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Renal medicine Flashcards

1
Q

Definition of complicated v uncomplicated UTI

A

Uncomplicated UTI: occurs in normal urinary tract and resolves rapidly with conventional antibiotics

Complicated UTI: occurs in patients with co-existing pathology (strictures, stones, DM, MS, SCI)

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2
Q

Definition of pyelonephritis

A

Significant bacteriuria in the presence of systemic illness and symptoms such as flank or renal angle pain, pyrexia, rigors, nausea and vomiting

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3
Q

Most common pathogens in UTIs

A 
E. Coli 80%
Staphylococcus saprophyticus 10%
Klebsiella 5%
Proteus less than 5%
Pseudomonas aeruginosa less than 1% (typically opportunistic or hospital-acquired due to catheters, instrumentation etc.)
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4
Q

Cause for increased UTIs during pregnancy

A

Ureteric dilatation

  • progestogenic relaxation of ureteric smooth muscle
  • pressure from expanding uterus

Overall effect = increased urinary stasis, compromised ureteric valves, vesicoureteric reflux

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5
Q

Reason for treating asymptomatic bacteriuria in pregnant women

A

Associated with low birth weight and pre-term delivery

Risk of ascent to pyelonephritis due to ureteric dilatation in pregnancy

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6
Q

CT findings in pyelonephritis

A

wedge-shaped areas of inflammation in renal cortex

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7
Q

Clinical features of pyelonephritis

A

Fever
Loin pain with renal/costovertebral angle tenderness
Systemic symptoms common (fever, rigors, nausea and vomiting)

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8
Q

Indications for investigations into anatomy for UTI in adults

A

Male
Women following 2 or more episodes of acute pyelonephritis
Anyone presenting with a proteus UTI

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9
Q

Management of non-pregnant woman with symptomatic UTI

A

Trimethoprim 3d
OR
Cephalexin, Augmentin or nitrofuratoin for 5d

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10
Q

Management of pregnant woman with UTI

A

While awaiting culture results:
Cephalexin, nitrofuratoin or Augmenin duo for 5d

Repeat MCS 48h post completion of antibiotics to ensure clearance of infection

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11
Q

Management of UTI in men

A

Empirical antibiotics while awaiting culture
- trimethoprim, cephalexin or augmentin for 14 days!

Investigate for underlying abnormality of the urinary tract

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12
Q

Management of pyelonephritis in a non-pregnant patient

A

Mild:
Oral Augmentin, cephalexin, trimethoprim for 10d

Severe: (septic, vomiting or pregnant with fever)
IV Gentamicin + amoxicillin (gent alone is ok if penicillin allergic)
If Gentamicin resistant: cefotaxime or cephtriaxone

Continue IV until afebrile for 24h, followed by 10-14d oral antibiotics guided by MCS

Repeat MCS 48h after completion of antibiotics to ensure clearance

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13
Q

Management of recurrent UTIS

A

Cranberry products
Intravaginal oestrogen (post-menopausal)
Prophylactic trimethoprim
Prophylactic cephalexin

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14
Q

Components of nephritic syndrome

A 
Haematuria (macro- or microscopic)
Proteinuria
Hypertension
Oedema
Temporary oliguria or uraemia
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15
Q

Causes of nephritic syndrome

A

Immune response to infection

  • Group A strep
  • chronic bacteraemia
  • sepsis
  • staph, pseudomonas, klebsiella
  • Hep B or C
  • varicella
  • coxsackie virus
  • EBV
  • Rubella
  • mumps

Drug induced:

  • gold
  • penicillamine

Other:

  • IgA nephropathy
  • SLE
  • Membranoproliferative glomerulonephritis (Type I, III - immune-mediated, Type II - complement-mediated)

Rapidly progressive (crescentic) glomerulonephritis

  • Goodpasture Syndrome
  • Churg-Strauss syndrome
  • Polyarteritis nodosa
  • idiopathic
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16
Q

Definition of IgA nephropathy

A

An immune complex-mediated glomerulonephritis characterised by IgA deposition in the glomerular mesangium due to exaggerated marrow and tonsillar IgA response to viral/other antigens

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17
Q

Clinical presentation of IgA nephropathy

A

Asymptomatic microscopic haematuria OR recurrent macroscopic haematuria sometimes following a viral URTI or GIT infection

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18
Q

Investigations in IgA nephropathy

A

Bloods: eGFR

Urinalysis

  • RBC casts
  • +++ protein, +++ blood
  • quantify proteinuria

Renal biopsy:

  • proliferation of mesangial cells
  • increased cellularity in mesangium
  • immune complexes in mesangium on immunoperoxidase staining
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19
Q

Management of IgA nephropathy

A

ACE-I or ARB

If more than 1-3g proteinuria/day with normal GFR: steroids

If GFR under 70: + fish oil OR prednisolone
AND cyclophosphamide for 3m

If recurrent tonsillitis - tonsillectomy

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20
Q

Prognosis of IgA nephropathy

A

up to 25% will undergo spontaneous remission

15-40% have slow progression to ESRD (5-20y)

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21
Q

Grades of lupus nephritis

A

Class I: minimal mesangial glomerulonephritis (5%)
- normal on light microscopy
- mesangial deposits on electron
Class II: mesangial proliferative lupus nephritis (20%)
- renal failure rare
- typically responds completely to corticosteroid
Class III: focal proliferative nephritis (25%)
- often responds successfully to high dose steroids
- renal failure uncommon
Class IV: diffuse proliferative nephritis (40%)
- renal failure common!
- treat with steroids and cyclophosphamide
Class V: membranous nephritis (10%)
- renal failure uncommon
- extreme oedema and protein loss

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22
Q

Important side effects of cyclophosphamide

A

Sterility
Immunosuppression
Bone marrow suppression

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23
Q

Definition of nephrotic syndrome

A

A disease of the glomerulus characterised by high urine protein excretion (3.5g/d), peripheral oedema, hypoalbuminaemia and hypercholesterolaemia

24
Q

Bland v active urine sediments in nephrotic syndrome

A 
Bland = without RBC casts
Active = with RBC casts
25
Most common primary glomerular causes of nephrotic syndrome
Children/ young adults: 1. Minimal change disease (80%) 2. Membranous nephropathy 3. Focal segmental glomerulosclerosis Adults: 1. Membranous nephropathy 2. Focal segmental
26
Investigations in nephrotic syndrome
Lipids Albumin 24h urine OR UACR eGFR, repeat few days later to identify rapidly progressive glomerulonephritis Investigate for primary and secondary causes - CBE - urine MCS - Renal USS - urine and serum electrophoresis - serum free light chains - ANA, dsDNA, ANCA, ENA - complement studies - Hep B and C serology - HIV serology - parathyroid hormone level
27
Secondary causes of nephrotic syndrome
Systemic diseases: - DM - SLE - Amyloidosis Cancers: - myeloma - lymphoma Drugs: - NSAIDs - captopril - tamoxifen - lithium Infections: - HIV - Hepatits B and C - Mycoplasma - Syphilis - Malaria Congenital causes - Alports syndrome - Denys-Drash syndrome - congenital nephrotic syndrome of the Finnish type
28
Complications of nephrotic syndrome (and why)
Thrombosis - urinary loss of anticoagulants (antithrombin III, protein C, protein S) - compensatory increase in coagulation factor/fibrinogen synthesis in response to hypoalbuminaemia Infection: - urinary loss of IgG - reduced complement activity - immunosuppressive therapy Volume depletion
29
General measures of management of nephrotic syndrome
Dietary Na restriction and thiazide diuretic (+frusemide if unresponsive) Normal protein intake Avoid prolonged bed rest, give long-term prophylactic anticoagulation Monitor for sepsis Statin to reduce lipid levels and CVD risk ACE-I or ARB to reduce proteinuria
30
Prognosis of membranous nephropathy
Almost half undergo remission | 40% develop CKD
31
Causes of membranous nephropathy
Idiopathic Drug-induced: - Gold - penicillamine - NSAIDs - captoptril Autoimmune disease: - thyroiditis - SLE Infectious disease: - Hep B or C - Schistosomiasis - malaria Neoplasm (atypical membranous nephropathy) - lung cancer - colon cancer - stomach cancer - breast cancer - lymphoma
32
Membranous nephropathy on renal biopsy
Immunofluorescence: - uniform granular capillary wall deposits of IgG and C3 Light microscopy: - late stage: deposits completely surrounded by basement membrane + undergoing resorption (uniform thickening of capillary basement membrane)
33
Management of membranous nephropathy
General management for nephrotic syndrome Corticosteroids Cyclophosphamide Rituximab
34
Prognosis of focal segmental glomerulosclerosis
50% will progress to end stage renal failure within 10 years Usually recurs in transplanted kidneys, sometimes within days of transplantation
35
Biopsy results of focal segmental glomerulosclerosis
``` Segmental glomerulosclerosis Focal tubular atrophy interstitial fibrosis Other glomeruli may be enlarged or normal +/- mesangial hyperplasia ``` Immunofluorescence: - C3 and IgM deposits in affected portions of glomerulus Electron microscopy: - capillary obliteration by hyaline deposits and lipids - foot process effacement, occasionally in patchy distribution
36
Management of focal segmental glomerulosclerosis
Low-dose prednisolone for 6m - cyclosporine if resistant after the 6m Second line: - cyclophosphamide - chlorambucil - AZA
37
Renal biopsy in minimal change disease
Appears normal on light microscopy Fusion of foot processes on electron microscopy No immune complexes nor anti-GBM antibodies on immunofluorescence
38
Prognosis of minimal change disease
Does NOT lead to chronic kidney disease response rate poorer in adults, may have to treat for longer (up to 24 weeks v 12 weeks) 2/3 children will relapse 1/3 of these will regularly relapse on steroid therapy Relapse is very rare if remission lasts 4y after steroid therapy
39
Management of minimal change disease
High dose corticosteroid therapy for 4-6 weeks, followed by 4-6 weeks steroids on alternate days (double the timeframe in adults) If regularly relapsing on steroid therapy, addition of cyclophosphamide after initial steroid induction Only 2 courses max of cyclosporine to children
40
Causes of acute kidney injury
Pre-renal (azotemia) = secondary to renal hypoperfusion - volume depletion (haemorrhage, GI fluid losses, burns) - volume overload with reduced renal perfusion (severe CCF, hepatorenal syndrome in liver failure) - systemic sepsis (peripheral vasodilation - medications (ACE-I, cyclosporine) Intrinsic/renal parenchymal disease - Acute tubular necrosis (ischaemia, medications, pregnancy-related e.g. PET) - surgery - acute interstitial nephritis - atheroembolism - acute glomerulonephritis (most common in children, e.g. post-strep) - HUS Post-renal (obstruction) - ureter obstruction (stones, tumours, fibrosis/stricture) - Bladder outflow obstruction (BPH, PCa, bladder Ca)
41
Establishing pre-renal kidney injury from ATN
``` Pre-renal: urinalysis normal Urine Na less than 20 Urine Na/Cr less than 20 Urine osmolality over 500 ``` ``` ATN: Urinalysis - red, pigmented granular cells Urine Na over 40 Urine Na/Cr over 40 Urine osmolality less than 350 ```
42
Clinical phases of acute kidney injury
Incipient phase - follows precipitating event - potentially reversible - oliguria develops - acid retention of sodium (urine Na less than 10) Oliguric/established phase - established ATN - lost ability to retain sodium (urine Na over 20) Diuretic phase - increase urine output preceded recovery of GFR - may lead to wasting of Na, K and Ca - tubular function still impaired, limited capacity to resorb water and sodium
43
Management of acute kidney injury
Incipient phase: - imaging (r/o obstruction) - correct fluid status with IV NS - high dose loop diuretic - if no response within several hours, patient has established AKI Established phase: - fluid replacement linked to urine output : 500mL + output per day - daily biochem monitoring - treat underlying cause Diuretic phase: - strict fluid balance chart - weight daily - daily biochemistry - fluid replacement: NS + K (insensible losses + output)
44
The 8 established risk factors for chronic kidney disease
- Diabetes mellitus - Hypertension - Smoking - Overweight/obesity - Age over 60 - Cardiovascular disease - Family history - ATSI
45
Risk of CVD with CKD
CKD is one of the most potent risk factors for CVD - 2-3 fold increased risk in cardiac death than those without CKD - risk of death due to CVD is 20x greater than the likelihood of surviving to the stage of needing dialysis or renal transplant
46
Micro v macro albuminuria lab values (UACR and 24h urine albumin)
Microalbuminuria: UACR - M: 2.5-25, F: 3.5-35 24h albumin: 30-300 Macroalbuminuria: UACR - M >25, F >35 24h urinary albumin: >300
47
Staging of chronic kidney disease
Based on GFR 1. over 90 2. 60-79 3a. 45-59 3b. 30-44 4. 15-29 5. less than 15 or on dialysis
48
Common symptoms in end stage kidney disease and optimum management
Fatigue - anaemia - EPO Pruritus (uraemia) - topical moisturisers - gabapentin or evening primrose oil - NOT antihistamines Nausea - exclude constipation - metoclopramide or haloperidol - levopromazine if refractory Dyspnoea: multifactorial (pulm oedema, anaemia, cardiac and pulmonary disease) - Sit upright - O2 if hypoxic - fan for cool air - gentle physio - low-dose opioid + low-dose benzo (e.g. lorazepam) Restless legs syndrome - dopamine agonists (ropinirole, gabapentin or pramipexole[second line])
49
Management of chronic kidney disease
Aggressive management of CVD risk factors Blood pressure management: target below 130/80 - reduces eGFR decline by 80% per year monitor every 6-12 weeks until sufficient improvement Dialysis
50
When to refer to a nephrologist
DAGGER: Decline in GFR of more than 5 over 6 months Albuminuria over 30 on at least 3 occassions Glomerular haematuria + proteinuria (G) EGFR less than 15 Resistant HTN in setting of CKD
51
Analgesics that are safe in CKD
``` Paracetamol Hydromorphone (reduced dose) Methadone Fentanyl Buprenorphine ``` NSAIDs, Codeine and Morphine are NOT safe Oxycodone and tramadol can be used at reduced doses, but the above listed are preferred
52
Dialysis outcomes in the elderly
Extends life, but negated by comorbidities and loss of independence Those with poorer functional status have no survival advantage with dialysis Outcomes are poor in NH patients initiated on dialysis (60% mortality in first year)
53
Withdrawing from dialysis
IS NOT euthanasia or physician-assisted suicide Mean survival time after withdrawing is 10 days (affected by comorbidities, hydration level and presence or absence of hyperkalaemia)
54
Stages of diabetic nephropathy
Early nephropathy - microalbuminuria - normal eGFR Overt nephropathy - macroalbuminuria - progressive decline in eGFR
55
Prevalence of CKD in diabetes
approx. 20-40% of DM patients over 25y Most common cause of end stage kidney disease in Australia and prevalence is increasing
56
How does CKD complicate DM management
Hypoglycaemia - reduced renal glucose production - reduced gluconeogenesis from alanine, pyruvate and glycerol - reduced glycogen reserve - reduced systemic response to adrenaline and glucagon - reduced insulin degradation by kidney - increased and prolonged action - reduced renal clearance of oral hypoglycaemic agents and their active metabolites

Medicine (12 decks)

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