Renal Disease Flashcards
What are causes of Renal Disease?
- 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
What are features of chronic renal disease?
- 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
What are features of Acute Renal Disease?
- Rapid (hours/days) onset of kidney failure caused by injury or illness.
- Usually reversible
- Potentially fatal
What is the definition of Chronic Kidney Disease?
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
What are risk factors/causes of Chronic Kidney Disease?
- Diabetes Mellitus
- CVD
- Smoking
- Hypertension
- Obesity
- Multisystemic disease such as SLE
- Structural renal disease/ Renal stones
- Family history
- Ethnicity
- Age
How does Chronic Kidney Disease present?
Asymptomatic in early stages
- Uraemic syndrome
- Progressive weakness, fatigue, loss of appetite, nausea, vomiting, tremors, altered mental function
- Nocturia,polyuria
- Pain
- Oedema.
What are some biochemical findings for CKD?
- 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)
What are renal causes, clinical features of each Biochemical finding in CKD?
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
How is Chronic Kidney Disease investigated and diagnosed?
- 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
What are investigations for CKD?
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.
How is the classification of Chronic Kidney disease derived?
Based on eGFR and albumin:creatinine ratio (ACR)
When is the eGFRcystatinC used?
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.
When should patients not be diagnosed with Chronic Kidney disease?
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.
Describe the progression of Chronic Kidney Disease worsen CKD?
- 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
What increases risk of CKD progression?
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
How is Chronic Kidney Disease managed?
No cure
Primary aim to:
- Manage/treat complications
- Slow progression
- Rzeduce risk of co-morbidities – CVD
What are methods to manage chronic kidney disease?
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
What is the laboratory monitoring of Chronic Kidney disease?
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
What is Acute Kidney injury?
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
What is the classification of Acute Kidney Injury?
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
What are risk factors for Acute Kidney Injury?
- Age
- Albuminuria
- Hypovolaemia/Hypotension
- Medication/Iondinated contrast
- Sepsis/Infection
- Previous AKI
- Liver Disease
- CKD
- Congestive Cardiac Failure
- Diabetes Mellitus
What are causes of Pre-Renal Acute Kidney Injury?
Pre-renal (inadequate blood supply)
- Hypovolaemia: Haemorrhage, Diuresis, GI fluid loss, Burns, Dehydration
- Reduced cardiac output: Heart failure
- Other: Sepsis, Vasodilatory drugs, ACEi
What are causes of Intrinsic Acute Kidney Injury?
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
What are causes of Post-Renal Acute Kidney Injury?
Post renal (urinary obstruction)
- Stones
- Bladder carcinoma
- Urethral stricture
- Prostate carcinoma
- Benign prostrate hypertrophy
What is the cause of Acute Tubular Necrosis?
Caused by ischaemia and nephrotoxins
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
What are biochemical features of Acute Kidney Injury?
- Increased urea/creatinine
- Hyponatraemia
- Hyperkalaemia
- Metabolic acidosis
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
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
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
What are symptoms suggesting acute on chronic disease?
- Anaemia
- Bone disease
- Skin disorders
- Neuropathy
- Sexual dysfunction
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
What are indicatons for commencing RRT?
- Hyperkalaemia
- Severe acidosis
- Uraemia
- Pulmonary oedema/neuropathy
- Stage 5 CKD
What are types of Renal Replacement Therapy?
- Haemodialysis
- Peritoneal dialysis
- Renal transplant
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)
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.
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.
How are complications of Renal Replacement Therapy monitored?
- Disequilibrium: U&E
- Anaemia: Hb, ferritin
- Malnutrition: Albumin, Prealbumin, Calcium, PO4, ALP, Mg, Aluminium
What are exclusions of Renal Replacement Therapy?
- Active malignancy
- Ischaemic Heart Disease
- Liver disease
- Peripheral vascular disease
- Obesity
- Substance abuse
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)
