Renal Disease Flashcards

1
Q

What are causes of Renal Disease?

A
  • Inflammatory: Infection, Drugs, Toxins, Autoimmune, Infiltration
  • Inherited: RTA, Polycystic kidney/tubulopathies
  • Metabolic Disease: Diabetes mellitus
  • Obstruction: Renal calculi, Carcinoma, Renal vein thrombosis

Affects any or all parts of the kidney (glomerular, interstitial, tubular and/or vascular

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2
Q

What are features of chronic renal disease?

A
  • Develops slowly (months/years)
  • Irreversible and Progressive. Loss of both glomerular and tubular function.
  • Leads to End Stage Renal Disease (ESRD)
  • Significant morbidity and mortality
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3
Q

What are features of Acute Renal Disease?

A
  • Rapid (hours/days) onset of kidney failure caused by injury or illness.
  • Usually reversible
  • Potentially fatal
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4
Q

What is the definition of Chronic Kidney Disease?

A

Abnormalities of kidney function or structure present for ≥3 months

  • Markers of kidney damage (albuminuria/haematuria/structural abnormalities)
  • and/or
  • GFR <60 ml/min/1.73 m2 on at least 2 occasions separated by a period of at least 90 days
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5
Q

What are risk factors/causes of Chronic Kidney Disease?

A
  • Diabetes Mellitus
  • CVD
  • Smoking
  • Hypertension
  • Obesity
  • Multisystemic disease such as SLE
  • Structural renal disease/ Renal stones
  • Family history
  • Ethnicity
  • Age
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6
Q

How does Chronic Kidney Disease present?

A

Asymptomatic in early stages

  • Uraemic syndrome
  • Progressive weakness, fatigue, loss of appetite, nausea, vomiting, tremors, altered mental function
  • Nocturia,polyuria
  • Pain
  • Oedema.
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7
Q

What are some biochemical findings for CKD?

A
  • Increased serumurea/creatinine
  • Hyponatraemia
  • Hyperkalaemia
  • Metabolic acidosis
  • Hyperphosphataemia
  • Hypocalcaemia
  • Glucose metabolism (Impaired glucose tolerance, Decreased insulin)
  • Lipid metabolism (Increased in triglycerides, Decreased HDL, Cardiovascular effects)
  • Protein metabolism (Patients are catabolic – protein loss)
  • Red cell production (Normocytic, normochromic anaemia,Decreased erythropoietin)
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8
Q

What are renal causes, clinical features of each Biochemical finding in CKD?

A

Increased serum urea/creatinine

  • Renal Cause: Reduced GFR
  • Clinical Feature: Uraemic syndrome

Hyponatraemia

  • Renal Cause: Reduced GFR (sodium retention), Reduced tubular function (sodium loss, inability to concentrate or dilute urine)
  • Clinical Features: Risk of over/under hydration, Polyuria/nocturia

Hyperkalaemia

  • Renal Cause: Reduced GFR
  • Clinical Features: Cardiac arrythmias, Cardiac arrest

Metabolic acidosis

  • Renal Cause: Reduced H ion excretion (GFR and reduced PO4 excretion), Reduced tubular function (bicarb reabsorption)
  • Clinical Features: Acidosis

Hyperphosphataemia

  • Renal Cause: Reduced GFR
  • Clinical Features: Renalosteodystrophy

Hypocalcaemia​

  • Renal Cause: Reduced 1,25 –vitamin D. (1a hydroxylase)
  • Clinical Features: Renalosteodystrophy
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9
Q

How is Chronic Kidney Disease investigated and diagnosed?

A
  • Non specific symptoms
  • Often diagnosed when in advanced stage – increased mortality and morbidity
  • Early diagnosis – slow progression / reduce number progressing to ESRD.
  • Screening of at risk populations – DM, CVD, hypertension, multisystemic disease (SLE), family history, nephrotoxic drugs.
  • Incidental finding – proteinuria and/or haematuria
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10
Q

What are investigations for CKD?

A

eGFR

  • Use the CKD-EPIcreat equation - previously most labs reported MDRD.
  • Use specific creatinine assays (enzymatic)
  • Advise people not to eat meat in the 12 hours before having a blood test for creatinine/eGFR.

Proteinuria

  • Use urine ACR in preference to PCR, if the ACR = 3 - 70 mg/mmol, confirm by a subsequent EMU. If the initial ACR ≥70 mg/mmol, repeat not required.

Other Markers

  • Urine sediment abnormalities,
  • Electrolyte and other abnormalities due to tubular disorders,
  • Abnormalities detected by histology,
  • Structural abnormalities detected by imaging, Ultrasound
  • History of kidney transplantation.
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11
Q

How is the classification of Chronic Kidney disease derived?

A

Based on eGFR and albumin:creatinine ratio (ACR)

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12
Q

When is the eGFRcystatinC used?

A

Consider using eGFRcystatinC at initial diagnosis to confirm or rule out CKD in people with:

  • eGFRcreatinine of 45–59 ml/min/1.73 m2, sustained for at least 90 days and
  • no proteinuria ACR<3 mg/mmol) or other marker of kidney disease.
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13
Q

When should patients not be diagnosed with Chronic Kidney disease?

A

Do not diagnose CKD in people with:

  • An eGFRcreatinine of 45–59 ml/min/1.73 m2 and
  • An eGFRcystatinC of more than 60 ml/min/1.73 m2 and
  • No other marker of kidney disease.
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14
Q

Describe the progression of Chronic Kidney Disease worsen CKD?

A
  • Kidney has a large reserve capacity. 50-60% loss of functioning kidney before symptom/biochemical abnormalities seen.
  • Adapts by hyperfiltration of remaining functioning nephrons
  • Hyperfiltration causes glomerular damage.
  • Initates an inflammatory response: Cellular infiltration and T-cell activation, Fibroblast activity increased leading to ECM synthesis – renal fibrosis, Disruption to renal blood flow which causes ischaemic damage
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15
Q

What increases risk of CKD progression?

A

Risk of progression:

  • ↑ACR
  • ↓eGFR
  • CVD, ­↑BP, DM, smoking, AKI, NSAIDs, ethnicity

Increased risk of progression to end stage kidney disease if they have either:

  • A sustained decrease in GFR of 25% or more over 12 months or
  • A sustained decrease in GFR of 15 ml/min/1.73 m2 or more over 12 months
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16
Q

How is Chronic Kidney Disease managed?

A

No cure

Primary aim to:

  • Manage/treat complications
  • Slow progression
  • Rzeduce risk of co-morbidities – CVD
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17
Q

What are methods to manage chronic kidney disease?

A

Dietary

  • Low Sodium, potassium intake
  • Phosphate binders
  • Protein restriction
  • Adequate energy intake - catabolic
  • Adequate fluid intake

Bone Disease

  • 1α vitamin D/Calcium
  • Bisphosphanates

Anaemia

  • Recombinant EPO

Hyperlipidaemia

  • Statins

Hypertension

  • Antihypertensive drugs - ACEi/ARB/Diuretics

Diabetes

  • Metformin

Lifestyle Changes

  • Smoking
  • Weight
  • Physical Activity
18
Q

What is the laboratory monitoring of Chronic Kidney disease?

A

eGFR

  • Monitor according to classification. Also consider:
  • past patterns of eGFR and ACR (but be aware that CKD progression is often nonlinear)
  • comorbidities, especially heart failure
  • changes to their treatment
  • intercurrent illness
  • whether they have chosen conservative management.

Calcium, phosphate, PTH in stages G4 and G5

Hb in stage G3b, G4 and G5

U&E – fluid balance, potassium, bicarbonate

Lipids

19
Q

What is Acute Kidney injury?

A

Must have ONE of the following criteria:

  • Serum creatinine rises by ≥ 26µmol/L within 48 hours
  • Serum creatinine rises ≥ 1.5 fold from the reference value*, which is known or presumed to have occurred within one week
  • Urine output is < 0.5ml/kg/hr for >6 consecutive hours

*reference value = lowest creatinine value recorded within 3 months of the event. If a reference value is not available within 3 months and AKI is suspected repeat serum creatinine within 24 hours

20
Q

What is the classification of Acute Kidney Injury?

A

Stage 1

  • SCr: Increase ≥ 26 μmol/L within 48hrs or Increase ≥1.5 to 1.9 X reference SCr
  • UOC: <0.5 mL/kg/hr for > 6 consecutive hrs

Stage 2

  • SCr: Increase ≥ 2 to 2.9 X reference SCr
  • UOc: <0.5 mL/kg/ hr for > 12 hrs

Stage 3

  • SCr: Increase ≥3 X reference SCr or increase ≥354 μmol/L or commenced on renal replacement therapy (RRT) irrespective of stage
  • UOc: <0.3 mL/kg/ hr for > 24 hrs or anuria for 12 hrs
21
Q

What are risk factors for Acute Kidney Injury?

A
  • Age
  • Albuminuria
  • Hypovolaemia/Hypotension
  • Medication/Iondinated contrast
  • Sepsis/Infection
  • Previous AKI
  • Liver Disease
  • CKD
  • Congestive Cardiac Failure
  • Diabetes Mellitus
22
Q

What are causes of Pre-Renal Acute Kidney Injury?

A

Pre-renal (inadequate blood supply)

  • Hypovolaemia: Haemorrhage, Diuresis, GI fluid loss, Burns, Dehydration
  • Reduced cardiac output: Heart failure
  • Other: Sepsis, Vasodilatory drugs, ACEi
23
Q

What are causes of Intrinsic Acute Kidney Injury?

A

Intrinsic Acute Kidney Injury

  • Glomerular: Glomerularnephritisis, ANCA vasculitis, SLE, Cryoglobulinaemia
  • Tubular: Nephrotoxins (ACEi, NSAIDS, antibiotics, amphotericin), Sarcoidosis, Ischaemia, Infection (pyelonephritis)
  • Contrast media
  • Poisoning
  • Rhabdomyolyis
  • Hepatorenal syndrome
24
Q

What are causes of Post-Renal Acute Kidney Injury?

A

Post renal (urinary obstruction)

  • Stones
  • Bladder carcinoma
  • Urethral stricture
  • Prostate carcinoma
  • Benign prostrate hypertrophy
25
Q

What is the cause of Acute Tubular Necrosis?

A

Caused by ischaemia and nephrotoxins

26
Q

What are symptoms/clinical features of Acute Kidney Injury?

A
  • Nausea/Vomiting
  • Cardiac Arrhythmias/Arrest
  • Muscle Weakness
  • Oliguria/Anuria
  • Oedema/Ascites/Pleural Effusion
  • Loss of consciousness
27
Q

What are biochemical features of Acute Kidney Injury?

A
  • Increased urea/creatinine
  • Hyponatraemia
  • Hyperkalaemia
  • Metabolic acidosis
28
Q

How is AKI diagnosed?

A
  • Diagnosis based on serum creatinine and urine output

Laboratory tests:

  • U&E including bicarbonate
  • Blood gases
  • Urinalysis – protein/Hb, Urine sodium, Urine/serum osmolality
  • Creatine kinase
  • BJP/serum electrophoresis
  • Blood / urine cultures
  • Virology
  • Auto antibodies (ANCA, Anti-GBM)

Imaging:

  • Ultrasound
  • CT
  • Chest x-ray
  • Renal angiography
  • Kidney biopsy
  • ECG
29
Q

What do investigations for Pre-Renal AKI show?

A

Pre-renal: (tubular function intact)

  • Increased serum urea/creatinine. Urea > creatinine
  • No proteinuria
  • Normal response to hypovolaemia – sodium and water retention
  • Urine sodium <20 mmol/L
  • Urine:Plasma Osmolalilty > 1.5 : 1
30
Q

What do investigations for Intrinsic AKI show?

A

Intrinsic

  • Increased urea/creatinine in proportion
  • Proteinuria
  • Sodium and water loss
  • Urine sodium >40 mmol/L
  • Urine:Plasma Osmolalilty > 1.1 : 1
31
Q

What are symptoms suggesting acute on chronic disease?

A
  • Anaemia
  • Bone disease
  • Skin disorders
  • Neuropathy
  • Sexual dysfunction
32
Q

How is AKI treated and managed?

A
  • Rapid diagnosis – identify and test patients at risk
  • ? Pre-renal / Post renal / intrinsic/?chronic
  • Hydration - Give fluids
  • Stop nephrotoxic drugs
  • Nephrology referral
  • Biochemical monitoring – U&E, fluid balance charts
  • Remove any obstruction / catheterise
  • Treat metabolic complications – hyperkalaemia
  • Treatment of underlying cause
  • Renal failure - RRT
33
Q

What are indicatons for commencing RRT?

A
  • Hyperkalaemia
  • Severe acidosis
  • Uraemia
  • Pulmonary oedema/neuropathy
  • Stage 5 CKD
34
Q

What are types of Renal Replacement Therapy?

A
  • Haemodialysis
  • Peritoneal dialysis
  • Renal transplant
35
Q

How is Haemodialysis conducted?

A

Home or hospital based

Regimens:

  • 3x weekly (3-5hrs)
  • Daily (2-3hrs)
  • O/N

Clearance based on principles of diffusion and ultrafiltration (negative hydrostatic pressure & osmosis)

36
Q

How is Peritoneal Dialysis conducted?

A
  • Continuous ambulatory peritoneal dialysis (CAPD).
  • Uses peritoneal membrane to exchange solutes. Dialysis fluid contains glucose/icodextrin as osmotic agent
  • Regimen – x4 2L per day
  • Automated PD (APD)
  • Simpler than HD, less restrictive. Risk of peritonitis, not as effective as HD.
37
Q

How is adequacy of Renal Replacement Therapy monitored?

A
  • Pre and Post dialysis serum urea
  • PD fluid urea
  • Creatinine clearance
  • PET (peritoneal equilibration test) - plasma & dialysilate fluid creatinine & glucose.
38
Q

How are complications of Renal Replacement Therapy monitored?

A
  • Disequilibrium: U&E
  • Anaemia: Hb, ferritin
  • Malnutrition: Albumin, Prealbumin, Calcium, PO4, ALP, Mg, Aluminium
39
Q

What are exclusions of Renal Replacement Therapy?

A
  • Active malignancy
  • Ischaemic Heart Disease
  • Liver disease
  • Peripheral vascular disease
  • Obesity
  • Substance abuse
40
Q

What is the role of the laboratory in Renal Transplant?

A
  • Pre-op: assess recipient to exclude those at risk of perioperative
  • Mortality: U&E, LFT, glucose, CRP, FBC, virology screen.
  • Tissue typing/blood group compatibility
  • Post-op: Graft rejection (U&E, evidence of acute renal failure), Immunosuppressant monitoring (tracrolimus/cyclosporin/sirolimus)