Nephro 1 Flashcards
What are the main functions of the kidney?
Filter and secrete waste/excess
Retain albumin and circulating cells
Reabsorb glucose, amino acids and bicarb
Control BP, fluid status and electrolyes
Activates 25-hydroxy Vit D –> 1,25 dihydroxy vitamin D (calcitriol)
Synthesis erythropoietin
What is the glomerular filtration rate?
Volume of fluid filtered from the glomeruli into Bowman’s space per unit time
120ml/min
7.2L/h
170L/day
What are characteristics of PCT?
Proximal Convoluted tubule
sugars, amino acids and bicarbonate get reabsorbed here
70% of Na+ absorbed and water follows
MOST vulnerable to damage
What is Fanconi syndrome?
not to be confused with FANCONI ANAEMIA
Proximal tubule insult (Wilson’s, tenofovir)
- glycosuria
- acidosis
- phosphate wasting = rickets/osteomalacia
- aminoaciduria
What are the functions of the loop of henle?
25% of Na+ absroved here and water follows
Thiazide diuretics work here
What are the functions of the distal convoluted tubule?
The juxtaglomerular apparatus
- a solute sensing organ, if it detects HIGH SOLUTES - GFR is low = releases RENIN
What are the actions of Renin?
- It converts angiotensinogen to angiotensin-I
- ACE from lungs converts angiotensin 1 to 2
- This causes vasoconstriction and release of aldosterone
What are functions of the collecting duct?
salt handling, tightly regulated by aldosterone (increases reabsorption of Na+ in exchange for K+)
Secrete K+ and H+ into the urine
Water handling is also done here via Aquaporin 2 channels (these regulated by vasopressin)
How is potassium handled by the kidney?
K+ freely filtered and mostly reabsorbed in PROXIMAL TUBULE/LOOP OF HENLE
Governed by Na+ and Aldosterone
Insulin and catecholamines drive K+ uptake
What drugs cause hypokalaemia?
Loop diuretics and thiazide diuretics
What drugs cause hyperkalaemia?
spironolactone
amiloride
ACE-I
ARB
Trimethoprim
What is urinating regulated neurally?
S3,4,5 via parasympathetic - contract detrusor relax urethra
How is storage of urine regulated neurally?
T10, L1, L2 via sympathetic nervous system - RELAX bladder CONTRACT urethral sphincter
What are the 3 main narrowings where renal stones can lodge themselves?
Pelviureteric Junction
Pelvic Brim
Vesicoureteric Junction
What are most renal stones made of?
Calcium oxalate and Phosphate
What are some risk factors for renal stones?
Anatomical abnormalities
Chemical composition of urine that favours stone crystallisation
Dehydration
Infection
Increased Ca, Oxalate, Urate
Primary renal disease
Drugs - diuretics, antacids, acetazolamide, corticosteroids
Chocolate, rhubarb
Gout
Fam Hx
How would renal stones/renal colic present?
Asymp
Renal Colic - rapid onset, loin to groin, comes and goes in waves, nausea and vomiting, worse with fluid loading
Dysuria, strangury (burning when peeing), frequency
Recurrent UTI’s
haematuria
How would you investigate renal colic?
Urinalysis - maybe normal, exclude other causes
FBC - WBC to rule out infection
Serum electrolytes, urea and creatinine - hypercalcaemia, hyperuricaemia
Urine pregnancy test - ectopic
non-contrast CT
How would you treat renal stones/colic?
Conservative - overhydration, low Ca, dietary intake, low sodium, reduced BMI, reduced animal proteins
Morphine
Ondansetron
Abx - trimethoprim/nitro
Surgical decompression
What are some pre-renal causes of AKI?
40-70%
Renal hypoperfusion (hypovolaemia or sepsis)
Hypotension without hypovolaemia (cirrhosis or septic shock)
Low cardiogenic output (cardiac failure/cardiogenic shock)
Renal hypoperfusion (NSAIDs, ACE-inhibitors)
What are some intrinsic renal causes of AKI?
10-50%
Renal parenchyma damage
Acute tubular necrosis (NSAIDs, radiological contrast, uric acid crystals, myeloma)
Vascular
- renal artery/vein thrombosis
- cholesterol
- vasculitis
- haemolytic uraemic syndrome
- malignant hypertension
Glomerular- glomerulonephritis, SLE, drugs, infection
What are some post-renal causes of AKI?
UTI
Luminal - stones, clots
Mural - malignancy, BPH, strictures
What are risk factors for AKI?
> 75
HF
Peripheral vascular disease
Sepsis
Poor fluid intake
CKD
Hypovolaemia
Diabetes
Prostate cancer
Nephrotoxic drugs
How does AKI present?
Oliguria
Arrythmias - hyperkalaemia
Uraemia - fatigue, weakness, anorexia, N&V, confusion, seizures and coma
Anaemia and pulmonary oedema - breathlessness
Pericarditis
Impaired platelet function
Postural hypotension
Thirst
How would you investigate AKI?
basic metabolic profile - elevated creatinine, high potassium
serum urea to creatinine ratio = 20:1 supports pre-renal
Urinalysis
urine culture
FBC - anaemia, leucocytosis, thrombocytopenia
VBG - met acidosis
fluid challenge - renal function will improve in pre-renal azotaemia
bladder catheterisation
What is a staging system for AKI?
KDIGO
based on serum creatinine and urine output
How would you treat AKI?
Volume expansion and/or red blood cell transfusion - normal saline
Vasopressor - dopamine/adrenaline
Diuretic - furosemide
Renal replacement therapy - haemodialysis for 4-6 hours
Hyperkalaemia - calcium gluconate + insulin and glucose to drive K+ into cells
Acidosis - sodium bicarb
What is acute nephritic syndrome characterised by?
also known as acute glomerulonephritis
Haematuria - visible or non-visible
Proteinuria (usually <2g in 24 hrs)
Hypertension
Oedema (periorbital, leg or sacral)
What are some causes/RFs of acute nephritic syndrome?
Often immune response to infection of another disease
IgA nephropathy (most common primary cause)
- bacterial (MRSA, typhoid, secondary syphilis)
- Hep B, C
- Schistomiasis
- Malaria
- Post-strep infection 0 classically 2 weeks after tonsilittis
- Infective endocarditis
- SLE
- ANCA assoc. vasculitis
- Goodpastures
What is IgA nephropathy?
Commonest cause of nephritic syndrome
Haematuria, IgA deposition in mesangium of kidney
Assoc. with tonsillitis and results in haematuria
What is goodpasture’s?
co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage, circulating antibodies directed against an intrinsic antigen to the basement membrane of both kidney and lung
How would you investigate acute glomerulonephritis?
Urinalysis - haematuria, proteinuria, dysmorphic RBCs, leukocytes and RBC casts
Met profile - creatinine, hypoalbunaemia
LFTs
GFR
FBC - normocytic normochromic anaemia
Lipid profile
USS of kidneys
How would you manage acute glomerulonephritis?
Phenoxymethylpenicillin
Furosemide
Prednisolone
IF SEVERE - plasmapheresis + corticosteroid + cyclophosphamide
What is the classical triad of nephrotic syndrome? What else might you see?
Proteinuria - frothy urine
Hypoalbunaemia
Oedema - pitting oedema of ankle, genital , abdo wall and sometimes periorbital
*severe hyperlipidaemia - liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and raised cholesterol
What are the causes/RFs of nephrotic syndrome?
Structural and functional abnorm of podocytes
Minimal change disease - commonest cause
Membranous nephropathy - penicillamine, gold, NSAIDs, SLE, thyroiditis, Hep B, C, schistomiasis, neoplasia
Focal segmental glomerulosclerosis
Diabetes
Amyloid
Infections
SLE, RA
How would you investigate nephrotic syndrome?
Renal biopsy - establish cause
urine dip - very high protein
CXR or USS for pleural effusion or ascites
Albumin low
Creatinine, eGFR, lipids and glucose
SLE - ANA, dsDNA, C3, C4
Hep B antigen, Hep C antibody
How would you manage nephrotic syndrome?
Oedema - furosemide, fluid and salt restriction
Proteinuria - ACEi, ARB
Complications - warfarin, simvastatin
What is minimal change disease? What are causes/RFs?
Commonest cause of nephrotic syndrome in children - boys under age of 5
characterised by minimal histological changes in the kidney
Idiopathic
Atopy - in 30%
Drugs - NSAIDs, lithium, Abx, Bisphos, Sulfasalazine
Hep C, HIV, TB
How would you treat minimal change disease?
Corticosteroid - prednisolone
Fluid restriction and low -salt
Albumin and furosemide
What is CKD?
longstanding, usually progressive, impairment in renal function for more than 3 months
GFR <60mL/min/1.73m2 for more than 3 months with/without evidence of kidney damage
Causes/RFs for CKD?
Diabetes HTN Atherosclerotic renal vascular disease PKD Tuberous sclerosis IgA nephropathy SLE Amyloidosis Smell and medium-sized vessel vasculitis
Fam Hx CKD
Presentation of CKD?
Early stages could be asymptomatic
Malaise Anorexia Weight loss Insomnia Nocturia Polyuria itching N&V and diarrhoea Amenorrhoea and ED in men
What are some complications assoc. with CKD?
anaemia - normochromic normocytic anaemia
bone disease - bone pain, osteo-malacia, hyperparathyroidism
neurological - autonomic dysfunction (postural hypotension, disturbed GI motility), peripheral paraesthesiae
CVS - MI, cardiac failure, sudden cardiac death and stroke
Skin disease - pruritus, brown discolouration of nails
How would you investigate CKD?
ECG - high potassium
Urinalysis - haematuria, proteinuria, MC&S, albumin to creatinine ratio
Biochem - urea, electrolytes, bicarb and creatine, low eGFR, raised ALK phos
Immunology - screen for SLE, scleroderma,and goodpastures
Hep B, C, HIV
USS - renal size
CT - detect stones
How is CKD staged?
According to GFR
Stage 1 = >90 normal
Stage 2 = 60-89
Stage 3A = 45-59
Stage 3B = 30-44
Stage 4 = 15-29
Stage 5 = <15
How would you treat CKD?
Stage 1-2 without uraemia
ACE/ARB
Statin
Atenolol
CCB - verapamil
Stage 3-4 without uraemia
ACE/ARB
Statin + ezetimibe
Atenolol
Educate about renal replacement therapy
Stage 5 or with uraemia
Dialysis
Kidney transplant
Sevelamer
Calcimimetic
What are the types of renal cystic disease?
AD PKD
AR PKD
What is the genetics behind PKD?
AD
Homozygous - die in womb
mutations in PKD1 (85%) gene in chromosome 16
mutations in PKD2 (15%) gene on chromosome 4
How does ADPKD present?
clinically silent for years
Symptoms normally 20s onwards
Loin pain haematuria loin or abdominal discomfort nocturia renal colic hypertension renal stones progressive renal failure
What are extra-renal presentation of ADPKD?
subarachnoid haemorrhage - berry aneurysm rupture
Polycystic liver disease (70%)
Pancreatitis
Mitral valve prolapse
Ovarian cysts
Diverticular disease
How would you investigate ADPKD?
Renal USS/CT
<30 y/o - atleast 2 unilateral or bilateral cysts
30-59 y/o - 2 cysts in each kidney
> 60 y/o - 4 cysts in each kidney
urinalysis
serum electrolytes, urea, creatinine
fasting lipid profile
ECG
CT head - check for ruptured intracranial aneurysm
Treatment of ADPKD?
nothing can slow progression
BP - control ACE-I
Laparoscopic removal of cysts
Serial monitoring of creatinine to track disease progression
What mutation for ARPKD?
PKHD1 mutation on long arm (q) of chromosome 6
Fam hx
What is acute interstitial nephritis? causes?
25% of drug-induced acute kidney injury.
penicillin rifampicin NSAIDs allopurinol furosemide
SLE sarcoidosis
How would you investigate acute interstitial nephritis?
urea and creatinine
Urine Hansel’s or Wright’s eosinophil stain - eosinophiluria
urinalysis - microhaematuria, sterile pyuria, proteinuria
trial of discontinuing offending medication
ANCA, ANA negative
How does acute interstitial nephritis present?
fever
rash
oedema
plus AKI and hypertension
Differences between IgA nephropathy and post-streptococcal glomerulonephritis?
Recent URTI
Haematuria
IgA after 1-2 days and PSG 1-2 weeks after URTI
PSG - proteinuria
For renal transplant, how are donors matched?
based on human leukocyte antigen
What is a typical renal transplant scar? What medications can be given for immunosuppression?
Hockey stick incision - hockey stick scar
Tacrolimus
Mycophenolate
Prednisolone
What is acute tubular necrosis?
damage and death of epithelial cells of the renal tubules - most common cause of AKI
takes 7-21 days to recover
What causes acute tubular necrosis? What would be typical on investigations?
Shock
Sepsis
Dehydration
Radiology dye
NSAIDs
Heroin
Muddy brown casts on urinalysis is pathognomonic!!
Aso renal tubular epithelial cells in urine
What are the different types of renal tubular acidosis?
Type 1 - distal tubule pathology (unable to excrete hydrogen ions)
Type 2 - proximal tubule pathology (unable to reabsorb bicarb from urine) Fanconis
Type 3 - combination of type 1 and type 2
Type 4 - reduced aldosterone (adrenal insufficiency, ACE, spironolactone, SLE) - treat with fludrocortisone, sodium bicarb and treat hyperkalaemia
Presentation of Rhabdo? Investigations?
Muscle aches and pain Oedema Fatigue Confusion Red-brown urine
CK - rises until 21 hrs and then remains elevated for 1-3 days
Myoglobinurea - red-brown colour in urine
U&Es
ECG - hyperkalaemia
Treatment of Rhabdo?
IV fluids
consider sodium bicarb
consider IV mannitol - to increase gfr and reduce oedema
Treat hyperkalaemia
