Renal Medicine Flashcards
5 functions of the kidney
Acid-base control (pumps out H+, reabsorbs bicarb)
Regulates blood/fluid volume
Waste, toxin and drug excretion
Produces erythropoietin (stimulating red cell production)
Vitamin D metabolism (Vit D to 1-Hydroxyvit D)
How do we measure kidney function?
Creatinine:
Albumin:creatinine ration (mg/mmol)
CKD staging
1: >90 (+evidence kidney damage)
2: 60-89 (+evidence kidney damage)
3a: 45-59
3b: 30-44
4: 15-29
5: <15
Takes into account albuminuria (<3, 3-30, >30)
How does renal failure lead to anaemia?
Reduced erythropoietin production
Reduced hepcidin clearance (waste product from liver which impairs iron absorption by duodenum)
Therefore give iron supplements (IV as duodenum absorption reduced)
Nephrotic syndrome proteinuria threshold
> 3g protein excreted per 24 hours
CKD timescale
> 3 months
Which patients should be started on ARB/ACE-i?
What should their BP target be?
Diabetic and ACR >3mg/mmol
Hypertensive and ACR >30mg/mmol
ACR >70mg/mmol
Target of 130/80
Management of acute hyperkalaemia?
Calcium gluconate 10ml 10% (protects myocardium)
Followed by salbutamol, insulin and dextrose to drive potassium into cells
Role of vitamin D
Increases calcium absorption
Increases renal tubular reabsorption
Increases osteoclast activity (releasing calcium from bone)
Stages of vitamin D activation
Cholecalciferol to calcidiol by liver
Calcidiol to calcitriol by kidneys
What acid-base changes might occur in CKD?
H+ ion retention leading to acidosis - treated with sodium bicarbonate
Possible complications of CKD
Anaemia
Fluid overload
Mineral and bone disorders
Hyperkalaemia
What type of anaemia would you see in CKD and how would you manage?
Normochromic normocytic
Erythropietin-stimulating agents e.g. epoetin alfa
Indications for dialysis in AKI
Refracatory hyperkalaemia
Refractory pulmonary oedema
Severe metabolic acidosis (<7.1)
Severe uraemia (>60mmol/L or CXR)
Complications of AKI
Hyperkalaemia
Fluid overload
Metabolic acidosis
Uraemic complications (pericarditis and encephalopathy)
Rhabdomyolysis signs and symptoms
Muscle pain
Dark brown urine (myoglobinuria)
Raised CK levels
Nephrotoxic drugs
ACE-i/ARBs NSAIDs penicillin Diuretics Furosemide Rifampicin Cephalasporins
Clinical definition of oliguria?
<0.5mls/kg/hr (35mls/hr in a 70kg patient)
If this persists >6hrs then is defined as AKI
How do NSAIDs adversely affect renal function?
Inhibition of COX1/2 leading to inhibition of prostaglandin synthesis. This causes constriction of afferent arterioles and reduced renal perfusion
Promotes natriuresis (sodium excretion in urine)
How is Stage 1 AKI diagnosed?
Serum creatinine (increase by >26umol/L in 48 hours or >1.5-1.9 in 7 days)
Urine output (<0.5mls/kg/hr over 6 hours)
Pre-renal causes of AKI and what can they lead to?
Cardiac output (cardiac failure)
Arteriolar changes (nephrotoxic drugs e.g. ACE-i or NSAIDs)
Systemic vasodilation (septic shock)
Reduced circulating volume (hypovolaemia)
This can lead to intrinsic damage due to prolonged ischaemia of renal parenchyma and development of acute tubular necrosis (ATN)
Intrinsic causes of AKI
Vascular:
Large vessel: atherosclerotic disease, thromboembolic disease, dissection, renal artery stenosis/thrombosis
Small vessel: vasculitides, malignant HTN, microangiopathic haemolytic anaemia (e.g. DIC), thromboembolic disease
Glomerular: primary or secondary. Can cause nephritic/nephrotic syndrome
Tubulointerstitial: acute tubular necrosis (ATN); acute interstitial nephritis (secondary to medication)
Post-renal causes of AKI
Obstructive uropathy (urolithiasis, malignancies, strictures and bladder neck obstruction)
Clinical features of pre-renal AKI
Evidence of dehydration/hypovolaemia:
Dry mucus membranes, reduced CRT, reduced urine output, low BP, reduced skin turgor, dizziness and thirst
Hypervolaemia (due to cardiac failure):
Pulmonary/peripheral oedema, orthopnoea, paroxysmal nocturnal dyspnoea, dyspnoea, raised JVP, ascites
Acute tubular necrosis clinical features
Brown muddy casts in urine (tubular cells)
AKI features
Clinical features of tubulointerstitial disease
Arthralgia
Rashes
Fever
Eosinophilia
Clinical assessment of patient with AKI
Fluid assessment (urine output) Urine osmolality and electrolytes MSU Urine dipstick ECG
Bloods: FBC, U&Es, bone profile, blood gas
Complement, vasculitis screen (ANCA, ANA), clotting, CK, blood film, Ig
ULTRASOUND, CXR, renal doppler, MRA
When would you discuss an AKI patient with a nephrologist?
<30 GFR, or decrease by >15 in a year
ACR >70mg/mmol
Rare or genetic cause of CKD
Renal artery stenosis
Persistent HTN despite 4 anti-hypertensives
Diagnosis that may require specialist intervention (e.g. glomerulonephritis, systemic vasculitis)
Management of AKI
Regular assessment and monitoring of urine output (catheter), weight, creatinine levels compared with baseline
Hypovolaemia: IV fluids
Hypervolaemia: fluid restriction/diuretics
Hyperkalaemia: 10ml calcium gluconate 10%, 10 units ACTRAPID insulin in 20% dextrose, 2.5mg salbutamol
Acidosis: sodium bicarbonate
RRT: if refractory pulmonary oedema/hyperkalaemia, severe uraemia (leading to encephalopathy or pericarditis), metabolic acidosis
RENAL DRS 26
Record baseline creatinine and regular U%Es Obstruction excluded (USS) Urinalysis +/- MSU Nephrotoxic drugs stopped Dry (IV fluids) or wet (furosemide) Urinary output monitoring Prescription review 26 (>26umol/L serum creatinine in 48 hours for diagnosis)
Triad of nephrotic syndrome (+ other features)
- Hypoalbuminaemia
- Proteinuria (>3.5g per day)
- Oedema (low oncotic pressure)
+ coagulopathy, sepsis, hyperlipidaemia, hypocalcaemia
Rapidly progressive glomerulonephritis features
Thrombosis and rupture of capillaries leading to glomerular crescent formation in >50% of glomeruli
50% reduction in GFR over 3 months
Primary and secondary causes of nephrotic syndrome
Caused by structural changes in the glomeruli
Primary: Minimal Change Disease (commonest in children), membranous GN (commonest in adults), focal segmental glomerulosclerosis (common in adults)
Secondary: SLE, diabetes mellitus, amyloidosis
Causes of nephritic syndrome?
Proliferative: IgA nephropathy, membrano-proliferative GN, post-strep GN
Proliferative with crescents (rapidly progressing): anti-GBM, Wegener’s, microscopic polyangitis
Treatment for minimal change disease
Glucocorticoids
Immunosuppressants (cyclophosphamide) if not responding
Minimal change disease clinical features
Fusion of podocyte foot processes
Nephrotic syndrome
Normotensive
Highly selective proteinuria
PUFFY FACE
Causes of minimal change disease
Idiopathic (majority)
Drugs: NSAIDs or rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononeucleosis
Causes of membranous glomerulonephritis
Thickened basement membrane
Idiopathic: anti-phospholipase A2 antibodies
Infections: hepatitis B, malaria, syphilis
Malignancy: lung cancer, leukemia
Drugs: penicillamine, NSAIDs
SLE, thyroiditis, rheumatoid
Management of membranous glomerulonephritis
ACE-i/ARBs to reduce proteinuria
Immunosuppression (corticosteroid + cyclophosphamide)
Anti-coagulation if high risk
1/3 spontaneous remission
1/3 ongoing proteinuria
1/3 ESRF
Nephritic syndrome clinical presentation
Haematuria
Mild proteinuria
HTN
Oliguria
What is nephritic urinary sediment?
Urinary red cell casts
Leucocytes
Dysmorphic red cells
Sub-nephrotic proteinuria (>3.5g/day)
Most common cause of glomerulonephritis worldwide?
IgA nephropathy
What conditions are associated with IgA nephropathy and how might a patient present?
Alcoholic cirrhosis, coeliac disease/dermatitis herpetiformis, Henoch-Schonlein Purpura
Presentation: young male following URTI, recurrent episodes of frank haematuria
Difference between IgA nephropathy and post-strep glomerulonephritis?
IgA is 1-2 days after URTI, post-strep 1-2 weeks
IgA young males with frank haematuria
Post-strep presents with proteinuria with haematuria less common
Management of IgA nephropathy
ACE-i; Steroids/immunosuppressants
Up to 50% will have ESRF and need RRT
Alport syndrome presentation
Childhood Progressive renal failure Microscopic haematuria Sensorineural deafness Ocular pathologies (lenticonus - protrusion of lens into anterior chamber)
Diagnosed by genetic testing (X-linked) and renal biopsy
What antibodies are found in 30% of cases of anti-GBM?
ANCA (associated with better response to treatment)
Anti-GBM management
Plasmapheresis (removes antibodies)
Corticosteroids
Cyclophosphamide
Complicated UTIs
Male Pregnant Diabetic Immunological abnormalities Catheter Structural abnormalities
Gram stain for E. coli
Gram negative bacillus
Organisms other than E. coli that might cause UTIs
Staph saprophyticus
Klebsiella pneumoniae
Proteus
What is urosepsis?
2 or more signs of systemic inflammatory response syndrome:
Temp: >38 or <36
HR: >90
RR: >20
WCC: >12 or <4
+ suspected urinary source of infection
What would you expect to see on urinalysis for a UTI?
Nitrites (90% +ve)
Leucocytes (50% +ve)
Bacteriuria definition
> 10^5 colony forming units/ml
Which UTI bacteria are associated with poorer outcomes and require broad spectrum ABx?
Extended spectrum beta lactamase producing E. coli
Use carbapenems
Which bacteria are more likely to lead haematogenous spread of UTI?
Staph aureus
Candida
Mycobacterium TB
What signs might you see with a UTI
Suprapubic tenderness Fever Rigors Costovertebral tenderness Flank pain Confusion
UTI diagnosis
In young, non-pregnant females usually clinical symptoms is enough, but you could also do a urine dip
Urine dip (leucocytes and nitrites) Urine microscopy, culture and sensitivity
FBC, U&Es, CRP
USS, CT (non-contrast) - abscesses, calculi, haemorrhages, obstruction
Management of uncomplicated UTI
Nitrofurantoin/trimethoprim BD 3 days female, 7-10 days male
Uncomplicated pyelonephritis: don’t admit, treat with fluoroquinoline e.g. ciprofloxacin 12-hourly for 14 days
Management of complicated UTI
Oral fluoroquinoline (e.g. ciprofloxacin)
IV co-amoxiclav if urosepsis or severe pyelonephritis
Which Ig protects mucosal surfaces, and what does that include?
IgA
Intestines, resp tracts, oral mucosa, urothilium
Who should you avoid trimethoprim in, and what adverse effects are there?
Pregnant women (or anyone with folate deficiency) - give nitrofurantoin instead
Nausea, vomiting, diarrhoea, rash, pruritis
How does rhabdomyolysis lead to AKI?
Causes myoglobinuria
Myoglobin causes tubular cell necrosis - ATN
When prescribing routine maintenance fluid, what is the normal requirement for chlorine, potassium and sodium?
1 mmol/kg/day
What symptoms might come with Henoch-Schonlein Purpura?
Abdominal pain
Palpable rash
Arthritis
Usually children
Pulmonary haemorrhage (chest pain/cough/haemoptysis) followed rapidly by haematuria - what is the disease and why does it present like this?
Goodpasture’s syndrome (anti-GBM)
Anti-GBM antibodies affect Type IV collagen found in lungs and kidneys leading to glomerulonephritis
Risk factors and management of Goodpasture’s syndrome?
Smoking, LRTI, pulmonary oedema, hydrocarbon inhalation, young age (20-30)
Mx: renal biopsy (IgG deposits along basement membrane), raised transfer factor secondary to pulmonary haemorrhage
Plasma exchange (plasmapheresis), steroids, cyclophosphamide
What do you use to prevent contrast-induced nephrotoxicity? When does it occur?
IV sodium chloride 0.9% 1ml/kg/hour for 12 hours pre- and post-procedure
Occurse 3-5 days post-procedure
What antibodies would you see in Granulomatosis with polyangitis (Wegener’s)?
ANCA
Inflammation of blood vessels around the body
Crystalloid vs colloid
Crystalloid: smaller molecules, immediate reuscitation, can cause oedema
Colloid: larger molecules, more expensive, quicker volume expansion in intravascular space but can cause allergic reactions, clotting disorders and kidney failure
Treatment of Henoch-Schonlein?
Analgesia for arthralgia
Supportive therapy for nephropathy
Usually good recover, 1/3 have relapse
What is Alport syndrome caused by
X-linked genetic defect in the gene which codes for type IV collagen (glomerular basement membrane)
What can a failed renal transplant in an Alport patient lead to?
Goodpasture syndrome presentation (pulmonary haemorrhage and haematuria caused by anti-GBM antibodies)
Potassium-sparing diuretics
Spironolactone
Eplerenone
NICE guidelines for IV fluid resus
IV sodium chloride 0.9% 500mls over 15 mins
SLE with proteinuria
Lupus nephritis
What is the risk with using metformin in renal failure?
Build up of metformin as it is usually cleared by the kidneys
Can lead to lactic acidosis
Use of aspirin in renal failure?
Has to be reduced to low dose (75mg per day)
Features of autosomal dominant polycystic kidney disease
HTN Abdominal pain and early satiety Recurrent UTIs Renal stones Haematuria CKD Liver cysts, berry aneyrsysm, pancreatic cysts, CV (mitral valve prolapse, aortic dissection, valve incompetence)
Cause of diabetes insipidus and what might you see on biochemistry results?
Lack of ADH production from posterior pituitary (cranial) or reduced sensitivity of kidneys to ADH (nephrogenic)
High/borderline plasma osmolarity (making patients thirsty to reduce osmolarity)
Inappropriately low urine osmolarity
How is DI diagnosed
Water deprivation test - leads to rise in plasma osmolarity and continued production of low urine osmolarity
In cranial DI, exogenous vasopressin will counteract this
In nephrogenic DI, exogenous vasopressin has no effect
What drugs remove potassium from the body?
Loop diuretics
Calcium resonium
Dialysis
What conditions lead to bilaterally enlarged kidneys?
Diabetic nephropathy
HIV-induced nephropathy
Amyloidosis
Autosomal-dominant polycystic kidney disease
Most common cause of viral infection following organ transplant, and what is the treatment?
Cytomegalovirus
Ganciclovir
Best way of distinguishing pre-renal uraemia from ATN?
Pre-renal: <20mmol/L urinary sodium
ATN: >40mmol/L
Maintenance fluid calculation for non-neonates
100ml/kg/day for first 10kg
50ml/kg/day for every kg from 10-20kg
20ml/kg/day for all weight after
Features of renal cell carcinoma
Triad: haematuria, loin pain, abdo mass
Pyrexia
Left varicocele (due to occlusion of left testicular vein)
Can secrete EPO (polycythaemia), PTH (hypercalcaemia), renin, ACTH
Chlamydia features
Majority asymptomatic
Urinary leucocytes and blood
Dysuria, cervicitis (discharge and bleeding)
Men: discharge and dysuria
Causes of haematuria
Persistent, non-visible: Cancer (bladder, renal, prostate) Prostatitis Cervicitis Stones Renal - IgA nephropathy, thin basement membrane
Sudden onset: Menstruation Sexual intercourse UTI Vigorous exercise
Spurious:
Rifampicin, doxorubicin
Beetroot
Indications for urgent referral
> 45 AND unexplained visible haematuria in absence of UTI or after successful treatment of UTI
> 60 AND unexplained nonvisible haematuria with either dysuria or raised WCC
Indications for non-urgent referral
> =60 with persistent UTIs
no referral needed if normotensive, normal renal function and no proteinuria
Test to assess diabetic nephropathy in a patient
Early morning ACR
Causes of haemolytic uraemic syndrome
E.coli
HIV
Pneumococcus
Cancer
Diagnosis and management of HUS
FBC (thrombocytopaenia, anaemia), U&E (AKI), stool culture
Management: Fluids, blood transfusion and dialysis if severe, eculizumab
Stage 2 AKI
2-2.9 baseline creatinine
Most common causes of acute interstitial nephritis
Drugs: rifampicin, penicillin, NSAIDs, allopurinol, furosemide
SLE
Sarcoidosis
Staph
Features of acute interstitial nephritis
Arthralgia
Rash
Fever
Eosinophilia
Mild renal impairment
Hypertension
Diagnosis of acute interstitial nephritis
Sterile pyuria
White cell casts
Features of tubulointerstitial nephritis with uveitis
Young women
Painful red eye
Weight loss
Fever
Urinalysis: leucocytes and protein
Indication for MRI in renal failure
Renal artery occlusion
Indication for abdo X-ray in renal failure
Renal stones
Maintenance fluid calculation for adults
25-30ml/kg/day
1mmol/kg/day of electrolyte
50-100g/day glucose
Recommended fluid challenge for patients with no signs of heart failure
500ml 0.9% saline STAT
Rhabdomyolysis treatment
IV saline to perfuse kidneys
Treatment for nephrogenic DI
Chlorothiazide (promotes sodium release into the urine)
EPO side effects
Flu-like symptoms HTN leading to encephalopathy Bone aches Skin rashes Pure red cell aplasia Increased risk of thrombosis
What abx can cause AKI
Gentamicin
