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PR2135 > Renal > Flashcards

Renal Flashcards

1
Q

Functions of Kidney

A

Excretory: excretion of metabolic waste products

Regulatory: maintain fluid & electrolyte homeostasis + interconversion of metabolic intermediates

Endocrine: synthesis/metabolism of hormones

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2
Q

Renal Failure

A

Increase in urea conc & SCr, decline in CrCl/eGFR & revelop uremic symptoms

*Know eqn to calculate CrCl

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3
Q

Chronic Kidney Disease (CKD)

A

Abnormalities of kidney structure/function, present >3 months (either of the following)

  • albuminuria
  • urine sediment abnormalities
  • electrolyte & other abnormalities
  • abnormalities by histology
  • structural abnormalities by imaging
  • history of kidney transplantation

-GFR<60ml/min/1.73 m^2

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4
Q

Azotemia

A
  • accumulation of nitrogenous waste products (increased urea, SCr) from reduction in renal function
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5
Q

Uremia

A
  • fluid, electrolyte, hormone imbalances & metabolic abnormalities due to deterioration of renal fn
  • azotemia + clinical signs & symptoms
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6
Q

CKD Classification

A 
Stage 1: GFR >= 90
Stage 2: GFR 60-89
Stage 3a: GFR 45-59
Stage 3b: GFR 30-44
Stage 4: GFR 15-29
Stage 5: GFR <15

Albuminuria A1: AER/ACR < 30
A2: AER/ACR 30-300
A3: AER/ACR >300

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7
Q

Causes of CKD/ESRD

A
  1. DM
  2. Glomerulonephritis (GN)
  3. Hypertension (HTN)
Others:
Urinary obstruction (kidney stones)
Chronic infections 
Genetic disorders
Immune diseases
Vascular diseases
Drugs
HIV-associated nephropathy
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8
Q

Clinical Presentation of CKD

A

Early stages: No clear signs with possible bubbles/blood in urine
Mid stage: loss of appetite, swelling ,fatigue
Late stage: ammonia breath, loss of appetite/diarrhoea, difficulty breathing, swelling, nausea/vomiting, loss of consciousness, anaemia

Uremic symptoms: fatigue, weakness, SOB, mental confusion etc

Signs: edema, changes in urine output, abdominal distension, pericardial rub, asterixis

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9
Q

Clinical Presentation of CKD (Lab abnormalities)

A
  • Increased: SCr, urea, K, P, PTH, BP, glucose, lipids, Ca (if on vit D therapy)
  • Decreased: GFR, CrCl, CO2 (metabolic acidosis), Hgb (anemia, iron stores, vit D, albumin, glucose, Ca (early stages), HDL
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10
Q

Complications with CKD

A 
CV disease
Fluid & electrolyte abnormalities
Metabolic acidosis
Malnutrition
Anemia
Secondary hyperparathyroidism; mineral & bone disorder 
Endocrine
GI
Dermatological
Uremic bleeding
Pulmonary
Immune system
Neurologic
Psychological
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11
Q

Goals in CKD Management

A
  • Slow down progression of disease + delay need for renal replacement therapy (RRT)
  • Maintain fluid & electorlyte homeostasis
  • Adequate nutritional & metabolic support
  • Prevent extra-renal (anemia & bone disease)
  • Reduce morbidity & mortality
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12
Q

DM Management in CKD
***Avoid use of glibenclamide in elderly & renal-impaired

SGLT2-i for Type 2 DM

A
  • SGLT2-i + metformin for HbA1c > 7% despite mono
  • SGLT2-i + sulfonylurea for HbA1c > 7% despite mono
  • SGLT2-i + metformin + sulfonylurea despite optimal doses of dual therapy
  • SGLT2-i + insulin +/- metformin

***eGFR<30 initiation not recommended for Canaglifozin, Dapaglifozin; Empagliflozin not recommended but may continue therapy

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13
Q

Benefits of SGLT2-i

A
  • Weight loss
  • Osmotic diuresis & natriuretic
  • Reduce eGFR
  • Reduce albuminuria
  • Synergistic effects with antiHTN therapies
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14
Q

How to manage DM in CKD

A
  • ACEi/ARB for pt with diabetes, HTN & albuminuria
  • quit smoking
  • consume diet high in veg, fruits, grains, fibre etc, lower process food & carbs
  • maintain protein intake of 0.8g protein/kg
  • Na intake <2g per day
  • moderate-intensity physical activity for at least 150 mins/wk
  • use HbA1c to monitor glycemic control
  • HbA1c target <6.5% to <8%
    more stringent if lower risk
  • Lifestyle therapy + metformin + SGLT-2i
  • if T2D + CKD + eGFR > 30: metformin, SGLT2-i
  • if metformin + SGLT2i not enough, use long-acting GLP-1 RA
  • discontinue metfomrin if eGFR<30/dialysis
  • do not initiate SGLT2i if eGFR<30 / discontinue if dialysis
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15
Q

Risk factors for CVD in CKD

A

Traditional: age, gender, smoking, DM, HTN, dyslipidemia

Non-traditional: malnutrition, uremic toxins, inflammation, oxidative stress, vascular calcification

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16
Q

CVD in CKD: HTN

A 
cause & complication of CKD
Goals of therapy:
1. lower bp
2. reduce risk of CVD
3. slow progression

Multiple interventions
- smoking cessation
DM & dyslipidemia management
- dietary & lifestyle modifications

Recommendation:
BP < 140/90 (no proteinuria; albumin excretion <30mg/24h)
BP < 130/80 (proteinuria; albumin excretion >30mg/24h)
ACEi/ARB (reduce BP, proteinuria, slow progression of CKD, prevent CVD events)
*avoid combi ACEi + ARB

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17
Q

CVD in CKD: HTN (side effects of ACEi & ARBs)

A
  1. Hypotension
  2. Worsening kidney function
  3. Hyperkalemia (more common with ACEi)
  4. Cough
  5. Angioneurotic edema
18
Q

AntiHTN agents: ACEi & ARBs

A
  • continued if increase in SCr < 25-30% from baseline value
  • continued if serum K <= 5.5 mmol/L

SHOULD NOT BE USED:
ACEi: pregnancy, history of angioedema, cough due to ACEi, allergy

ARB: allergy, pregnancy, cough due to ARB

19
Q

AntiHTN agents: Diuretics

A
  • Reduce extracellular vol
  • Lower BP
  • Used w ACEi, ARB
  • Thiazide-type diuretic in all patients
  • Excessive diuresis –> worsening renal function
20
Q

AntiHTN agents: Beta blockers

A

Atenolol, bisoprolol - undergo renal elimination

21
Q

AntiHTN agents: CCBs - DHP / non DHP

A

DHP: SE: peripheral edema, flushing, HA

Less potent BP reduction but can reduce proteinuria

22
Q

AntiHTN agents: Direct acting vasodilators

A

SE: fluid retention, tachycardia

23
Q

AntiHTN agents: alpha-blockers

A

good for pts with BPH, SE: postural hypotension

24
Q

CVD in CKD: Dyslipidemia

A
  • increased risk for CVD
  • common complication esp pts with nephrotic syndrome
  • some pts may present with low serum cholesterol
  • high & low LDL increase mortality risk in CKD
  • as eGFR declines, magnitude of excess risk with increased LDL decreases –> LDL levels not used to determine if CKD pts should receive statin therapy

**When CrCl is < 30ml/min (stage 4/5), fibrates are contraindicated

25
Q

Lipid Management in CKD

A
  • Adults > 50 yo with eGFR<60 (non-dialysis/transplant) –> statin/statin + ezetimibe
  • Adults > 50 yo with eGFR>60 –> statin
  • **for adults on dialysis, statins/statin+ezetimibe not recommended
  • if already receiving statins/statins+ezetimibe at time of dialysis can continue
  • adult kidney transplant pt should receive statin
  • CKD (dialysis/transplant) & hypertriglyceridemia –> fibrates not recommended, TLC
  • statins CI in pregnancy, use non-pharm/omega 3
26
Q

Lipid Management in CKD

A

DDI:

  • macrolide antibiotics
  • cyclosporine
  • colchicine
  • amlodipine (+ simvastatin)
  • grapefruit juice

Fibrates not recommended

  • unless pt have v high fasting TG (>11.3)
  • Gemfibrozil preferred
  • Fenofibrate associated w elevated SCr
27
Q

Other CV complications from dyslipidemia

A
  • CHF
  • Atherosclerosis
  • Vascular calcification
  • Pericarditis –> req dialysis
28
Q

Fluid & Electrolyte Abnormalities (Water)

A
  • gradual narrowing in upper & lower limits of water excretion –> excess water intake: fluid retention, rapid reduction of water intake: vol depletion
  • urine output decrease –> edema
  • diuretic therapy to control edema/fluid overload/HTN
29
Q

Fluid & Electrolyte Abnormalities (Sodium) 135-150mmol/L

A

CKD pt unable to adjust rate of Na excretion

  • net Na retention –> increased intravascular vol, circulatory overload, edema, HTN, CHF
  • Na restriction necessary: <2g of Na/day (1 teaspoon salt)
30
Q

Fluid & Electrolyte Abnormalities (Potassium) 3.5-5 mmol/L

A
  • freely filtered at glomerulus, reabsorbed at proximal tubule, LOH, secreted into urine
  • after ingestion of K –> shifting of extracellular K into cells, increased distal tubular K secretion, increased K excretion in colon, increased renal excretion of K
  • as GFR decreases, renal excretion of K impaired –> hyperkalemia
31
Q

Other potential causes of hyperkalemia

A
  • metabolic acidosis
  • catabolic states
  • dietary indiscretion
  • salt substitutes
  • administration of stored blood
  • sudden decrease in urine output
  • drug eg. penicillin, beta-blockers, succinylcholine, ACEi/ARBs
32
Q

Clinical presentation of hyperkalemia

A
  1. Neuromuscular –> initial increase in excitability of neural/muscle cell membranes then decrease
    - muscle weakness: lower extremities then trunk, upper extremities & muscles of respiration
    - initial muscle twitching >6.5mmol/L
    - end result: muscle paralysis & areflexia
  2. Cardiovascular
    - Sustained depolarization of conduction system
    - Cardiac disturbances observed when levels > 7-7.5 mmol/L
    - S&S: bradycardia, hypotention, VF
    - EKG changes: peaked T waves, widened ARS interval
33
Q

Management of Hyperkalemia (1)

A
  • Dietary restriction
  • drug causes
  • Calcium gluconate (shifting of K from extracellular to intracellular to remove amt of K in the blood directly) –> antagonise effects on heart, used when dangerous EKG abnormalities, given IV when K>6.5 & peaked T waves
  • ———- CI: hypercalcemia & high/toxic digoxin conc
  • Sodium polystyrene sulfonate (Resonium) (remove K from the body)
  • —- K-Na exchange resin, each g of resin binds 1 mmol of K in exchange for Na, given PO/rectally
  • —– SE: constipation/diarrhea, Na overload, GI necrosis
  • do not take with fruit juice
34
Q

Management of Hyperkalemia (1)

A
  • Glucose & insulin (shift K intracellularly)
  • Beta2-adrenergic agonist: shift K intracellularly, IV, SE: tachycardia
  • Sodium bicarb: shift K intracellularly, IV, useful for severe metabolic acidosis
  • Patiromer: exchange Ca for K in gut, increase K excretion, SE: GI, hypoMg
  • SZC: exchange Na & H for K, increase K excretion, SE: edema, drug interactions
  • Dialysis: remove K from body
35
Q

Uric Acid in CKD

A
  • renal excretion of uric acid is impaired
  • hyperuricemia can be cause/consequence of CKD
  • xanthine oxidase inhibitors (allopurinol, febuxostat), colchicin short course of oral steroids may be indicated
  • uricosuric agents (probenecid, benzbromarone) generally ineffective
  • avoid NSAIDs, take steroids instead
36
Q

Mg in CKD

A
  • renally excreted
  • hypermagnesemia –> reduced neuromuscular activities
  • avoid Mg-containing medications (eg. laxatives, antacids, multivitamins)
37
Q

Metabolic Acidosis in CKD

A
  • decr H+ excretion –> decr pH & serum bicarb
  • decr NH3 excretion
  • decr PO4 excretion
  • retention of SO4
  • CaCO3 released from bone to buffer excess H+
  • reduction in serum bicarb (22-26 mmol/L), compensatory fall in pCO2 & decrease in arterial pH
  • anorexia, nausea, lethargy
38
Q

Management of metabolic acidosis

A
  • alkalinizing salts to replenish bicarb stores
  • initiated when CO2 < 20-22 mmol/L
  • —– sodium bicarb (PO/IV):
  • —– citrate/citric acid prep (req liver metabolism to bicarb, CO2, water)
  • —– use higher conc of bicarb/acetate for dialysis pt
  • —– SE: metabolic alkalosis, lethargy/cardiac depression, GI distress
39
Q

Malnutrition

A
  • protein-energy malnutrition common in pt w advanced CKD (low serum albumin)
  • Causes: poor dietary intake, loss of nutrients from dialysis, hypercatabolism, blood loss
40
Q

Protein req for malnutrition

A
  • lower in predialysis pt due to dietary restrictions + inability to excrete nitrogenous wastes
  • higher in dialysis pt due to protein loss from dialysis
  • maintain adequate amt of energy for optimal utilization –> recommended 25-35 kcal/kg/day
  • water soluble vitamins are low –> dialyzed out; low dietary intake, supplementation with renal vitamins
41
Q

Vitamins in malnutrtition

A
  • increased amt of vit A & E in ESRD
  • low vit D
  • iron & zinc deficiency
  • Al overload
  • use enteral feeds if inadequate PO intake
  • total parenteral nutrition (TPN)/intradialytic parenteral nutrition (IDPN)

PR2135 (2 decks)

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