Renal Flashcards
How can you prevent calcium stones?
This is caused by hypercalcuria hence you can:
- High fluid intake
- Add lemon juice to water
- Avoid carbonated drinks
- Limit salt intake
- K citrate may be useful
- Thiazide diuretics - increases distal tubular ca resorption ***
How can you prevent oxalate stones?
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion
How can you reduce uric acid stones?
allopurinol
urinary alkalinization e.g. oral bicarbonate
podocyte fusion and effacement of the podocyte foot processes on renal biopsy
What diagnosis?
Mx?
Minimal change disease
mx- oral corticosteroids (80% of cases) -> cyclophosphamide in steroid resistant cases
What does focal segmental glomerulosclerosis cause?
cause of nephrotic syndrome and chronic kidney disease
typically presents in younger adults
What are some causes of focal segmental glomerulosclerosis?
idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell
Also high recurrence rate in renal transplants
What are the main extra-renal manifestations of ADPKD?
Liver cysts - 70% most common feature
Berry aneurysms - can rupture -> SAH
CVS - MV prolapse, M / T valve incompetence, aortic root dilatation, aortic dissection
Cysts in other organs - pancreas, spleen
Rarely - thyroid, oesophagus and ovary
In children presenting suspectingly for minimal change disease what is mx?
1st line oral pred
If steroid non-responsive, high suspicion of alternative diagnosis or declining renal func (on calcuerin inhibitor) -> renal biopsy
Which immunosuppression can cause tremor?
Tacrolimus
Which renal stones are radio-opaque?
Calcium oxalate
Mixed calcium oxalate / phosphate
Triple phosphate
Calcium phosphate
Which renal stones are radio-lucent?
Urate stones
Xanthine stones
Which renal stones are semi-opaque? what do they look like?
Cystine stones - ground glass appearance
Why do you get mineral bone disease in ckd?
Basic problems in chronic kidney disease (CKD):
> 1-alpha hydroxylation normally occurs in the kidneys → CKD leads to low vitamin D
> the kidneys normally excrete phosphate → CKD leads to high phosphate
This, in turn, causes other problems:
> the high phosphate level ‘drags’ calcium from the bones, resulting in osteomalacia
> low calcium: due to lack of vitamin D, high phosphate
> secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D
How is mineral bone disease risk reduced in CKD?
The aim is to reduce PO4 and PTH levels.
reduced dietary intake of phosphate is the first-line management
phosphate binders
vitamin D: alfacalcidol, calcitriol
parathyroidectomy may be needed in some cases
MoA of Spironolactone?
Aldosterone antagonist: acts on the cortical collecting ducts as a diuretic via inhibition of mineralocorticoid receptor
What is the most common type of glomerulonephritis in adults? how does this present / biopsy
Membranous glomerulonephritis - third most common cause of ESRF
Nephrotic syndrome / proteinuria
What are the causes of membranous glomerulonephritis?
idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
Young female, hypertension and asymmetric kidneys → what diagnosis?
Fibromuscular dysplasia
HTN is secondary to renal artery stenosis (this is the 2nd most common cause after renal vascular disease)
Why does lithium cause DI?
Causes nephrogenic DI - densitises kidneys ability to respond to ADH in collecting ducts
Features of Goodpasture syndrome?
Goodpastures syndrome = Anti-GBM disease - small vessel vasculitis associated with:
pulmonary haemorrhage
rapidly progressive glomerulonephritis
this typically results in a rapid onset acute kidney injury
nephritis → proteinuria + haematuria
Ix findings in Goodpastures syndrome?
renal biopsy: linear IgG deposits along the basement membrane
raised transfer factor secondary to pulmonary haemorrhages
Anti-GBM antibodies
Main mx for rhabdomyolysis?
IV fluids
Urinary alkalinization used sometiems
Which drugs to stop in AKI?
DAMN
D diuretics
A ace/ arbs + aminoglycosides (eg gent)
M metformin
N nsaids except aspirin at low dose 75mg
What are some adverse effects associated with aldosterone antagonists? how can you reduce this risk?
Hyperkalaemia
Gynaecomastia - less common with eplerenone (more selective with less afinity for androgen receptors)
Which medication can be used in ADPKD and when?
Tolvaptan (Vasopression receptor 2 antagonist) - slows progression of cyst development + renal insufficiency to be used if:
> CKD 2 /3 at start of tx
> Evidence of rapidly progressive disease
> + company provides it with discount agreed in patient access scheme
In hyperkalaemia which medications can be used to remove K from the body?
Calcium resonium (oral / enema) -> enema more effective than oral as K is secreted by rectum
Loop diuretics
Dialysis - considered in patients w AKI and persistent hyperkalaemia
What are the indications for renal replacement therapy in AKI?
The following if refractory to medical mx:
1. Hyperkalaemia
2. Met acidosis
3. Sx or complications of uraemia - pericarditis / encephalopathy
4. severe pulmonary oedema
Screening test for ADPKD?
USS Urinary system
clinically is characterized by fever, deranged transaminases, leukopenia and thrombocytopenia
Important to consider in those with renal transplant recipients
Diagnosis? Ix? Mx?
CMV infection
Ix - Viral PCR
Mx - Ganciclovir
Which condition can cause AKI following initiation of ACEi
Younger females?
Older patients?
Younger females - Fibromuscular dysplasia
Older - Atherosclerosis of renal arteries
What are the biopsy findings in Amyloidosis?
Congo red stain shows apple-green birefringence under polarised light
What are the features of acute interstitial nephritis?
What is a common cause?
Sterile pyuria and white cell casts in the setting of rash and fever is suggestive of acute interstitial nephritis - also eosinophilia
Commonly due to abx therapy (penicillins , rifampicin, NSAIDs, allopurinol, furosemide)
What blood results should have you considering rhabdomyolysis?
Lactic acidosis
Hyperkalaemia
+ features of ATN
What are the features of HIV-associated nephropathy (HIVAN)
There are five key features of HIVAN:
> massive proteinuria resulting in nephrotic syndrome
> normal or large kidneys
> focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
> elevated urea and creatinine
> normotension
Alport syndrome - inheritance?
X-linked dominant
Man like alport is dominant in the air, got that x factor
What is Calciphylaxis? when is it seen? what increases risk of this?
Rare complication of ESRF -> deposition of ca in arterioles -> microvascular occlusion + necrosis of tissue hence presenting with painful necrotic skin leisons
Risk is seen with:
Hypercalaemia, hyperphosphataemia + hyperparathyroidism
Warfarin can cause / exacerbate in high risk patients
tx involves reducing levels of this and controlling hyperparathyroidism + avoiding contributing drugs
HLA matching for renal transplants which are the most important HLA antigens?
when HLA matching for a renal transplant the relative importance of the HLA antigens are as follows DR > B > A
DR Berry Aneurysm
Indications for use of spironoloactone?
ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
hypertension: used in some patients as a NICE ‘step 4’ treatment
heart failure - NYHA III + IV already on ACEi (reduces all cause mortality)
nephrotic syndrome
Conn’s syndrome
Most common cause of peritonitis secondary to peritoneal dialysis?
Coagulase -ve staph eg staph epidermis (also staph aureus)
What murmur is associated with mitral valve prolapse?
late systolic murmur accompanied by a mid-systolic click
What are some possible complications of nephrotic syndrome?
> Increased VTE risk due to loss of antithrombin III and plasminogen - DVT, PE or renal vein thrombosis -> sudden decline in renal func.
hyperlipidaemia - increased risk of ACS + Strokes
CKD
Increased risk of infection due to Ig loss
Hypocalcaemia secondary to Vit D and binding protein loss
What electrolyte changes cause nephrogenic DI?
Hypercalcaemia
Hypokalaemia
RFs for urothelial (transitional cell) caricinoma of bladder?
Smoking
Aniline dyes
Rubber manufacturing
Cyclophosphamide
RFs for SCC of bladder?
Smoking
Schistosomiasis
History of chronic sinusitis, haemoptysis + microscopic haematuria + raised IFMs
cANCA +ve
What is the diagnosis? what kidney disease does this cause? renal biopsy shows what?
Granulomatosis with polyangiitis (GPA), formerly known as Wegener’s granulomatosis
Causes rapidly progressive glomerulonephritis - cresenteric glomerulonephritis
How can you distinguish between prerenal uraemia and ATN?
Urinary sodium:
- Prerenal uraemia -> kidneys respond to reduced perfusion by conserving Na hence low urinary Na
- ATN -> kidneys can’t reabsorb Na hence high urinary Na
When does PSGN and IgA nephropathy develop ?
PSGN develops 1-2 weeks after URTI.
IgA nephropathy develops 1-2 days after URTI
What are some causes of membranous glomerulonephritis?
Idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
Glomeruli with epithelial crescents are suggestive of?
Rapidly progressive glomerulonephritis
Rapidly progressive glomerulonephritis with upper respiratory signs is suggestive of which dx? ab?
Granulomatosis with polyangiitis
cANCA ab
Mx of choice for HIV associated nephropathy?
Anti-retroviral therapy
How to distinguish between typical and atypical HUS?
typical caused by Ecoli - shiga toxin
atypical isn’t caused by this usually complement dysregulation - can be normal though
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 (1/2 their weight) for more than 6 hours in adults and more than
How long does it take for AV fistula to develop?
6-8 weeks
How long before effects of Finasteride for BPH can be seen?
6 months
a1 agonists work much faster
fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension
Is suggestive of which type of kidney damage?
Acute interstitial nephritis
What is Fanconi syndrome? What happens in it?
Fanconi syndrome is a reabsorptive defect in PCT
This leads to increased excretion of nearly all amino acids, glucose, bicarbonate and phosphate (T2 Proximal RTA)
In a patient with hypercalciuria and renal stones, calcium excretion and stone formation
can be decreased by the use of what? eg?
Thiazide diuretics eg indapamide
Potassium citrate can also be useful
Prevention of oxalate stones?
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion
Prevention of Urate stones?
allopurinol
urinary alkalinization e.g. oral bicarbonate
Respiratory issues + some / all of: HTN, HyperCa and haematuria is suggestive of what?
Renal cell carcinoma
can metastasise to lungs
What are the different classess of SLE related renal disease?
WHO classification
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis
Class IV - most common and severe version
Young, recurrent UTIs and CKD
What is the likely underlying cause? ix?
Reflux nephropathy
Ix - Micturating cystography, DMSA scan to check for renal scarring
Grading of VUR?
I Reflux into the ureter only, no dilatation
II Reflux into the renal pelvis on micturition, no dilatation
III Mild/moderate dilatation of the ureter, renal pelvis and calyces
IV Dilation of the renal pelvis and calyces with moderate ureteral tortuosity
V Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity
Anion gap in RTA?
Normal
Epididymo-orchitis abx of choice?
IM ceftriaxone stat + oral doxycycline for 2 weeks
Causes of raised anion gap met acidosis?
lactate:
shock
sepsis
hypoxia
ketones:
diabetic ketoacidosis
alcohol
urate: renal failure
acid poisoning: salicylates, methanol
bicalutamide MoA?
non-steroidal anti-androgen
blocks the androgen receptor
Factors that increase the risk of pulmonary haemorrhage in Goodpastures syndrome (Anti-GBM disease)?
smoking
lower respiratory tract infection
pulmonary oedema
inhalation of hydrocarbons
young males
Why do patients with chronic kidney disease have a raised phosphate level?
Decreased renal excretion
What is thin basement membrane disease?
Inherited disorder of type IV collagen
Diagnosis based on persistent haematuria, normal kidney function and fhx of haematuria w/out kidney failure
haemoptysis + AKI/proteinuria/haematuria
What disorder?
Anti-GBM disease
Modification of Diet in Renal Disease (MDRD) equation is a widely used formula to estimate the glomerular filtration rate (eGFR) in patients with chronic kidney disease
What variables does it use?
What factors can affect the results?
CAGE - Creatinine, Age, Gender, Ethnicity
Factors which may affect the result
> pregnancy
> muscle mass (e.g. amputees, body-builders)
> eating red meat 12 hours prior to the sample being taken
ABG abnormality in excess 0.9% NaCL use?
Hyperchloraemic metabolic acidosis
Contrast-induced nephropathy
time frame?
Occurs 2 -5 days after administration
Which tumour marker is raised in testicular seminomas?
hCG
Causes of nephrogenic DI?
Genetic
Electrolytes - hypercalcaemia, hypokalaemia
Lithium
Demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
Disorders associated with glomerulonephritis and low serum complement levels?
post-streptococcal glomerulonephritis
subacute bacterial endocarditis
systemic lupus erythematosus
mesangiocapillary glomerulonephritis
What is the most likely outcome following the diagnosis of minimal change nephropathy in a 10-year-old male?
Full recovery but 2/3 have relapses - 1/3 frquent and 1/3 infrequent
CKD proteinuria ix?
Spot ACR sample
the NICE guidelines state ‘regard a confirmed ACR of 3 mg/mmol or more as clinically important proteinuria’
‘if the initial ACR is between 3 mg/mmol and 70 mg/mmol, this should be confirmed by a subsequent early morning sample. If the initial ACR is 70 mg/mmol or more, a repeat sample need not be tested.’
NICE recommendations for referral to a nephrologist for proteinuria when?
a urinary albumin:creatinine ratio (ACR) of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated
a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection
consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease
Subendothelial and mesangial immune deposits resulting in a ‘tram-track’ appearance
renal biopsy findings - dx?
T1 membranoproliferative glomerulonephritis
focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
Seen in what dx?
HIV nephropathy
Thickened basement membrane with subepithelial electron-dense deposits creating a ‘spike and dome’ appearance
dx?
membranous glomerulonephritis
Common causes of chronic kidney disease?
diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease
Most likely cause of death in CKD with haemodialysis?
most likely cause of death is IHD
Diffuse proliferative glomerulonephritis - presentation?
classical post-streptococcal glomerulonephritis in child
presents as nephritic syndrome / acute kidney injury
most common form of renal disease in SLE
Membranoproliferative glomerulonephritis (mesangiocapillary)
types?
type 1: cryoglobulinaemia, hepatitis C
type 2: partial lipodystrophy
Benign prostatic hyperplasia - ethnicity?
Black > white > asian
GnRH agonists - what should be given alongside when used in mx of prostate ca?
Lead to lower LH levels long term by causing overstimulation -> -ve feedback
initially causes rise in testosterone which can lead to tumour flare
Hence need anti-androgen therapy in meanwhile eg cyproterone acetate
Stages of diabetic nephropathy?
5 stages - this is for T1DM, T2DM is same but can progress to later stages quicker
1 - hyperfiltration (rise in GFR) ?reversible
2 - silent / latent - most dont develop microalbuminuria for 10 y - can see persistent rise in GFR
3 - incipient nephropathy - microalbuminuria - dipstick -ve
4 - overt neprhropathy - persistne proteinuria >300 albumin and dipstick +ve, HTN in most
Histology: diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)
5 - ESRD <10 GFR, RRT needed
Which organ can be dysfunctioning in RCC?
paraneoplastic hepatic dysfunction syndrome
(Stauffer syndrom)e
- a paraneoplastic disorder associated with renal cell cancer
- typically presents as cholestasis/hepatosplenomegaly
- it is thought to be secondary to increased levels of IL-6
What endocrine effects can RCC have?
may secrete erythropoietin (polycythaemia)
parathyroid hormone-related protein (hypercalcaemia), renin
ACTH
Features and associations of retroperitoneal fibrosis?
Lower back/flank pain is the most common presenting feature. Fever and lower limb oedema is also seen in some patients.
Associations
- Riedel’s thyroiditis
- previous radiotherapy
- sarcoidosis
- inflammatory abdominal aortic aneurysm
- drugs: methysergide
SLE kidney disease mx in pregnancy
Azathioprine
However if this doesnt work consider Ciclosporin but associated w premature delivery and LBW
Which BPH med reduces PSA levels?
Finasteride
What can increase PSA?
Prostate ca
benign prostatic hyperplasia (BPH)
prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at least 6 weeks after treatment)
ejaculation (ideally not in the previous 48 hours)
vigorous exercise (ideally not in the previous 48 hours)
urinary retention
instrumentation of the urinary tract
Ix of renal artery stenosis?
MR angiography
How to distinguish between ATN and acute interstitial nephritis?
Urine dip - ATN = proteinuria minimal haematuria
Nephritis = haematuria
Mx of HUS?
Largely supportive - Fluids, blood transfusion and dialysis if required
No ABX
Plasma exchange in rare cases - more often if not associated w diarrhoea + severe HUS
Eculizumab C5 inh MAb - better than plasma exchange in adult atypical HUS
The cyanide-nitroprusside test - when is it +ve
The cyanide-nitroprusside test +ve = Homocystinuria + cystinuria
Differentiation = renal stones in latter
Causes of normal anion gap met acidosis?
GI bicarb loss - prolonged diarrhoea, ureterosigmoidoscopy, fistula
RTA
Drugs eg acetazolamide
Ammonium chloride injections
Addisons
Light microscopy renal biopsy:
Mesangium: normal, with no hypercellularity. The capillary walls are thickened. Subepithelial deposits are seen. (‘spike and dome’ appearance)
Suggestive of ? mx?
Membranous glomerulonephritis
Mx = ACEi / ARB -> improves prognosis and reduces proteinuria
RFs for renal stones?
dehydration
hypercalciuria, hyperparathyroidism, hypercalcaemia
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, polycystic kidney disease
beryllium or cadmium exposure
RFs for urate stones?
gout
ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid
drugs that promote calcium stones?
drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline
Hepcidin in CKD?
CKD -> raised hepcidin due to reduced renall clearance
Hepcidin -> preventing iron absorption by blocking the action of ferroportin, a transmembrane protein that maintains iron homeostasis hence reduced iron absorption
RFs for contrast nephropathy?prevention?
known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs
prevent with 1ml/kg/hr for 12hr pre + post procedure + hold metformin 48h before due to risk of lac acidosis
Requirements for maintainence fluids per 24h?
Sodium - 1mmol/kg
Potassium - 1 mmol/kg
Water - 30ml/Kg
Glucose - 50-100g
Prognosis in IgA nephropathy?
markers of good prognosis: frank haematuria
markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD
25% develop ESRF
Complications of plasma exchange?
hypocalcaemia: due to the presence of citrate used as an anticoagulant for the extracorporeal system
metabolic alkalosis
removal of systemic medications
coagulation factor depletion
immunoglobulin depletion
Histology in IgA nephropathy?
mesangial hypercellularity, positive immunofluorescence for IgA & C3
urpuric rash on the extensor surfaces of his lower legs. He also has a history of abdominal pain and an urticarial rash
Urine dip ++ blood
dx? renal biopsy?
HSP aka IgA vasculitis -> mesangial hypercellularity due to the deposition of IgA immune complexes within the mesangium.
PLEX indications?
Guillain-Barre syndrome
myasthenia gravis
Goodpasture’s syndrome
ANCA positive vasculitis if rapidly progressive renal failure or pulmonary haemorrhage
TTP/HUS
cryoglobulinaemia
hyperviscosity syndrome e.g. secondary to myeloma
When is AA and AL amyloidosis seen?
AL - more common - L = light chain seen with myeloma, MGUS + Waldenstroms
AA - A = acute phase reactant - seen in chronic infection / inflammation
eGFR and CKD stage?
1 Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a 45-59 ml/min, a moderate reduction in kidney function
3b 30-44 ml/min, a moderate reduction in kidney function
4 15-29 ml/min, a severe reduction in kidney function
5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
(patients classically have a loss of subcutaneous tissue from their face),
Condition? renal issue?
Partial lipodystrophy
Renal - Membranoproliferative glomerulonephritis T2
Alcohol bingeing effect on kidneys?
ADH suppression in the posterior pituitary gland subsequently leading to polyuria
+ raised urinary sodium and reduced urinary osmolality
