Renal Medicine Flashcards
Causes of non-visible haematuria
Transient: UTI, menstruation, vigorous exercise, sexual intercourse
Permanent: cancer, stones, BPH, prostatitis, urethritis, IgA nephropathy, thin BM disease
2-week-wait criteria for ?bladder or renal cancer
For bladder or renal -
>=45 AND: unexplained visible haematuria without UTI, or visible haematuria that persists after successful treatment of UTI
For bladder -
>=60 AND have unexplained non-visible haematuria and either dysuria or a raised WCC on a blood test
non-urgent referral for bladder cancer criteria
Aged >=60 with recurrent or persistent unexplained UTI
4 types of casts seen in urine, and the conditions that cause them
- Hyaline cast: seen in normal urine, after exercise, during fever or with loop diuretics
- Red cell cast: glomerulonephritis (nephritics)
- White cell cast: pyelonephritis, interstitial nephritis, glomerulonephritis
- Granular cast: CKD, acute tubular necrosis
Investigations for UTI
Investigations for the following groups ->
- ?uncomplicated cystitis
- ?complicated cystitis
- systemically unwell
- recurrent/atypical/male pyelonephritis
Non-pregnant: >=3 symptoms (or 1 severe) -> empirical abx without Ix.
Dipstick if any uncertainty (nitrites + leukocytes). Dont dipstick if pregnant or elderly.
If pregnant/male/child/failure to respond to empirical abx -> MSU
If systemically unwell -> FBC, U+E, CRP, blood culture, fasting glucose
If recurrent/atypical/male pyelonephritis -> USS and urology assessment
Common causative organisms of UTI
E coli, Staphylococcus saprophyticus, Proteus mirabilis, Klebsiella pneumonia
Management for UTI
- non-pregnant cystitis
- pregnant cystitis
- male cystitis
- non-pregnant pyelonephritis
- pregnant pyelonephritis
Non-pregnant cystitis: 3 days trimethoprim or nitrofurantoin
- avoid nitrofurantoin if eGFR <30
- if failure to respond -> MSU
Pregnant cystitis: 7 days nitrofurantoin if not at term (amoxicillin or cefalexin second line)
- avoid nitrofurantoin in tri 3
- avoid trimethoprim in tri 1
- avoid ciprofloxacin throughout
Male cystitis: 7 days trimethoprim or nitrofurantoin
Non-pregnant pyelonephritis: 7-10 days co-amoxiclav/ trimethoprim/ cefalexin
Pregnant pyelonephritis: admit to hospital, send MSU
Risk factors for UTI
sex, incontinence, constipation, menopause, reduced oestrogen, spermicides, dehydration, obstruction, DM, stones, immunosuppression, catheter, pregnancy, tract malformation
Stage 1 vs stage 2 vs stage 3 AKI
Stage 1: rise of serum creatinine >26.5 or 1.5-1.9x baseline, and urine output <0.5ml/kg/hour for 6-12hrs
Stage 2: serum creatinine 2.0-2.9x baseline, or UO <0.5ml/kg/hr for >12 hours
Stage 3: serum creatinine >3x baseline, or UO <0.3ml/kg/hour for >24 hours
Pre-renal causes of AKI
Renal artery stenosis, haemorrhage, D+V, pancreatitis, burns, shock, MI, sepsis, drugs (NSAIDs, ACEI), hepatorenal syndrome
Intrinsic causes of AKI
glomerulonephritis, acute tubular necrosis, drugs (gentamicin, contrast media), infection, tumour lysis syndrome, rhabdomyolysis, HUS, TTP, DIC
Post-renal causes of AKI
Stones, malignancy, stricture, clot, prostatic hypertrophy, retroperitoneal fibrosis
eg. BPH -> acute urinary retention -> bilateral hydronephrosis
Signs and symptoms of AKI
May be asymptomatic
Reduced urine output
Pulmonary and peripheral oedema (fluid overload)
There may be pain/signs of acute urinary retention if obstruction
Arrhythmias secondary to K+ and acid-base balance changes
Uraemia (pericarditis, encephalopathy)
Investigations for AKI
UEs
Urinalysis
Renal ultrasound
ABG will show acidosis and maybe hyperkalaemia
Management of AKI
- If Pre-renal: correct fluid depletion and.or increase renal perfusion via circulatory support, treat any underlying sepsis
- If intrinsic: refer for likely biopsy and specialist treatment of intrinsic renal disease
- If post-renal: catheter, nephrostomy or urological intervention to relieve retention
Supportive treatment:
- Fluid boluses
- Careful fluid balance (catheter and UO hourly, daily weights)
- Check K+ and treat any hyperkalaemia urgently
- Review drug chart
- RRT is not responding to medical management
- Urology review if obstruction is suspected
- Nephrology review if cause unknown or AKI severe
Cause and management of fluid overload
Caused by aggressive fluid resuscitation, oliguria and sepsis due to increased capillary permeability
Mx: O2 if needed, fluid restriction, diuretics if symptomatic, RRT
Management of hyperkalaemia >6.5 or any with ECG changes
- 10ml 10% calcium chloride
- 10units actrapid in 50ml 50% glucose infusion
- +/- salbutamol nebs
- Renal replacement therapy
Indications for RRT in AKI
fluid overload not responding to Mx, severe/prolonged acidosis, recurrent/persistent hyperkalaemia despite management, uraemia
ECG changes with hyperkalaemia
Tall tented T waves -> prolonged PR -> small/absent P -> wide QRS -> sine wave -> asystole
Classification of CKD
1: eGFR >90 with some sign of kidney damage on other tests
2: eGFR 60-89 with some sign of kidney damage on other test
3a: eGFR 45-59
3b: eGFR 30-44
4: eGFR 15-29
5: eGFR <15. ESRF. Dialysis or transplant needed.
Clinical features of CKD
Oedema, weight loss, SOB, tiredness, pruritis (uraemia), encephalopathy (uraemia), rash, N+V (uraemia), anorexia (uraemia), restless legs, muscle cramps, bone disease (osteitis fibrosa cystica, osteomalacia, osteosclerosis, osteoporosis)
Low Vit D (lack of hydroxylation)
High phosphate (lack of excretion)
Hypocalcaemia (due to low vit D and high phosphate)
Secondary hyperparathyroidism (due to hypocalcaemia)
High ALP due to bone turnover
Hyperkalaemia
Normochromic normocytic anaemia (lack of EPO)
Management of CKD
Optimise BP and DM, lifestyle
Reduce risk of complications: lifestyle, atorvastatin, low dose aspirin
CKD diet: high protein, low potassium, low sodium, low phosphate
Manage complications:
-Anaemia: erythropoietin
-Acidosis: sodium bicarb if eGFR<30 and bicarb <20
-Oedema: fluid and sodium restriction, consider loop diuretics
Bone mineral disorders: reduce phosphate in diet first line, phosphate binders, vit D (calcitriol/alfacalcidol), parathyroidectomy
-Restless legs: consider neuropathic analgesia
Renal replacement therapy
Indications for dialysis in CKD
eGFR usually 5-10 inability to control fluid balance (pulm oedema) Inability to control HTN Serositis Acide base or electrolyte disturbance Pruritus N+V or nutritional deterioration Cognitive impairment
How does haemodialysis work
- when is the AV fistula created
- where is it done, how many sessions per week, how long per session
- Blood passed from AV fistula into a machine over a semi-permeable membrane against a dialysis fluid. Blood is filtered and then put back in body
- AV fistula created 8 weeks before dialysis
- Requires at least 3 sessions/week, lasting 3-5 hours each session
How does peritoneal dialysis work
-where is the session done
Dialysis solution is injected into the abdo cavity through a permanent catheter, the blood is then filtered using the peritoneum as a semipermeable membrane
what is STEAL syndrome
inadequate blood flow to the limb distal to the AV fistula, causing distal ischaemia
Haemodialysis complications
Site infection, endocarditis, stenosis of fistula, hypotension, stenosis thrombosis, cardiac arrhythmia, air embolus, anaphylactic reaction to sterilising agents, disequilibrium syndrome
Peritoneal dialysis complications
Peritonitis, sclerosing peritonitis, catheter infection, catheter blockage, constipation, fluid retention, hyperglycaemia, hernia, back pain
Renal transplantation complications
- Surgical complications: haemorrhage, thrombosis, infection, urinary leak, hernia
- Delayed graft function (requires dialysis)
- Acute rejection (T cell mediated or antibody mediated -> high dose methylprednisolone or plasma exchange and IVIg)
- Chronic rejection
- Opportunistic infection
- Malignancies
- Bone marrow suppression
- Recurrence of original disease
- Urinary tract obstruction
- Cardiovascular disease
Indications and contraindications for renal transplant
Indications: ESRF or progressing towards ESRF
CI: active metastatic cancer, active infection, HIV, unstable CVD, heart failure
Different types of renal transplant
DBD: brain death donor
DCD: circulatory death donor
Live related
Live unrelated
Renal transplant immunosuppression
Monoclonal antibodies (basiliximab): selectively inhibits T cell activation to reduce risk of rejection
Calcineurin inhibitors (tacrolimus, ciclosporin): inhibits T cell activation. Narrow therapeutic index. Nephrotoxic so close monitoring required. CYP450 clearance
Antimetabolites: Mycophenolate mofetil, azathioprine
Prednisolone
Investigations for glomerulonephritides
RENAL BIOPSY IS REQUIRED FOR DIAGNOSIS
Bloods - FBC, U+E, LFT, CRP, immunoglobulins, electrophoresis, complement, autoantibodies (ANA, ANCA, anti-dsDNA, anti-GBM), blood cultures, hepatitis serology, ASOT (anti-streptolysin O titre for post strep glomerulonephiritis)
Urine - MC+S, bence jones, A:CR or P:CR, RBC casts
Imaging - CXR (pulm haemorrhage), renal USS
Examples of nephritic syndromes
IgA nephropathy (Bergers), Henoch-Schoönlein purpura, post-strep glomerulonephritis, anti-GBM disease (Goodpasture’s), rapidly progressive glomerulonephritis, Alport syndrome
Examples of nephrotic syndromes
- primary renal causes
- secondary causes
Primary: Minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, membranoproliferative glomerulonephritis
Secondary: DM, SLE, myeloma, amyloid, pre-eclampsia
IgA Nephropathy (Berger’s)
- what is it/what happens?
- presentation
- associated conditions
- progression to ESRF
- management
- Commonest cause of glomerulonephritis worldwide
- Deposition of IgA complexes (=IgA and C3) in the mesangium
- Young adult male with haematuria 1-2 days post URTI. Associated with high levels of complement.
- Associated with alcoholic cirrhosis, coeliacs, and HSP
- Renal failure may occur decades later
- Mx: control BP (lifestyle, anti-HTN), prednisolone (prevent IgA complex formation)
Henoch-Schönlein purpura
- what is it
- presentation
- diagnosis
- management
-IgA mediated small vessel vasculitis (systemic version of IgA nephropathy) -> IgA complex deposits in skin, gut, kidney, joints
-Seen in children following infection -> palpable purpuric rash over buttocks/arms/legs, abdo pain, polyarthritis, haematuria, renal failure
-clinical diagnosis. Positive immunofluorescence for IgA and C3 in skin. Renal biopsy shows IgA.
-Mx: analgesia, supportive treatment for nephropathy. (inconsistent evidence for use of steroids and immunosuppressants).
Good prognosis.
Post-streptococcal glomerulonephritis
- nephrotic or nephritic
- when does it occur and in who
- features
- diagnosis
- mx
- causes a mixed nephritic and nephrotic picture
- A child presents with haematuria 1-2 weeks after strep pyogenes URTI
- features: headache, malaise, haematuria, proteinuria (<3g/day), oedema, HTN, -Diagnosis: starry sky appearance on immunofluorescence, low C3 levels, raised ASOT (anti-streptolysin O titre)
- supportive management (manage HTN and oedema) +/- abx (penicillin)
- good prognosis
Nephritic syndrome clinical features
Haematuria, hypertension, oliguria, some oedema
Nephrotic syndrome clinical features
Proteinuria (P:CR >300), hypoalbuminaemia (<30g/L), oedema, intravascular fluid depletion, hypercholesterolaemia
Goodpasture’s syndrome (anti-GBM disease)
- cause
- age and gender most at risk
- presentation
- investigations
- management
-Caused by type 4 collagen autoantibodies, which attack the GBM
- bimodal age 20-30 and 60-70, males more common
- Rapidly progressive. Within weeks/months -> pulmonary haemorrhage, haematuria, anuria, AKI, renal failure. often dialysis-dependent at diagnosis
-Ix: biopsy shows crescents in the glomerulus (linear IgG deposits along GBM)
Anti-GBM antibodies in the blood. Raised transfer factor (due to pulm haemorrhage)
-Mx: plasma exchange, steroids, cyclophosphamide
Rapidly progressive glomerulonephritis
- 3 types
- management
Group of glomerulonephritides causing rapid reduction in renal function over days/weeks
Type 1: anti-GBM (goodpasture)
Type 2: immune-complex mediated (post-strep, SLE, IgA nephropathy, HSP)
Type 3: Pauci-immune/cANCA (wegener)/pANCA (churg-strauss), idiopathic
Mx: coricosteroids, cyclophosphamide, plasma exchnage if anti-GBM or ANCA, monoclonal ab if SLE
Alport syndrome
- inheritance pattern
- what is it
- features
- diagnosis
- management
-X-linked dominant (85%) or autosomal recessive
-Abnormal type 4 collagen (affects GBM, cochlear BM, eye BM).
Abnormal GBM is leaky -> haematuria -> protein eventually leaks through too -> GBM eventually undergoes sclerosis -> renal failure and HTN
-Features: SN hearing loss, myopia, cataracts, anterior lenticlonus (lens capsule cant maintain shape), renal failure, haematuria, proteinuria, HTN
-Diagnosis: clinical signs, FHx, renal or skin biopsy
-Mx: ACEI/ARB for proteinuria, lens replacement for anterior lenticlonus, RRT and supportive Mx for kidney failure
Complications of nephrotic syndrome
VTE: due to urinary loss of anticoagulants anti-thrombin III, protein C+S) III, and increased clotting factors -> LMWH and warfarin
Infection due to urinary loss of immunoglobulins and immune mediators, and oedema fluid acting as a culture medium -> pneumococcal vaccine
Hyperlipidaemia as a result of hypoproteinaemia leading to reactive hepatic synthesis of proteins (including lipoproteins) -> atherosclerosis
Hypocalcaemia (not a true hypocalcaemia) due to low albumin
HTN due to fluid retention and reduced kidney function
Malnutrition due to oedema of the gut and ascites causing impaired absorption
Minimal change disease
- causes
- features
- management
- prognosis/progression to ESRF
- causes: idiopathic, drugs (lithium, NSAIDs), hodgkins, thymoma, infectious mononucleosis
- only intermediate sized proteins are lost (albumin), BP normal, minimal change to glomerulus on biopsy
- manage with steroids for 1-4 months
- no progression to ESRF
Focal segmental glomerulosclerosis
- causes
- at risk age group
- investigations
- management
- prognosis/progression to ESRF
- Idiopathic, secondary to other renal pathologies, HIV, heroin, alports, sickle cell
- occurs in young adults
- biopsy shows scarring of certain segments of glomerulus
- Mx: ACEI/ARBS (for proteinuria and HTN), steroids, calcineurin inhibitors
- At risk of developing renal failure
What drug/drugs can be used to treat proteinuria?
ACEI/ARBs
Membranous glomerulonephritis
- how common
- causes
- Ix
- Mx
- prognosis/progression to ESRF
- Commonest type of GN in adults, and third most common cause of ESRF
- Causes: idiopathic (antiphospholipase A2 antibodies), hep B, malaria, syphilis, lung cancer, lymphoma, leukaemia, gold, penicilamine, NSAIDs, autoimmune (SLE, thyroiditis, RA)
- Ix: biopsy shows thickened GBM due to subepithelial deposits of Ig
- Mx: ACEI/ARB to reduce proteinura, combination of corticosteroids and cyclophosphamide for severe disease, consider anticoag for high risk patients
- prognosis: rule of thirds. one third have spontaneous remission, one third remain proteinuric, one third develop ESRF
Membranoproliferative glomerulonephritis
- 3 types
- management
- prognosis
- Type 1 (90%): caused by cryoglobulinaemia or hep C, shows subendothelial and mesangium deposits (tram-track appearance) on renal biopsy
- Type 2: causes by partial lipodystrophy, factor H deficiency. Low C3 levels. Biopsy shows dense deposits (intramembranous immune complexes)
- Type 3: caused by hep B and hep C
- management: steroids may be effective
- prognosis is poor
Diabetic nephropathy
- pathophysiology
- features
- investigations/screenin
- management
- Patho: hyperglycaemia -> increased growth factors, RAAS, oxidative stress -> increased glomerular capillary pressure, podocyte damage, endothelial dysfunction
- Features: albuminuria, glomerulosclerosis, nodules, fibrosis -> reduced renal function
- Co-existing HTN accelerates disease
- Ix: annual A:CR screening. A:CR shows microalbuminuria
- Mx: DM control, BP <130/80 (ACEI/ARB), statins, sodium restriction
Lupus nephritis
- pathophysiology
- SLE features
- diagnosis
- management
- Autoimmune dsDNA and ANA antibodies -> deposition -> inflammation and tissue damage
- renal disease, malar rash, photosensitivity, serositis, ulcers, arthritis, CNS effects, cytopenia
- diagnosis: antibody scren (ANA, ds-DNA), renal biopsy if A:CR>30 or P:CR >50
- Mx: ACEI/ARBs, hydroxychloroquine for extra-renal disease, immunosuppression (rituximab, MMF, steroids, cyclophosphamide)
Granulomatosis with polyangitis
- what is it
- features
- investigations
- management
- prognosis
- (wegeners) Small-medium vessel vasculitis
- Epistaxis, saddle shaped nose, sinusitis, nasal crusting, haemoptysis, dyspnoea, proptosis, rash, rapidly progressive glomerulonephritis
- Ix: c-ANCA, CXR (cavitating lesions), renal biopsy (epithelial crescents)
- Mx: steroids, cyclophosphamide, plasma exchange
- prognosis: median survival 8-9 yrs
Eosinophilic granulomatosis with polyangitis
- what is it
- features
- investigations
- management
- (churg-strauss) small-medium vessel vasculitis
- Features: asthma, eosinophilia, pasanasal sinusitis, mononeuritic multiplex, dyspnoea
- Leukotriene receptor antagonists may precipitate disease
- Ix: p-ANCA, eosinophilia, CXR (vasculitic damage and eosinophil infiltration), Lung function tests (asthma), biopsies of affected tissues, ECG
- Mx: prednisolone, inhaled steroids, cyclophosphamide/rituximab if unresponsive, azathioprine/methotrexate to allow for steroid reduction,
Autosomal dominant polycystic kidney disease
- mutation
- renal clinical features
- extrarenal clinical features
- diagnostic criteria
- management
- Mutation in PKD1 most common (ESRF by 50y) or PKD2 (ESRF by 70y)
- 2/3 people need transplant
- Asymptomatic until cysts or large or they haemorrhage -> loin pain, haematuria, cyst infection, renal calculi, HTN, CKD, ESRF
- Extrarenal features: liver cysts, intracranial aneurysm (SAH), mitral valve prolapse, ovarian cyst, diverticulosis
- USS diagnostic criteria in patients with positive FHx: <30yrs old requires two cysts (unilateral or bilateral), aged 30-59 requires two cysts in both kidneys, aged >60 requires 4 cysts in both kidneys
- Mx: vasopressin antagonist (tolvaptan), RRT, transplant, increased fluid intake suppresses cyst growth, BP <130/80 (ACEI/ARB)
Autosomal recessive polycystic kidney disease
- Which is more common, ARPKD or ADPKD?
- Which chromosome is the defect on?
- How is it usually diagnosed and when?
- Associated condition
- When does ESRF occur?
- Other organ involvement
-Much less common than ADPKD, due to defect on chromosome 6 (fibrocystin)
Prenatal USS diagnosis
Associated with Potter’s syndrome secondary to oligohydramnios
ESRF in childhood
Patients also typically have liver fibrosis
Acute interstitial nephritis
- causes
- features
- investigations
- management
- Causes: drugs most common (penicillin, rifampicin, NSAIDs, allopurinol, furosemide), SLE, sarcoidosis, Sjögrens, staph infection
- features: eosinophilia (30%), mild AKI, HTN, 10% have allergic triad (rash, fever, arthralgia)
- Ix: sterile pyuria, white cell casts
- Mx: treat underlying cause, steroids
Rhabdomyolysis
- typical presentation
- clinical features
- lab results
- causes
- management
- A patient who has had a fall or prolonged epileptic seizure and is found to have AKI on admission
- Clinical features: muscle pain.swelling, AKI, red/brown urine, history of trauma/ immobility/ dehydration
- Lab results: AKI with disproportionately raised creatinine, elevated CK, myoglobinuria, hypocalcaemia (myoglobin binds calcium)< elevated phosphate (released from myocytes), hyperkalaemia (due to renal failure), met acidosis
- Causes: seizure, collapse/coma, ecstasy, crush injury, statins (esp if prescribed with clarithromycin)
- Mx: IV fluids to maintain UO, urinary alkalisation sometimes, manage hyperkalaemia, ?RRT
Acute tubular necrosis
- causes
- investigations
Most common cause of AKI
Ischaemic causes: shock, sepsis
Nephrotoxins: gentamicin (aminoglycosides), myoglobin (rhabdomyolysis), contrast, lead
Ix: AKI (raised urea, raised creatinine, raised potassium), muddy brown casts in urine
Renal artery stenosis features
HTN, CKD, flash pulmonary oedema (rapid onset pulm oedema)
Accounts for 90% of renal vascular disease, with fibromuscular dysplasia being the most common cause of the remaining 10%
