Renal & Urology Overview Flashcards Preview

• regulation of blood pressure & volume via RAAS
   
• acid-base balance

• electrolyte balance

• production of new RBCs stimulated by Epo

• contains 1-alpha-hydroxylase, which is needed to produce the active form of vitamin D

• acts as a filter for the excretion of water-soluble waste products 

• the prohormone, 25(OH)D is produced in the liver 

• the kidney contains 1-alpha-hydroxylase, which will hydroxylate the prohormone to produce the active hormone

• active vitamin D leads to increased calcium absorption in the gut and the bone 

renal function = flow rate from the glomerulus into the Bowman's capsule

• this is the glomerular filtration rate (GFR)
  • ​it is a measure of the volume of blood being filtered by the glomerulus each minute

• any value of GFR > 90 ml/min is considered normal
  • this means that the glomerulus is filtering 90ml of blood each minute

• GFR typically reduces at a rate of 1 ml/min/year 

• the only way that GFR can be measured is with inulin clearance

• inulin is freely filtered by the glomerulus, not secreted or reabsorbed in the tubules and is not synthesised or metabolised by the kidney

• calculations involve concentrations of inulin in the urine and serum

• urea is a by-product of protein metabolism that is freely filtered at the glomerulus

• it has variable reabsorption (30-60%) depending on nutritional state, hepatic function and GI bleeding 
  • e.g. GI bleed can raise serum urea 

• raised serum urea can indicate poor kidney function

• creatinine is derived from muscle cells, freely filtered at the glomerulus and not reabsorbed

• the Cockcroft-Gault equation is used to estimate creatinine clearance and eGFR
  • this estimates how much creatinine is being cleared from the blood

• creatinine clearance is affected by age, sex, ethnicity and weight
  • ​more creatinine is produced when there is more muscle mass 

• urea is reabsorbed by the tubules, but creatinine is not

• normal urea to creatinine ratio is 40:1 to 100:1

• this ratio is used when looking at different types of kidney injury

• it is used to measure creatinine clearance as a measure of eGFR

• it often overestimates the true GFR, especially when < 30 ml/min

• creatinine clearance (eGFR) is important to measure when giving drugs that are renally cleared

• if the drugs are not being cleared sufficiently, it can lead to renal toxicity 

500ml of 0.9% saline over 15 minutes 

• this looks like a pre-renal AKI

• need to give an IV fluid bolus and maintenance fluids

• hold nephrotoxic medications
  • metformin
  • NSAIDs
  • ACE-inhibitors

DAMN

• D - diuretics

• A - ACEi / ARBs

• M - metformin (can predispose to lactic acidosis)

• N - NSAIDs

• a rapid decline in renal function over hours to days

there is failure to maintain homeostasis of:

• fluid - leading to oliguria or volume overload

• electrolytes - leading to hyperkalaemia

• acid-base balance - leading to metabolic acidosis 

• it is measured by looking at urea and creatinine 

• the easiest way to recognise AKI is that the patient stops peeing

• look at creatinine as this will be acutely raised

• it is potentially reversible

• this is a chronic and irreversible process with 5 stages

• there must be impaired renal function for > 3 months based on:
  • abnormal structure or function
  • or GFR < 60 ml/min for > 3 months
  • +/- evidence of kidney damage 

• this is progressive and irreversible, ending in end-stage renal failure

• it is monitored by looking at eGFR

symptoms depend on underlying cause, but typically:

• oliguria / anuria
  • abrupt anuria suggests a post-renal cause 

• nausea & vomiting

• dehydration

• shortness of breath

• confusion
  • encephalopathy from uraemia (build-up of urea in the brain)

• hypertension

• distended bladder
  • typically seen with an obstructive cause

• postural hypotension due to dehydration

• if they have fluid overload - raised JVP, peripheral / pulmonary oedema
  • ​i.e. in cirrhosis, heart failure, nephrotic syndrome

• if they have vascular disease - bruising, rash, pallor 

KDIGO classification system

• need to check the patient's baseline creatinine to determine whether a rise is significant 

Stage 1:

• 1.5x rise in creatinine compared to baseline 
• OR urine output <0.5 ml/kg/hr for > 6 hours

Stage 2:

• 2x rise in creatinine compared to baseline 
• OR urine output <0.5 ml/kg/hr for > 12 hours 

Stage 3:

• 3x rise in creatinine compared to baseline
• OR urine output < 0.3 ml/kg/hr for > 24 hours
• OR anuria for > 12 hours 

CHARD CH

• C - chronic kidney disease 
• H - hypovolaemia
  • this is the most common cause of AKI
• A - age > 75
• R - renal transplant
• D - diabetes

• C - contrast administration
• H - heart ailure 

there is inadequate perfusion to the kidney

when there is decreased blood flow to the glomerulus, there is decreased blood filtration

• this is most commonly due to hypovolaemia

• systemic vasodilatation (e.g. in sepsis)

• decreased cardiac output

• intrarenal vasoconstriction 

Renal loss:

• loss of fluid from diuretic overuse

• osmotic diuresis (e.g. diabetic ketoacidosis)

Extrarenal loss:

• vomiting and/or diarrhoea

• burns

• sweating

• blood loss 

Systemic vasodilatation:

• sepsis
• neurogenic shock

Decreased cardiac output:

• heart failure
• myocardial infarction

• cardiorenal syndrome

• hepatorenal syndrome

• renal artery stenosis

• reduced urine output
  • if there is no bloodflow to the kidney, urine cannot be produced

• urea is raised much higher than creatinine so urea:creatinine > 100:1​

• this is due to dehydration and urea resabsorption by the kidneys
  • urea is still being reabsorbed as the kidneys themselves are not damaged 

• start with NEWS monitoring and observe for life-threatening complication
  • should be able to identify hyperkalaemia / hypovolaemia 

• need to treat hypovolaemia 

• catheterise the patient to monitor fluid balance

• need to monitor K⁺, lactate (for signs of sepsis) and daily creatinine

Urine dipstick:

• proteinuria and/or haematuria could be a sign of glomerulonephritis 

USS:

• should be performed within 24 hours unless there is an obvious cause 

VBG:

• check electrolytes, glucose & lactate
• check platelets to rule out thrombotic cause like HUS or TTP

• if AKI does not improve, consider investigations for intrinsic renal disease 

• bolus fluid and maintenance fluid

• treat the underlying cause e.g. sepsis

• stop nephrotoxic medications

• stop / change medications that are heavily renally excreted
  • e.g. LMWH
  • if eGFR < 30 then use another form of prophylactic VTE 

• avoid radiological contrast

aminoglycosides

(e.g. amikacin, gentamicin)

these can cause acute tubular necrosis 

• this is caused by cellular / intrinsic damage to the kidney

• the different types depend on where the damage is located
  • tubular
  • glomerular
  • interstitial
  • vascular 

acute tubular necrosis

• ischaemia

• drugs
  • NSAIDs
  • paracetamol
  • ACE inhibitors

• toxins
  • contrast
  • myoglobulinuria in rhabdomyolysis 

• these cause death of the tubular epithelial cells than form the renal tubules of the kidneys