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RENAL > A. KIDNEY DISEASE > Flashcards

A. KIDNEY DISEASE Flashcards

1
Q

what is AKI

A
  • an abrupt decrease in kidney function that occurs within 7 days (no structural abnormalities)
  • an increase in SCr by 50% within 7 days or
  • an increase in SCr by 0.3mg/dl (26.5 micromol/l) within 2 days or
  • oliguria for ≥6 hours

*included in AKD and CKD

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2
Q

what is AKD

A
  • patients who have functional/structural abnormalities with implications for health
  • ≤ 3 months
  • AKI or
  • GFR <60ml/min/1.73m2 or
  • decrease in GFR by ≥35% or
  • increase in SCr by >50%
  • marker of kidney damage (albuminuria, hematuria, pyuria)
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3
Q

what is CKD

A
  • abnormalities in kidney structure or function that persists for >3 months
  • GFR < 60ml/min/1.73m2
  • marker of kidney damage (albuminuria)
  • can include AKI and AKD

*classified according to CGA classification

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4
Q

kidney disease progression

A
  • AKI to AKD (both can have recovery)
  • AKD to CKD to (AKI-on-CKD during progression) ESRD which requires renal replacement therapy (dialysis, transplant)
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5
Q

what is maladaptive repair

A
  • development of fibrosis
  • delayed resolution of pathology/inflammation
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6
Q

what is adaptive repair

A
  • clear debris by macrophages
  • proliferation to restore tubular epithelial cell layer
  • resolution of pathology/inflammation
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7
Q

what risk factors contribute to progression

A
  • severity/frequency of AKI (AKI-on-CKD if have a number of times)
  • age
  • sex (males have faster rate)
  • pre-existing CKD
  • albuminuria
  • hypoalbuminaemia
  • hypertension
  • obesity
  • DM
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8
Q

AKI

A
  • rapid loss of kidney function
  • sudden onset of renal impairment – (within 7 days)
  • range from mild renal dysfunction to the need for renal replacement therapies (RRTs)
  • outcomes: recovery, AKD with recovery, CKD (possibly to ESRD), ESRD or death
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9
Q

what are the 3 types of causes of AKI

A
  1. pre-renal: occurs before the kidney - reduced perfusion to kidney (80%)
  2. intrinsic (or intrarenal): nephrons
  3. post-renal: ureter, bladder, urethra
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10
Q

main causes of pre-renal AKI

A
  • low renal perfusion
  • dehydration (esp elderly)
  • medicines which can impact on hydration, will further decrease perfusion (diuretics, antihypertensives, laxatives) - withhold if have AKI
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11
Q

what drugs exacerbate AKI or are unsafe to use and so should be withheld

A

DAMN
- Diuretics
- ACE inhibitors, AIIRAs
- Metformin
- NSAIDs

CANDA
- Contrast media
- ACE inhibitors
- NSAIDs
- Diuretics
- AIIRAs

*dose adjustment guided by clinical judgement and drug monitoring

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12
Q

definition of CKD

A
  • long-term, progressive, irreversible loss of nephrons
  • either through disease/damage or ageing
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13
Q

clinical definition of CKD

A
  • presence of kidney damage or
  • GFR < 60 m L/min/1.73m2
  • persisting for ≥ 3 months
  • irrespective of cause
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14
Q

prevalence of CKD in UK

A
  • 13-14% adults (age ≥16)
  • 6% UK (age ≥16) with CKD stages 3-5
  • higher prevalence in males
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15
Q

difference in CKD vs AKI

A
  • long duration of symptoms
  • absence of acute illness
  • anaemia
  • hyperphosphataemia, hypocalcaemia (but similar laboratory findings may complicate AKI)
  • reduced renal size and cortical thickness on renal ultrasound (but renal size is typically preserved in patients with diabetes)
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16
Q

causes of CKD

A
  • DM (1 - most common cause to ESKD), hypertension (2), obesity
  • renal vascular disorders: atherosclerosis, nephrosclerosis
  • immunological disorders: SLE, glomerulonephritis (3)
  • infections: pyelonephritis, TB
  • nephrotoxins (NSAIDs, heavy metals)
  • UT obstruction (kidney stones, hypertrophy of prostate)
  • polycystic kidney disease (4)
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17
Q

cycle of how CKD leads to ESRD

A
  • primary kidney disease
  • decreased nephron number
  • hypertrophy and vasodilation of surviving nephrons (surviving nephrons adapt as there is an increase in structural features) ADAPTIVE CHANGES
  • increased glomerular pressure and/or filtration
  • maintain excretion of water/solutes (near normal function)

*over time these functional changes may lead to further injury

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18
Q

how is an asymptomatic patient with CKD diagnosed (adaptation)

A
  • blood/urine tests
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19
Q

when do clinical symptoms show with CKD

A
  • 75%-80% nephron loss
  • stage 4/5 (near ESKD)
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20
Q

how can CKD lead to ESKD

A
  • primary kidney disease
  • decreased nephron number
  • increased arterial pressure caused by decreased fluid excretion
  • hypertrophy and vasodilation of surviving nephrons (surviving nephrons adapt as there is an increase in structural features) ADAPTIVE CHANGES
  • increased glomerular pressure and/or filtration
  • glomerular sclerosis (stress on capillaries and scarring, less elastic and able to cope with pressures)
  • decreased nephron number
  • ESRD
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21
Q

what drugs slow down progressive loss of kidney function (by decreasing glomerular pressure)

A
  • ACEIs
  • AIIRAs (renoprotective)
  • SGLT2 inhibitors (dapagliflozin)
22
Q

how is angiotensin II converted to angiotensin I IN RAAs

A
  • renin from JG cells
23
Q

how is angiotensin I converted to angiotensin II

A
  • angiotensin-converting enzyme (ACE)
24
Q

what does angiotensin II trigger

A
  • vasoconstriction
  • aldosterone release from adrenal cortex
25
Q

what does vasoconstriction cause

A
  • efferent arteriole being narrower than afferent arteriole
  • increased filtration pressure and GFR
26
Q

what effect does aldosterone cause

A
  • increased Na+ and water reabsorption
  • increased K+ (from P-cells) and H+ secretion (from H+ cells)
27
Q

how do ACEIs act as renoprotective agents

A
  • block ACE
  • hence decreases angiotensin II levels
  • decreases vasoconstriction at efferent arteriole
  • decrease in blood pressure, renal blood flow, GFR
  • decreased intraglomerular pressure and glomerular sclerosis
  • decreases aldosterone levels
  • decreased Na+ and water reabsorption
  • decreased K+ and H+ secretion so get a decreased blood volume and hyperkalaemia
28
Q

ACEIs causing renal impairment

A
  • patients with reduced renal perfusion such as renal vascular disease, bilateral renal artery stenoses
  • get a further decrease in GFR ie further ischaemia of kidney
29
Q

how do SGLT2 inhibitors work in CV

A
  • mild natriuresis and glucose-induced osmotic diuresis
  • decrease in blood volume and blood pressure
  • decrease in intraglomerular pressure
  • decrease in glomerular sclerosis

*Cardiovascular & renal benefits manifest rapidly, unlikely to be related to improvement in glycaemic control

*SGLT2 inhibitors are used in the management of T2DM, CHF and CKD

29
Q

how do SGLT2 inhibitors work in renal impairment (flozins - dapagliflozin, canagliflozin, empagliflozin)

A
  • reversibly inhibit SGLT2 in renal PCT to reduce glucose reabsorption and increase urinary glucose excretion so there is a decrease in blood glucose
30
Q

signs and symptoms of CKD

A
  • none, often asymptomatic (stages 1-3)
  • nausea, vomiting (acidosis)
  • loss of appetite and weight loss
  • itching
  • confusion, seizures
    *uraemic toxins
  • ankle swelling (oedema)
  • shortness of breath (oedema, anaemia, acidosis)
  • weakness, fatigue (anaemia)
  • altered urine output
31
Q

what factors cause progression of chronic renal disease and how can we control the modifiable risks

A
  • advancing age
  • sex (male, AMAB>female, AFAB)
  • race (black African/caribbean, asian)
  • socio-economic status (if lower, faster rate)
  • hypertension: blood pressure control
  • proteinuria: ACEIs or AIIRAs by decreased intraglomerular pressure and hence the rate
  • obesity: weight loss
  • dyslipidaemia; statins
  • smoking: smoking cessation
  • diabetes control: good glycemic control
32
Q

what are the aims of management

A
  • identify patients with CKD
    differentiate from AKI
    establish aetiology if possible
    establish severity
  • treat underlying reversible causes
  • reduce CV risk (controlling modifiable risk factors)
  • delay or prevent progression (controlling modifiable risk factors)
  • treat complications
  • dialysis preparation for those with progressive disease
33
Q

how do you treat renal anaemia

A
  • supplemental iron (and folate) may be required
  • erythropoiesis-stimulating (RBC production) agents (ESA) such as epoetin alfa, beta
34
Q

how do you treat renal bone disease

A
  • vitamin D analogues (alfacalcidol and calcitriol)
  • phosphate binders (e.g. calcium carbonate, sevelamer)
  • dietary restriction of high phosphate foods (low protein, low dairy)
35
Q

what is alfacalcidol

A
  • l-hydroxy attached to vitamin D so need metabolism to get 25-hydroxy added to make it calcitriol
36
Q

how do phosphate binders work

A
  • collate phosphate in stomach and gut to decrease absorption from food substances
  • if you have hyperphosphatemia or if you break down bone to get calcium you get increased phosphate levels)
37
Q

how do you treat CV disease

A

statins

38
Q

what are renal replacement therapies

A
  • long term dialysis: haemodialysis (connected to machine) and peritoneal dialysis (in patients own body to remove toxins) which relieves uraemia symptoms and detoxify
  • kidney transplantation: therapy of choice for ESRD - cadaveric or living donor transplantation
39
Q

what substances are affected by altered glomerular filter integrity and what are the consequences

A
  • protein: proteinuria
  • RBCSs: haematuria
40
Q

what substances are affected by decreased excretion and what are the consequences

A
  • creatinine: increased serum creatinine conc and decreased eGFR
  • uraemia toxins: excess of amino acids and protein metabolic end-products: uraemia
  • salt/water: hypertension, oedema
  • acid: metabolic acidosis
  • potassium: hyperkalaemia
  • phosphate: hyperphosphatemia
41
Q

what substances are affected by decreased biosynthesis (stages 4/5) and what are the consequences

A
  • EPO: anaemia
  • activation of vitamin D: osteodystropy (hypocalacaemia)
42
Q

how does erythropoietin work

A
  • decreased oxygen delivery to the kidney
  • peritubular fibroblast-like cells produce EPO (interstitium of cortex/outer medulla)
  • EPO stimulates erythropoiesis by the bone marrow stem cells
  • increased red blood cell production restores oxygen levels back to normal (homeostasis)
43
Q

how is EPO production affected in chronic renal failure

A
  • decreased
  • leads to renal anaemia due to insufficient production of RBCs
44
Q

how is activated vitamin D made

A
  • vitamin D3 (cholecalciferol) from skin (made from radiation) and diet (egg yolk, fish, fortified cereals)
  • converted to 1,25-dihydroxycholecalciferol (1,25-dihydroxyvitamin D3, calcitriol)
  • by the liver (25alpha-hydroxylase) then the kidney (1alpha-hydroxylase)
45
Q

what homeostatic mechanism is activated vitamin D involved in

A

calcium homeostasis

46
Q

what effect does activated vitamin D have on the body

A
  • intestines: increased calcium and phosphate absorption (from digested foods)
  • kidneys (weak): increased calcium and phosphate reabsorption
47
Q

what effect does PTH have on actions of vitamin D

A
  • permissive actions
  • 1alpha-hydroxylase synthesis and activity (and hence synthesis of calcitriol) requires PTH
48
Q

how can we elevate plasma calcium levels

A
  • increase in intestinal calcium absorption by vitamin D
  • increase in renal calcium reabsorption by PT§H and vitamin D
  • increase resorption of calcium and phosphate from bone by PTH
49
Q

how is vitamin D synthesis affected in advanced CKD (chronic renal failure)

A
  • low levels of calcitriol as not a lot of 1alpha-hydroxylase activity
  • hence decreased plasma calcium leads to increased PTH secretion (acts to increase calcium levels)
50
Q

how does decreased calcitriol levels in chronic renal failure

A
  • hypocalacaemia leads to hyperparathyroidism
  • increased PTH leads to: resorption of bone and calcium release and hence impaired bone mineralisation
    (renal osteodystrophy/renal bone disease - bone pain, joint pain, bone deformation, bone fracture, poor mobility)

RENAL (13 decks)

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