renal Flashcards
most common infection in solid organ trasnplant
cytomegalovirus tx ganciclovir
ATN fx
Acute tubular necrosis Urine sodium > 40 mmol/L Urine osmolality < 350 mOsm/kg Fractional sodium excretion* > 1% Response to fluid challenge Poor Serum urea:creatinine ratioNormal Fractional urea excretion** >35% Urine:plasma osmolality < 1.1 Urine:plasma urea < 8:1 Specific gravity < 1010 Urine Brown granular casts
cause of peritonitis in peritoneal dialysis
staphylococcus epidermidis
causes of polyuria
Common (>1 in 10) diuretics, caffeine & alcohol diabetes mellitus lithium heart failure
Infrequent (1 in 100)
hypercalcaemia
hyperthyroidism
Rare (1 in 1000)
chronic renal failure
primary polydipsia
hypokalaemia
Very rare (<1 in 10 000) diabetes insipidus
mechanism of thiazide for nephrogenic DI
In simple terms DI leads to the production of vast amounts of dilute urine which is dehydrating and raises the plasma osmolarity, stimulating thirst. The effect of the thiazide causes more sodium to be released into the urine. This lowers the serum osmolarity which helps to break the polyuria-polydipsia cycle.
alports syndrome
Alport’s syndrome usually presents in childhood. The following features may be seen:
microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biospsy: splitting of lamina densa seen on electron microscopy
complication of mephrotic syndrome
higher risk of VTE
acute interstitial nephritis
caused by drugs
presence of white cells in urine as they infiltrate- differentiates from ATN
s/e of epo
accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients)
bone aches
flu-like symptoms
skin rashes, urticaria
pure red cell aplasia* (due to antibodies against erythropoietin)
raised PCV increases risk of thrombosis (e.g. Fistula)
iron deficiency 2nd to increased erythropoiesis
maximum K+ infusion rate
The maximum recommended rate of potassium infusion via a peripheral line is 10 mmol/hour, whereas rates above 20 mmol/hour require cardiac monitoring
urea creatinine ratio raised in
pre renal causes of AKI
proteinuria and hepatomegaly
amyloidosis
post strep vs iga nephropathy
iga delayed 1-2days, post strep 1-2weeks
iga macroscopic haematuria young males
PSGN Proteinuria low complement
both: recent urti, haematuria
screening for polycystic kidneys
The screening investigation for relatives is abdominal ultrasound:
Ultrasound diagnostic criteria (in patients with positive family history)
two cysts, unilateral or bilateral, if aged < 30 years
two cysts in both kidneys if aged 30-59 years
four cysts in both kidneys if aged > 60 years
ADPKD fx
Features hypertension recurrent UTIs abdominal pain renal stones haematuria chronic kidney disease
Extra-renal manifestations
liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly
berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
drugs causing interstitial nephritis
drugs: the most common cause, particularly antibiotics penicillin rifampicin NSAIDs allopurinol furosemide
Membranous glomerulonephritis histology
basement membrane thickening on light microscopy
subepithelial spikes on sliver stain
positive immunohistochemistry for PLA2
causes of haematuria
Causes of transient or spurious non-visible haematuria
urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse
Causes of persistent non-visible haematuria
cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease
matabolic acidosis with normal anion gap
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease (with hyperkalaemia due to low aldo)
kidney size in diabetic nephropathy
Chronic diabetic nephropathy will have large/normal sized kidneys on ultrasound whereas most patients with chronic kidney disease have bilateral small kidneys
fibromuscular dysplasia fx
Renal artery stenosis secondary to atherosclerosis accounts for around 90% of renal vascular disease, with fibromuscular dysplasia being the most common cause of the remaining 10%.
Epidemiology
90% of patients are female
Features
hypertension
chronic kidney disease or more acute renal failure e.g. secondary to ACE-inhibitor initiation
‘flash’ pulmonary oedema
calcium acetate
calcium-based binder used to treat hyperphosphataemia. This patient is suffering from symptoms of hypercalcaemia as a result of a side effect of using a calcium-based binder. Patients with chronic kidney disease (CKD) may suffer from hyperphosphataemia since the kidneys are unable to excrete excess phosphate. Calcium-based binders are used to reduce phosphate levels in patients with CKD. Symptoms of hypercalcaemia include ‘bones, stones, groans and psychic moans’.
Hereditary haemochromatosis causes
cranial diabetes insipidus
acute vs chronic graft rejection
Acute rejection occurs within 6 months and typically presents with signs and symptoms of infection. The diagnosis can only be confirmed with biopsy of the transplanted kidney. The best initial management is to increase the steroid dose. Chronic rejection presents insidiously with deteriorating renal function. This can occur after 6 months from transplant.
HSP fx
palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure
staging of AKI
Stage Creatinine Urine production
1 Increase 1.5-1.9x baseline < 0.5ml/kg/h for >6 consecutive hours
2 Increase 2.0-2.9x baseline < 0.5ml/kg/h for >12 consecutive hours
3 Increase > 3x baseline or >354 µmol/L < 0.3ml/kg/h for > 24h or anuric for 12h
contraindication for peritoneal dialysis
crohns
causes of crescentic glomerulonephritis
Causes
Goodpasture’s syndrome
Wegener’s granulomatosis
others: SLE, microscopic polyarteritis
Features
nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria
features specific to underlying cause (e.g. haemoptysis with Goodpasture’s, vasculitic rash or sinusitis with Wegener’s)
bisphosphonates used in ckd why
to prevent draggin of Ca from bones in hyperphsophataemia
rxfor ascites
spironolactone
causes of DI
Causes of cranial DI idiopathic post head injury pituitary surgery craniopharyngiomas histiocytosis X DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome) haemochromatosis
Causes of nephrogenic DI
genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes: hypercalcaemia, hypokalaemia
drugs: demeclocycline, lithium
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
left varicolcele associated ith
renal cell carcinoma
path proteins lost in nephrotic syndrome
Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis. Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels.
how to differentiate Primary and secondary aldosteronism
looking at the renin levels. If renin is high then a secondary cause is more likely, i.e renal artery stenosis.
hyaline casts
loop diuretics
stop ACEi in ckd pt when…
AKI
GFR less than 30
