Miscellaneous Flashcards

1
Q

What is eGFR?

A

-Measure of how fast the kidney is filtering through its 1 million glomeruli.
-GFR is the most useful test of overall kidney function
-However because it is not straightforward to measure GFR directly, most of the time we use estimated GFR, eGFR, to give an approximate idea of how good kidney function is.

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2
Q

Describe the MDRD equation

A

-It is an estimate not a precise measure. It is most accurate in people who are quite well and in reasonable health. People at extremes – amputees, body builders, people who have lost a lot of weight during an illness – are likely to get the least accurate results.
-It was worked out from results in white and black patients in the US. It may not be so accurate for other races.
-It’s least accurate at good levels of kidney function, and gets better the worse kidney function is.
-It shouldn’t be used in under-18s, in pregnancy, or relied on in acute illnesses.

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3
Q

Using eGFR

A

CKD stages: eGFR is used to categorise reduced kidney function into 5 CKD stages.

Prescribing: eGFR is very useful for identifying patients who might be at risk from drug overdoses because their kidneys don’t get rid of the drug as fast as usual. However most drug datasheets only have instructions for adjusting dose according to creatinine clearance – so in some circumstances you may need to work that out before calculating the dose. More on measuring renal function

Improvements to come: research to identify more accurate equations, and to test MDRD and other methods with patients of different countries and races, is under way.

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4
Q

Drug interactions of Tacrolimus and cyclosporine

A
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5
Q

Mycophenolate mofetil

A
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6
Q

Azathioprine

A
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7
Q

CTKUB

A
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8
Q

Nephrotic vs Nephritic

A

-Nephrotic:
=Injury to podocytes
=Changed architecture: scarring, deposition of matrix or other elements
=PROTEINURIA

-Nephritic:
=Inflammation
=Reactive cell proliferation
=Breaks in GBM
=Crescent formation
=HAEMATURIA

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9
Q

Describe nephritic syndrome

A

The nephritic syndrome is characterised by the presence of haematuria in association with hypertension, oliguria, fluid retention and reduced/declining renal function. Many patients with glomerulonephritis, particularly those with milder disease, do not exhibit all of these features; however, their combined presence is typical of a rapidly progressive glomerulonephritis and warrants urgent investigation. In many cases, investigation will include a renal biopsy to confirm diagnosis and guide management, but less invasive investigations may also be useful

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10
Q

Cause and investigation of nephritic syndrome

A

-Rapidly progressive glomerulonephritis
=Post-infectious glomerulonephritis (C3, C4)
=Anti-GBM disease (antibody)
=Small-vessel vasculitis (p-ANCA, c-ANCA)
=Lupus nephritis (ANA, dsDNA, C3, C4)

-Mild glomerulonephritis presentation
=IgA nephropathy (serum IgA)
=Mesangioproliferative glomerulonephritis (C3, C4, HEP B, C, HIV, ANA, dsDNA, PPE)
=Alport syndrome (genetic screening, hearing test)

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11
Q

USS of kidneys

A

-Kidney size (small kidneys are seen in CKD)
-Echogenicity (the cortical area is usually darker than the medulla and cortical thinning or increased echogenicity suggests an intrinsic problem rather than pre- or post-renal disease)
-Renal shape (irregularity of the kidney surface may be due to local scars such as in reflux nephropathy)
-Renal asymmetry (points to a developmental failure of one kidney or a reduced blood supply such as with unilateral renal artery stenosis/occlusion)
-Renal cysts (such as in polycystic kidney disease, when the kidneys are enlarged, though degenerative cysts can also be observed, when the kidney size is typically normal or reduced)
-Hydronephrosis (dilated pelvicalyceal system in obstruction)

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12
Q

Slowing progression of CKD

A

-Disease-specific therapies, such as glycaemic control for diabetic nephropathy
-Immunosuppression for auto-immune diseases such as vasculitis or tolvaptan
-Anti-diuretic hormone receptor antagonist to reduce cyst enlargement in polycystic kidney disease
-RAAS blockade represents the anti-hypertensive therapy of choice; problematic in patients with pre-renal AKI, therefore we advise them to stop the medication if they are unwell
-Lifestyle measures such as low salt diet, weight loss for those with BMI >25 and stopping smoking are beneficial for all forms of CKD

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13
Q

Managing complications of CKD

A

-Anaemia due to deficiency of erythropoietin (EPO) becomes common in stage 4 CKD and many patients will need injections of recombinant EPO after excluding other causes
-Bone metabolism disorders such as hyperparathyroidism are common. Many patients will be on phosphate binders to prevent phosphate absorption and on supplements of activated vitamin D to suppress the overactive parathyroid glands.
-Hyperkalaemia is common in stage 4-5 CKD and may limit the use of RAAS inhibitors. It can be managed by low potassium diet and occasionally with potassium binders, which inhibit potassium absorption. Loop and thiazide diuretics may also help by promoting kaliuresis
-Fluid retention is common in advanced CKD and treated with diuretics and fluid and salt restriction. Patients are weighed at each clinic and this can be helpful to monitor fluid status. As dietary or fluid restriction is commonly required, many patients will also see a dietician when they attend the renal clinic.

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