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Year 6 Nephrology > PassMed > Flashcards

PassMed Flashcards

1
Q

AKI definition

A
  • rise of baseline serum creatinine >26 umol/L in 48 hrs, 50% over baseline
  • >1.5 fold increase in serum creatinine within 1 week
  • children and young people = 25%+ decline in eGFR within 7d

Associated with low UO → <0.5 ml/kg/hour

  • more than 6 hours in adults, 8 hours in children
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2
Q

Pre-renal causes of AKI

A

Ischaemia:

  • hypovolaemia 2o to diarrhoea/vomiting
  • renal artery stenosis
  • heart failure
  • cirrhosis
  • sepsis
  • dehydration
  • excessive blood loss
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3
Q

Renal causes of AKI

A

damage to glomeruli, renal tubules, interstitium of kidneys

toxins (drugs, contrast) or immune-mediated glomerulonephritis

  • glomerulonephritis
  • acute tubular necrosis (ATN)
  • acute interstitial nephritis (AIN)
  • rhabdomyolysis
  • tumour lysis syndrome
  • gentamicin
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4
Q

Post renal causes of AKI

A

Obstruction → backing up:

  • kidney stone in ureter or bladder
  • benign prostatic hyperplasia (BPH)
  • external compression of the ureter
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5
Q

Risk factors for AKI

ACEi and AKI

A
  • CKD if eGFR <60
  • organ failure/chronic disease (e.g. HF, liver disease, DM)
  • hx of AKI
  • nephrotoxic drugs (NSAIDs, aminoglycosides, ACEi, ARBs, diuretics) within the past week
  • use of iodinated contrast agents within past week
  • emergency surgery i.e. risk of sepsis or hypovolaemia
  • 65 or older

ACEi = worsen renal function and provoke hyperkalaemia

  • mechanism: lowers BP by preventing AT1 → AT2 conversion
  • AT2 peptide hormone for vasoconstriction and fluid retention through stimulating vasopressin release
  • use with caution in in patients with declining renal function
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6
Q

Causes of oliguria (3 genres)

A
  • neurological
  • cognitive impairment
  • disability
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7
Q

2 ways to detect an AKI

A
  • reduced UO <0.5 ml/kg/hour
  • fluid overload
  • rise in molecules that kidney normally excretetes/maintains a careful balance of → sodium, potassium, urea, creatinine (U+Es)
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8
Q

How do we detect an AKI?

A

AKI criteria = serum creatinine and UO

U+Es = Na, K, urea, creatinine

urinalysis = all patients with suspected AKI

imaging = no identifiable cause or risk of UTO → renal USS within 24 hours of assessment

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9
Q

AKI mx

A

largely supportive = careful fluid balance, review medication list

  • fluids if dehydrated
  • abx if an infection
  • stop taking certain medicines = NSAIDs should be stopped in AKI except aspirin at cardio-protective dose
  • urinary catheter to drain bladder if there’s a blockage

Monitor with regular blood tests if unwell or starting new medication

RRT (e.g. haemodialysis) = used when patients is not responding to medical treatment of complication e.g. hyperkalaemia, pulmonary oedema, acidosis, uraemia

  • e.g. uraemia encephalopathy and pericarditis (reduced GCS, new onset confusion/drowsiness, pericardial rub) → inability to protect airway

specialist input from nephrologist for cases where cause is unknown or severe AKI

A helpful mnemonic to remember the drugs to stop in AKI is DAMN AKI:

  • *D**iuretics
  • *A**minoglycosides, ARBs and ACE inhibitors
  • *M**etformin
  • *N**SAIDs.

all patients with suspected AKI 2o to urinary obstruction require prompt review by a urologist

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10
Q

What mx is NOT recommended for an AKI

A

loop diuretic (to artificially boost UO) = only for SIGNIFICANT fluid overload

low-dose dopamine (to increase renal perfusion)

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11
Q

AKI mx and hyperkalaemia

A

mx to avoid arrhythmias. 3 categories to tx hyperkalaemia

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12
Q

AKI staging criteria (KDIGO): three stages

A
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13
Q

AKI staging criteria (KDIGO): three stages

A
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14
Q

AKI referral criteria

A
  • renal transplant
  • ITU with unknown cause of AKI
  • vasculitis/glomerulonephritis/tubulointersitital nephritis/myeloma
  • AKI with unknown cause
  • inadequate response to tx
  • complications of AKI
  • stage 3 AKI
  • CKD stage 4/5
  • qualify for RRT, hyperkalaemia, metabolic acidosis, complications of uraemia, fluid overload (pulmonary oedema)
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15
Q

Symptoms of AKI

A
  • feeling sick/being sick
  • diarrhoea
  • dehydration
  • peeing less than usual
  • confusion
  • drowsiness
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16
Q

AKI complications

A

high potassium (normal 3.5 - 5 mmol/L)

  • muscle weakness, paralysis, arrhythmias

pulmonary oedema

metabolic acidosis

  • N+V, drowsiness, breathlessness
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17
Q

CKD vs AKI

A

Renal USS = most patients with CKD have bilateral small kidneys except:

  • ADPCKD
  • Diabetic nephropathy (early stage)
  • Amyloidosis
  • HIV-associated nephropathy

Hypocalcaemia in CKD (due to lack of vitamin D)

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18
Q

Mx of hyperkalaemia (including staging and ECG features)

A

As a result of AKI (e.g. mainly from ACEi)

Staging:

  • mild = 5.5 - 5.9 mmol/L
  • moderate = 6 - 6.4 mmol/L
  • severe = >6.5 mmol/l

ECG done in all patients with new hyperkalaemia, features:

  • peaked/tall-tented T waves (occurs first)
  • loss of P waves
  • broad QRS complexes
  • sinusoids wave pattern

Management (principles)

stabilise cardiac membrane

  • IV CaGl = does NOT lower serum k levels, reserved for severe >5.5 mmol/L or associated ECG changes

Short term shift in K from ECF to ICF

  • Combined insulin/dextrose infusion
  • Nebulised salbutamol

Removal of potassium from the body

  • Calcium resonium (orally/enema) = enema more effected than oral as K is secreted by the rectum
  • Loop diuretics
  • Dialysis = haemofiltration/haemodia;ysis considered for patients with AKI and persistent hyperkalaemia

practical tx

severe hyperkalaemia (>6.5) or ECG changes should have emergency treatment

  • IV CaGl
  • insulin/dextrose infusion

Further mx:

  • stop exacerbating drugs
  • tx any underlying cause
  • lower total body potassium (calcium resonium, loop diuretics, dialysis)
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19
Q

Pathophysiology of CKD: Mineral bone disease

A

1a-hydroxylation normally occurs in kidneys → CKD leads to low Vit D

kidneys normally excrete phosphate → CKD leads to high phosphate (hyperphosphataemia)

Effects:

  • high phosphate drags Ca from bones → osteomalacia
  • low Ca = from lack of vit D, high phosphate
  • 2o HPT = due to low Ca (hypocalcaemia), high PO, low Vit D
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20
Q

CKD: Mineral bone disease management

A

Overview: reduce PO and PTH levels

  • reduces dietary intake of PO = 1st line
  • phosphate binders
  • Vit D = alfacalcidiol, calcitriol
  • parathyroidectomy in some cases

Phosphate binders

  • aluminium-based less common
  • Ca-based binders = problems → hypercalcaemia, vascular calcification
  • sevelamer = non-Ca based binder, binds to dietary PO to prevent its absorption, reduces uric acid levels, improve lipid profiles

Osteomalacia mx

  • alendronic acid (bisphosphonate) = reduce rate of bone turnover and strengthens bone
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21
Q

Metabolic acidosis

A

Anion gap = (Na + K) - (CI + HCO3). 10-18 mmol/L

Normal gap = hyperchloraemic metabolic acidosis

  • GI bicarbonate loss: prolonged diarrhoea (hypokalaemia), ureterosigmoidostomy, fistula
  • renal tubular acidosis
  • drugs e.g. acetazolamide
  • ammonium chloride injection
  • Addison’s disease

Raised anion gap

  • lactate = shock, sepsis, hypoxia, burns, metformin
  • ketones = DKA, alcohol
  • urate = renal failure
  • acid poisoning = salicylates, methanol
  • 5-oxoproline = chronic paracetamol use

Metabolic acidosis 2o to high lactate levels subdivided into 2 types:

  • type A = sepsis, shock, hypoxia, burns
  • type B = metformin
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22
Q

Rapidly progressive/crescentic glomerulonephritis (definition, causes, features)

A

Rapid loss of renal function associated with formation of epithelial crescents in the majority of glomeruli

Causes:

  • Goodpasture’s syndrome (anti-GBM)
  • Wegener’s granulomatosis (cANCA PR3 +ve)
  • SLE, microscopic polyarteritis

Features:

  • nephritic syndrome = haematuria, red cell casts, proteinuria, HTN, oliguria
  • features specific to underlying cause (haemoptysis with Goodpasture’s, vasculitic rash or sinusitis with Wegener’s)
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23
Q

AKI: ATN vs pre-renal uraemia vs acute tubular necrosis

A
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24
Q

Adult maintenance fluid

A
  • 25-30 ml/kg/d of water
  • 1 mmol/kg/d K, Na, CI
  • 50-100 g/d glucose to limit starvation ketosis

Example:

  • 80 kg patient in 24 hours = 2 L of water
  • 80 mmol K
  • When prescribing for routine maintenance alone, consider using 25-30 ml/kg/day sodium chloride 0.18% in 4% glucose with 27 mmol/l potassium on day 1 (there are other regimens to achieve this)*
  • Specific points:*
  • 0.9% saline = if large volumes used → increased risk of hyperchloraemic metabolic acidosis
  • Hartmann’s = contains K → do NOT use in patients with hyperkalaemia
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25
Q

Fibromuscular dysplasia

A

RAS 2o to atherosclerosis = 90% of renal vascular disease, older persons

  • atherosclerosis of renal arteries

Fibromuscular dyplasia = 10% of renal vascular disease, young female patient develop AKI after initiation of ACEi

  • proliferation of cells in arterial wall -→ vessels buldge/narrow
  • ‘string of beads’ appearance
  • Features = HTN, CKD or AKI 2o to ACEi initiation, ‘flash’ pulmonary oedema
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26
Q

CKD: eGFR and classification

A

creatinine not accurate estimate of renal function due to differences in muscle. eGFR takes in:

  • serum creatinine, age, gender, ethnicity

Factors affecting the result:

  • pregnancy
  • muscle mass (e.g. amputees, body-builders)
  • eating red meat 12 hours prior to the sample being taken

CKD needs to have markers of kidneys disease as well = proteinuria, haematuria, electrolyte abnormalities, structural abnormalities

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27
Q

Renal transplant: HLA typing and graft failure

post-op problems of grafting

hyper acute rejection (minutes to hours)

acute graft failure (<6m)

chronic graft failure (>6m)

A

The human leucocyte antigen (HLA) system is the name given to the major histocompatibility complex (MHC) in humans. It is coded for on chromosome 6.

Some basic points on the HLA system:

  • class 1 antigens include A, B and C. Class 2 antigens include DP,DQ and DR
  • when HLA matching for a renal transplant the relative importance of the HLA antigens are as follows DR > B > A
  • HLA-C and HLA-DP cross match preferable but not requirement

Post-op problems:

  • ATN of graft
  • vascular thrombosis
  • urine leakage
  • UTI

Hyperacute rejection (minutes to hours):

  • from pre-existing abs against ABO or HLA antigens
  • T2HR
  • → widespread thrombosis of graft vessels → ischaemia and necrosis of transplanted organ
  • no tx is possible and graft MUST be removed

Acute graft failure (<6m):

  • from mismatched HLA, cell-mediated (cytotoxic T cells)
  • usually asx and picked up by rising creatinine, pyuria and proteinuria
  • other causes are CMV infection
  • may be reversible with steroids and immunosuppressants

Causes of chronic graft failure (>6m):

  • both ab and cell-mediated mechanisms causes fibrosis to the transplanted kidney (chronic allograft nephropathy)
  • recurrence of original renal disease (MCGN > IgA > FSGS)
28
Q

ADPKD features

A
  • HTN
  • abdominal pain and early satiety
  • bilateral palpable flank masses
  • systolic apical murmur (mitral valve disease)
  • renal stones
  • haematuria
  • CKD

Extra-renal manifestations:

  • liver cysts (70%) → hepatomegaly
  • berry aneurysms → rupture can cause subarachnoid haemorrhage
  • CVS = mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilatation, aortic dissection
  • cysts in other organs = pancreas, spleen, very rarely thyroid/oesophagus/ovary
  • diverticulosis
29
Q

HSP

A

IgA mediated small vessel vasculitis

Features:

  • palpable purpuric rash (with localised oedema) over buttocks and extensor surfaces of arms and legs
  • abdominal pain
  • poly arthritis
  • features of IgA nephropathy (Berger’s disease) may occur e.g. haematuria, renal failure

Mx:

  • analgesia for arthralgia
  • supportive (inconsistent evidence for use of steroids and immunosuppressants)

Prognosis:

  • usually excellent, self-limiting
  • BP and urinalysis monitored to detect progressive renal involvement
  • ⅓rd have relapse

Henoch-Schonlein purpura => Type III hypersensitivity reaction => immune complex deposition in small vessels => local damage to blood vessels => purpura. Not necessarily thrombocytopenia

30
Q

MCD

A

Most common in children, Develops faster than other glomerular disease, affects podocytes within BM of kidneys → increased permeability → albumin leakage into urine → oedema

Causes:

  • IDIOPATHIC
  • drugs = NSAIDs, rifampicin
  • Hodgkin’s lymphoma, thymoma
  • infectious mononucleosis

Pathophysiology:

  • T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
  • the resultant reduction of electrostatic charge → increased glomerular permeability to serum albumin

Features

  • nephrotic syndrome = proteinuria, oedema, hypoalbuminaemia
  • NORMOTENSION
  • highly selective proteinuria = only intermediate-sized proteins e.g. albumin and transferrin leak through the glomerulus
  • renal biopsy = normal glomeruli on LM, fusion of podocytes and effacement of foot processes on EM

Mx:

  • oral corticosteroids = 80% steroid responsive, 6wk course of full-dose prednisolone followed by 6wk course of reduced dose
  • cyclophopshamide 2nd line

Prognosis = good, relapse common (⅓ rule)

  • ⅓ one episode
  • ⅓ infrequent relapses
  • ⅓ frequent relapses stop before adulthood
31
Q

Causes of haematuria

A

Transient or spurious non-visible haematuria:

  • UTI
  • menstruation
  • vigorous exercise (settles after 3d)
  • sexual intercourse

Persistent non-visible haematuria:

  • cancer (bladder, renal, prostate(
  • stones
  • BPH
  • prostatitis
  • urethritis e.g. chlamydia
  • renal causes: IgA nephropathy, thin BM disease

Spurious causes: red/orange urine, where blood is not present on dipstick

  • foods = beetroot, rhubarb
  • drugs = rifampicin, doxorubicin
32
Q

Testing for haematuria

A
  • persistent non-visible haematuria = blood present in 2 out of 3 samples tested 2-3 weeks apart
  • renal function, ACR or PCR and BP should also be checked
  • urine microscopy may be used but time to analysis significantly affects the number of RBCs detected
33
Q

Urgent vs non-urgent referral for haematuria

A

Urgent

>45 AND:

  • unexplained visible haematuria without UTI, or
  • visible haematuria that persists or recurs after successful tx of UTI

>50 AND unexplained non-visible haematuria and either dysuria or a raised WBC on a blood test

Non-urgent

>60 with recurrent or persistent unexplained UTI

patients <40 with normal renal function, no proteinuria, normotensive do not need to be referred and may be managed in in primary care

34
Q

Renal investigations

A

Examination = abdominal examination, external genital examination, fluid/hydration assessment

Bedside = set of observations (BP), urinalysis (haematuria, leukocytes, nitrates, proteinuria, pyuria) for MC+S, UO, weight

Bloods = FBC (WCC, Hb, plts), blood film, RFTs (creatinine, ACR/PCR/UCR, eGFR), U+Es (urea, Na, K, phosphate, Ca, Vit D), ABG, stool culture (STEC?)

Imaging = CT KUB, renal USS, DMSA, MCUG

35
Q

HUS

A

young children triad:

  • AKI
  • MAHA
  • thrombocytopenia

Most cases are secondary: typical HUS

  • STEC 0157:H7 (verotoxigenic, enterohaemorrhagic), most common cause in children
  • pneumococcal infection
  • HIV
  • rare = SLE, drugs, cancer

Primary HUS atypical = complement dysregulation

Ix:

  • full blood count: anaemia, thrombocytopaenia, fragmented blood film
  • U&E: acute kidney injury
  • stool culture
    • looking for evidence of STEC infection
    • PCR for Shiga toxins

Management:

  • supportive - fluids, blood transfusion, dialysis if required
  • no role for abx
  • plasma exchange = reserved for severe HUS not associated with diarrhoea
  • eculizumab (C5 inhibitor monoclonal ab) = greater efficiency than plasma exchange alone in tx of adult atypical HUS
36
Q

How do we manage salicylate poisoning?

A

raised anion gap metabolic acidosis

initially presents as = N+V, tinnitus, headache

Severe OD = hyperventilation → 2o respiratory alkalosis → metabolic acidosis and hypokalaemia → confusion, coma, seizures, hypoglycaemia, fever

Mx:

  • recent = activated charcoal
  • minor = supportive
  • significant OD = alkalisation with IV sodium bicarbonate to maintain blood pH at 7.5-8 and enhance salicylate excretion
37
Q

pre-renal AKI and low UO, which fluids?

A

crystalloid containing sodium 130-154 mmol/L with initial bolus of 500mL over less than 15 minutes

Give 0.9% saline = no potassium as hyperkalaemia is a concern in AKI

Hartmann’s is a NO NO (has K)

38
Q

What is the most common cause of peritonitis secondary to peritoneal dialysis?

A

Coagulase-negative staphylococcus e.g. staphylococcus epidermidis

39
Q

Peritoneal Dialysis (PD) and complications

A

Form of RRT, CAPD = continuous ambulatory peritoneal dialysis, 4x 2L exchanges/day

Stop-gap to haemodialysis OR younger patients who do not want to visit hospital 3x/week

Complications = peritonitis and sclerosing peritonitis

Peritonitis

  • CoNS staph epidermidis most common cause, then staph aureus
  • abx should cover both G+ve and G-ve (vancomycin/teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth
  • aminoglycosides are sometimes used to cover the G-ve organisms instead of ceftazidime (cephalosporin)
40
Q

U:C ratio calculation to find out pre-renal AKI

A

divide urea by the creatinine divided by 1000

>100 means pre-renal AKI

41
Q

Acute interstitial nephritis (AIN)

A

commonly caused by drugs

  • fever, rash, arthralgia
  • eosinophilia
42
Q

Acute tubular necrosis

A

Most common cause of AKI = ischaemia, haemorrhage and nephrotoxins → tubule cannot reabsorb urea

  • another cause = compartment syndrome (tibial fracture + fasciotomy → myoglobinuria)
  • haemorrhage → hypotension with compensatory tachycardia
  • normal U:C ratio
  • MUDDY BROWN CASTS (cell injury → red cell casts → brown urine)
43
Q

Acute tubular necrosis

A

Most common cause of AKI = ischaemia and nephrotoxins → tubule cannot reabsorb urea

  • normal U:C ratio
44
Q

Rhabdomyolysis chemical pathology

A

Within hours and a fall/prolonged epileptic seizure

  • raised Cr
  • hypocalcaemia
  • elevated phosphate
  • hyperkalaemia
45
Q

ADPKD: Diagnosis and Mx

A

PDK½ = polycystin-1 and 2, T1 more common and presents with renal failure earlier

US diagnostic criteria (in pt with +ve FHx):

  • 2 cysts, uni/bi, <30 years
  • 2 cysts bi 30-59 years
  • 4 cysts bi >60 years

Mx:

tolvaptan (VR2A) = slows progression of cyst development and renal insufficiency only if

  • CKD stage ⅔ at start of tx
  • evidence of rapidly progressing disease
  • company provides it with the discount agreed in the patient access scheme
46
Q

IgA nephropathy (Berger’s disease): features and pathophysiology and vs post-strep

A

Commonest cause of glomerulonephritis worldwide

Macroscopic haematuria, young male people, after URTI

Renal failure unusual

Associated conditions:

  • alcoholic cirrhosis
  • coeliac disease/dermatitis herpetiformis
  • HSP

Pathophysiology:

  • mesangial deposition of IgA immune complexes
  • pathological overlap with HSP
  • histology: mesangial hypercellularity, positive IF for IgA and C3
47
Q

IgA nephropathy (Berger’s disease): management and prognosis

A

Isolated haematuria, no or minimal proteinuria, and normal GFR

  • no tx needed, f/u to check renal f(x)

persistent proteinuria, normal or slightly reduced GFR

  • active tx with ACEi

Active disease (e.g. failing GFR) or failure to respond to ACEi

  • immsupp with corticosteroids

Prognosis:

  • 25% develop ESRF
  • good prognosis = frank haematuria
  • poor prognosis = male gender, proteinuria (>2g/d), HTN, smoking, hyperlipidaemia, ACE genotype DD
48
Q

3 types of renal replacement therapy and decision to pick which one

A

RRT:

  • haemodialysis
  • PD
  • renal transplant

Consider:

  • predicted QoL
  • predicted life expectancy
  • patient preference
  • co-existing medical conditions

Haemodialysis:

  • most common, in hospital 3x week 3-5 hours each
  • AV fistula surgery 8wk beforehand (lower arm)
  • some patients trained to perform home haemodialysis

PD:

  • filtration via abdomen
  • dialysis solution into Abdo cavity through permanent catheter, high dextrose solution draws waste products from blood into the abdominal cavity across peritoneum → dwell time → dialysis solution then drained, removing waste products from body, and exchanged for new dialysis solution
  • Type 1 = CAPD, exchange lasts 30-40 minutes, dwell time 4-8 hours, can do normal activities with dialysis solution inside their abdomen
  • Type 2 = APD, machine fills and drains abdomen while patient sleeping, 3-5 exchanges over 8-10 hours each night

Renal transplantation

  • live/deceased donor
  • 3 year wait time (pt can receive kidneys donated by cross-matched friends or family)
  • transplanted into groin with renal vessels connected to external iliac vessels
  • failing kidneys NOT removed
  • LIFE-LONG immunosuppressants to prevent kidney rejection
  • 10-12 year kidney life span from deceased, 12-15 from living
49
Q

Complications of RRT

A

Dialysis disequilibribrium syndrome rare complication

  • on those starting RRT
  • headache and increasingly drowsy
  • caused by cerebral oedema, mechanism unclear, diagnosis of exclusion
50
Q

Anti-GBM (Goodpasture’s syndrome)

A

small vessel vasculitis. 2:1 male:female

  • pulmonary haemorrhage
  • rapidly progressing gloemrulonephritis (rapid onset AKI(, nephritis → proteinuria + haematuria

Ix:

  • renal biopsy: linear IgG deposits along BM, anti-GBM abs against T4 collagen
  • raised transfer factor 2o to pulmonary haemorrhage

Mx:

  • plasma exchange (plasmapheresis)
  • steroids
  • cyclophosphamide

Complications: pulmonary haemorrhage. Risks:

  • smoking, LRTI, pulmonary oedema, inhalation of hydrocarbons, young males
51
Q

CKD: anaemia

A

Mainly reduced EPO levels = normocytic anaemia + LVH , apparent when GFR >60 ml/min

Other causes:

  • reduced erythropoiesis due to toxic effects of uraemia on bone marrow
  • reduced iron absorption
  • anorexia/nausea due to uraemia
  • reduced red cell survival (especially in haemodialysis)
  • blood loss due to capillary fragility and poor pet function
  • stress ulceration leading to chronic blood loss

Mx:

  • target Hb 10-12 g/dl
  • determination and optimisation of Fe status carries out prior to administration of erythropoiesis-stimulating agents (ESA) → IV iron
  • ESAs = EPO and darbepoetin
52
Q

Hypokalaemia: causes, features and mx

A

Causes

Increased potassium loss

  • drugs: thiazides, loop diuretics, laxatives, glucocorticoids, abx
  • GI losses: D+V, ileostomy
  • renal causes: dialysis
  • endocrine disorders: hyperaldosteronism, Cushing’s syndrome

Transcellular shift

  • insulin/glucose therapy
  • salbutamol
  • theophylline
  • metabolic alkalosis

Decreased K intake

Mg depletion (associated with increased K loss)

Features

  • ECG = U waves, T flattening or absent, ST segment (prolonged PR) changes, ST depression
  • muscle weakness/hypotonia, leg cramps, palpitations 2o to cardiac arrhythmias and ascending paralysis
  • predisposes its to digoxin toxicity, care should be taken if patients are also on diuretics

Mx

Depends on severity, causative agents removed, ideally PO

  • mild moderate 2.5-3.4 with PO K (no symptoms, no ECG changes)
  • severe <2.5 = IV, high care area w/ cardiac monitoring, 3 bags 0.9% saline with 40mmol KCI. No CI to fluid therapy (volume overload, HF), K diluted to low concentrations as high concentrations can be phlebitic
53
Q

Focal segmental glomerulosclerosis (FSGS)

A

Nephrotic syndrome and CKD, young adults mainly, high recurrence rate in renal transplants

Causes:

  • idiopathic
  • 2o to other renal pathology e.g. IgA nephropathy, reflux neprhotpathy
  • HIV
  • heroin
  • Alport’s syndrome
  • sickle-cell

Ix:

  • renal biopsy = focal and segmental sclerosis and hyalinosis on LM, effacement of foot processes on EM

Mx:

  • steroids +/- immunosuppressants

Prognosis

  • untreated FSGS has a <10% chance of spontaneous remission
54
Q

What virus is most common and important viral infection in solid organ transplant recipients

A

CMV

mx with ganciclovir

55
Q

Complications of nephrotic syndrome

A

Complications

increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine

  • deep vein thrombosis, pulmonary embolism
  • renal vein thrombosis, resulting in a sudden deterioration in renal function

hyperlipidaemia

  • increasing risk of acute coronary syndrome, stroke etc

chronic kidney disease

increased risk of infection due to urinary immunoglobulin loss

hypocalcaemia (vitamin D and binding protein lost in urine)

56
Q

Renal artery stenosis (secondary to atherosclerosis)

A

90% of renal vascular disease, 10% is fibromuscular dysplasia

giving an ACEi = worsen stenosis → drop in eGFR

ix: raised renin:alodsterone from 2o hyperaldosteronism → presents as refractory HTN in younger patients

features:

  • HTN
  • CKD
  • ‘flash pulmonary oedema’
57
Q

Rhabdomyolysis

A

Rhabdomyolysis will typically feature in the exam as a patient who has had a fall or prolonged epileptic seizure and is found to have an acute kidney injury on admission.

Features

  • acute kidney injury with disproportionately raised creatinine
  • elevated creatine kinase (CK)
  • myoglobinuria
  • hypocalcaemia (myoglobin binds calcium)
  • elevated phosphate (released from myocytes)
  • hyperkalaemia (may develop before renal failure)
  • metabolic acidosis

Causes

  • seizure
  • collapse/coma (e.g. elderly patients collapses at home, found 8 hours later)
  • ecstasy
  • crush injury
  • McArdle’s syndrome
  • drugs: statins (especially if co-prescribed with clarithromycin)

Management

  • IV fluids to maintain good urine output
  • urinary alkalinization is sometimes used
58
Q

Diabetic nephropathy: management

A

Screening

  • annual using urinary ACR
  • early morning specimen
  • ACR >2.5 = microalbuminuria

Management

  • dietary protein restriction
  • tight glycemic control
  • BP aim <130/80 mmHg
  • ACEi or ARB = should start if urinary ACR >3 mg/mmol, dual therapy ACEi and ARB should not be started
  • control dyslipidaemia e.g. statins
59
Q

Diabetes Insipidus

A

Decreased ADH secretion from pituitary (cranial DI) or insensitivity to ADH (nephrogenic DI)

Causes of cranial DI:

  • idiopathic
  • post head injury
  • pituitary surgery
  • craniopharyngiomas
  • infiltrative = histiocytosis X, sarcoidosis
  • DIDMOAD = cranial DI, DM, optic atrophy and deafness (Wolfram’s syndrome)
  • haemochromatosis

Causes of nephrogenic DI:

  • genetic = ADH-r, AQP2
  • hypercalcaemia, hypokalaemia
  • lithium = sensitises kidney’s ability to respond to ADH in the CD
  • demclocycline
  • tubulo-interstitial disease = obstruction, sickle-cell, pyelonephritis

Features = polyuria, polydipsia

Ix = high plasma osmolality + low urine osmolality, urine osmolality >700 mOsm/kg excludes DI, water deprivation test

Mx =

  • nephrogenic DI: thiazides, low salt/protein diet
  • cranial DI: desmopressin
60
Q

Acid-base disorders

A
61
Q

Alport’s Syndrome

A

Childhood, X-linked dominant, defects T4 collagen, anti-GBM abs → abnormal GBM

M>F in severity → renal failure

Features:

  • microscopic haematuria
  • progressive renal failure
  • bilateral sensorineural deafness
  • lenticonus = protrusion of lens surface into anterior chamber
  • retinitis pigments
  • renal biopsy = splitting of lamina dense seen on EM

Diagnosis:

  • molecular genetic testing
  • renal biopsy: EM = splitting of lamina dense of GBM → ‘basket-weave’ appearance
62
Q

Post-streptococcal glomerulonephritis

A

2-3 wk after group A b-haemolytic Streptococcus infection (usually Streptococcus progenies), immune complex (IgG/M, C3) deposition in glomeruli, young children

Features

  • general = headache, malaise
  • visible haematuria
  • proteinuria → oedema
  • HTN
  • oliguria
  • bloods = low C3, raised ASOT

Renal biopsy features

  • acute, diffuse, proliferative glomerulonephritis
  • endothelial proliferation with neutrophils
  • EM = subepithelial ‘humps’ caused by lumpy immune complex deposits
  • IF = granular or ‘starry sky’ appearance
63
Q

AV fistulas

A
64
Q

CKD: proteinuria and ACR

A

Sign of diabetic nephropathy

ACR used as well

Collecting an ACR sample = spot sample early morning first-pass urine specimen

  • ACR >3 mg/mmol is clinically important

NICE recommendations for referral to a nephrologist:

  • a urinary albumin:creatinine ratio (ACR) of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated
  • a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection
  • consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease
65
Q

Indications and adverse effects for spironolactone

A

Spironolactone is an aldosterone antagonist which acts in the cortical collecting duct.

Indications

  • ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
  • hypertension: used in some patients as a NICE ‘step 4’ treatment
  • heart failure (see RALES study below)
  • nephrotic syndrome
  • Conn’s syndrome

Adverse effects

  • hyperkalaemia
  • gynaecomastia: less common with eplerenone

RALES study

  • NYHA III + IV, patients already taking ACE inhibitor
  • low dose spironolactone reduces all cause mortality
66
Q

RCC (hypernephroma)

A

arises from proximal renal tubular eptihlium

  • most common subtype is clear cell

Associations:

  • middle-aged men
  • smoking
  • VHL syndrome
  • tuberous sclerosis
  • ADPKD

Features:

  • Triad = flank pain, flank mass, haematuria (advanced disease)
  • PuO
  • endocrine effects = EPO secretion (polycythaemia), PTH (hypercalcaemia), renin, ACTH
  • 25% metastasis at presentation
  • paraneoplastic hepatic dysfunction syndrome
  • varicocele (bag of worms texture) → renal USS. Majority left sided, tumour compresses veins, increased IL-6 levels → cholestasis/hepatosplenomegaly

Management:

  • confined disease = partial/total nephrectomy depending on tumour size. T1 tumour (<7cm) → partial
  • a-interferon + IL-2 to reduce tumour size and tx patients with metastases
  • receptor TK inhibitors (sorafenib, sunitinib)
67
Q

Immunosuppression regime (solid)

A

Induction agent = alemtuzumab, basiliximab

maintenance agent = tacrolimus, mycophenolate mofetil, predisolone

Year 6 Nephrology (1 decks)

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