Renal Medicine Flashcards

1
Q

What are the 3 major categories of AKI?

A

Pre-Renal:
- Lower vascular volume due to haemorrhage, D and V…
- Decreased CO ( HF, MI,…)
- Systemic vasodilation due to sepsis/drugs.
- Renal vasoconstriction due to NSAID’s, ACEi/ARBs or hepatorenal syndrome.

Renal:
- Acute tubular necrosis
- Glomerulonephritis
- Infection

Post-Renal:
- Obstruction by malignancy, stones, strictures…
- Extrinsic compression of the tubes from malignancy, prostatic hypertrophy…

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2
Q

Recognition of AKI

A
  • Creatinine levels and urine output to be monitored so the injury can be staged.
  • Watch for confusion and drowsiness
  • General nausea, emesis and diarrhoea.
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3
Q

Investigations for AKI

A
  • Urine dipstick to check for proteinuria or haematuria which overall checks for intrinsic renal disease.
  • Ultrasound unless cause is obvious. This checks for CKD ( if kidneys are small), and if kidneys are asymmetrical this will check for renal vascular disease.
  • Check for intrinsic renal disease with immunoglobulin, autoantibodies etc…
  • Check liver function
  • Check platelet count, low may indicate haemolysis therefore you need a blood film.
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4
Q

Management and support for AKI-

A
  • Discontinue any nephrotoxic drugs
  • Ensure volume status is normal and consider urinary catheter to monitor urine output.
  • Adjust any current drug medications to the level of kidney function
  • Treat underlying cause of the AKI and consider sending to ICU if condition is not helped or is deteriorating
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5
Q

What is CKD and what are the common causes?

A
  • CKD is abnormal kidney structure or function present for over 3 months with implications on health.
  • Presents with a lowering GFR and albuminuria, (higher levels indicate a higher amount of kidney damage).
  • Most common causes are glomerulonephritis, high blood pressure and renovascular disease.
  • Lower GFR increases the risk of mortality, especially relating to the heart, kidney and it increases the chance of AKI.
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6
Q

Recognition of CKD

A
  • Check whether patients eGFR has been adjusted to the correct values for ethnicity etc..
  • Check past medical history focusing in on previous urological problems. Lower UTI’s especially.
  • Check for major risk factors; high blood pressure, diabetes, ischaemic heart disease…
  • Family history
  • Drug history, especially looking at when drugs where started.
  • Systems review to rule out malignancy. Ask, when was the last tie you felt well?
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7
Q

Symptoms of CKD

A
  • Typically symptoms only start when the GFR is below 30
  • Can present with peripheral oedema
  • Nausea and vomiting
  • Weight loss and fatigue
  • Change in mental state
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8
Q

Complications of CKD

A
  • Hypertension
  • CVD
  • Bone disease and hyperparathyroidism as kidney can’t activate vitamin D therefore less calcium is absorbed so more bone needs to be broken down in order to replenish the stores.
  • Anaemia of Chronic Disease as the kidney isn’t producing as much erythropoietin
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9
Q

Monitoring and Referral for CKD

A
  • Monitor the albuminuria and the eGFR at least annually, more frequently if the patient is higher risk, (high BP, diabetes, etc…)
  • Refer to nephrology when the GFR drops below 30 ( stage 4), stage 5 when the GFR drops below 15, then classed as kidney failure. Also refer if there’s a sudden drop in GFR by more than 25% or if there’s significant proteinuria with haematuria.
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10
Q

Treatment of CKD

A
  • Treat to SLOW disease progression. Primarily done by the control of blood pressure below 140/90 or 130/80 if diabetic or high albumin to creatinine ratio. Done with ACEi or ARBs. Also control hyperglycaemia, and make lifestyle changes such as more exercise, stop smoking and reducing salt intake
  • Treat RENAL complications. Major ones are anaemia, ( check Hb, iron and EPO levels and supplement where necessary). Consider bicarbonate supplement if acidotic. Reduce fluid and salt intake to control oedema, give diuretics if becomes more severe. Phosphate may become high as less activated Vit D therefore can cause bone disease and vascular calcification therefore give calcium free phosphate binders and control dietary intake.
  • Treat for CARDIO complications as CKD increases CVD risk due to higher BP, oxidative stress… Give aspirin as an antiplatelet and 20mg of Atorvastatin.
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11
Q

How to plan for Renal Replacement Therapy

A
  • Should start in CKD patients when the risk of renal failure is 10-20% within the year.
  • Patients should be listed for a deceased organ donation 6 months before the anticipated start of RRT
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12
Q

Cause of Diabetic Nephropathy

A
  • Hyperglycaemia increases RAAS activation, growth factors, and increases oxidative stress.
  • All of these factors increase glomerular capillary pressure causing podocyte damage therefore epithelial dysfunction.
  • This results in albuminuria.
  • Overtime scarring occurs ( glomerulosclerosis), causing overall lower renal function. This process is quickened with higher blood pressure.
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13
Q

Investigation for Diabetic Nephropathy

A
  • Urine dipstick checking for albuminuria. Starts with microalbuminuria ranging from 3-30mg of albumin. Can still regress at this stage.
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14
Q

Management of Diabetic Nephropathy- Su

A
  • Tight control of diabetes to prevent progression of albuminuria and any other microvascular progression.
  • Control of blood pressure to control albuminuria
  • Salt restriction to less 2g of sodium a day.
  • Statins to reduce cardiovascular risk. These can be continued if patient on dialysis but shouldn’t be started at this point.
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15
Q

What is Nephrotic Syndrome

A
  • Type of glomerulonephritis
  • Classified by a triad of Oedema, Hypoalbuminemia, and proteinuria ( less than 3g in a day).
  • Caused either by primary inflammation, ( minimal change disease, membranous nephropathy…) or secondary to DM, lupus nephritis, myeloma…
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16
Q

Recognition and Investigations of Nephrotic Syndrome

A
  • Pitting oedema which can appear severe and sudden.
  • Do a systems check to rule out malignancy
  • Check for chronic infection
  • Do a urinalysis to check for irregularities.
  • Blood film can check for hypoalbuminemia.
17
Q

Management of Nephrotic Syndrome

A
  • Reduce oedema with diuretics and fluid restriction. Reduce weight by 0.5-1kg per day to avoid intravascular fluid depletion and potential AKI.
  • Treat the underlying cause. Find this out with a biopsy, made need diuresis before biopsy as oedema can get in the way.

Most common cause in children is MINIMAL CHANGE DISEASE. Corticosteroids puts this into remission, therefore start with them and if no results take a biopsy. Start with biopsy in adults.
- ACEi/ARB’s to reduce proteinuria.

18
Q

Management of Complication of Nephrotic Syndrome

A
  • Thromboembolism: Increased risk as higher concentration of clotting factors and platelet abnormalities. Therefore give heparin unless the patient has a high bleeding risk.
  • High cholesterol production by the liver in response to low oncotic pressure, therefore give statins to reduce cardiovascular risk.
  • Urinary losses of immunoglobulins and immune mediators lead to high vulnerability for urinary infections. Therefore ensure patient has received all pneumococcal vaccinations, (not if immunocompromised).
19
Q

Which patients require specialist renal care?

A
  • When an AKI is not responding to treatment, is stage 3 ( creatinine is over 3 times the baseline), or there are severe complications, (hyperkalaemia, acidosis, accompanying HTN, or fluid overload).
  • When eGFR drops below 30 in CKD you should refer, also if proteinuria becomes severe. Sudden drops in eGFR (25%) should also be sent to nephrology.
  • Unexplained haematuria should be referred to nephrologists and a renal biopsy will be done.
20
Q

Treatment of low blood pressure

A
  • Low blood pressure will mean lower renal perfusion. Therefore give 500mL of any crystalloid over 15 minutes. Reassess after this and if not fixed give 250-500mL more. Seek expert help if patient isn’t euvolemic after 2L. Blood components should be given too in a haemorrhage.
  • Before filling the intravascular space check the low blood pressure isn’t due to congestive heart failure or sepsis etc. As this would make the condition worse.
21
Q

Treatment of fluid overload

A
  • Usually occurs due to aggressive fluid resuscitation therefore always monitor persons bodyweight when giving them fluid replacement therapy.
  • Treat if symptomatic, ( high blood pressure, lung crepitations, peripheral oedema…) Treat with diuretics.
  • Also treat if fluid overload occurs in AKI with renal replacement therapy.
22
Q

Renal replacement therapy

A
  • Long term treatment is started to tackle one of the uncontrollable complications of kidney failure, ( inability to control fluid status, inability to control blood pressure, electrolyte imbalances…)
  • Types include Haemodialysis, Peritoneal dialysis, and Hemofiltration.
  • Some elect to not receive RRT, instead they try and preserve residual kidney function and and prepare for end of life care.
23
Q

Common complications of RRT

A
  • Largest RF is cardiovascular disease due to higher blood pressure, calcium/phosphate dysfunction, vascular stiffness…
  • Protein and calorie malnutrition, often linked to metabolic acidosis as this lowers protein synthesis.
  • Renal bone disease
  • Infection as uraemia causes granulocyte and T cell dysfunction leaving the body more prone to infection.
  • Amyloid accumulates in long term dialysis causing carpal tunnel syndrome, arthralgia ( joint stiffness), and visceral effects.
24
Q

RRT: Transplantation

A
  • Should be considered when patient is approaching stage 5 CKD
  • Should be avoided if patient has cancer metastases, bad congestive HF/ CVD, and should be postponed if patient has current infection, unstable CVD or HIV with viral replication.
  • Live donor is preferred.
  • Immunosuppressants should be given before transplant as body will recognise the new kidney as foreign.

Give minimal effective dose with lowest drug-related toxicity. Type of immunosuppression depends on recipient individual risk and type of donated kidney.

25
Q

Complications of renal transplantation

A
  • Surgical. Bleed, thrombosis, infection, urinary leaks…
  • Delayed graft function. When new kidney doesn’t start working properly straight away. Happens in 40% of cases.
  • Rejection. ( 90% survive for a year)
    Acute: Either antibody related or cellular. Treat with more immunosuppression and corticosteroids. 15% of cases.
    Chronic: Antibody mediated attack. Results in gradual loss of kidney function as more and more damage is caused over time. Usually the graft degrades by ~4% per year.
  • Infection. Higher chance of all infections. Firstly in hospital then opportunistic risk for first 6 months,. Increased chance of community infections in months 6-12 months.
  • Malignancy. 25x chance of cancer especially skin due to the immunosuppression used.
  • 3-5x more chance of premature CVD.