Lecture 10 - renal diseases Flashcards

1
Q

What is the primary function of the kidneys?

A

Regulation of water and electrolytes, acid/Base balance, waste excretion, blood pressure control, and hormone secretion (erythropoietin, vitamin d, renin)

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2
Q

List the major factors associated with CKD progression according to the 2021 NICE guideline

A

increasing age, cardiovascular disease, proteinuria, previous AKI, hypertension, diabetes, smoking, African/african-caribbean or asian family origin, chronic NSAIDs, untreated urianry outflow tract obstruction

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3
Q

How is renal function commonly measured?

A

cockcroft gauld - uses IBW, age, and weight. use correction factor 0.4 + IBWif obese. limitatiosn are if patient is in catabolic stress, extensive oedema, very poor or good renal fucntion, rapidly changign rena fucntion, pregannt women or children and icnreased creatine consumption.

eGFR - uses age, race, BSA, gender, albumin. limitations are if patient has a transplant, serious comorbidiotes eg diabetes, all races, very poor or good renal fucntion, rapidly changign renal fucntion, pregnant women or children and icnreased creatine consumption

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4
Q

what is renal disease ?

A

renal disease can be acute or chronic kidney disease. eGFR, CrCl and CKD-EPI can all be used to estimate the severity. we don’t just look at the current serum CR - need to look at a trend for what is normal for the patient

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5
Q

chronic kidney disease - what is it, who is at risk and how do we manage it ?

A

chronic kidney disease is deteriorating progression, irreversible loss of kidney function, that may require renal replacement therapy. people at risk are: diabetes, HTN, AKI, CVD, structural renal disease tract, Polycystic kidney disease, Glomerulonephritis, family history of ESRD, opportunistic detection of haematuria, longterm nephrotoxic medication - ciclosbrin, NSAID etc, covid 19 infection.
what can we do - Accurate diagnosis, monitor & treat underlying causes
✅ Prevent progression:
ACE inhibitors, ARBs, SGLT2 inhibitors
Lifestyle advice
Aggressive BP control
✅ Preserve kidney function: avoid nephrotoxins
✅ Control symptoms
✅ Manage cardiovascular risk:
BP target <140/90 (<130/80 if diabetic/proteinuria)
Consider statin

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6
Q

what should be considered when starting an ace inhibitor in renal of CKD

A

ACE inhibitors or an ARB slows renal function even in advanced CKD. there may be an initial fall in eGFR up to 30%. check the bloods initially and after dose changes. there is more likely to be a decline in GFR due to volume depletion eg on high dose diuretic. the main caution is bilateral renal artery stenosis and hyperkalaemia. Must remember SICK day rules.

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7
Q

describe SGLT2 inhibitors in renal disease and safety advice

A

SGLT2 inhibitors improve cardiac control, renal outcomes and glycemic control.

safety advice - the tibial fall in eGFR can be up to 30%. SGLT2 inhibitors have a risk of diabetic ketoacidosis, and mycotic genital infections. requires caution if patient is dehydrated, has UTIs or peripheral vascular disease.

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8
Q

what are they intervention for CKD management

A

Accurate diagnosis, preventing progression with ACE inhibitors, ARBs, and SGLT2 inhibitors, symptom control, and lifestyle modifications.

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9
Q

What are some biological actions altered in CKD that impact medication management?

A

Hypovalameia: enhanced antihypertensive effects. start at low dose and increase to max.
Hyperkalaemia: increased side effects with ace inhibitors and potassium salts
uraemia: can cause excess bleeding
enhanced sensitivity to centrally acting eg analgesics especially morphine - start at lower doses.
variation in electrolytes eg digoxin toxicity

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10
Q

what are drugs used to treat hyperkalaemia ?

A

Patiromer 16.8 g once daily or Lokelma – 5-10 g x 1-3 daily
Calcium Resonium – 15 g x 3 daily (o), 30 g (PR)
Salbutamol Nebules – 5 mg x 4 daily
Calcium Gluconate 10% - 30 mls over 5-10 mins
Insulin/Dextrose – 8 units actrapid in 100 mls 20% dextrose over 15 - 30 mins
Sodium Bicarbonate 1.26%, 500 mls - over 1 hour

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11
Q

what are drugs that you must take care with

A

Low therapeutic window drugs
Drugs that are really excreted for example, aminoglycosides and vancomycin
Active metabolites which are really excreted for eg morphine
antibiotics especially cephalasporins and penicillins. lower dose is required as nephrotoxic. ciprofloxacin and macrolides can cause nausea if the dose is too high.
antiviral eg acyclovir need to be drastically reduced otherwise very nephrotoxic and will cause nausea

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12
Q

what are hyperparathyroidism causes

A

reduced phosphate excretion, reduced calcium absorption, reduced calcitriol production by the kidney, uraemia reduces sensitivity of parathyroid gland to calcium, inhibitors of binding oc calitriol to receptor in parathyroid gland

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13
Q

what are CKD mineral and bone disorders?

A

hyperparathyroidism, osteomalacia, dynamic bone disease, osteoporosis

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14
Q

what are secondary causes of hyperparathyroidism?

A

Secondary causes of hyperparathyroidism are reduced phosphate excretion, reduced calcium excretion, reduced calcitriol production from the kidneys, uraemia reduces sensitivity of parathyroid gland to calcium, and inhibiting of binding of calcitriol to receptors to the parathyroid gland.

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15
Q

what are symptoms of raised calcium or phosphate product

A

pruritic, conjunctival calcification, bone pain, skeletal deformity, increased risk of fractures

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16
Q

what are treatment option of raised phosphate or calcium

A

diet - food rich in protein
phosphate binders, vitamin D and cinacelet
control of aluminium levels
Surgery

17
Q

give examples of phosphate binders

A

calcium based - calcichew , calcium acetate
heavy metal based - lanthanum carbonate
iron based - velphoro
polymer based - sevelamer carbonate and hydrochloride

18
Q

What are the treatment options for CKD-related Mineral and Bone Disorder (CKD-MBD)?

A

Vitamin D analogues: Alfacalcidol (1α-hydroxycholecalciferol, oral/IV), Calcitriol (1,25-dihydroxycholecalciferol, oral), Paricalcitol (vitamin D analogue, oral/IV).
Calcimimetics: Cinacalcet (oral), Etelcalcetide (IV).

19
Q

what are the causes of renal anaemia ?

A

Lack of erythropoietin production
Iron deficiency (TSATS > 20, Ferritin: 200-500)
Increased red blood cell breakdown due to uraemia
Blood loss
Hyperparathyroidism
Aluminium toxicity
Infection or Inflammation
Inadequate dialysis

20
Q

what are symptoms of anaemia ?

A

Fatigue
Breathlessness
LVH
Impaired cognitive function
Loss of libido
Decreased cold tolerance

21
Q

Treatment of anaemia

A

ESA’s e.g. Epoetin alfa, beta & zeta, Darbepoetin, Mircera – SC/IV
HIF-Inhibitors e.g. Roxadustat – oral option

IV Iron: e.g. iron sucrose, iron dextran, Ferinject, ferric derrisomaltose
Oral iron (not at same time as phosphate binders)

22
Q

Renal Replacement Therapy Modalities

A

Haemodialysis (HD) / Haemodiafiltration (HDF)

Haemofiltration – mainly done in ICU

Peritoneal dialysis – CAPD, APD

Transplantation

Conservative care

23
Q

What are some common problems associated with HDF (Hemodiafiltration)?

A

Hypotension (“crash”) - 25-60%
Cramps - 5-25%
Itch - 1-5%
Clotting & blocked lines
Nausea & vomiting - 5-15%
Exhaustion
Anaemia
Hair loss
Infections
Issues with dementia patients - confusion, pulling needles/lines out
Restless legs
Boredom

24
Q

what are risk factors for AKI

A

Increasing age
Diabetes
CKD
Cardiac failure
Dehydrated
On more than 1 nephrotoxin
Chronic liver disease

People with reduced renal blood flow

25
Q

what are signs and symptoms of an Aki ?

A

reached urinary output, dehydration or thirst, SOB, fatigue, confusion or drowsiness, coma if severe, abdominal pain, nausea or vomiting, swelling in legs, ankles or around eyes

26
Q

what is are physiological and nephrotoxins of pre renal failure

A

type of AKI

physiological causes are
volume depletion,fluid loss, reduced CO, vascular insufficiency and hepatic failure

nephrotoxicity - drugs
ciclosphpirs, laxative, ace inhibitors, diuretics, NSAIDs, beta blockers high dose dopamine

27
Q

what is pre renal failure ?