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Nephrology Flashcards

1
Q

What are the causes of metabolic acidosis:

A

Normal anion gap (hyperchloraemic)

  • GI bicarbonate loss - diarrhoea, uterosigmoidostomy, fistula
  • renal tubular acidosis
  • drugs e.g. acetazolamide
  • ammonium chloride injection
  • Addison’s

Increased anion gap

  • lactate: shock, hypoxia
  • ketonones: DKA, alcohol
  • urate: renal failure
  • acid poisoning: salicylates, methanol
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2
Q

Causes of metabolic alkalosis:

A

Loss of hydrogen ions or gain of bicarbonate due to kidney or GI problems:

  • vomiting/aspiration
  • diuretics
  • liquorice, carbenoxolone
  • hypokalaemia
  • primary hyperaldosteronism
  • Cushing’s syndrome
  • Bartter’s syndrome
  • congenital adrenal hyperplasia
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3
Q

Causes of respiratory acidosis:

A
  • COPD
  • decompensation other resp conditions
  • sedatives: benzodiazepines, opiate overdose
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4
Q

Causes of respiratory alkalosis:

A
  • anxiety
  • PE
  • salicylate poisoning
  • CNS disorders: stroke, SAH, encephalitis
  • altitude
  • pregnancy
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5
Q

What causes type A lactic acidosis?

A
  • sepsis
  • shock
  • hypoxia
  • burns
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6
Q

What causes type B lactic acidosis?

A

metformin

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7
Q

What are the causes of acute interstitial nephritis?

A

Drugs:

  • penicillin
  • rifampicin
  • NSAIDs
  • allopurinol
  • furosemide
  • systemic: SLE, sarcoidosis, Sjogren’s
  • infection: Hanta virus, staphylococci
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8
Q

What are the features and investigations of acute interstitial nephritis?

A
  • fever, rash, arthralgia
  • eosinophilia (casts)
  • mild renal impairment
  • HTN
  • sterile pyuria and white cell casts
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9
Q

Pre-renal causes of AKI:

A

ischaemia: e.g. hypovolaemia secondary to diarrhoea/vomiting, renal artery stenosis etc.

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10
Q

Renal causes of AKI:

A
  • intrinstc damage to glomeruli, renal tubules or interstitium
    e. g. toxins (drugs, contrast), GN, ATN, AIN, rhabdomyolysis, tumour lysis syndrome
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11
Q

Postrenal causes of AKI:

A

obstruction to urine: e.g. stones, hydronephrosis, external compression etc.

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12
Q

Risk factors of AKI:

A
  • CKD
  • other organ failure/chronic disease e.g. HF, liver disease, diabetes
  • history of acute AKI
  • nephrotoxic drugs: NSAIDs, aminoglycosides, ACEi, ARBs and diuretics in past week
  • iodinated contrast agent
  • > =65yo
  • oliguria (<0.5ml/kg/hr)
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13
Q

Symptoms and detection of AKI:

A

Symptoms:

  • reduced urine output
  • pulmonary and peripheral oedema
  • arrhythmias (secondary to changes in K+)
  • features of uraemia (e.g. pericarditis or encephalopathy)

Detection:

  • creatinine increase by >=26micromol/L in 48 hours
  • 50% or greater rise in serum creatinine or within 7 days
  • reduced urine output <0.5ml/kg/hr for more than 6 hours
  • urinalysis
  • renal US within 24 hours
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14
Q

Drugs which should be stopped in AKI:

A

-NSAIDs
-aminoglycosides
-ACEi
-ARB
-diuretics
(metformin, lithium, digoxin)

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15
Q

How do you treat hyperkalaemia e.g. in AKI?

A
  • IV calcium gluconate
  • combined insulin/dextrose infusion
  • nebulised salbutamol
  • calcium resonium (oral or enema)
  • loop diuretics
  • dialysis
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16
Q

Criteria for diagnosing AKI:

A
  1. rise in creatinine of 26micromol/L or more in 48 hours OR
  2. > =50% rise in creatinine over 7 days OR
  3. fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults (8 in children) OR
  4. > =25% fall in eGFR in children/young adults in 7 days
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17
Q

When do you refer AKI to a nephrologist?

A
  • renal transplant
  • ITU with unknown cause AKI
  • vasculitis/GN/tuberointerstitial nephritis/myeloma
  • AKI with no known cause
  • inadequate response to treatment
  • complications of AKI
  • stage 3 AKI
  • CKD stage 4 or 5
  • qualify for renal replacement hyperkalaemia/metabolic acidosis/complications of uraemia/fluid overload (pulmonary oedema)
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18
Q

How can you differentiate between acute and chronic renal failure?

A

-renal US
-most chronic have bilateral small kidneys
EXCEPT ADPKD, diabetic nephropathy, amyloidosis, HIV associated nephropathy
-chronic has hypocalcaemia due to reduced vit D

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19
Q

What are the types of ADPKD?

A 
Type I:
-polycysitn-1
-85% of cases
-chromosome 16
-presents with renal failure earlier
Type II:
-polycystin-2
-chromosome 4
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20
Q

Features and extra renal manifestations of ADPKD:

A
  • HTN
  • recurrent UTIs
  • abdominal pain
  • renal stones
  • haematuria
  • CKD
  • extra-renal: liver cysts, berry aneurysms (SAH), mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
  • cysts in other organs: pancreas, spleen, rarely thyroid, oesophagus and ovary
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21
Q

How do you manage ADPKD:

A
  • tolvaptan (vasopressin receptor 3 antagonist)

- if CKD stage II or III, evidence of rapidly progressing disease

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22
Q

What is Alport’s syndrome? (incl features)

A
  • x-linked dominant
  • defect gene coding for type IV collagen (abnormal GBM)
  • more severe in males
  • presents in childhood

Features:

  • mircoscopic haematuria
  • progressive renal failure
  • bilateral sensorineural deafness
  • leticonus
  • retinitis pigmentosa
  • renal biopsy: splitting of lamina densa
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23
Q

What is Amyloidosis?

A
  • extracellular deposition of insoluble fibrillar protein - amyloid
  • also apolipoprotein E and heparin sulphate proteoglycans
  • accumulation of amyloid fibrils - tissue/organ dysfunction
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24
Q

How do you diagnose amyloidosis?

A
  • congo red staining - apple-green birefringence
  • serum amyloid precursor scan
  • biopsy of rectal tissue
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25
Q

What is an anion gap?

A

(sodium+potassium) - (bicarbonate+chloride)

normal: 8-14mmol/L

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26
Q

What is anti-GBM disease?

A
  • Goodpasture’s
  • rare, small vessel vasculitis
  • associated with pulmonary haemorrhage and rapidly progressive GN
  • antibodies against type IV collagen
  • more common in men 2:1
  • HLA DR2
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27
Q

How do you test for and manage anti-GBM disease?

A
  • renal biopsy: linear IgG deposits along BM
  • increased transfer factor secondary to pulmonary haemorrhages
  • manage with: plasma exchange, steroids, cyclophosphamide
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28
Q

What increases the risk of pulmonary haemorrhage in anti-GBM?

A
  • smoking
  • lower RTI
  • pulmonary oedema
  • inhalation of hydrocarbons
  • young males
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29
Q

What is ARPKD?

A
  • autosomal recessive version
  • much less common
  • defect in gene on chromosome 6 which encodes fibrocytin
  • end stage renal failure in childhood
  • liver involvement (portal and interlobular fibrosis)
  • renal biopsy shows multiple cylindrical lesions
  • diagnosis on prenatal US: abdominal masses and renal failure, consistent with Potter’s syndrome secondary to oligohydramnios
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30
Q

Complications of AV fistulae?

A
  • infection
  • thrombosis (absence of bruit)
  • stenosis (acute limb pain)
  • steal syndrome
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31
Q

What is diabetes insipidus and what are the features and investigation?

A
  • either deficiency of ADH (cranial) or insensitivity to ADH (nephrogenic)
  • polyuria and polydipsia
  • increased plasma osmolality and decreased urine osmolality
  • urine osmolality >700mOsm/kg excludes DI
  • water deprivation test
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32
Q

What causes cranial diabetes insipidus and what is the management?

A

-idiopathic
-post HI
-pituitary surgery
-craniopharyngiomas
-histiocytosis X
-DIDMOAD (Wolfram’s syndrome)
-haemochromatosis
manage with desmopressin

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33
Q

What are the causes of nephrogenic diabetes insipidus and the management?

A

-genetic (ADH receptor or aquaporin 2 channel)
-electrolytes (hypercalcaemia and hypokalaemia)
-drugs: demeclocycline, lithium
-tubulo-interstitial disease: obstruction, sickle cell, pyelonephritis
manage with thiazides, low salt/protein diet

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34
Q

Side effects of erythropoietin therapy and indication:

A 
-used for anaemia associated with CKD 
can cause:
-accelerated HTN - encephalopathy and seizures
-bone aches
-flu-like
-skin rashes, urticaria
-pure red cell aplasia
-increased PCV - thrombosis
-iron deficiency secondary to increased erythropoiesis
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35
Q

Why might someone be unresponsive to erythropoietin therapy?

A
  • iron deficiency
  • inadequate dose
  • concurrent infection/inflammation
  • hyperparathyroid bone disease
  • aluminium toxicity
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36
Q

What is Fanconi syndrome, features and causes?

A
  • generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule
  • polyuria, type II RTA, aminoaciduria, glycosuria, phosphaturia, osteomalacia
  • causes: cystinosis, Sjogren’s, multiple myeloma, nephrotic syndrome, Wilson’s
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37
Q

What is fibromuscular dysplasia?

A
  • renal artery stenosis secondary to atherosclerosis
  • 90% female
  • causes HTN, CKD and flash pulmonary oedema
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38
Q

Maintenance fluids:

A
  • 25-30ml/kg/day water
  • 1mmol/kg/day of potassium, sodium and chloride
  • 50-100g/day of glucose to limit starvation ketosis
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39
Q

What is the risk of using large volumes of NaCl 0.9%?

A

increased risk of hyperchloraemic metabolic acidosis

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40
Q

In which patients is Hartmann’s contraindicated?

A

hyperkalaemic patients

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41
Q

What is focal segmental glomerulosclerosis and the causes?

A
  • causes nephrotic syndrome and CKD
  • young adults
  • idiopathic
  • secondary to other renal pathology
  • HIV
  • heroin
  • Alport’s syndrome
  • sickle cell
  • high recurrence rate in renal transplants
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42
Q

What are the investigations and management for focal segmental glomerulosclerosis?

A
  • renal biopsy: focal and segmental sclerosis and hyalinosis, effacement of foot processes
  • manage with steroids (and immunosuppressants)
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43
Q

Causes of transient or spurious non-visible haematuria:

A
  • UTI
  • menstruation
  • vigorous exercise (resolves in 3 days)
  • sexual intercourse
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44
Q

Spurious causes of haematuria (red/orange urine)

A
  • beetroot, rhubarb
  • rifampicin
  • doxorubicin
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45
Q

Urgen referral criteria for haematuria:

A
  • > =45yo with unexplained visible haematuria without UTI or visible haemautria that persists after successful treatment of UTI
  • > =65yo and unexplained non-visible haematuria and dysuria or increased WCC
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46
Q

Non-urgent referral criteria for haematuria:

A
  • > =60yo with recurrent or persistent unexplained UTI

- <40yo with normal renal function, no proteinuria and normotensive (no referral - manage in primary care)

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47
Q

Presentation of HUS:

A
  • triad: AKI, microangiopathic haemolytic anaemia, thrombocytopaenia
  • bloody diarrhoea few days after onset
  • most cases secondary to:
  • shiga toxin producing e-coli (STEC) O157:H7 - most common in children
  • pneumococcal infection
  • HIV
  • rare: SLE, drugs, cancer
  • primary HUS - atypical - complement dysregulation
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48
Q

Management of HUS:

A
  • supportive e.g. dialysis, fluids, blood transfusion
  • no Abx
  • eculixumab - C5 inhibitor monoclonal antibody
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49
Q

What is Henoch-Schonlein Purpura and the features?

A
  • IgA mediated small vessel vasculitis
  • some overlap with IgA nephropathy (Berger’s)
  • usually in children following infection
  • palpable purpuric rash (with localised oedema) over buttocks and extensor surfaces of arms and legs
  • abdominal pain
  • polyarthritis
  • features of IgA nephropathy
  • good prognosis - self-limiting
50
Q

Treatment of HSP:

A
  • analgesia for arthralgia

- supportive Tx for nephropathy

51
Q

What is IgA nephropathy, associations, pathophysiology and presentation?

A
  • Berger’s
  • most common cause of GN
  • associated with: alcoholic cirrhosis, coeliac disease/dermatitis herpetiformis, HSP
  • mesangial deposition of IgA immune complexes, mesangial hypercellularity, positive immunofluorescence for IgA and C5
  • typically young male with recurrent episodes of macroscopic haematuria following a RTI
  • nephrotic range proteinuria rare
  • renal failure unusual
52
Q

IgA nephropathy vs post streptococcal:

A
  • post strep results in low complement
  • post strep main symptom proteinuria
  • interval between URTI and post-strep onset (1-2 weeks)
53
Q

Prognosis of IgA nephropathy:

A
  • 25% ESRF
  • frank haematuria - good prognosis
  • male, proteinuria, HTN, smoking hyperlipidaemia, ACE genotype DD - poor prognosis
54
Q

How does membranoproliferative GN/mesangiocapillary GN present?

A
  • nephrotic syndrome, haematuria or proteinuria
  • poor prognosis
  • involves mesangium as well as BM (unlike membranous)
55
Q

Type I membranoproliferative GN:

A
  • 90% cases
  • caused by cryoglobulinaemia, hepatitis C
  • renal biopsy: sub endothelial and mesangium immune deposits of electron dense material - tram track appearance
56
Q

Type II membranoproliferative GN:

A
  • dense deposit disease
  • caused by partial lipodystrophy and factor H deficiency
  • persistent activation of alternative complement pathway
  • low circulating levels of C3
  • C3b nephritic factor found in 70%
  • renal biopsy: intramembranous immune complex deposits with dense deposits
57
Q

Type III membranoproliferative GN is caused by:

A

hepatitis B and C

58
Q

How do you treat membranoproliferative GN?

A

steroids

59
Q

Membranous GN

A
  • most common type in adults
  • presents as nephrotic syndrome or proteinuria
  • renal biopsy: basement membrane thickened with sub epithelial electron dense deposits (spike and dome)
60
Q

Causes of membranous GN:

A
  • idiopathic: antiphospholipase A2 antibodies
  • infections: hep B, malaria, syphilis
  • malignancy: prostate, lung, lymphoma, leukaemia
  • drugs: gold, penicillamine, NSAIDs
  • autoimmune: SLE, thyroiditis, rheumatoid
61
Q

Management of membranous GN:

A
  • ACEi or ARB
  • immunosuppression (corticosteroid and cyclophosphamide)
  • consider anticoagulation
62
Q

Prognosis of membranous GN:

A

1/3 spontaneous remission
1/3 remain proteinuric
1/3 ESRF

63
Q

Minimal change disease (presentation, causes, features, biopsy, management)

A
  • presents as nephrotic syndrome
  • causes: idiopathic, drugs, Hodgkin’s lymphoma, thymoma, infectious mononucleosis
  • T cell and cytokine mediated damage to GBM - polyanion loss
  • normotension, high selective proteinuria (albumin and transferrin leak through glomeruli)
  • renal biopsy: normal glomeruli on light microscopy, fusion of podocytes and effacement of foot processes on electron microscopy
  • management: majority steroid responsive or cyclophosphamide if steroid resistant (do biopsy)
64
Q

Prognosis of minimal change disease:

A
  • 1/3 only 1 episode
  • 1/3 infrequent relapses
  • 1/3 frequent relapses which stops before adulthood
65
Q

Features of nephrotic syndrome:

A
  • triad: proteinuria, hypoalbuminaemia, oedema
  • loss of antithrombin III, protein C and S and associated increase in fibrinogen predisposes to thrombosis
  • loss of thyroxine - binding globulin decreased total but not free thyroxine
66
Q

Complications of nephrotic syndrome:

A
  • increased risk of thromboembolism due to loss of antithrombin III and plasminogen in urine
  • hyperlipidaemia - increased risk of ACS, stroke etc.
  • CKD
  • increased risk of infection due to urinary immunoglobulin loss
  • hypocalcaemia (vita and binding protein lost in urine)
67
Q

Sign of nephrotoxicity contrast media:

A

25% increase in creatinine within 3 days of intravascular administration

68
Q

Nephrotoxicity contrast media risk factors and prevention:

A
  • know renal impairment
  • > 70 yo
  • dehydration
  • cardiac failure
  • use of nephrotoxic drugs

Prevention:

  • IV 0.9% NaCl at 1ml/kg/hr of 12 hours pre- and post-op
  • isotonic sodium bicarbonate
  • N-acetylcysteine not effective
69
Q

Complications of peritoneal dialysis:

A
  • peritonitis: coagulase negative staph e.g. staph epidermis most common, also aureus
  • sclerosing peritonitis
70
Q

Post-streptococcal glomerulonephritis presentation and features:

A
  • 7-14 days following group A beta haemolytic strep infection (usually pyogenes)
  • immune complex deposition in glomeruli
  • mostly young hcildren
  • general headache, malaise, visible haematuria, proteinuria, oedema, HTN, oliguria, low C3 and raised ASO titre
  • good prognosis
71
Q

What does the renal biopsy show in post-streptococcal GN?

A
  • acute diffuse proliferative GN
  • endothelial proliferation with neutrophils
  • electron microscopy: sub epithelial humps cause by lumpy immune complex deposits
72
Q

Rapidly progressive glomerulonephritis causes and presentation:

A
  • rapid loss of renal function with formation of epithelial crescents in majority of glomeruli
  • causes: Good pasture’s, vasculitic rash or sinusitis with Wegener’s
73
Q

Reflux nephropathy:

A
  • chronic pyelonephritis secondary to vesico ureteric reflux
  • commonest cause of chronic GN
  • scanning first 5 year
  • strong genetic component
  • renal scars may produced increased quantities of renin - HTN
  • diagnosis by micturating cystography
74
Q

Renal artery stenosis:

A
  • secondary to atherosclerosis (90% of renal vascular disease)
  • HTN, CKD, flash pulmonary oedema
75
Q

Renal papillary necrosis incl causes and features:

A
  • coagulative necrosis of renal papillae due to variety of causes
  • caused by: severe acute pyelonephritis, diabetic nephropathy, obstructive nephropathy, analgesic nephropathy, sickle cell anaemia
  • visible haematuria, loin pain, proteinuria
76
Q

Types of renal replacement therapy:

A
  • haemodialysis
  • peritoneal dialysis
  • renal transplant
77
Q

Haemodialysis:

A
  • most common RTT
  • most need 3 per week
  • surgery to create AV fistula 8 weeks before commencing
78
Q

Peritoneal dialysis:

A
  • filtration within abdomen
  • dialysis solution injected into abdominal cavity through a permanent catheter
  • high dextrose concentration of solution draws waste products out
  • 2 types: continuous ambulatory and automated peritoneal dialysis
79
Q

Renal transplant:

A
  • into groin and renal vessels connected to external iliac
  • failing kidneys not removed
  • life-long immunosuppressants
  • average lifespan 10-12 years
80
Q

Haemodialysis complications:

A
  • site infection
  • endocarditis
  • stenosis at site
  • hypotension
  • cardiac arrhythmias
  • air embolus
  • anaphylactic reaction to sterilising agents
  • disequilibration syndrome (cerebral oedema)
81
Q

Peritoneal dialysis complications:

A
  • peritonitis (staph epidermis)
  • sclerosing peritonitis
  • catheter infection
  • catheter blockage
  • constipation
  • fluid retention
  • hyperglycaemia
  • hernias
  • back pain
  • malnutrition
82
Q

Renal transplantation complications:

A
  • DVT/PE
  • opportunistic infection
  • malignancies (particularly lymphoma and skin cancer)
  • bone marrow suppression
  • recurrence of original disease
  • urinary tract obstruction
  • CVD
  • graft rejection
83
Q

Hyperacute rejection of transplant:

A
  • pre-existing Ab against ABO or HLA antigens
  • type II hypersensitivity
  • widespread thrombosis of graft vessels -ischaemia and necrosis
  • remove graft
84
Q

Acute graft failure of transplant:

A
  • <6 mo
  • usually mismatched HLA, cell mediated cytotoxic T cells
  • or CMV infection
  • may be reversible with steroids and immunosuppressants
85
Q

Chronic graft failure of transplant:

A
  • > 6 mo
  • both AB and cell mediated mechanisms cause fibrosis to transplanted kidney
  • recurrence of renal disease
86
Q

Immunosuppression in renal transplantation:

A
  • intial: ciclosporin/tacrolimus with monoclonal Ab
  • maintenance: ciclosporin/tacrolimus with MMF or sirolimus
  • add steroids if more than one steroid responsive acute rejection episode
87
Q

Rhabdomyolysis features:

A
  • AKI with disproportionately increased creatinine
  • elevated CK
  • myoglobulinuria
  • hypocalcaemia (myoglobin binds calcium)
  • increased phosphate (from myocytes)
  • hyperkalaemia (before renal failure)
  • metabolic acidosis
88
Q

Causes of rhabdomyolysis:

A
  • seizure
  • collapse/coma
  • ecstacy
  • crush injury
  • McArdle’s syndrome
  • drugs: statins (especially with clarithromycin)
89
Q

Management of rhabdomyolysis:

A
  • IV fluids to maintain good urine output

- urinary alkalisation sometimes used

90
Q

Causes of sterile pyuria:

A
  • partially treated UTI
  • urethritis e.g. chlamydia
  • renal tuberculosis
  • renal stones
  • appendicitis
  • bladder/renal cell cancer
  • APKD
  • analgesic nephropathy
91
Q

SLE renal complications WHO classifications:

A
  • class I: normal kidney
  • class II: mesangial glomerulonephritis
  • class III: focal and segmental proliferative GN
  • class IV: diffuse proliferative GN
  • class V: diffuse membranous GN
  • class VI: sclerosis GN

class IV most common and severe

92
Q

What produces hyaline casts:

A
  • Tamm Horsfall protein secreted by distal convoluted tubule

- normal urine, exercise, fever or loop diuretics

93
Q

What is visible in the urine in ATN?

A

brown granular casts

94
Q

How does the urine appear in prerenal uraemia:

A

bland urinary sediment

95
Q

What is visible in the urine with nephritic syndrome?

A

red cell casts

96
Q

Symptoms of anaemia in CKD:

A
  • tachycardia
  • fatigue
  • pallor
  • aortic flow murmur
97
Q

What causes anaemia in CKD:

A
  • usually normochromic normocytic anaemia
  • prediposes to left ventricular hypertrophy
  • decreased erythropoietin
  • reduced erythropoiesis due to toxic effects of uraemia on bone marrow
  • reduced iron absorption
  • anorexia/nausea due to uraemia
  • reduced red cell survival
98
Q

Management of anaemia in CKD:

A
  • determination of iron status before erythropoiesis stimulation agents
  • many patients esp haemodialysis requires IV iron
  • ESAs e.g. erythropoietin and darbepoietin
99
Q

Clinical manifestations of bone disease in CKD:

A
  • osteitis fibrosa cystica (hyperparathyroid bone disease)
  • adynamic: cellular activity decreased, may be due to over treatment with vit D
  • osteomalacia
  • osteoscelerosis
  • osteoporosis
100
Q

Management of bone disease in CKD:

A
  • aim to decrease phos and PTH
  • 1st line: decrease phosphate dietary intake
  • phosphate binders (sevelamer, calcium based)
  • vit D: alfacalcidol (does not require activation in kidneys), calcitriol
  • sometimes parathyroidectomy
101
Q

CKD stage I

A
  • GFR greater than 90ml/min

- some sign of kidney damage

102
Q

CKD stage II

A
  • 60-90ml/min

- some sign of kidney damage

103
Q

CKD stage IIIa and b

A 
a
-45-59ml/min
-moderate reduction kidney function
b
-30-44ml/min
-moderate reduction kidney function
104
Q

CKD stage IV

A
  • 15-29ml/min

- severe reduction in kidney function

105
Q

CKD stage V

A
  • less than 15ml/min
  • establish kidney failure
  • dialysis or kidney transplant needed
106
Q

What can affect MDRD formula for calculating CKD stage?

A
  • pregnancy
  • muscle mass
  • eating red meat 12 hours before sample
107
Q

At what eGFR does a nephrologist need to be called?

A

<30ml/min

108
Q

What ratio is used to determine proteinuria in CKD?

A

ACR over PCR (greater sensitivity)

109
Q

How should a urine sample be collected for CKD?

A
  • spot sample
  • first pass morning urine
  • if initial ACR 3-70mg/mmol, subsequent early morning sample (higher no repeat sample needed)
110
Q

Which ACR values should be referred to a nephrologist?

A
  • > =70mg/mmol unless caused by diabetes
  • > =30mg/mmol with persistent haematuria (2 of 3 dipsticks) after exclusion of UTI
  • 3-29mg/mmol with persistent haematuria and risk factors consider
111
Q

Management of coexistent HTN and CKD:

A
  • ACEi or ARB

- ACR >70mg/mmol regardless of BP

112
Q

Which medication which CKD patients take can lead to abdominal pain, back pain, muscle weakness etc?

A
  • calcium binders e.g. calcium acetate

- hypercalcaemia and vascular calcification

113
Q

What kind of murmur can you hear with anaemia?

A

soft ejection systolic murmur (aortic flow murmur)

114
Q

Maintenance fluid regime rate:

A

500ml 0.9% saline at 100ml/hr

115
Q

Resuscitation fluids:

A

500ml 0.9% saline in 15 mins

116
Q

What should you consider in young females who develop an AKI after taking ACEi? (string bead appearance)

A

fibromuscular dysplasia

117
Q

How to distinguish primary and secondary aldosteronism:

A

high renin - secondary e.g. renal artery stenosis

118
Q

Most common extra renal manifestation of ADPKD:

A

liver cysts

119
Q

How do you treat nephrogenic diabetes?

A

chlorthiazide

120
Q

How do you treat hypokalaemia?

A
  • cardiac monitoring

- 3 x 1 litre bags of 0.9% saline with 40mmol KCL per bag over 24 hours

121
Q

What variables does the MDRD equation include?

A
  • creatinine
  • age
  • gender
  • ethnicity

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