Learning objectives: Renal Flashcards
Learning Objectives: Renal
Renal function:
What is urea? What is it a indicator od?
DDX Decreased urea?
Increased urea DDx - List 6 causes 3 marks
What is creatinine? Why is a good indicator of renal function:
What is
What are the stages of renal disease: Stage 1-5
Write out stages in accordance with impairment and eGFR
How can osmolality be measured?
What is Urea:creatinine ratio? Why is it important?
List 3 causes from each catergory and expected U+Cs? Pre-renal, renal, post renal.
What else can decrease the ratio?
What is normal urine pH?
What is urine specific gravity represents? List 2 causes of low specific gravity? List 2 causes of high urinary specific gravity
What is urine osmolality? High? Normal?
Protienuria DDx: List 4 causes: Renal? CV? Pregnancy? Drugs?
Nitrites & WBC/leukocytes esterase- causing of an increase in urinary dipstick? give 2
Hameturia:- List DDx- Pre renal, renal, post renal -
What are causes of increased ketones in urine? list 3 1.5 marks
What is bilirubin? Wgat are causes of an increased conjugated bilirubin? Pre hepatic? hepatic, post-hepatic?
What is urobilinogen? When is it evevated? when is it decreased?
Proteinuria: What does it meausre?
What are indication for testing proteinuria?
DDx for protienuria: Renal - list 4 causes? list 4 other causes?
What is Albumin creatining ratio? What is it an indicator of?
Electrolyte: Overview:
How should you correct fluids and electrolytes
What are broad syustems which can affect electrolyte balance? Just read:
What is third space loss? What are examples of these?
Outline different common fluids:
What are limitations of normal saline?
Hartmans? Lactated ringers? Dextrose solutions
What is hyponatraemia?
List 5 causes: Renal? endocrine? GIT and Loss? Skin? 3rd spacing?
Euvolemic hyponatraemia? Hypervolemic hyponatraemia (dilutional)
Clinical features: List 4 (think cerebral oedema) - 2 marks, MSK- 1 mark? Complications? list 2
Investigation? +findings and importance ?
Management of hyponatremia? (why is it rarely treated with aggressive fluids)
How do you manage SIADH?
What is hypernatremia? What is it caused by? list 3 common causes?
What is REGS? What are caises of excessive Na load? (e.g hyperaldosteronism)
Clinical features? List 4
Asssessment? WHat should it include?
Investigation: And importance and findings?
Management? What are precautions to be taken when replacing fluids?
What is hyperkalemia? What are mechanisms that cause it? (increased intake, increased production, shifts, decreased excretion) List 2 from each
Symptoms/clinical features of hypokalemia? List 4 ; 2 marks
ECG findings in hyperkalemia? (2 mark)
Management strategies for hyperkalemia: 3 marks - non-pharm? mostly medical management
Hypokalaemia: What are 3 most common causes:
REGS- ?
Symptoms/clinical features? List 4 - 2 marks
ECG findings in hypokalaemia? list 4 features
Management principles: 3 marks: Non-pharm (think monitoring)
What are 5 causes of hypocalcemia? Renal? endocrine? GI?
What are 4 clinical signs of hypocalcemia? What is the first common clinical sign (2.5 marks) What are two specific MSK signs for hypocalcemia?
CNS features?
ECG? 0.5 marks
Management? 1 mark
What are 2 most common causes for hypercalcemia?
Symptoms? BSGMP?
ECG features?
Acute management? 2 marks
What relationship does magnesium, potassium and calcium have in terms of electrolyte balances:
What relationship does magnesium, potassium and calcium have in terms of electrolyte balances
Hyperphosphatemia?
Hypermagnesemia? Hypomagnesemia?
Outline steps needed to work out cause of hyponatremia:
What is SIADH? Patho? Diagnosis? What are common causes?
Dddx?
Management?
What is an AKI? Define: 0.5 marks
List 4 limitation of eGFR?
Most common causes of AKI? List 4 - 2 mark
Risk factors? list
Aetiology: Pre-renal? Renal? Post renal : list 2 causes from each - 3marks
Clinical features- Symptoms: list 4 - 2 marks
What are key questions on history to ask? (think DDx)
Examination findings: List from whole exam: VS? Monitoring? Fluid status assessment ? Skin? CVS? Lungs? abdo? peripheries?
First line investigations - list 4 ; 2 marks
Diganosis? (different definition)
Management: General. Specifics, monitoring, ongoing investigations? Specific investigations?
Acute Kidney Injury
Acute kidney injury (AKI) is an acute reduction in renal function (within 48 hours) as measured by an increase in serum creatinine, decrease in urine output, and/or need for renal replacement therapy.
- Normal Adult urine output ≥0.5mL/kg/hr
Epidemiology:
- Risk factors – Pre-existing CKD, increasing age, male sex.
- Most common causes:
- Sepsis
- Major surgery
- Shock – cardiogenic, hypovolaemic
- Drugs
- Hepatorenal syndrome
- Obstruction.
Aetiology:
- Pre-renal: ↓ perfusion of kidneys (60%)
- Hypovolaemia – Haemorrhage, Diarrhoea/vomiting, burns, pancreatitis.
- Hypotension – Cardiogenic shock, MI, Haemorrhage
- Renal Vasoconstriction or stenosis – NSAIDs (constriction of afferent), ARB/ACEi (dilation/prevents constriction of efferent), hepatorenal syndrome
- Renal: intrinsic renal disease (30%)
- Glomerulonephritis, acute tubular necrosis (prolonged hypoperfusion causing intrinsic, renal damage, or toxins), vasculitis, infiltration (e.g. sarcoidosis).
- Post-renal: obstruction to urine (10%
- BPH/Prostatic Ca., Renal calculi, Bladder cancer, UTI, prolonged incorrect catheterisation.
Clinical Features:
Mild-to-moderate acute kidney injury can have no symptoms at all. Severe cases are symptomatic
Sign/Symptom
Pathophysiological Explanation
Abnormal urine output
- Anuria
- Oliguria
- Polyuria
Oedema
Weight gain
Confusion
Lethargy
Fatigue
History / Key questions:
- Hx of V/D, haemorrhage, shock => Systemic volume depletion
- Trauma/immobilisation => Rhabdomyolysis
- Fever, maculopapular erythematous rash, and arthralgias => acute interstitial nephritis
- Flank pain and history of kidney stones.
- Dysuria, suprapubic pain, slow urine stream, increased frequency of urination = Lower urinary tract disease
- Medication history = Most important.
Examination:
- BP
- Daily weights
- Fluid status assessment
- JVP
- Mucosal membranes, CAP, skin turgor
- Skin examination – many causes associated with rashes
- CVS examination – CCF, ?source of emboli, endocarditis.
- Lungs –CCF & pulmonary renal syndrome.
- Abdo – masses, vascular disease, liver disease
- Peripheries – oedema, distal pulses, muscle tenderness (rhabdomyolysis), arthritis
Investigations:
- FBC
- EUC – Decreased GFR
- Blood urea nitrogen – Increased
- Creatinine – Increased
- Urinalysis
Diagnosis:
Diagnose acute kidney injury in patients with any of the following:
- Increase in serum creatinine by ≥ 0.3 mg/dL (≥ 26.5 mcmol/L) within 48 hours
- Increase in serum creatinine to ≥ 1.5 times baseline, which is known or presumed to have occurred within prior 7 days
- Urine volume < 0.5 mL/kg/hour for 6 hours
Management:
Summary:
- Stop exposure to nephrotoxic agents if possible
- Identify and treat any infectious cause
- Monitor and adjust fluid and electrolyte balance to address volume depletion or overload, hyponatraemia, hyperkalaemia, hyperphosphatemia, and hypermagnaesemia
- Reserve diuretics for patients with volume overload
Expanded:
- Monitoring
- Fluid balance (catheter + hourly urine output).
- Give IV fluids if hypovolaemic: 500mL crystalloid over mins (Hartmann’s, Plasma-Lyte, Ringers lactate)
- Give crystalloid not normal saline to avoid hyperchloraemic acidosis).
- If Hypervolaemic (fluid overloaded), give O2, restrict fluids, give diuretics
- Give IV fluids if hypovolaemic: 500mL crystalloid over mins (Hartmann’s, Plasma-Lyte, Ringers lactate)
- Monitor K+ for hyperkalaemia (VBG, ECG) → Tx: calcium gluconate, glucose, insulin, salbutamol. May require renal replacement/dialysis if severe
- Lactate for signs of sepsis
- Daily serum creatinine
- 4 hourly obs
- Investigations
- Bedside: ECG, urine dispstick
- Bloods: FBC, UECs, LFTs (hepatorenal syndrome), CMP, CRP .
- Ix for intrinsic renal disease → autoantibodies (ANCA, ANA, anti-GBM), ABG (acidosis)
- Imaging: US-KUB, CXR(pulmonary oedema in fluid overload
- Other – urinalysis, urine M/C/S
- Support
- Treat sepsis
- Cease nephrotoxic medications: SADMANs
- S sulfonylureas
- A ACE-inhibitors
- D diuretics
- M metformin
- A angiotensin receptor blockers
- N non-steroidal anti-inflammatory
- S SGLT2 inhibitors
- Avoid radiological contrast (nephrotoxic
- Correct acidosis (sodium bicarbonate)
- Renal replacement (haemodialysis or haemofiltration). Indicated if severe acidosis, persistent hyperkalaemia, uraemia, or fluid overloaded (unresponsive to medical treatment)
- In intrinsic renal disorders → biopsy kidney and refer to renal team
- In post-renal disorders → catheterise and refer to urology
AKI table:
AKI definitions:
DDx? Pre renal, renal, post renal:
Blood ure:creatinine ratio: useful in determining cause of AKI:
Principle? Pre-renal? renal? post renal?
Risk factors?
Pre-renal causes? Renal causes? Post renal causes: List 2 from each
Clincal features:
History: Look for pre-renal factors, look for ATN, look for GN factors, obstructive factors?
Exam: VOLUME status, What should be done to optimise measurement of urine output?
Investigation? Bedside?
Labs? Urine? Bloods? Specific diagnosis? Imaging?
Management of AKI:
1) Primary survery and resus”:
2) Address-life threats: Think do they need fluid, do they need restriction, think electrolytes, think blood gases?
3) Active management? Pre-renal, intrinsic, post-renal, haemodialysis
What are indications for haemodialysis: AEIOU
4) Supportive management?
5) Communication, safety net, follow-up and referral
What is acute tubular necrosis? What are they two types? What are causes?
Clinical featurs? What will be found on urinalysis? Patho:
What is characteristic of ATN on urinalysis?
What is Acute interstial nephritis? Eitology? Clinical features? Investigations?
What is analgesic nephropathy? Patho?
What is CKD?
Definition?
Epidemiology?
Presentation: List 5 symptoms? List examination +finding?
Screening? WHo and what?
Investigations? Bloods? Urine? Imaging?
What are conditions where eGFR may be unreliable?
What are other causes of increased ACR?
Chronic Kidney DIsease (CKD)
CKD is defined as the occurrence of kidney damage and/or reduced kidney function that lasts for three months or more.
It is defined as >3 months of either a GFR <60 mL/minute/1.73m2 or other evidence of kidney damage including albuminuria, abnormal kidney structure detected by imaging, or a history of a renal transplant.
Epidemiology
- 1 in 10 adults have chronic kidney disease (N.B less than 10% are diagnosed)
- 1 in 3 adults are at risk.
- 1 in 1400 are on dialysis or living with transplant.
- Prognosis:
- 9th leading cause of death.
- CKD > DM as a risk factors of future coronary event and all-cause mortality
Aetiology
Most common causes of end stage kidney disease
- Diabetic kidney disease – 36%
- Glomerulonephritis – 19%
- Hypertensive vascular disease – 12%
- Polycystic kidney disease (pkd) – 5%
- Other – 28%
Presentation
- Up to 90% of kidney function may be lost prior to symptoms
- Stage 4-5 = most common time symptoms arise)
- Annual screening is essential.
- First symptoms:
- HTN
- Pruritis
- Nocturia, haematuria, proteinuria
- SOB, peripheral oedema
- N/V, anorexia, malaise, lethargy
- Examination
- BP & weight – Serial measurements
- Hydration & fluid status – peripheral & dependent oedema, lung bases, ascities.
Investigaitons:
Following screening the following investigations should be performed to assess for underlying and reversible causes of CKD.
- Bloods:
- Repeat (within 1 week) – UEC + RFTs
- Continued decrease in eGFR => AKI (most likely), and manage accordingly
- FBC, CRP, ESR
- Fasting lipids BSL, HbA1c
- Repeat (within 1 week) – UEC + RFTs
- Urine:
- ACR (preferably first morning void to minimise postural effects on albumin excretion, although random urine is acceptable.)
- M/C/S – microscopy for dysmorphic red cells, red cell casts or crystals.
- Renal USS
***Conditions where eGFR may be unreliable:
- Acute changes in kidney function – e.g. AKI
- Dialysis
- Recent consumption of cooked red meat (within 4hrs)
- High muscle mass (may underestimate eGFR)
- Severe liver disease
- Drugs interacting with creatinine excretion – fenofibrate, trimethoprim.
- Pregnancy
***Validity of eGFR in pregnancy is unknown. Serum Creatinine = GOLD standard.
Other causes of increased ACR:
- UTI
- High dietary protein intake
- CCF
- Acute febrile illness or heavy exercise (within 24hrs)
- Menstruation or vaginal discharge
- Drugs – especially NSAIDs.
What tests should be completed to workup cause of CKD? (need 3 things)
What are special tests to do if
1) Pt has signs of systemic disease (rash, features of CT disease, pulmonary symptoms, )
2) Risk factors - infectious disease
3) age>40 and myeloma possible cause
Outline management of CKD: Refer? Slow progression? treat complications? (list complications - 5 - 2.5 marks)? + management- 2.5 marks , Renal replacement?
GP management of CKD? Nutrition? fluid restrictions?referral?
What relationship does CKD and HTN have? What is the management?
When is referral to nephrologist indicated? What should be done in your pre-referral work-up?
Managment
Mx Summary:
- Refer to nephrology (CKD stage 4 – 5)
- Slow renal disease progression
- Tx HTN – ACEi/ARB
- Tx DM
- Smoking cessation, reduced Na+, K+, and protein diet
- Treat complications
- Anaemia → Iron / B12 / folate supplementation, EPO
- Acidosis → sodium bicarbonate
- Oedema → restrict sodium + fluids. High dose loop diuretic
- Osteoporosis (due to ↑ serum phosphate + ↓hydroxylation of vitamin D by kidneys)
- → measure CMP, PTH, and vit D levels.
- Restrict dietary phosphate (e.g. dairy products), give vitamin D supplement.
- If hyperparathyroidism, give calcitriol
- Restless legs / cramps → exclude IDA as a cause. Give sleep hygiene advice. Treat with magnesium
- CVD → increased risk of CVD in CKD due to HTN, vascular stiffness, inflammation, and abnormal endothelial function.
- Give antiplatelets, statins
- Infections(uraemia alters effectiveness of WBCs)
- Renal replacement therapy
- Dialysisis commenced when GFR is ~5–10mL/min
- Two main options: haemodialysis Vs peritoneal dialysis
- Register for renal transplantation
GP:
Absolute cardiovascular risk assessment is vital!
- Lifestyle intervention
- Pharmacotherapy – ACEi/ARB
Nutrition:
- eGFR >30 = Australian dietary guidelines.
- eGFR<30 = Special nutritional targets.
- Dietitian referral.
- Low protein diet – reduces urea levels.
- Low Na+, Low K+ diet
- Fluid restrictions – assess based on urine output.
CKD + Hypertension:
- First line – ACEi/ARBs (safe at all stages of CKD)
- Should be ceased during acute illness (increased risk of AKI)
- Recommence when condition stabilises.
- Second line
- Non-loop (e.g. thiazide) & loop diuretics = safe at all stages of CKD
- Frusemide = useful for managing fluid overload.
- OD up to 80mg PO; then split to BD to improve efficacy if required.
- In severe decompensated fluid overload IV albumin with IV frusemide chaser improves efficacy. Albumin binds frusemide and increases filtration in the kidney thus improving frusemide effectiveness.
- Frusemide = useful for managing fluid overload.
- ß-blockers = useful in people with CAD, tachyarrhthmias and CCF.
- CI = asthma and heart block
- CCBs = useful in people with angina & elderly with SBP hypertension.
- Non-loop (e.g. thiazide) & loop diuretics = safe at all stages of CKD
ACEi/ARB = renal protective, however eGFR may reduce in the first 2 months due to reversible reduction in glomerular blood flow.
- Reductions <25% = normal, therefore continue medications.
Reductions >25% = abnormal, cease medication and refer to nephrologist. - Caution if K+ ≥5.5mmol/L
- Early treatment & reduction in BP –> decrease CVD risk and ESKD progression by 50%
Indications for Nephrology Referral:
Anyone with rapidly declining eGFR and/or signs of acute nephritis (oliguria, haematuria, acute hypertension and oedema) should be regarded as a medical emergency and referred without delay.
- eGFR < 30 mL/min/1.73m2 (Stage 4 or 5 CKD of any cause)
- Persistent significant albuminuria (urine ACR ≥30 mg/mmol)
- A sustained decrease in eGFR of 25% or more OR a sustained decrease in eGFR of 15 mL/min/1.73m2 within 12 months
- Normal decline in CKD = 5 eGFR units per year.
- CKD with hypertension that is hard to get to target despite at least three anti-hypertensive agents
Pre-referral workup:
- Current blood chemistry and haematology
- Urine ACR and urine microscopy for red cell morphology and casts
- Urine culture not necessary on referral form – can be managed by GP, unless abnormal bacteria.
- Current and historical blood pressure
- USS KUB
CKD and medications:
What are 5 common nephrotoxics? 2.5 marks
What is a triple whammy? explain?
When should metformin be ceased?
Algorithm for intial detection of CKD:
Risk factors?
tests? How often?
How is then staged?
What should be done next?
Counseling CKD 5: Education? Transplant? Dialysis? PD vs HD
What is definiton of CKD?
Epidemiology Australia?
What is Azotaemia? What is Uraemia?
What is age related renal decline? What is the significance?
What are the 5 most common causes of CKD? list 2.5 marks
What are major causes in children?
How can you classify? (same as AKI) Pre-renal? Chronic rebal, chronic post renal
What are risk factors CKD? (think same as screening indications) List 5 - 2.5 marks
Pathogenesis of CKD: Loss of nephrons-
What relationship does CKD and minberal and bone denisty have? What does it result in? What is the disease called? What are complications of this?
What is renal osteodystrophy? How does this lead to secondary hyperparathyroidism?
CKD pathology: Gross? Microscopi?
Screening for CKD? Who is it recommended for?
What does screening test involve? 1.5 marks?
What do this tests indicated? Management dependant on staging
Staging of CKD (colour coding)
What are limitations eGFR?
What conditions are classified as CKD even with normaleGFR and albumin?
Clinical features of CKD: list 6 classic symptoms:
Fetaures based on causes:
Uraemic symptoms: List 4
Anaemia of CKD? When?
FLuid overload?
Electolyte & pH abnormalites?
sexual?
Urinary?
Complications: List 4 ; think from each disturbances?
Assessment of CKD:
History: HPC, PmHX, Social, family hx.
Examination: Use? General? Vital signs? hands? Arms? Eyes? Mouth? Neck? Chest? Abdo? Back? Legs? (list a fetaure from each)
Other exams? List 4: and why?
Distinguishing AKI vs CKD
CKD features? (imaging, US and symptoms)
ARF features?
What investigations should be done in a newly diagnosed CKD patient?
Bedside? (1 mark +findings)
Urine sample tests:
Urine tests? List 3 and expected finding
What are expected findings in various renal conditions: READ!
Bloods and expected findings: FBC, U+Ecs, ALP? (secondary hyperparathyroidism) PTH levels, fasting lipids and glucose
Imaging: USS KUB - essential, other images?
Biopsy?
Creatinine vs GFR in CKD:
What are long term management prinicples for CKD: (e.g what investigations, active management, actively manage CV risk, lifestyle, BP management, statin, Management, lifestyle, prescriptions, DM optimization:
Treat complications:
Fluid overload? Proteinuria? Electrolytes? HAGMA? Renal osterodystrophy? Anemia of CKD?
Ongoing monitoring? Frequency depends on what? Assessing how often and what?
When should you refer to nephrologist?
Renal replacement therapy:
Indications for diaylsis: AEIOU
What about CKD?
What are types of renal replacement therapy?
What are benefits and limitations to peritoneal diaylsis?
What are benefits and limitations to haemodiaylsis?
Problems with fistulas?
Risks/ complications: List 4
- stenosis
- thrombosis
- aneurysmal diltation
Haematuria:
DDx gross haematuria: Painless? List 4 causes?
Painful haematuria? ddx?
Pseudohematuria: DDx:
History of painless haemturia: SOCRATES? explain, Associated symptoms (important), Pmhx
Examination findings: Inspection, Vitals, growth, peripheries, face, abdo, resp
First line investigations for haemturia? Dipstick? Labs? 2nd line investigations?
Normal nephron histology:
What is glomerulonephritis? Primary and secondary?
What are the pathological stages of GN? minimal change, proliferaitve, membranous, membranoproliferative, crescentic, sclerosing, necrotizing
What investigations need to be done? Think specific to pathology
Outline pre-procedure, post-procedure management when undertaking a renal biopsy? What does the result provide?
Glomerulonephritis
Definitions:
Glomerular disease is categorised as:
- Primary and secondary
- Primary glomerular diseases – Diseases in which the kidney is the only or predominant organ involved.
- Secondary glomerular disease – Diseases where glomerular disease is a complication; not the main part of the disease
- Immunological
- Glomerular antigen (anti-GBM)
- Non-glomerular antigen
- Immune complex
- Morphological
- Diffuse – All glomeruli
- Focal – Some glomeruli
- Global – Whole of glomeruli
- Segmental – Part of glomeruli
- Clinical
- Nephritic syndrome
- Nephrotic syndrome
- Pathology
- Minimal Change – Normal appearing glomerulus
- Proliferative – Increased cells, inflammation
- Membranous – Thickening of BM
- Membranoproliferative – Combination
- Crescentic – FSGS, rapidly progressive GN – accumulation of cells in the Bowman’s space
- Sclerosing – scarring of the glomerulus
- Necrotizing = cell death within the glomerulus.
Investigations
- Bedside – urine dipstick
- Bloods:
- FBC, UECS, LFTs, CRP,
- Immunoglobulins (IgG, IgA, IgM)
- Electrophoresis (?Multiple myeloma)
- Completement (C3, C4)
- Autoantibodies (ANCA, anti-GBM, etc.)
- Urine – M/C/S, ACR/PCR, Microscopy for casts
- Imaging – CXR (APO & pulmonary haemorrhages), USS KUB
-
Renal biopsy
- Percutaneous biopsy = most common
- Rarer – Surgical and trans-jugular biopsies.
Renal Biopsy:
- Pre-procedure:
- Measure BP. Order FBC, coagulation studies.
- Discuss complications with patient
- Back/ loin pain, visible haematuria, bleeding, need for transfusion
- Cease anticoagulants prior to procedure
- Post-procedure:
- Bed rest for 4 hours minimum.
- Monitor pulse, BP, symptoms + urine colour.
- Do not discharge until haematuria has settled.
- Anticoagulants can be restarted the day after the procedure (if uncomplicated)
- Result:
- Gives information regarding proportion of glomeruli involved (focal vs diffuse), how much of each glomerulus is affected (segmental vs global), sclerosis, etc.
- Immunohistology of the sample (Ig, light chains, complement) should also be performed.
- Electron microscopy can show deposits and podocytes
- Requires specialist Renal Pathologist to interpret accurately. Most samples are sent to Brisbane.
Generally:
Presentation differences in nephritic vs nephrotic syndrome
List 4 features of each: Nephritic syndrome
List 4 features of nephrotic syndorme: 2 marks
List 3 causes of nephritic syndrome? List 3 causes nephrotic syndrome?
What is the prognosis following various GN?
Normal Glomerular histology:
Patho of GN: Immune complexes? Anti-GBM ab, Ab reacting to ag (PSGN)
Patho explained: Read:
Nephritic vs Nephrotic syndrome:
List 3 clinical correlations to nephritic syndrome:
List 3 clinical correlations to Nephrotic syndrome: list?
Morphological changes/classification:
Pathological classification:
What are the 4 ways GN presents: List all 4 - 2 marks
Proteinuria: if in non-neprhotic range- HWat should be done? What tests?
What is classified as microalbuminuria? Macroalbuminuria? Nephrotic range?
DDx for proteinuria? (think- physiological, overproduction, GN, Tubulointerstial)
What are primary vs secondary causes of proteinuria?
GN eitology:
Primary causes: List 4: 2 marks
Secondary causes: List 4: 2 marks
Nephritic vs nephrotic spectrum:
Nephrotic vs nephritic: Eitology?
Clinical features of each? Symptoms? Complications? Lab findings?
BP in each? eGFR in each?
Complications of each? List 2 from each - 2 marks
Outline Assessment for Nephritic vs nephrotic syndrome:
Investigations for GN: Workup? Urine, Bloods- Nephritic? Nephrotic? Imaging? Renal biopsy?
Progression of GN to chronic GN?
Nephritic vs nephrotic case examples:
Nephrotic syndromes:
DDx for generalise oedema? List 5 - 2.5 marks
List nephrotic syndromes: What is the most common cause in children?
Clinical features of minimal change disease? Complications of minimal change?
Ix for nephrotic syndrome? Examinations findings?
Management of nephrotic syndrome (unknown cause)
Primary survey? Active management? (edema), Specific? prophylaxis? Ongoing? Long term
List 6 complications of steroid use in children?
What is Membranous nephropathy? (most common cause in adults) - Autoimmune:
Eitology? Explain, primary vs secondary
Patho: Read:
Morphology on histology:
Clinical?
Management:
What is focal segment glomerularsclerosis (FSGS)
Primary vs secondary? Patho?
Morphology: Micro?
Investigations? Prognosis?
What is membranoproliferative?
Management principles of nephrotic syndrome: treating underling cause? Fluids? HTN & proteinuria? statins? VTE prophylaxis?
Nephritic syndrome: GN with nephritic features:
What are clinical features: list 4 major: 2 marks
What role does complement have in diagnosing nephritic syndromes: Explain:
What two condition cause a positive anti GBM?
What nephritic syndromes cause a decrease in C3 levels?
What is IGA nephropahty? (bergers disease) Eitology? Patho? Morphology? Clinical features? What are clinical features? Management?
What is Post-streptococcus GN (PSGN)
What is it? What relevance does it have in children?
Patho? Micro?
Clinical features? - preceding events?
Complications: List 4 - 2 marks?
Investigations: list 4 and importance: 2 marks
Management: Admit, acute management, after discharge?
What is Henoch scholein purpura? (HSP) - Who does it occur in?
Clinical features? lis 3 specific to condition:
What is rapidly progressing GN (RPGN) ?
General overall management of Nephritic syndromes: list - 2 marks
Common secondary causes of GN: list 4
