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77 Cards in this Set

  • Front
  • Back
types of renal stones
ca-oxalate (60% most common): radio opaque
cystine: cystinuria
urate: not radioopaque
mg-ammonium: associated with infections (klebsiella, proteus, ..)
haematuria - DDx
renal tract (stones, tumors, infection, cyclophosphamide induced haemorraghic cystitis)
glomerulonephritis
rhabdomyolysis
malaria (blackwater fever)
suspected acute rejection of renal graft
check ciclosporin levels - if normal need biopsy
water deprivation test urinary osmolality
(result in DI, other cause)
if not >750 then DI
desmopressin test urinary osmolality
(result in central DI, nephrogenic DI)
central DI: >50% increase after 2micromol desmopressin
central pontine myolinolysis - how fast can you correct Na?
1mmol/hour
ACE-I and renal function - what's the catch?
- non-progressive rise in creatinine 20-30% can be accepted
- guideline: check creatinine 1 week and 1 month
- if deteriorates rapidly consider renal artery stenosis
diabetic nephropathy and pregnancy - change of deterioration?
dending on creatinine there is a chance of worsening.
see study Katz et alhi
General points in measuring acute severe renal failure
(uraemic emergency, creatinine very high)
1. sort out potassium if high
ECG -> if cardiotoxicity then Ca gluconade
insulin+dextrose, neb salbutamol
2. sort out fluid status:
urinary cathether
CVP line
start IV saline at 100ml per hour and titrate
3. further management:
urgent USS
liaise for renal replacement therapy
tubulointerstitial nephritis
causes
70-90% drugs (penicillin, NSAIDs, etc)
15% infections (hantavirus - haemorrghic fever, pyelonephritis)
8% idiopathic
TINU (with uveitis)
systemic inflammatory disorders
tubulointestitial nephritis clinical features
drug reaction 5 days - 5 months
fever, arthralgia, skin rashes, acute renal failure
eosinophilia/eosinophiluria
chronic TIN causes
analgetic abuse, DM, SSD
sloughed papillae can cause urinary obstruction.
tubulointestitial nephritis def
inflammation affecting the interstitium around the tubules either acute or chronic
consequences of TIN depending on location
prox tubulus affected -> T2 renal tubulus acidosis
dist tubulus affected -> loss of concentrating function and salt wasting.
general: loss of excretory function
TIN management & prognosis
stop offending drug
steroid treatment not successful
dialysis if severe renal function
usually recovery but may have rresidual chronic impairment (degree of fibrosis)
analgetic nephropathy and flank pain and deterioration of renal function
sloughed papillae
renal artery stenosis causes
fibromuscular disease 20-40%
artherosclerosis
artherosclerotic renal artery stenosis clinical features
>60 years
30% in patient with other vascular manifestations
patient with HTN, renal failure
patient with flash pulm. oedema without cardiac disease
clinical signs: abdominal bruit (or other vascular bruit incurring the possibility)
renal artery stenosis diagnosis
ultrasound: difference in size >1.5cm, intrarenal vascular resistance to predict success of intervention
MRA/CTA
renal artery stenosis indications for revascularisation
stenosis >75%
single functioning kidney
recurrent flash pulmonary oedema
intracable hypertension
progressive renal failure
patient requiring ACE-I for CCF
analgetic nephropathy and flank pain and deterioration of renal function
sloughed papillae
renal artery stenosis causes
fibromuscular disease 20-40%
artherosclerosis
artherosclerotic renal artery stenosis clinical features
>60 years
30% in patient with other vascular manifestations
patient with HTN, renal failure
patient with flash pulm. oedema without cardiac disease
clinical signs: abdominal bruit (or other vascular bruit incurring the possibility)
renal artery stenosis diagnosis
ultrasound: difference in size >1.5cm, intrarenal vascular resistance to predict success of intervention
MRA/CTA
renal artery stenosis indications for revascularisation
stenosis >75%
single functioning kidney
recurrent flash pulmonary oedema
intracable hypertension
progressive renal failure
patient requiring ACE-I for CCF
when to investigate further in renal stones?
young patient
recurrent stones
further investigations in renal stones
serum Ca (hypercalcaemia -> investigate further if high)
uric acid (urate stones)
HCO3-/urine pH (RTA)
chemical analysis (cystine, urate stones)
urine screening for cystinuria
urinary calcium, oxalate and uric acid output
urine culture
renal imaging
prohpylaxis of renal stones
adequate fluid intake (2-3L)
especially in cystine stones (5L)
limit oxalate containing food (if oxalate stones)
limit animal protein and salt (Ca stones)
thiazide (ca stones)
allopurinol (urate stones)
penicillamine (cystine stones)
ADPKD complications
cyst infection
renal calculi
HTN
progressive renal failure
hepatic cysts 30%
intracranial aneurysm 10%
mitral valve prolapse 20%
ADPKD genetic basis
PKD 1 on chromosome 16 85%
PKD 2 on chromosome 4 rest
ADPK presenting features
acute loin pain, haematuria (bleeding, infection, stone in cyst)
general abdo discomfort and loin pain (cyst growing)
complications of SAH
complication of HTN
complications of liver cysts
chronic renal failure
medullary sponge disease clinical features
intermittent renal colic with passage of small stones, haematuria
renal function is well maintained
(unless obstructive uropathy ensues)
medullary sponge disease diagnosis
diagnostic: excretion urography
RCC def
malignant tumor arising from proximal tubular epithelium
RCC clinical features
M>F 55yr (rarely before 40)
haematuria, loin pain, mass in flank
rarely L sided varicocele with L sided tumour (invaded renal vein)
5% polycythaemia
30% HTN/anaemia
25% present with mets
RCC diagnosis
USS/IVU may miss if <3cm
measure patency of renal vein and IVC
MRI/CT for tumour staging
urine cytology no value
RCC treatment
nephrectomy (even if metastatic)
partial nephrectomy if solitary kidney
IL2, beta-INF 20% remission
urothelial malignancy risk factors
cigarrette smoking
carcinogens (chemical, rubber industry)
chinese herbs (aristocholic acid)
drugs (phenacetin, cyclophosphamide)
schistosomiasis
TCC clinical features
M>F >40yr
painless haematuria
TCC investigations
urine cytology
cystoscopy (for lower urinary tract)
USS/CT for upper urinary tract
TCC treatment
(bladder)
superficial: transurethral resection, bladder instillarion for recurrences. 5-yr survival: 80-90%
invasive: <70yr radical cystectomy, >70 radical radiotherapy - 5% survival rate in metastatic disease.
benign prostate hyperplasia clinical features
M >60
nocturia (first), frequency, hesitancy, reduced stream, post-void dribbling
haematuria
urinary retention/renal failure
BPH management
(mild sx, moderate sx, urinary obstruction)
mild sx: watchful waiting
medium sx: medical Rx - tamsulosin, finasteride
worsening renal failure: surgery
urinary retention: either prostatectomy or perm. cath
Prostate Ca clinical features
urinary tract obstruction
metastatic disease (bone)
high PSA >16 in screening
irregular hard gland on rectal exam
Prostate Ca investigations
transrectal USS+biopsy
gleasson scoring based on histology
USS (hydronephrosis)
bone scan (metastasis)
Prostate Ca treatment
confined to gland: radical prostatectomy
locally extensive: radio + androgen ablation
metastases: orchidectomy/LHRH analogues
what is the "normal" renal function in patients in their 80s?
GFR 50-60
cave: reduced muscle mass, hence creatinine falsly low. Use eGFR!
urinary incontinence
urge incontinence (UTI, stone, stroke, dementia, PD)
stress incontinence (cough, sneeze)
overflow incontinence
funtional incontinence
incontinence management
examine for local problems
urinalysis (glucose, culture for infection)
Rx contributing factors: constipation, drug
urge incontinence
bladder training, antimuscarinics (oxybutinine, tolterodine)
stress incontinence
pelvic floor exercises
overflow incontinence
treat obstruction
functional
improve facilities, regular voiding, absorbent padding
causes of normal anion gap metabolic acidosis
loss of bicarb in GI tract: diarrhoe
loss of bicarb renal: RTA Type 2, azetazolamide, ATN, hyperparathyroidism
inability to excrete H+ renally: RTA Type 1 and 4
normal anion gap
10-18
causes of Type 2 RTA
Fanconis (glycosuria, aminoaciduria, phosphaturia, high urate excretion)
Wilson's
hereditary fructose intolerance
osmolar gap
osmolality = 2(Na+K)+glucose+urea
normal gap is <10
what to do before epo therapy
ensure iron storages are high
(ferritin >100)
blood pressure is controlled
analgetic nephropathy
= chronic TIN
60% have hypertension
sloughed papillae can cause acute obstruction
recurrent UTIs
salt losing nephropathy
analgetic nephropathy findings
IVU: clubbed calyces, ring signs, filling defects in urether
microscopy: papillary cells
management of malignant hypertension
if signs of hypertensive encephalopathy or aortic dissection:
rapid BP reduction with IV nitroprusside/labetolol
otherwise, oral antihypertensive
aim for diastolic 100-120mmHg
management strategies for RCC
nephrectomy even if mets
(exception - solitary kidney or bilateral tumor)
IL2 or small molecule kinese inhibitors for mets
radio or chemo no role!
causes of RTA type 1
auto immune (e.g. SLE)
drugs (e.g. amphotericin)
inherited
idiopathic
management of RTA 1
correct hypoK before acidosis!!!
bicarbonate 1-3mmol/kg per day to correct acidosis.
Familial mediterranean fever
clinical features
autosomal recessive
Jews, Arab, Turk, Greece
<18 years with first presentation
fever and serositis that occurs in attacks (relapsing/remitting course):
95% abdominal attack: peritonitis (with all signs)
75% joint attack: arthritis, large joint
40% chest attack: pleuritis/pericarditis
rare: scrotal attack, myalgia
25% fever alone
FMF complications
AA amyloidosis leading to renal failure
FMF diagnosis
mainstay: clinical
CRP raised
genetic test available
FMF management
monitor renal function
treat symptomatically with NSAIDS
colchicin 1-2mg can reduce attack frequency and amyloidosis.
Renal tubular acidosis type II associations
Fanconi's, Wilson's, fructose intolerance, Lowe's, heavy metal poisoning.
IgA nephritis diagnosis
renal biopsy
NOT IgA levels!
Liddle's syndrome
clinical features
autosomal dominant
presenting mostly with hypertension in childhood
ENaC defect: uncontrolled Na reabsorption, hence K loss and metabolic alkalosis
aldosterone low (response)
Liddle's treatment
low sodium diet
amiloride
Renal tubular acidosis Type IV
hyperkalaemic RTA
low aldosterone/failure to respond
RTA Type IV associations
spironolactone, ACEI, ARB, trimethoprim, heparin, pentamin, NSAIDs
SLT, amyloidosis
How to manage early hyperparathyroidism in chronic renal disease? (Ca low-normal)
if PTH > twice normal try alfacalcidiol
if not successful consider surgery.
cinacalcet for patients who are not fit for surgery only (NICE)
How to manage anaemia in chronic renal disease?
load iron storages
ferritin >100
start epo
aim for Hb 10.5 - 12.5
How to manage late hyperparathyroidism in chronic renal disease? (PTH high, Ca high)
cinacalcet and low phosphate diet plus sevelamer