Renal Medicine Flashcards
(107 cards)
5 functions of the kidney
Acid-base control (pumps out H+, reabsorbs bicarb)
Regulates blood/fluid volume
Waste, toxin and drug excretion
Produces erythropoietin (stimulating red cell production)
Vitamin D metabolism (Vit D to 1-Hydroxyvit D)
How do we measure kidney function?
Creatinine:
Albumin:creatinine ration (mg/mmol)
CKD staging
1: >90 (+evidence kidney damage)
2: 60-89 (+evidence kidney damage)
3a: 45-59
3b: 30-44
4: 15-29
5: <15
Takes into account albuminuria (<3, 3-30, >30)
How does renal failure lead to anaemia?
Reduced erythropoietin production
Reduced hepcidin clearance (waste product from liver which impairs iron absorption by duodenum)
Therefore give iron supplements (IV as duodenum absorption reduced)
Nephrotic syndrome proteinuria threshold
> 3g protein excreted per 24 hours
CKD timescale
> 3 months
Which patients should be started on ARB/ACE-i?
What should their BP target be?
Diabetic and ACR >3mg/mmol
Hypertensive and ACR >30mg/mmol
ACR >70mg/mmol
Target of 130/80
Management of acute hyperkalaemia?
Calcium gluconate 10ml 10% (protects myocardium)
Followed by salbutamol, insulin and dextrose to drive potassium into cells
Role of vitamin D
Increases calcium absorption
Increases renal tubular reabsorption
Increases osteoclast activity (releasing calcium from bone)
Stages of vitamin D activation
Cholecalciferol to calcidiol by liver
Calcidiol to calcitriol by kidneys
What acid-base changes might occur in CKD?
H+ ion retention leading to acidosis - treated with sodium bicarbonate
Possible complications of CKD
Anaemia
Fluid overload
Mineral and bone disorders
Hyperkalaemia
What type of anaemia would you see in CKD and how would you manage?
Normochromic normocytic
Erythropietin-stimulating agents e.g. epoetin alfa
Indications for dialysis in AKI
Refracatory hyperkalaemia
Refractory pulmonary oedema
Severe metabolic acidosis (<7.1)
Severe uraemia (>60mmol/L or CXR)
Complications of AKI
Hyperkalaemia
Fluid overload
Metabolic acidosis
Uraemic complications (pericarditis and encephalopathy)
Rhabdomyolysis signs and symptoms
Muscle pain
Dark brown urine (myoglobinuria)
Raised CK levels
Nephrotoxic drugs
ACE-i/ARBs NSAIDs penicillin Diuretics Furosemide Rifampicin Cephalasporins
Clinical definition of oliguria?
<0.5mls/kg/hr (35mls/hr in a 70kg patient)
If this persists >6hrs then is defined as AKI
How do NSAIDs adversely affect renal function?
Inhibition of COX1/2 leading to inhibition of prostaglandin synthesis. This causes constriction of afferent arterioles and reduced renal perfusion
Promotes natriuresis (sodium excretion in urine)
How is Stage 1 AKI diagnosed?
Serum creatinine (increase by >26umol/L in 48 hours or >1.5-1.9 in 7 days)
Urine output (<0.5mls/kg/hr over 6 hours)
Pre-renal causes of AKI and what can they lead to?
Cardiac output (cardiac failure)
Arteriolar changes (nephrotoxic drugs e.g. ACE-i or NSAIDs)
Systemic vasodilation (septic shock)
Reduced circulating volume (hypovolaemia)
This can lead to intrinsic damage due to prolonged ischaemia of renal parenchyma and development of acute tubular necrosis (ATN)
Intrinsic causes of AKI
Vascular:
Large vessel: atherosclerotic disease, thromboembolic disease, dissection, renal artery stenosis/thrombosis
Small vessel: vasculitides, malignant HTN, microangiopathic haemolytic anaemia (e.g. DIC), thromboembolic disease
Glomerular: primary or secondary. Can cause nephritic/nephrotic syndrome
Tubulointerstitial: acute tubular necrosis (ATN); acute interstitial nephritis (secondary to medication)
Post-renal causes of AKI
Obstructive uropathy (urolithiasis, malignancies, strictures and bladder neck obstruction)
Clinical features of pre-renal AKI
Evidence of dehydration/hypovolaemia:
Dry mucus membranes, reduced CRT, reduced urine output, low BP, reduced skin turgor, dizziness and thirst
Hypervolaemia (due to cardiac failure):
Pulmonary/peripheral oedema, orthopnoea, paroxysmal nocturnal dyspnoea, dyspnoea, raised JVP, ascites