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APhase 3b flashcards > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Manifestations of high phosphate

A

Itch/pruitus

Osteodystrophy

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2
Q

Kidney stone disease name

A

Nephrolithiasis

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3
Q

Types of kidney stone composition

A

Calcium stones - either calcium oxalate, calcium phosphate.

Others:
Struvite (magnesium, ammonium, phosphate from bacterial infection)
Uric acid (low urine pH)
Cystine (genetic cause).

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4
Q

Risk factors for kidney calculi

A 
Male
Obese
Dehydration
Diet = high animal protein diet
Deformity = horseshoe kidney
Drugs = vitamin D supplements
Diseases = hyperparathyroidism
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5
Q

3 common sites of renal stones

A

Pelvic-ureteric junction
Mid-ureter at cross over of iliac vessels
Vesicoureteric junction

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6
Q

Signs and symptoms fo renal calculi

A

Renal colic = sudden onset severe unilateral pain in the loin area and radiated to groin/labia area.
Pain can occur in spasms/intervals but usually constant.
Nausea, vomiting, haematuria.
Hx of dysuria, frequency or straining.

O/E - restless (peritonitis pts are still), pyrexi

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7
Q

Investigations for renal calculi

A

Non-contrast helical CT of KUB.

Urine dipstick = ++RBC
MSU for ms+c
FBC, CRP, U+Es, serum calcium, phosphate, urate
Pregnancy test in females

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8
Q

Management of renal calculi

A

1) Analgesia - IM diclofenac.
Anti-emetic - IM Metoclopramide.
2) Hydration - fluids will pass out stones <5mm.
3) Medical expulsion therapy for stones: CCB e.g. Nifedipine or alpha blocker e.g. tamsulosin.
4) ESWL - Extracorporeal shock wave lithotripsy.
5) Ureteroscopy and laser break down.
6) Surgical nephrolithotomy.

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9
Q

Types of polycystic kidney disease

A 
Autosomal dominant (ADPKD) usually adult presentation.
Autosomal recessive (ARPKD) much more rare and presents in childhood.
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10
Q

Genes in autosomal dominant polycystic kidney disease

A

PKD1 coding for protein polycystin 1 (85%) and PKD2 coding for polycystin 2.

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11
Q

Signs and symptoms of PKD

A

Can be asymptomatic until complication.

ADPKD = nocturia and polyuria
ARPKD = childhood onset, abdo mass and renal failure, portal HTN and hepatic fibrosis..
History:
Lumbar pain (esp females)
Flank discomfort.
Dysuria
Haematuria
LUTS e.g. urgency
Symptoms of HTN e.g. headaches.
FHx of PKD/ESRD.
O/E:
Palpable kidney/mass in flank area.
HYPERTENSION
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12
Q

Investigations for PKD

A

KUB USS
Genetic testing.
CT abdo pelvis non-contrast.

Screen for complications:

  • intracranial aneurysms with MRI
  • ECG or echocardiogram.
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13
Q

Treatment of PKD

A

SCREEN FAMILY!
Ensure adequate water intake.
Treat symptoms e.g. HTN with ACE-i.
Renal replacement therapy - dialysis, transplant list.
Surgery on cysts
Genetic counselling.
Safety-net advise on SAH and cerebral aneurysms.

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14
Q

Glomerular filtration barrier components

A

Podocyte
Glomerular basement membrane
Fenestrated capillary endothelium

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15
Q

Flow of blood in nephron

A

Glomeruli –> proximal convoluted tubule –> descending loop of Henle –> ascending loop of Henle –> distal convoluted tubule –> collecting tubule –> collecting duct.

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16
Q

What makes up the renal corpuscle

A

Glomerulus and Bowman capsule

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17
Q

Name some functions of the kidney

A 
Eliminate waste products
Regulate acid-base balance
Regulate blood pressure
Regular electrolyte balance
Produce erythropoietin
Produce renin (juxtaglomerular apparatus)
Activate vitamin D
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18
Q

Quick description of RAAS

A
  1. Low renal perfusion or increased sympathetic drive = kidneys produce RENIN.
  2. In liver angiotensinogen is converted to angiotensin I.
  3. Conversion of angiotensin I to angiotensin II via ACE mostly in lungs.
  4. Angiotensin II is vasoconstrictor.
  5. Aldosterone secretion of adrenal cortex under influence of angiotensin II.
  6. Aldosterone increases sodium and warmer reabsorption in kidneys.
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19
Q

Causes of end stage renal failure

A

Pyelonephritis
Polycystic kidney disease
Glomerulonephritis
Diabetes

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20
Q

Fanconi syndrome

A
  • Proximal tubule dysfunction leading to acute tubular acidosis.
  • Urine has high levels of:
    Glucose, phosphate, uric acid, amino acid and high protein:creatinine ratio.
  • S+S: growth impairment, muscle weakness, Rickets, hypoglycaemia
  • Ix: serum anion gap on ABG is normal.
  • Rx: need to replace phosphate.
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21
Q

Hydronephrosis

A

Dilation of renal pelvis commonly due to urine obstruction.
Can be unilateral or bilateral.
If kidney function is affected from urine obstruction = obstructive nephropathy.

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22
Q

Common causes of hydronephrosis

A 
Renal calculi (unilateral)
BPH (bilateral)
Prostate cancer
Bladder cancer
Iatrogenic e.g. gynae surgery
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23
Q

Presentation of hydronephrosis

A 
Flank pain
Dysuria
LUTS
Haematuria
Fever

O/E:
Distended abdomen and palpable bladder

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24
Q

Ix for hydronephrosis and Mx

A

Lab:
Urea and creatinine
Urine dipstick
FBC

Imaging:
USS KUB
Non-contrast CT

Mx = treat cause. Analgesia, antibiotics. Ureteric stent, nephrostomy.

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25
Q

Why measure creatinine for kidney function

A
  • Serum creatinine is usually constant.
  • Creatinine is freely filtered by glomerulus and not reabsorbed so marker of GFR.
  • Estimate GFR with serum creatinine level and a timed urine collection.
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26
Q

Definition for acute kidney injury 💦

A

Sudden onset renal dysfunction.
KDIGO definitions:
- Rise in creatinine >26micromol/L in 48hrs
- Rise in creatinine >1.5 times baseline creatinine within 7 days.
- Urine output <0.5ml/kg/hr for >6 consecutive hours.

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27
Q

Causes of acute renal failure

A

·PRE-RENAL = hypovolaemia, reduced cardiac output
e.g. burns, haemorrhage, cardiac failure, cariogenic shock, ACE inhibitors.
·RENAL = vascular glomerular, tubular and interstitial
e.g. thrombosis, scleroderma, glomerulonephritis, rhabdomyolysis, acute tubular necrosis due to SEPSIS, interstitial nephritis.
·POST-RENAL = obstruction
e.g. renal calculi, bladder cancer, BPH
·DRUGS (NSAID, contract, diuretics, ACE inhibitors, penicillins).

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28
Q

Acute tubular necrosis

A
  • Decrease perfusion - sepsis, shock, contrast agents.
  • VVVV common cause of intrinsic/renal AKI.
  • Ix =Hyperkalaemia, hyperuraemia, high creatinine. Urinalysis = brown granular casts.
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29
Q

Name some nephrotoxic drugs 🤪

A 
Iodinated contrast agents
Diuretics
ACE inhibitor and Angiotensin receptor blockers
NSAIDS
Gentamycin
Acyclovir
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30
Q

Complications of AKI

A 
Hyperkalaemia
Metabolic acidosis 
Pulmonary oedema
Uraemia
CKD and ESKD
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31
Q

S+S of AKI

A

Decreased urine output
Nausea and vomiting
Dizziness, drowsiness, fatigue, altered mental state (uraemia).
Hx of risk factors or causes (DM, prescribed drugs, CHF, muscle cramps).

O/E:
tachycardia, hypotensive, pedal oedema.

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32
Q

AKI and not responsive to fluids cause…

A

Hepatorenal syndrome

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33
Q

Ix for suspected AKI

A

· Bloods: ABG or VGB, serum creatinine, U+E (esp potassium!!), LFT, FBC. Find cause e.g. ANCA, ANA antibodies, creatinine kinase (rhabdomylosis)
· Catheterise: urine dipstick, urine sample for microscopy (bence jones protein, cellular casts), urine osmolality, urine sodium.
· Other: ECG, CXR
· Imaging: KUB USS (within 24hrs)

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34
Q

Management of AKI

A
  1. Stop nephrotoxic drugs.
  2. A to E resuscitation including IV fluid bolus (500ml 0.9% normal saline STAT) and catheter.
  3. Investigate ABG + ECG + KUB USS + urine dipstick.
  4. Sodium bicarbonate for metabolic acidosis + good ventilatory support.
  5. If uraemia, severe met acidosis, severe hyperkalaemia = renal replacement therapy e.g. dialysis.
  6. If due to obstruction - stent.
  7. Consider need for ITU and vasopressors if not responding to fluid.
  8. RRT.
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35
Q

Management of hyperkalaemia and what level of K is worrying?

A

If potassium is >6.5mmol/L or >6mmol/L + ECG changes: ACT NOW 🆘⚠️🆘
·Nebulise salbutamol
·IV 10% calcium gluconate - repeat ECG. This protects the heart but does not treat high potassium.
·10units ACTRAPID + 50ml 50% glucose over 30mins - can do this twice before getting senior, specialist help.

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36
Q

Complications of polycystic kidney disease

A

Hypertension
Cyst infection
ESRF
Cardiac = aortic root dilation, mitral valve prolapse and other valvular diseases.

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37
Q

metformin and the kidneys

A

Won’t be exact cause of an AKI but will worsen the injury and increase acidosis.

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38
Q

Why metabolic acidosis in AKI?

A

Unable to excrete waste organic acids

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39
Q

Definition of chronic kidney disease

A

Chronic abnormal function or structure of the kidney which goes on for 3 months or more of:

  • haematuria +/- proteinuria
  • GFR <60ml/minute/1.73m2.
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40
Q

Common causes of CKD

A 
Diabetes mellitus
Glomerulonephritis
Hypertension
Polycystic kidney disease
Nephrotic and nephritic syndromes; focal segmental glomerulosclerosis.
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41
Q

GFR and end-stage kidney disease

A

Stage 5 CKD = GFR <15ml/mine/1.73m2.

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42
Q

Who should be screened/routinely tested for CKD?

A 
Diabetics
HTN
CHF or IHD
SLE
Recurrent UTI e.g. BPH
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43
Q

Presentation of CKD

A

Asymptomatic (apart from symptoms of causative disease), most picked up on routine checks.

Fatigue (anaemic)
Oedema (water and salt retention)
Nausea, pruritus and anorexia (uraemia)
Recurrent UTI

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44
Q

Investigating CKD

A 
Serum creatinine
Estimation of GFR using serum creatinine
Albumin:creatinine ratio
Urine dipstick
Urine microalbumin
KUB USS
Look for cause - OGTT, BP, antibodies for glomerulonephritis cause.
Prevent complications - FBC.
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45
Q

Management of CKD

A

1) Information, education and lifestyle advice: exercise, stop smoking, dietary advice (low salt diet).
2) Blood pressure control (target 140/90mmHg) e.g. ACE-inhibitor.
3) Optimum blood glucose control HbA1c <7%.
4) Prevent CVD in CKD patients with QRisk score and anti-platelet agent e.g. apixaban and statin.
5) Treat complications - ferrous sulphate for anaemia, diuretics for oedema, calcitriol or bisphosphonate for bone disease.
6) Stage 5 or uraemia = RRT.

46
Q

Complications of CKD

A

Anaemia from reduced EPO action
Uraemia
Metabolic acidosis
Oedema
Low bone mineralisation (high phosphate, low vit D, secondary hyperparathyroidism)
Cardiovascular disease - left ventricular hypertrophy.
Hyperkalaemia

47
Q

Monitoring of CKD patient

A

Annual creatinine for eGFR, urine dipstick.

48
Q

Name some renal replacement therapies

A

Renal transplant
Peritoneal dialysis
Haemodialysis

49
Q

What to do in the assessment of a patient for potential RRT?

A 
Neurocognitive issues
Psycho-social evaluation
Understanding of process
Interference with daily life
Type of RRT patient has a preference for
Is there a matched donor 👯‍♂️
50
Q

Indications for dialysis in AKI

A 
Uraemia
Pulmonary oedema
Severe hyperkalaemia
Metabolic acidosis, unresponsive to sodium bicarbonate
Severe renal failure.
51
Q

Overview of haemodialysis

A

Requires AV fistula to bypass capillary network.
Blood passes over semi-permeable membrane in opposite direction to dialysis fluid.
Counter-current mechanism draws solutes out of blood into dialysis fluid along concentration gradient.
Constant infusion of heparin during procedure!

Need to come into hospital 3 times a week for around 4 hours.

52
Q

Complications of haemodialysis

A

Infection
Hypotension
Disequilibration syndrome (tremor, fits, restless, coma)

53
Q

Overview of peritoneal dialysis

A

Intermittent drainage and infusing.
Dialysate infused into peritoneal cavity and works with the semi-permeable peritoneum to filter solutes.
Ultrafiltration can be achieved by adding osmotic agents to the dialysate fluid e.g. glucose.

Need to do it twice a day but can be done at home, no admission.

54
Q

Complications of peritoneal dialysis

A

Infection at catheter site
Peritoneal-dialysis related peritonitis
membrane function declines over time
Hernia

55
Q

Possible sources for renal transplants and what needs to be matched

A

Deceased donor or living donor.

Match: ABO blood group, tissue HLA, antibody screening.

56
Q

Contraindications for renal transplant

A

Cancer with metastasis
HIV with viral replication
Unstable CVD

57
Q

Immunosuppression for renal transplant

A

Induction with basiliximab + IV methylprednisolone

Maintenance with prednisolone, calcineurin inhibitors e.g Tacrolimus and anti-metabolites e.g. Azathioprine.

58
Q

Risks of renal transplant

A

Oppertunistic infections due to immunosuppression.
Surgical Cx e.g. thrombosis, infection, hernia.
Malignancy: post-transplant lymphoproliferative disorder, small increase in RCC.
Increased CVD risk
REJECTION - hyper-acute, accelerated, acute, chronic.

59
Q

Young child with easy bruising, AKI symptoms and pale/anaemic. Hx of diarrhoea episode

A

· Haemolytic uraemia syndrome = microangiopathic haemolytic anaemia + thrombocytopenia (low platelets) + AKI.
· Shiga toxin-producing E.coli 0157:H7
· Ix = FBC, peripheral blood smear = schistocytes, serum creatinine, PT, stool sample for E.coli, U+E.
· Resuscitation with IV fluids, red cell transfusion, dialysis/RRT.

60
Q

Accelerated HTN + AKI

A

Scleroderma renal crisis in patients with systemic sclerosis. Rapidly progressive glomerulonephritis.
Ix = kidney biopsy = onion skin thickening of arterioles, collapsed glomeruli.
Rx = ACE inhibitors, IV vasodilators.

61
Q

Treatment of renal disease + small vessel vasculitis (?respiratory symptoms + renal symptoms)

A

High-dose glucocorticoids + cyclophosphamide/rituximab.

62
Q

Diabetic nephropathy

A

Hyperfiltration, thickening of glomerular basement membrane and intercapillary glomerulosclerosis (Kimmelstiel-Wilson nodules).

Screen DM annually with

1) First-pass early morning urine specimen for estimation of the albumin:creatinine ratio
2) U+E for eGFR.

63
Q

Common organism in pyelonephritis

A

E.coli

64
Q

RFx for pyelonephritis

A 
Hx of UTI
DM
Elderly
Immunocompromised e.g. renal transplant, HIV.
Sexual activity
Anatomical deformity in kidneys 
Catheterisation
65
Q

S+S of pyelonephritis

A

main 3:
Fevers
Flank pain
Costo-vertebral angle/renal tenderness

Vomiting
UTI symptoms e.g. cloudy urine, frequency, dysuria.

66
Q

Ix and Mx for pyelonephritis

A

Ix = Urine dipstick, mid-stream urine sample microscopy, culture and sensitivity (incl gram stain), CRP, FBC, blood cultures, procalcitonin, KUB USS or CT.

Mx = adequate hydration, empiracal ABx until sensitivity known e.g. Ciprofloxacin.

67
Q

What is glomerulonephritis?

A

Injury to glomerular capillaries and glomerular basement membrane cause proteinuria, haematuria and CKD.
Most are immune mediated injuries.

68
Q

Most common glomerulonephritis

A

Focal segmental glomerulonsclerosis in nephrotic syndrome

69
Q

Examples of nephrotic glomerulonephritis

A

Minimal change disease
Focal or segmental glomerulonephritis
Membranes nephropathy
Secondary causes e.g amyloidosis, SLE, HIV, diabetes.

70
Q

Examples of nephritic syndromes

A

IgA nephropathy
Henoch-Schonlein Purpura
post-streptococcal glomerulonephritis
Anti-glomerular basement membrane disease

71
Q

Pathophysiology of nephrotic syndrome

A

Proteinuria >3g/24hrs
Hypoalbuminaemia (<30g/L)
Peripheral oedema

Hyperlipidaemia
Non-proliferative

72
Q

Pathophysiology of nephritic syndrome

A

Oligouria/AKI
Hypertension
Haematuria (red cells and casts)

Can have proteinuria but less than 3g/day
Inflammation
Proliferative

73
Q

Investigating glomerulonephritis

A

Serum: FBC, U+E, albumin, creatinine (estimate GFR), LFT, CRP, autoantibodies, immunoglobulins, electrophoresis for complement, blood sugar.
Urine: dipstick, protein:creatinine ratio, microscopy for casts, mid stream urine MC+S.
BP
Renal USS
Renal biopsy.

74
Q

Management of glomerulonephritis

A

Treat underlying cause!!

Fluid and salt restriction.
Treat HTN (ACE inhibitor)
Diuretics e.g. furosemide
Corticosteroids 
Renal transplant
75
Q

Minimal change disease

A 
Not a massive cause of CKD
Majority of patients are young children.
Light microscopy = normal
Electron microscopy = fusion of podocyte foot processes.
Mx = prednisolone
76
Q

Focal segmental glomerulosclerosis

A

Rx with high-dose prednisolone.
Control BP
Cause of CKD
Associated with HIV

77
Q

IgA nephropathy

A

IgA antibodies deposit in mesangium.
S+S = haematuria, hypertension, <1g proteinuria, Hx of resp or GI infection.
Ix = biopsy shows IgA deposits in mesangium.
Rx = prednisolone, ACEi for BP.

78
Q

Rash on extensor surface of legs, arthritis, high BP, low urine output

A

Henoch-Schonlein purpura.

79
Q

Complications of Glomerulonephritis esp Nephrotic syndrome

A

Thromboembolism (high lipids)
UTI
Hypercholesterolaemia

80
Q

Histology of renal cell cancer

A

Renal cell carcinoma, most are clear cell.
Proximal renal tubule epithelium in renal cortex.
Often seen as yellow because of high lipid content.

Mutation in Chr3 at VHL gene causes increase in IGF1 (angiogenesis and dysfunctional cell growth)

81
Q

RFx for renal cell carcinoma

A

Male
Smoking
Obesity
Hypertension

Hereditary = Von Hippel-Lindau syndrome, polycystic kidney disease.

82
Q

S+S of renal cell carcinoma

A

Asymptomatic

Abdominal mass
Haematuria
Loin pain
Anorexia, malaise, weight loss.
Left varicocele from left RCC compressing on venous drainage of left testis.

Paraneoplastic syndromes = HTN from renin, polycyathaemia from EPO, hypercalcaemia from PTHrP, Cushing’s from ACTH.

S+S of met to lung and bone.

83
Q

Common locations to renal cell carcinoma to metastasis

A

LUNGS
Bone
Liver

84
Q

Ix for renal cell carcinoma

A

Bloods: FBC - Polycythaemia from EPO, U+E, ESR, LFT.
Urine: cytology for red blood cells. Exclude UTI with mc+S.
Imaging: CT/MRI
Other: CXR for cannon-ball metastasis, skeletal survey for boney met.

∆ urine dipstick, KUB USS then CT (high enhancement of tumour).

85
Q

Mx for renal cell carcinoma

A

Dependent on stage.

1) local tumour = laparoscopic partial or total nephrectomy.
2) If not suitable for invasive surgery consider radio-frequency or cryotherapy ablation.
3) Adjuvant monoclonal antibodies. Anti-VEGF biologics.

86
Q

Complications of renal cell carcinoma

A

Compression of testicular vein = varicocele.

Paraneoplastic syndromes e.g. Cushing’s, Polycythaemia.

87
Q
  1. Action of aldosterone?

2. Why do you get hypokalaemia and alkalosis in Conn’s?

A
  1. Distal convoluted tubule. Increase sodium reabsorption and potassium excretion.
  2. H+ is excreted along with potassium. If high potassium excretion will get loss of protons = alkalosis. Will get hypertension as high sodium retention leads water to follow.
88
Q

What would an ABG and U+E show in Addisons?

A

Low aldosterone, less potassium and thus H+ excretion, less sodium reabsorption.

  • Hyperkalaemia
  • Acidosis
  • Hypotension
89
Q

Where do loop diuretics act?

A

Na+-K+-2Cl− symporter (NKCC2) in the thick ascending limb of the Loop of Henle.
Inhibit sodium, chloride and potassium reabsorption.

90
Q

Where do thiazide diuretics act?

A

Inhibit of the sodium-chloride (Na/Cl) channel in the proximal segment of the distal convoluted tubule.

91
Q

Have HTN resistant to Rx

A

Renal artery stenosis.

Kidneys are not well perfused from stenotic artery so activate RAAS despite rest of body adequately perfused.

92
Q

Subarachnoid haemorrhage renal cause

A

Autosomal dominant polycystic kidney disease.

Can cause Berry aneurysms.

93
Q

Someone has polycystic kidney disease, can you assess their risk of malignancy?

A

Bozniak staging

94
Q

What do you need to do before dialysis and what are some complications?

A

Arteriovenous fistula.

Complications = infection, stenosis, thrombosis, Steal syndrome (ischaemia).

95
Q

Indications for dialysis in AKI

A 
Metabolic acidosis refractive to Rx (sodium bicarb)
Hyperkalaemia
Pulmonary oedema
Uraemic pericarditis
Severe uraemia
96
Q

What is an amyloid deposit?

A

Histology specimen which binds to cotton wool dye, Congo red dye and shows green birefringence under polarised light.

97
Q

Presentation of amyloidosis

A 
Dependent on organ affected.
Fatigue, weight loss, easy bruising, breathlessness, postural hypotension.
Peripheral oedema.
Massive proteinuria
Hepatomegaly
Heart failure, raised JVP
Sensory glove + stocking polyneuropathy.
Racoon eyes, peri-orbital purpura
Carpel tunnel syndorme
98
Q

Ix and Mx for amyloidosis

A

Biopsy of affected organ = stains red with Congo red dye, is green birefringence under polarised light.
Immunofixation electrophoresis.

Mx = symptomatic e.g. diuretics, beta-blockers.
May have role for chemotherapy or stem cell transplant.

99
Q

What is amyloidosis a good ∆∆ for?

A

MGUS/myeloma.

100
Q

Pathology of lymphoedema

A

Increased vascular permeability from inflammation.
Obstruction to lymph drainage.
Liver failure and nephrotic syndrome =
Hypoalbuminaemia and decreased oncotic pressure in plasma.

101
Q

Acidotic with high chloride, low bicarbonate but normal anion gap…?

A

Renal tubular acidosis.

102
Q

When do look at renal replacement therapy in CKD?

A

eGFR <15ml/min/1.73m2 (ESKD) or uraemia

103
Q

Normal eGFR

A

eGFR >90 ml/minute/1.73 m2

104
Q

Normal eGFR

A

eGFR >90 ml/minute/1.73 m2

105
Q

Managing complications of CKD

  1. Anaemia
  2. CVD risk
  3. Osteoporosis
  4. Malnutrition
  5. Acidosis
  6. Oedema
  7. Hyperkalaemia
A
  1. Ferrous sulphate or if severe erythropoietin.
  2. Qrisk, statin, anti-platelet.
  3. Calciferol, bisphosphonate.
  4. Maintain healthy BMI, sodium salt restriction, exercise advise.
  5. Sodium bicarbonate.
  6. Loop diuretics
  7. Dialysis if over 7mmol/L
106
Q

Uraemia clinical features and management

A

Symptoms:
Vomiting, nausea, fatigue, drowsiness, anorexia, pruritus, muscle cramps.
Altered mental state from uraemia encephalopathy

Signs:
Uraemic frost on forehead and scalp
Skin gets grey yellow tinge.
Pallor
Hypertension
Elevated JVP
Bruising
Pericardial friction rub from pericarditis.
107
Q

The causes of death in AKI

A

Volume overload e.g. flash pulmonary oedema
Metabolic acidosis
Hyperkalaemia

108
Q

Chocolate or tea coloured urine in a catheter nag of an elderly patient who fell

A

Rhabdomyolysis.

109
Q

Complications of nephrotic syndrome

A

Thromboembolic event e.g. DVT, MI
Infection e.g. cellulitis
AKI

110
Q

Muddy brown cellular casts in urine

A

Acute tubular acidosis such as Fanconi’s syndrome

APhase 3b flashcards (16 decks)

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