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106 Cards in this Set
- Front
- Back
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What are the features of Goodpasture's syndrome
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IgG deposits in renal biopsy
anti-GBM pulmonary hemorrhage |
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What do you lose in nephrotic syndrome that predisposes you to clotting?
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anti thrombin III
protein C and S rise in fibrinogen |
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How do you decide between HUS and TTP?
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neuro + purpura leans towards a TTP dx
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Pathogenesis of TTP
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* abnormally large and sticky multimers of von Willebrand's factor cause platelets to clump within vessels
* in TTP there is a deficiency of caspase which breakdowns large multimers of von Willebrand's factor * overlaps with haemolytic uraemic syndrome (HUS) |
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Features of TTP
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* rare, typically adult females
* fever * fluctuating neuro signs (microemboli) * microangiopathic haemolytic anaemia * thrombocytopenia * renal failure |
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Treatment of minimal change disease to reduce proteinuria
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prednisolone
ACEi if not responding |
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Dx test in amyloidosis
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rectal biopsy (+ in 80%)
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Difference between IgA nephropathy and post-strep GN
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post strep has low complement levels
main symptom of post-strep is proteinuria typically time interval between URTI and post strep GN |
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How does membranous GN present? Cause?
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* presentation: proteinuria / nephrotic syndrome / chronic kidney disease
* cause: infections, rheumatoid drugs, malignancy * 1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop chronic kidney disease |
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How does diffuse proliferative GN present? Cause
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* classical post-streptococcal glomerulonephritis in child
* presents as nephritic syndrome / acute kidney injury * most common form of renal disease in SLE |
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What causes minimal change disease? How does it present?
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* typically a child with nephrotic syndrome (accounts for 80%)
* causes: Hodgkin's, NSAIDs * good response to steroids |
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Complications of nephrotic syndrome
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increased infection - Ig loss
increased risk of thromboembolism - loss antithrombin III and plasminogen hyperlipidemia hypocalcemia - vit D and binding protein loss in urine ARF |
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What is the most common viral infection in solid organ transplant recipients?
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CMV
occur 1-6 month post transplant |
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Causes of persistent non-visible hematuria
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bladder, renal, prostate cancer
stones BPH prostatitis urethritis eg chlamydia renal: IgA, thin basement membrane disease |
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Causes of transient non-visible hematuria
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UTI
menstruation vigorous exercise sex |
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What is the commonest cause of GN
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membranous
usu presents w proteinuria or nephrotic syndrome |
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What is Goodpasture's syndrome?
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pulmonary hemorrhage
rapidly progressive GN |
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How do you calculate the anion gap?
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Na + K - Cl - HCO3
Usually = 15 +/- 4 |
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What can cause an increased anion gap?
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lactic acidosis
ketoacidosis DM Starvation Methanol Aspirin Ethylene glycol |
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Does RTA give you an increased anion gap?
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NO
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What is Bartter's syndrome?
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Usually autosomal recessive - defect in thick ascending limb (Na-K-2Cl)
Mild volume depletion, RAS activated, Increased distal tubular flow leads to increased K and H secretion Low K Metabolic alkalosis Hypercalciuria High renin and aldosterone Juxta Glomerular Apparatus hypertrophy Normal BP +/- low Mg Mental retardation, short stature Young presentation |
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Symptoms of acute hyponatraemia?
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Relate to cerebral oedema (when plasma osmlolaity falls rapidly water flows into cerebral cells which become swollen and ischaemic)
Headache, N, malaise, lethargy, weakness, mm cramps, anorexia, somnolence disorientation, personality changes, depressed reflexes, decreased LOC NB: if occurs over time cerebral cells have time to respond by reducing intracellular osmolality to reduce gradient |
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How do you treat hyponatraemia?
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Treat the cause
Rate of correction shoudl be proportional to the rate of development If they have cerebral oedema they developed hyponatraemia rapidly so correct quickly If they have cerebral euilibrium the brain has adapted so correct slowly |
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What signs does hypernatraemia present with
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brain cell shrinkage
altered mental status, weakness, neuromuscular irritability, focal neurological deficits, seizures, coma, death +/- poluyruia, thirst, signs of hypovolaemia |
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What are the complications with hypernatraemia?
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increased risk of vascular rupture resulting in intracranial haemorrhage
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What are the risks of rapid resusctiation with hyponatraemia?
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Osmotoc demyelination
sx flaccid paralysis, dysarthria, dysphagia Rapid correction - sudden osmotic shrinkage of brain cells - demyelination |
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What is the risk of rapid resuscitation with hypernatraemia?
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cerebral oedema
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What signs might you see in a hypertensive crisis?
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focal signs
severe headache confusion seizures nausea vomiting papilloedema retinal haemorrhage |
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What is the goal reduction in BP in hypertensive emergencies?
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Reduce BP by no more than 25% within the first 2 hours, then toward 160/100 within 2-6 hours
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What can lowering BP too quickly result in?
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renal, coronary, cerebral ischaemia
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What pharmacological management should be used to lower BP in an ICU setting?
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Sodium nitroprusside
Diazoxide Hydralazine Clonidine Glyceryl trinitrate |
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What pharmacological management is appropriate in less urgent settings to lower BP?
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amlodipine or nifedpiein or methyldopa or prazosin or captopril
If MI also present give BB + CCB (dihydropyridine) |
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Does acidosis or alkalosis cause hyperkalaemia or hypokalaemia?
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Acidosis causes hypernatraemia
Alkalosis causes hypokalaemia |
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How may a person with hyperkalaemia present?
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Usually asymptomatic but may develop
N, paliptations mm weakness, mm stiffness, paraesthesias, areflexia, ascending paralysis and hypoventilation |
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What are the ECG changes associated with hyperkalaemia?
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Peaked T waves
Short QT prolonged PR interval VF, asystole |
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How do you manage hyperkalaemia?
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Calcium gluconate - no effect on serum K just antagonises cardiac toxicity of hyperkalaemia -
Sodium bicaronate if metabolic acidosis as well Correct volume depletion to optimise renal function Insulin - if severe CKD when a sodium load is CI Beta agonists - if CKD - potential to precipitate cardiac arrthmias Loop diuretics Sodium polystyrene sulfonate - binds to potassium secreted into the colon - slow lowering of potassium over 1-6 hours Dialysis - only when hyperkalaemia is extreme as in extensive tissue breakdown due to rhabdomyloysis or none of above approaches effective |
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What is a big cause of hyperkalaemia that you don't want to miss?
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Adrenal insufficiency
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what features of hypokalaemia do you see on ECG?
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U waves most important
Flattened or inverted T waves Prolonged QT |
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What life threatening conditions are associated with hypokalaemia?
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mm necrosis
diaphragmatic weakness cardiac arrhythmias |
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At what K level should you start supplemental K?
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if < 3 mmol/L
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Which form of IV potassium is the most commonly used?
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Potassium Chloride
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What urine output suggests inadequate renal perfusion?
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< 0.5ml/kg/hr OR < 30 ml/hr
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What is rapidly progressive glomerulonephritis?
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Subset of neprhitic syndrome in which renal failure progresses in weeks to months
There are 3 types all caused by other types of glomerulonephritis |
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What is usually seen on biopsy in patients with rapidly progressive glomerulonephritis?
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crescent formation
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How do you manage rapidly progressive glomerulonephritis?
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Start empirial therapy straight away to minimise extent of irreversible injury
Give IV pulse methylpred + oral or IV cyclophosphamide + consider plasmaphresis |
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How do patients with rapidly progressive glomerulonephritis present?
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Usually insidious onset with fatigue or oedema
BUT can present with acute onset of macroscopic haematuria, decreased urine output, and oedema |
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Indications for dialysis in acute kidney injury?
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Hyperkalaemia (refractory)
Pulmonary oedema/volume overalod Metabolic acidosis Uraemia (> 35-50) Pericarditis Encephalopathy |
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Causes of increased anion gap
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lactic acidosis (DKA, starvation, alcohol)
ingestions (methanol, ethylene, aspirin) chronic kidney disease |
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Causes of normal anion gap
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diarrhea
RTA carbonic anhydrase inhibitors some chronic kidney disease |
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What are causes of acute renal graft failure
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* usually due to mismatched HLA
* other causes include cytomegalovirus infection * management: give steroids, if resistant use monoclonal antibodies |
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What are causes of chronic renal graft faiilure
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* chronic allograft nephropathy
* ureteric obstruction * recurrence of original renal disease (MCGN > IgA > FSGS) |
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What electrolyte disturbance is LMWH associated with if patient has renal impairment?
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hyperkalaemia
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Which drugs commonly cause acute kidney injury?
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NSAIDs
ACEI or ARB Gentamicin (aminoglycoside) Sulphonamides Penicillin Digoxin Contrast Lithium Cephalosporins Gold Cyclosporin |
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How do you tell the difference based on tests between pre renal and renal failure?
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Urine osmolality is high in prerenal failure and plasma like in renal failure
Sodium in the urine is decreased in pre-renal failure and increased in renal failure FE Na < 1% in pre renal and > 1% in renal |
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What does the urine/plasma creatinine ratio measure?
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It can be used to estimate tubular water reabsorption
Creatinine concentration in the filtrate = that in the plasma and then rises progressively as water is reabsorbed Patients with prerenal disease have a U/P creat ratio > 40 because a higher percent of filtered water has been reabsorbed Water reabsorption is less efficient in renal ATN failure so U/P creat is < 20 |
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What GFR in CKD do you get biochemical derangements?
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Stage 3a GFR < 45-59 - you start to see serum biochemical derangements
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ACE I can cause an increase in serum creatinine when initiated in patients with CKD. What % increase is ok?
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30%
and should stabilise within 2 months If rises above 30% consider bilateral renal artery stenosis |
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What is first line management for proteinuria?
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ACE I or ARB
Reduction in sal output through reducing salt intake |
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What are the 3 drugs that you do not want to give together in CKD?
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ACE I (or ARB)
NSAID (low dose aspirin seems to be ok) Diuretic |
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What is the target BP for patients with CKD?
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130/80
OR 125/75 if > 1g proteinuria Urine protein: creatinine ratio of 100mg/mmol |
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How can you manage acidosis in patients with stage 4-5 CKD?
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Supplementation with sodium bicarbonate
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Which compound are phosphate binders composed of?
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Calcium carbonate
Binds phosphate in the gut |
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What is cinacalcet?
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Used to suppress PTH secretion in CKD
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When does IV contrast induced nepropahty occur? (time period)
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12-24 hours after contrast study
Majority are nonoliguric and then recover renal function over 3-5 days |
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What are people with CKD most likely to die from?
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IHD
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What is the screening test for adult polycystic kidney disease?
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Abdominal US
2 cysts (unilateral or bilateral ( < 30 2 cysts in both kidneys 30-59 4 cysts in both kidneys > 60 |
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Which gene mutations are involved in polycystic kidney disease?
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(PKD) Polycystein 1 (chromsome 16)
polystein 2 (chromosome 4) |
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Is polycystic kidney disease autosomal dominant or recessive?
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dominant
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What are the extrarenal manifrestations of polycystic kidney disease?
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Polycystic liver disease (usually asymptomatic)
Mitral valve prolapse Berry aneurysms Diverticulosis Cysts less commonly found in pancreas, spleen, thyroid, ovary, seminal vesicles, aorta |
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Why do patients with polycystic kidney disease get HTN?
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due to focal compression of intrarenal arteries by cysts
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Is Hb high or low in polycystic kidney disease
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High due to increased secretion of EPO from functioning renal cysts
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How do you manage acute abdominal flank pain/dull lumbar back pain caused by polycystic kidney disease?
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narcotics for acute episodes
Can surgically aspirate large cysts |
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Should patients with polycystic kidney disease be screening for aneurysms?
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Only if family history of aneurysm or SAH, previous aneurysm rupture, pre-op for elective surgery, high risk occupations (pilots)
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Which gene involved in polycystic kidney disease is more aggressive?
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PKD 1
Most PKD1 patients will experience renal failure by age 70 50% of PKD2 patients will experience renal failure by 70 |
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What are the side effects of EPO?
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Accelerated hypertension - encephalopathy and seizures
bone ahces flu like symptoms Iron deficincy secondary to increased erythoporiesis |
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Can you diagnose CKD based on eGFR alone?
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NO
In stage 1 and 2 there must be accompanying signs of CKD in addition to the lower GFR If low GFR but all tests are normal then no CKD |
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Which drugs are most associated with proteinuria?
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gold
penicillin |
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Is autoimmune disease a CI for being a live organ donor?
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yes
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What medications are used to treat restless legs?
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First line - levodopa + carbidopa or benserazide
More severe sx manage with dopamine agonists or oxycodone 3rd line drugs - benzos or antiepileptics (gabapentin or clonazepam) |
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Is your life expectancy near normal after a renal transplant?
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yes!
It's the only way to increase survival in ESKD patients Highest rate of mortailty is in the first 12 months |
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What kind of complications can you get with immunsuppressant therapy?
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Skin cancers
kaposi sarcoma post transplant lymphoproliferative disorder |
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At what stage do CMV infectiosn usually occur post renal transplant
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1-6 months
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What is type 1 RTA?
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Inability to excrete H+
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What is type 2 RTA?
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Inability to absorb HCO3
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What is type 4 RTA
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defective ammoniagenesis due to decreased aldosterone or hyporesponsiveness or hyperkalaemia
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Features of nephritic syndrome?
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Proteinuria (not as bad as nephrotic)
haematuria Azotemia RBC casts oliguria hypertension |
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Features of nephrotic syndrome?
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Severe proteinuria
oedema hypoalbuminaemia hyperipidaemia hypercoagulable state oval fat bodies (microscopy) |
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Which virus is cryoglobulinaemia associated with?
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hep C
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How does cryogolgbulinaemnia present?
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fever
purpura Raynaud's arthralgias |
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What antibody is present in Wegner's granulomatosis?
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c-ANCA
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What are the antibodies against in Goodpasture's disease?
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Type 4 collagen present in lungs and GBM
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What do high levels of urobilinogen in the urine suggest?
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haemolytic anaemia
hepatitis cirrhosis if negative in patient with bilirubin or liver dysfunction indicates presence of hepatic or biliary obstructrion |
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Which renal disease are fatty casts seen in?
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nephrotic syndrome
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What is the use of the urine protein/creatiine ratio?
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Measures protein loss in comparison to creatinine which is normally excreted into the urine at a constant rate
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What variables does the MDRD take into account when measuring renal function?
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Creatine
Age Gender Race |
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Most common sites of renal calculi
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Ureteric vesico junction
under vas deferns/broad ligament Ureteric Pelvic Junction - staghorn pelvic brim |
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When do you treat renal stones conservatively?
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<5 mm
conserv mx = fluids >2L/day |
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Medical treatment for calcium kidney stones
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cellulose phosphate
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Indications for stent in renal calculi that is found in renal pelvis
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if stone 1.5-2.5 cm, stent
ESWL (electric shock wave lithotripsy) if stone <2.5 cm >2.5 cm, percutaneous nephrolotomy |
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Management of renal calculi in ureters
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ESWL (electric shock wave lithotripsy) if >5 mm
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Prevention of renal calculi
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increase fluids >2 L/day
increase K+ intake reduce animal protein, oxalate, sodium, sucrose, fructose avoid vitamin C Meds: thiazides (hypercalcemia), allopurinol (hyperuricosuria), potassium citrate (hypocitraturia) |
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Which types of renal calculi are radioLUCENT (not seen on KUB xray)?
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uric acid
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T/F All types of kidney stones are seen on CT
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True
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painless gross hematuria is ____ until proven otherwise
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bladder cancer
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Gold standard dx test for bladder cancer
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cystoscopy with bladder washings
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Indications for acute hemodialysis
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refractory hyperkalemia
acidosis uremia fluid overload pericarditis encephalopathy pulmonary edema |
