CKD and Glomerulonephritis Flashcards

1
Q

What is chronic kidney disease?

A

Progressive stepwise deterioration of renal function over months to years, that is often irreversible.

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2
Q

What values for eGFR dictate each stage of CKD?

A
Stage 1 -90+. (Evidence of anatomical defect or CKD)
Stage 2 - 60-89.
Stage 3a - 45-59.
Stage 3b - 30-44.
Stage 4 - 15-29.
Stage 5 - <15.
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3
Q

What is used to determine if a patient has proteinuria?

A

Albumin creatinine ratio. Value of 30-290mg/g indicates microalbuninurua, whereas >300mg indicates overt proteinuria

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4
Q

What are primary causes of CKD?

A

Polycystic kidney disease,
Acute tubular necrosis,
Recurrent pyelonephritis,
Glomerulonephritis.

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5
Q

What are secondary causes of CKD?

A

Diabetes mellitus (lead cause),
Hypertension,
Renovascular disease,
Autoimmune (eg lupus).

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6
Q

What is the gross pathology of CKD?

A

atrophy and loss of renal parenchyma (kidney appears shrunken and cortex is replaced by extracellular matrix)

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7
Q

Why is HbA1c not used to measure diabetic control of a patient with CKD?

A

it is haemaglobin dependant and CKD commonly causes anaemia due to chronic disease, iron deficiency or lack of EPO secretion.

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8
Q

What type of diuretics should be used to treat oedema secondary to fluid overload caused by CKD?
What dosage should be used?

A
Loop diuretics (eg furosemide).
Greater dosage required
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9
Q

Why may metabolic acidosis occur in patients with CKD?

A

Renal loss of bicarbonate. Treated with oral sodium bicarbonate tablets.

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10
Q

Why might a patient with CKD develop secondary hyperparathyroidism?

A

Kidney no longer activates vitamin D, so hypocalcaemia occurs. PTH rises to supply the body with calcium from bone in abscence of the negative feedback provided by calcium.

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11
Q

What skeletal problems are common in CKD?

A

Osteomalacia or rickets - due to bone resorption and high PTH levels.

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12
Q

What may occur after bone resorption in CKD and a rise in circulating free calcium?

A

Calcium deposition in tissues eg blood vessels or joints, leading to necrotic lesions - calciphylaxis

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13
Q

What may be required in a patient with CKD to manage calcium levels?

A

Parathyroidectomy

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14
Q

At what point do patients often require dialysis to survive?

A

End stage renal failure - when eGFR is around 8-10

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15
Q

What three treatment options does a person with end stage renal failure have?

A

Haemodialysis,
Peritoneal dialysis,
Renal transplant.

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16
Q

What are the benefits of haemodialysis?

A

Less responsibility placed upon the patient - good if young or elderly.
Proven to be effective long term.
Does not have to be undertaken every day - gives some freedom.

17
Q

What are the drawbacks of haemodialysis?

A

Time consuming,
Rigid dialysis timing,
Access problems with fistulae,
Fluid and sodium restrictions to diet are often difficult to follow.

18
Q

What are the benefits of peritoneal dialysis?

A

More independace - patients can change their own bags.
Less fluid and food restrictions.
More flexible schedule,
May preserve renal function better initially.

19
Q

What are the drawbacks of peritoneal dialysis?

A

Infection (peritonitis).
Frequent overnight changes required.
Responsibility is placed on patient.
Less long term survival data.

20
Q

What are the downsides of renal transplant? (This is still always the best option)

A

Life long immunosuppressants.
Risks of surgery.
Not enough kidneys - may have to wait forever.

21
Q

What is 4 structures may be damaged in glomerulonephritis?

A

Capillary endothelium,
Glomerular basement membrane,
Mesangial cells,
Podocytes.

22
Q

What is NephrOtic Syndrome?

What is the most common sign of this?

A

Podocyte damage leading to glomerular charge-barrier disruption.
Causes massive proteinuria and oedema.

23
Q

What triad of signs characterises nephrotic syndrome?

A

Proteinuria (>350mg/mmol),
Hypoalbumianaemia,
Oedema.
(Also often high cholesterol)

24
Q

How does diabetic nephropathy occur?

A

Glycated proteins at the efferent arteriole lead to hyaline atherosclerosis and decreased perfusion, activating RAAS. Mesangial cells over time secrete mor matrix which thickens the basement membrane, decreasing GFR.

25
Q

How is diabetic nephropathy managed?

A

Treatment of hypertension and control of glycaemic index. ACEi, ARB

26
Q

What is minimal change disease?

A

Autoimmune process resulting in fusion of podocyte foot processes. Named as no significant renal change on light microscopy. Common cause of nephrotic syndrome in children under 6

27
Q

What is membranous glomerulonephritis?

A

Subepithelial deposition of immune complexes leading to thickening of the basement membrane. Treated via immunosuppressants and managing underlying causes.

28
Q

What are the causes of Focal Segmental Glomerulosclerosis?

A

Primary: idiopathic.

Can be secondary to sickle cell disease, HIV, heroin abuse, kidney hyper perfusion.

29
Q

What is FSGS

A

Damage of podocytes and protein buildup in glomerulus, leading to hyalinosis and sclerosis. Treated via steroids.

30
Q

How is nephrotic syndrome broadly managed?

A

Diuretics for oedema,
ACEi for proteinuria,
Lifestyle changes to reduce cholesterol,
Treatment of underlying condition eg steroids.

31
Q

What triad is commonly found in Nephritic syndrome?

A

Haematuria,
Reduced GFR (presenting as oliguria)
Hypertension.

32
Q

What is Bergers disease (IgA nephropathy)?

A

Hypertension and raised IgA levels leading to deposition in the mesangium. Sclerosis of damaged segments. Managed by antihypertensives and steroids.

33
Q

What is rapidly progressive glomerulonephritis?

A

Severe glomerular injury due to leakage of fibrin and macrophage/epithelial proliferation. Causes loss of renal function on days to weeks. Treated with steroids, immune suppressants and plasma exchange.

34
Q

What is GoodPastures syndrome?

A

Antibodies to type IV collage. build up in glomerular basement membrane and lead to rapid progressive glomerulonephritis, acute renal failure and lung haemorrhage. Treated with plasma exchange and corticosteroids.

35
Q

What is post streptococcal glomerulonephritis?

A

Occurs after infection of group A beta haemolytic strep at pahrynx, tonsils or skin. May migrate to kidney. Treated with antibiotics.

36
Q

How is nephritic syndrome treated?

A
ACEi or ARBs,
Diuretics for oedema,
Immune suppressants,
Cardiovascular risk management (eg stopping smoking),
Dialysis if required (short term).