Renal Disease Flashcards
(40 cards)
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
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
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
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
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
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.
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)
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
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
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.
11
Q
How is the classification of Chronic Kidney disease derived?
A
Based on eGFR and albumin:creatinine ratio (ACR)
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.
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.
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
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
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
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
What is the cause of Acute Tubular Necrosis?
Caused by ischaemia and nephrotoxins
26
What are symptoms/clinical features of Acute Kidney Injury?
* Nausea/Vomiting
* Cardiac Arrhythmias/Arrest
* Muscle Weakness
* Oliguria/Anuria
* Oedema/Ascites/Pleural Effusion
* Loss of consciousness
27
What are biochemical features of Acute Kidney Injury?
* Increased urea/creatinine
* Hyponatraemia
* Hyperkalaemia
* Metabolic acidosis
28
How is AKI diagnosed?
* **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
What do investigations for Pre-Renal AKI show?
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
What do investigations for Intrinsic AKI show?
Intrinsic
* Increased urea/creatinine in proportion
* Proteinuria
* Sodium and water loss
* Urine sodium \>40 mmol/L
* Urine:Plasma Osmolalilty \> 1.1 : 1
31
What are symptoms suggesting acute on chronic disease?
* Anaemia
* Bone disease
* Skin disorders
* Neuropathy
* Sexual dysfunction
32
How is AKI treated and managed?
* 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
What are indicatons for commencing RRT?
* Hyperkalaemia
* Severe acidosis
* Uraemia
* Pulmonary oedema/neuropathy
* Stage 5 CKD
34
What are types of Renal Replacement Therapy?
* Haemodialysis
* Peritoneal dialysis
* Renal transplant
35
How is Haemodialysis conducted?
**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
How is Peritoneal Dialysis conducted?
* 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
How is adequacy of Renal Replacement Therapy monitored?
* Pre and Post dialysis serum urea
* PD fluid urea
* Creatinine clearance
* PET (peritoneal equilibration test) - plasma & dialysilate fluid creatinine & glucose.
38
How are complications of Renal Replacement Therapy monitored?
* **Disequilibrium:** U&E
* **Anaemia:** Hb, ferritin
* **Malnutrition:** Albumin, Prealbumin, Calcium, PO4, ALP, Mg, Aluminium
39
What are exclusions of Renal Replacement Therapy?
* Active malignancy
* Ischaemic Heart Disease
* Liver disease
* Peripheral vascular disease
* Obesity
* Substance abuse
40
What is the role of the laboratory in Renal Transplant?
* **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)
