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Renal Medicine Flashcards

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1
Q

Causes of non-visible haematuria

A

Transient: UTI, menstruation, vigorous exercise, sexual intercourse
Permanent: cancer, stones, BPH, prostatitis, urethritis, IgA nephropathy, thin BM disease

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2
Q

2-week-wait criteria for ?bladder or renal cancer

A

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

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3
Q

non-urgent referral for bladder cancer criteria

A

Aged >=60 with recurrent or persistent unexplained UTI

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4
Q

4 types of casts seen in urine, and the conditions that cause them

A
  • 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
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5
Q

Investigations for UTI

Investigations for the following groups ->

  • ?uncomplicated cystitis
  • ?complicated cystitis
  • systemically unwell
  • recurrent/atypical/male pyelonephritis
A

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

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6
Q

Common causative organisms of UTI

A

E coli, Staphylococcus saprophyticus, Proteus mirabilis, Klebsiella pneumonia

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7
Q

Management for UTI

  • non-pregnant cystitis
  • pregnant cystitis
  • male cystitis
  • non-pregnant pyelonephritis
  • pregnant pyelonephritis
A

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

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8
Q

Risk factors for UTI

A

sex, incontinence, constipation, menopause, reduced oestrogen, spermicides, dehydration, obstruction, DM, stones, immunosuppression, catheter, pregnancy, tract malformation

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9
Q

Stage 1 vs stage 2 vs stage 3 AKI

A

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

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10
Q

Pre-renal causes of AKI

A

Renal artery stenosis, haemorrhage, D+V, pancreatitis, burns, shock, MI, sepsis, drugs (NSAIDs, ACEI), hepatorenal syndrome

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11
Q

Intrinsic causes of AKI

A

glomerulonephritis, acute tubular necrosis, drugs (gentamicin, contrast media), infection, tumour lysis syndrome, rhabdomyolysis, HUS, TTP, DIC

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12
Q

Post-renal causes of AKI

A

Stones, malignancy, stricture, clot, prostatic hypertrophy, retroperitoneal fibrosis

eg. BPH -> acute urinary retention -> bilateral hydronephrosis

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13
Q

Signs and symptoms of AKI

A

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)

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14
Q

Investigations for AKI

A

UEs
Urinalysis
Renal ultrasound

ABG will show acidosis and maybe hyperkalaemia

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15
Q

Management of AKI

A
  • 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
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16
Q

Cause and management of fluid overload

A

Caused by aggressive fluid resuscitation, oliguria and sepsis due to increased capillary permeability

Mx: O2 if needed, fluid restriction, diuretics if symptomatic, RRT

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17
Q

Management of hyperkalaemia >6.5 or any with ECG changes

A
  1. 10ml 10% calcium chloride
  2. 10units actrapid in 50ml 50% glucose infusion
  3. +/- salbutamol nebs
  4. Renal replacement therapy
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18
Q

Indications for RRT in AKI

A

fluid overload not responding to Mx, severe/prolonged acidosis, recurrent/persistent hyperkalaemia despite management, uraemia

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19
Q

ECG changes with hyperkalaemia

A

Tall tented T waves -> prolonged PR -> small/absent P -> wide QRS -> sine wave -> asystole

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20
Q

Classification of CKD

A

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.

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21
Q

Clinical features of CKD

A

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)

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22
Q

Management of CKD

A

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

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23
Q

Indications for dialysis in CKD

A 
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
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24
Q

How does haemodialysis work

  • when is the AV fistula created
  • where is it done, how many sessions per week, how long per session
Study These Flashcards
A
  • 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
25
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
26
what is STEAL syndrome
inadequate blood flow to the limb distal to the AV fistula, causing distal ischaemia
27
Haemodialysis complications
Site infection, endocarditis, stenosis of fistula, hypotension, stenosis thrombosis, cardiac arrhythmia, air embolus, anaphylactic reaction to sterilising agents, disequilibrium syndrome
28
Peritoneal dialysis complications
Peritonitis, sclerosing peritonitis, catheter infection, catheter blockage, constipation, fluid retention, hyperglycaemia, hernia, back pain
29
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
30
Indications and contraindications for renal transplant
Indications: ESRF or progressing towards ESRF CI: active metastatic cancer, active infection, HIV, unstable CVD, heart failure
31
Different types of renal transplant
DBD: brain death donor DCD: circulatory death donor Live related Live unrelated
32
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
33
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
34
Examples of nephritic syndromes
IgA nephropathy (Bergers), Henoch-Schoönlein purpura, post-strep glomerulonephritis, anti-GBM disease (Goodpasture's), rapidly progressive glomerulonephritis, Alport syndrome
35
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
36
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)
37
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.
38
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
39
Nephritic syndrome clinical features
Haematuria, hypertension, oliguria, some oedema
40
Nephrotic syndrome clinical features
Proteinuria (P:CR >300), hypoalbuminaemia (<30g/L), oedema, intravascular fluid depletion, hypercholesterolaemia
41
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
42
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
43
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
44
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
45
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
46
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
47
What drug/drugs can be used to treat proteinuria?
ACEI/ARBs
48
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
49
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
50
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
51
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)
52
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
53
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,
54
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)
55
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
56
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
57
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
58
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
59
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%

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