardiomyocyte stiffening, hypertrophy and interstitial fibrosis.
How is cardio-renal syndrome classified?
T1 - Acute cardiac
T2 - Chronic cardiac
T3 - Acute renal
T4 - Chronic renal
T5 - Systemic illness fucking both organs at once
What can be the result of prolonged diuretic use?
Can lead to decrease in ANP + diuretic resistance - which requires higher doses of diuretics which Ps can resist
Why can hyponatremia occur in severe HF?
Due to inc fluid levels in the body diluting the levels of Na in the serum
How can ACEIs damage the kidney?
Stop AGTI to AGTII (potent vasoconstrictor).
AGTII - constricts the efferent arterioles (maintaining GFR) - thus ACEIs cause dilation of efferent arterioles - reducing glomerular pressure and GFR - can decrease kidney function - can be damaging if already have compromised kidney perfusion.
If Ps have renal artery stenosis - the kidneys rely on AGTII to maintain adequate perfusion - removing this with ACEIs can severely reduce renal BF = acute renal failure
ACEIs - can cause hyperkalaemia - by reducing aldosterone secretion (which normally promoted K excretion in the kidneys).
When are ACEIs highly beneficial for protecting kidney function?
In Ps with DM or HT - they reduce proteinuria and slow progression of kidney disease.
The kidney is very sensitive to nephrotoxic drugs when Ps have HF. Which drugs in particular should you you be wary of?
NSAIDs
ACEIs
Aminoglycosides
How does liver cirrhosis affect the kidney?
Cirrhosis -> inc resistance in the portal system = portal hypertension = vasodilation in the abdominal circulation. This reduces circulating volume = activation of RAAS by the kidney which senses decreased volume.
RAAS -> inc aldosterone -> decreased excretion of Na. This causes hypernatremia -> water retention -> oedema and ascites.
How does liver cirrhosis cause increased ANP?
Atrial Natriuretic Peptide (ANP) is a hormone produced by the atria of the heart that promotes natriuresis (excretion of sodium in the urine), diuresis (increased urine production), and vasodilation.
Patients with cirrhosis often have elevated levels of ANP. This is likely due to increased atrial stretch from hypervolemia and increased cardiac output commonly seen in cirrhosis.
What is an important thing to control when managing ascites.
Sodium = needs restricting
What is it called when both the liver and kidney are dysfunctional?
Hepatorenal syndrome
What is hepatorenal syndrome?
Functional AKI - where there is severe renal vasoconstriction without evidence of structural kidney disease
Why can the Cr be misleading as to kidney dysfunction in Ps with hepatorenal syndrome?
Ps with chronic liver disease - often have reduced muscle mass, lower protein intake - therefore Cr levels can be influenced by this and appear better than they would be with normal protein levels in the body.
There are two types of hepatorenal syndrome - 1 and 2. What is the difference between them?
1 = Acute - oliguric with doubled creatinine within 2 weeks. Outcome poor (days-weeks).
2 = Chronic - diuretic resistant - less rapid deterioration in renal function - associated refractory ascites. Less poor but still crap survival (months).
How is hepatorenal syndrome treated?
Mainly supportive - Na and H20 restriction.
Can give human albumin solution
Terlipressin (ADH analogue) - acts as a vasoconstrictor in the splanchnic circulation
TIPS procedure
Dialysis - only to support until transplantation if needed.
Why can sepsis damage the kidneys?
Endotoxins are released in sepsis -> systemic vasodilation -> reduced renal perfusion = AKI
AKI in sepsis is very common
How can systemic infections damage the kidney?
Can get immune complexes which stick in the kidney = immune complex nephritis -> post infectious glomerulonephritis
Which is the most common infection to cause post infectious glomerulonephritis?
Post streptococcal infection = post-streptococcal glomerulonephritis
MRSA or S. aureus are also becoming more common
What are the most common viral causes of nephrotic syndrome or glomerulonephritis?
HIV
Hep B
Hep C
Which cancers can affect the glomerulus?
Lymphoma
Leukaemia
Myeloma
Lung, GI, Uterine, Prostate carcinomas
What is haemolytic uraemic syndrome?
Thrombosis of small blood vessels throughout the body
Triad of
- Haemolytic anaemia
- AKI
- Thrombocytopenia
What often triggers HUS?
Shiga toxin - E Coli 0157 most common
Also produced by shigella
What are the S&S of HUS?
Initially brief gastroenteritis, often + bloody diarrhoea
5 days later
- reduced urine output
- haematuria / dark brown urine
- abdominal pain
- lethargy and irritability
- confusion
- HT
- bruising
What is the management of HUS?
Supportive treatment - but medical emergency - 10% mortality.
Anti-hypertensives
Blood transfusions
Dialysis if needed
70-80% make a full recovery
What are the most common causes of glomerular disease?
DM
HT
Genetic conditions
Malignancy
Recent infection - streptococcus
Drugs/toxins - NSAIDs, heroin
How much protein does a normal kidney excrete in a day?
<150mg
What is the definition of nephrotic syndrome in terms of proteinuria?
Proteinuria >3.5g/1.73m2 body surface area / day
What is greater in the urine - blood or protein - in
1) nephrotic syndrome
2) nephritic syndrom?
Nephrotic = excess protein in the urine
Nephritic = excess blood in the urine
What can nephrotic syndrome cause?
Low albumin
Oedema
High lipids (hyperlipidaemia)
Vascular thromboses
What is the most common cause of nephrotic syndrome in children?
Minimal change disease (Minimal Change Glomerulonephritis)
What can cause nephrotic syndrome in adults?
Membranous Glomerulonephritis
Focal Segmental Glomerulosclerosis
What are secondary causes of nephrotic syndrome?
DM
SLE
Amyloidosis
What are the clinical signs of nephritic syndrome?
Haematuria
HT
Decreased urine output
Oedema
What are the biggest cause of nephritic syndrome?
IgA nephropathy
What systemic causes can cause nephritic syndrome?
Vasculitis
Goodpastures Syndrome
SLE
What is AKI?
Sudden decline in GFR over days
What is pyonephrotis?
Pus in the collecting system of the kidney
When should US be done in the following situations:
- Suspected pyonephrosis
- No idenfied cause of AKI
- At risk of urinary tract obstruction
Within 6 hours
2&3 = Within 24 hours
If there is an upper urinary tract obstruction - how should a nephrostomy or stent be done?
Within 12 hours
What is hydronephrosis?
Dilation of the renal collecting system - caused by obstruction of the kidney.
What imaging is used for AKI to determine whether there is an obstructive cause?
CT KUB
What imaging is used for CKD?
Ultrasound
What imaging is used for diagnosing renal artery stenosis?
Renal angiogram
What rare reaction can occur with gadolinium contrast?
Nephrogenic Systemic Fibrosis - fibrosis of skin, joints, eyes and internal organs
How long can it take to develop Sx of NSF?
Hours - Years
Which Ps are more likely to get an AKI from contrast?
Those with existing renal impairment
How is renal obstruction treated?
Nephrostomy
What is pyelonephritis?
Acute infection of the upper urinary tract
What does streaky or wedge shaped enhancement in the kidney on CT mean?
Pyelonephritis
What is the difference between renal or peri-nephric abscesses?
Peri-nephric = pus filled collection around the kidney resulting from unresolved pyelonephritis
Renal abscess = pus fulled collection within the kidney
